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With Contributions of
Dear Colleagues,<br />
INTRODUCTION and WELCOME<br />
We are very proud to invite you and to have the honour to host you at the “4 th International Congress on<br />
Psychopharmacology” which will be held in Antalya on November 23-27, 2011 as the Turkish Association for Psychopharmacology<br />
(TAP) Conference.<br />
The theme of the congress is: “Innovations and continuity in psychiatry & psychopharmacology: better care for better<br />
health.”<br />
We haven chosen to combine two key concepts as the main theme of this conference: ‘Innovations” and “Continuity”. This<br />
is simply to reflect the fact that the field of psychopharmacology has been progressing rapidly with very novel psychotropic<br />
medications being launched faster then ever.<br />
Furthermore, many patients with mental illness present with a wide-range of psychiatric and medical co-morbidities which<br />
require the treating clinician to have an up-to-date knowledge of psychotropic medications to be able to provide effective and<br />
optimal treatments. Therefore, “continuity” refers to the fact that there is a gap between evidence-based practice guidelines<br />
and actual care in clinical practice for patients with mental illnesses, a lack of “continuity” of knowledge to be shared with the<br />
clinician. One of the objectives of this conference is to fill this gap by our rich scientific programme!<br />
This year’s conference will help participants and clinicians to be able to discuss and to gain insight into translating the latest<br />
evidence-based research into actual clinical practice, to assess where new psychotropic medications fit into patient-centred<br />
treatment strategies and to get direct guidance on the toughest clinical challenges to help patients presenting with complex<br />
psychiatric needs.<br />
This conference will be a wonderful opportunity, not only to present the results of your work, but also to meet, to<br />
communicate and to discuss research issues with other colleagues from the field in a beautiful and sunny part of the World.<br />
There is no doubt that the 4 th International Congress on Psychopharmacology will provide a warm and an elite atmosphere<br />
in Antalya for discussions, solutions, and practical suggestions about daily practice problems and issues. We hope that<br />
this will an opportunity for you, to refresh, update, and expand your knowledge in the major and challenging domains of<br />
psychopharmacology, biological psychiatry, neuroscience and neuroimaging, by contributions from Turkish and international<br />
researchers and clinicians. The Congress aims to create an interactive platform, where all participants are encouraged to ask<br />
questions and share their experiences about difficult and treatment resistant cases.<br />
As always and as expected, the Congress will bring together scientists from Turkey and other internationally renowned<br />
scientists to share experiences and ideas on the latest developments in psychopharmacology at the conference, symposia,<br />
debates, bilateral and multilateral discussion sessions, and satellite symposia. This congress will also dedicate time to ‘meet the<br />
specialist’ sessions and courses, which will be held by distinguished scientists in the field.<br />
Furthermore, the traditional “The Poster Presentation Research Incentive Awards” will also be presented at the 4 th<br />
International Congress on Psychopharmacology to the top three posters selected by the jury.<br />
The most exciting and novel aspect of this Congress is that it is the first International conference organized by TAP.<br />
We will be hosting fellow Associations, and fellow participants who are part of these Associations, from all over the world<br />
including Canada, Malaysia, India, The Czech Republic, Greece, China, Hungary, USA, The UK, Australia, Israel, Iran, Russia,<br />
Germany, The Netherlands, and The Ukraine.<br />
Furthermore, there will be joint symposia with International Fellow and Partner Associations at this meeting. It is hoped that<br />
this will increase International research collaborations.<br />
Abstracts of all the presentations submitted to the 4 th International Congress on Psychopharmacology will be published in<br />
the latest issue of the Bulletin of Clinical Psychopharmacology as a supplement. This will ensure that these presentations are<br />
available to be accessed at the SCI-E.<br />
We hope that the conference will be a fruitful and enjoyable experience for all participants and we are looking forward to<br />
meeting you in beautiful and sunny Antalya, Turkey!<br />
The 4 th ICP Organizing Committee
Turkish Association for Psychopharmacology<br />
4 th International<br />
Congress on Psychopharmacology<br />
“Innovations and continuity in psychiatry &<br />
psychopharmacology: better care for better health”<br />
November 23-27, 2011<br />
Antalya, Turkey<br />
PROGRAM<br />
www.psychopharmacology2011.org
Cengiz Han AÇIKEL<br />
Feyza ARICIOĞLU<br />
Murad ATMACA<br />
Glen BAKER (Canada)<br />
Cengiz BAŞOĞLU<br />
Alican DALKILIÇ (USA)<br />
Rasim Somer DİLER (USA)<br />
Serdar DURSUN (Canada)<br />
Servet EBRİNÇ<br />
Atila EROL<br />
Ayhan ALGÜL<br />
M. Alpay ATEŞ<br />
İsmail AK<br />
Lütfullah BEŞİROĞLU<br />
Mustafa BİLİCİ<br />
Sunar BİRSÖZ<br />
Ömer BÖKE<br />
M. Emin CEYLAN<br />
Mecit ÇALIŞKAN<br />
Murat DEMET<br />
Nesrin DİLBAZ<br />
H. Murat EMÜL<br />
Cüneyt EVREN<br />
Ömer GEÇİCİ<br />
Erdal IŞIK<br />
Fatih KARAASLAN<br />
Nesrin KARAMUSTAFALIOĞLU<br />
CO-CHAIRS<br />
Mesut ÇETİN<br />
Oğuz KARAMUSTAFALIOĞLU<br />
PROGRAM COMMITTEE MEMBERS<br />
Ömer GEÇİCİ<br />
Ali Saffet GÖNÜL<br />
Hasan HERKEN<br />
Numan KONUK<br />
Samet KÖSE (USA)<br />
David OSSER ( USA)<br />
Haluk A. SAVAŞ<br />
Tahir TELLİOĞLU (USA)<br />
Tümer TÜRKBAY<br />
Ömer YANARTAŞ<br />
SECRETARIAT TREASURERS<br />
EXECUTIVE COMMITTE<br />
Yasin BEZ<br />
Gökay ALPAK<br />
Nazmiye KAYA<br />
Selim KILIÇ<br />
Selçuk KIRLI<br />
Erhan KURT<br />
Ömer ÖZBULUT<br />
Bengi SEMERCİ<br />
Ümit Başar SEMİZ<br />
Aytekin SIR<br />
M. Zihni SUNGUR<br />
M. Hakan TÜRKÇAPAR<br />
Özcan UZUN<br />
İlhan YARGIÇ<br />
Ümit YAŞAR<br />
Kazım YAZICI<br />
Mustafa YILDIZ<br />
COMMITTEES
Nihat ALPAY<br />
Rüstem AŞKIN<br />
Ömer AYDEMİR<br />
İbrahim BALCIOĞLU<br />
Mustafa BAŞTÜRK<br />
Erhan BAYRAKTAR<br />
Meral BERKEM<br />
Can CİMİLLİ<br />
Ali ÇAYKÖYLÜ<br />
Orhan DOĞAN<br />
M. Kerem DOKSAT<br />
Ali DORUK<br />
Alaattin DURAN<br />
Engin EKER<br />
Ercan ABAY<br />
Mehmet Yücel AĞARGÜN<br />
Fisun AKDENİZ<br />
Tunç ALKIN<br />
Köksal ALPTEKİN<br />
Jules ANGST (Switzerland)<br />
Zehra ARIKAN<br />
Çiğdem AYDEMİR<br />
Cahide AYDIN<br />
Nazan AYDIN<br />
İsmail Hakkı AYHAN<br />
Glen BAKER (Canada)<br />
David BALDWIN (UK)<br />
Reha BAYAR<br />
Oğuz BERKSUN<br />
Mansur BEYAZYÜREK<br />
Michel BOURIN (France)<br />
Charles BOWDEN (USA)<br />
Adnan CANSEVER<br />
John COOKSON (UK)<br />
Behçet COŞAR<br />
Duran ÇAKMAK<br />
Abdülkadir ÇEVİK<br />
Ali Savaş ÇİLLİ<br />
Ayşen ÇOŞKUN<br />
Bülent ÇOŞKUN<br />
Bill DEAKIN (UK)<br />
Melissa DELBELLO (USA)<br />
Yunus Emre EVLİCE<br />
Max FINK (USA)<br />
Guy GOODWIN (UK)<br />
ORGANIZING COMMITTEE<br />
Hayriye ELBİ METE<br />
Hüsnü ERKMEN<br />
Ertuğrul EŞEL<br />
Erol GÖKA<br />
Mustafa GÜLTEPE<br />
Hayrettin KARA<br />
İsmet KIRPINAR<br />
Işın Baral KULAKSIZOĞLU<br />
Bekir Aydın LEVENT<br />
Özgür ÖNER<br />
Aytekin ÖZŞAHİN<br />
Mücahit ÖZTÜRK<br />
M. Kemal SAYAR<br />
Sefa SAYGILI<br />
INTERNATIONAL SCIENTIFIC ADVISORY BOARD<br />
Başak ÖZÇELİK<br />
Erol GÖKA<br />
Peykan GÖKALP<br />
Bahar GÖKLER<br />
Ayça GÜRDAL KÜEY<br />
Hatice GÜZ<br />
David GREENBERG (Israel)<br />
Çiçek HOCAOĞLU<br />
İlkin İÇELLİ<br />
Rene S. KAHN (The Netherlands)<br />
Ayhan KALYONCU<br />
Emine KILIÇ<br />
Neşe KOCABAŞOĞLU<br />
Stan KUTCHER (Canada)<br />
Levent KÜEY<br />
Lee Wei LIM (Netherlands)<br />
Karl LOOPER (Canada)<br />
Herbert MELTZER(USA)<br />
Levent METE<br />
Hasan MIRSAL<br />
Nahit MOTAVALLI MUKADDES<br />
Norbert MULLER (Germany)<br />
Donald Hugh MYRICK (USA)<br />
Ziad NAHAS (USA)<br />
Andrew NIERENBERG (USA)<br />
David NUTT (UK)<br />
Jim Van OS (The Netherlands)<br />
David OSSER (USA)<br />
Timuçin ORAL<br />
Süha ÖZAŞKINLI<br />
Haluk ÖZBAY<br />
Ayşegül ÖZERDEM<br />
COMMITTEES<br />
Levent SEVİNÇOK<br />
Vedat ŞAR<br />
Cem ŞENGÜL<br />
Lut TAMAM<br />
Bilgen TANELİ<br />
Ertan TEZCAN<br />
Musa TOSUN<br />
Tayfun TURAN<br />
Raşit TÜKEL<br />
Müfit UĞUR<br />
Medaim YANIK<br />
Yankı YAZGAN<br />
Ayşegül YILDIZ<br />
Salih ZOROĞLU<br />
Fuat ÖZGEN<br />
Mine ÖZKAN<br />
Sedat ÖZKAN<br />
Mine ÖZMEN<br />
Nurgül ÖZPOYRAZ<br />
Özden PALAOĞLU<br />
Özkan PEKTAŞ<br />
Jorge A. QUIROZ (USA)<br />
Gary SACHS (USA)<br />
Armağan SAMANCI<br />
Bilgin SAYDAM<br />
Seher SOFUOĞLU<br />
Haldun SOYGÜR<br />
Atilla SOYKAN<br />
Ahmet Rıfat ŞAHİN<br />
Rajiv TANDON (USA)<br />
Işık TUĞLULAR<br />
Zeliha TUNCA<br />
Ömer TUNCER<br />
Hamdi TUTKUN<br />
Ümran TÜZÜN<br />
Berna ULUĞ<br />
Aylin ULUŞAHİN<br />
Tayfun UZBAY<br />
Alp ÜÇOK<br />
Süheyla ÜNAL<br />
Simavi VAHİP<br />
Hans Peter VOLZ (Germany)<br />
Axel WÜRZ (UK)<br />
Olcay YAZICI<br />
Nevzat YÜKSEL<br />
Joseph ZOHAR (Israel)
JOINT SYMPOSIUMS WITH INTERNATIONAL PARTNER SOCIETIES<br />
Canadian College of<br />
Neuropsychopharmacology (CCNP)<br />
Czech NeuroPsychopharmacological<br />
Society (CNPS)<br />
Hellenic Society for the Advancement<br />
of Psychiatry and Related Sciences<br />
Ian ANDERSON<br />
Kandasamy ARUN<br />
Glen BAKER<br />
Tanja BRUECKL<br />
Ingolf CASCORBI<br />
C. Robert CLONINGER<br />
Alican DALKILIÇ<br />
Rasim Somer DİLER<br />
Serdar DURSUN<br />
Serdar GÜNER<br />
Mohamed Husain HABIL<br />
Stefan HOFMANN<br />
Jirí HORÁCEK<br />
Cyril HOSCHL<br />
Alan Leslie HUDSON<br />
Nikolaos KAZANTZIS<br />
INVITED INTERNATIONAL SPEAKERS<br />
CV’s of international guest speakers can be found at<br />
www.psychopharmacology2011.org<br />
Irving KIRSCH<br />
Adrián LLERENA<br />
Peter R. MARTIN<br />
Pavel MOHR<br />
Tomas PALENICEK<br />
Thomas J. PAPARRIGOPOULOS<br />
Antigone S. PAPAVASILIOU<br />
Rusdi Abd. RASHID<br />
Umi Adzlin SILIM<br />
Constantin R. SOLDATOS<br />
A. Shyam SUNDAR<br />
Tahir TELLİOĞLU<br />
Manickam THIRUNAVUKARASU<br />
Axel WÜRZ<br />
Hazli ZAKARIA<br />
Joseph ZOHAR<br />
SPEAKERS<br />
The International Union of Basic and<br />
Clinical Pharmacology (IUPHAR)<br />
Turkish Association for Cognitive<br />
Behaviour Psychotherapy (TACBP)<br />
International Association for<br />
Cognitive Psychotherapy (IACP)<br />
Indian Psychiatric Society Malaysian Psychiatric Association
NOVEMBER 23, 2011 WEDNESDAY<br />
TIME HALL A HALL B HALL C<br />
13.30 ARRIVING TO HOTEL - REGISTRATION<br />
15.00-16.00<br />
OPENING CONFERENCE<br />
Evolution of human brain functions: Identifying<br />
psychobiological targets for promoting well-being<br />
Claude Robert Cloninger, USA<br />
16.30-17.00 COFFEE BREAK<br />
17.30-19.30<br />
PS-01<br />
Epigenetics or genetics: Gene-environment<br />
interactions over the life - span<br />
PS-02<br />
Behavioral addictions and treatments:<br />
Review of recent data<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
AT A GLANCE<br />
PS-03<br />
Painful syndromes in psychiatry and their<br />
managements
NOVEMBER 24, 2011 THURSDAY<br />
TIME HALL A HALL B HALL C HALL D HALL E<br />
09.00-10.30<br />
KL-01<br />
Treatment of opioid<br />
dependence<br />
during pregnancy<br />
Peter R. Martin, USA<br />
PS-04<br />
Adult attention - deficit<br />
hyperactivity disorder<br />
(ADHD) and comorbidity<br />
10.30-11.00 COFFEE BREAK<br />
11.00-12.30<br />
MD-01: DEBATE<br />
Antidepressants are not<br />
associated with suicide risk<br />
Serdar Dursun, Canada<br />
Nesrin Dilbaz, Türkiye<br />
Hakan Türkçapar, Türkiye<br />
PS-06<br />
Neuroimaging in<br />
psychopharmacology: An<br />
update<br />
12.30-13.30 LUNCH<br />
13.30-14.30<br />
14.30-16.00<br />
SATELLITE SYMPOSIUM<br />
MD-02: DEBATE<br />
Antidepressants are useful<br />
in treatment of depression<br />
M. Zihni Sungur, Türkiye<br />
Ian Anderson, UK<br />
Irving Kirsch, UK / USA<br />
16.00-16.30 COFFEE BREAK<br />
16.30-18.00<br />
KL-02<br />
Benzylpiperazine; a major<br />
contaminant of ecstasy,<br />
induces marked changes<br />
in rat brain neurochemistry<br />
and behavior<br />
Alan Leslie Hudson, Canada<br />
JS-01<br />
International Association for<br />
Cognitive Psychotherapy (IACP)<br />
Advances and problems in<br />
Cognitive Behavior Therapy<br />
(CBT)<br />
18.00-18.30 COFFEE BREAK<br />
18.30-20.30<br />
20.30-22.30<br />
JS-02<br />
Malaysian Psychiatric<br />
Association<br />
Malaysian perspective of<br />
substance dependence<br />
PS-07<br />
The rationale of<br />
antipsychotic combinations<br />
in schizophrenia:<br />
Epidemiological and clinical<br />
evidences<br />
PS-05<br />
Brain mapping, TMS, NVS,<br />
biofeedback and deep brain<br />
stimulation in treatment of<br />
psychiatric disorders<br />
POSTER SESSIONS<br />
ORAL SESSIONS<br />
PS-08<br />
Advances in complementary<br />
alternative psychotropic<br />
drugs: Fish oil (omega-3<br />
fatty acids), vitamine B12,<br />
folate ve other add-on<br />
therapies in psychiatric<br />
disorders<br />
KC-04<br />
Mindfulness and acceptance<br />
based therapies<br />
Kültegin Ögel, Türkiye<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
COURSE<br />
KC-01<br />
Biostatistics - Basic<br />
part 1<br />
Selim Kılıç, Türkiye<br />
KC-02<br />
Biostatistics -<br />
Intermediate part 1<br />
Cengiz Han Açıkel, Türkiye<br />
AT A GLANCE<br />
THERAUPATIC ALLIENCE<br />
EDUCATION PROGRAM<br />
15.00-19.00<br />
THERAUPATIC ALLIENCE<br />
EDUCATION PROGRAM<br />
Hakan Türkçapar<br />
Sponsored by
NOVEMBER 25, 2011 FRIDAY<br />
AT A GLANCE<br />
TIME HALL A HALL B HALL C HALL D HALL E<br />
09.00-10.30<br />
KL-03<br />
Unipolar versus bipolar depression<br />
in children: What do we know<br />
about the etiology, diagnosis, and<br />
treatment?<br />
Rasim Somer Diler, USA<br />
PS-09<br />
From preclinical studies to clinical<br />
practice in anxiety disorders<br />
10.30-11.00 COFFEE BREAK<br />
11.00-12.30<br />
MD-03: DEBATE<br />
Antidepressants are useful in the<br />
treatment of bipolar disorders<br />
Haluk Savaş, Türkiye<br />
Selçuk Kırlı, Türkiye<br />
Kaan Kora, Türkiye<br />
PS-11<br />
Psychotropic drug treatments<br />
during pregnancy and lactation<br />
12.30-13.30 LUNCH<br />
13.30-14.30<br />
14.30-16.00<br />
SATELLITE SYMPOSIUM<br />
PS-13<br />
Hormones and psychiatric<br />
disorders<br />
PS-14<br />
Clinical course of psychiatric<br />
disorders associated with trauma<br />
and treatment issues<br />
16.00-16.30 COFFEE BREAK<br />
16.30-18.00<br />
KL-04<br />
Transcultural psychiatry (a<br />
comparison of USA - Türkiye and<br />
sample cases)<br />
Alican Dalkılıç, USA<br />
JS-03<br />
Hellenic Society for the Advancement<br />
of Psychiatry and Related Sciences<br />
Disorders of sleep and wakefulness<br />
and their pharmacological<br />
management<br />
18.00-18.30 COFFEE BREAK<br />
18.30-20.30<br />
20.30-22.30<br />
21.30<br />
JS-04<br />
The International Union of Basic<br />
and Clinical Pharmacology<br />
(IUPHAR)<br />
Pharmacogenomics of<br />
psychoactive drugs<br />
“DÜŞÜNEN ŞARKILAR”<br />
SOSYAL PROGRAM<br />
PS-16<br />
Marijuana; from mellow to<br />
madness<br />
PS-10<br />
Will glutamatergic modulators be<br />
a target for the future therapy of<br />
depression?<br />
PS-12<br />
Vitamin and mineral<br />
supplementation in treatment of<br />
childhood psychiatric disorders<br />
COURSE<br />
KC-03<br />
CBT in somatization disorders<br />
Axel Würz, UK<br />
PS-15<br />
Depression and pain<br />
PS-17<br />
Overcoming treatment resistance:<br />
An update<br />
WS-01<br />
Management of panic disorder<br />
Serdar Güner, The Netherlands<br />
COURSE and WORKSHOP<br />
KC-01<br />
Biostatistics - Basic<br />
part 2<br />
Selim Kılıç, Türkiye<br />
KC-02<br />
Biostatistics -<br />
Intermediate part 2<br />
Cengiz Han Açıkel, Türkiye
NOVEMBER 26, 2011 SATURDAY<br />
NOVEMBER 27, 2011 SUNDAY<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
AT A GLANCE<br />
TIME HALL A HALL B HALL C HALL D HALL E<br />
09.00-10.30<br />
JS-05<br />
Indian Psychiatric Society<br />
Current concept of obsessive<br />
compulsive disorder (OCD)<br />
KL-05<br />
Medical marijuana use in<br />
psychiatry<br />
Tahir Tellioğlu, USA<br />
10.30-11.00 COFFEE BREAK<br />
11.00-12.30<br />
KL-06<br />
Early intervention in anxiety and<br />
depression: What we know, what<br />
we don’t know and what we<br />
should know?<br />
Joseph Zohar, Israel<br />
PS-19<br />
Are the effects of<br />
psychopharmacological and<br />
other therapeutic approaches<br />
neuroregenerative or<br />
neurodegenerative? Review of<br />
recent data<br />
12.30-13.30 LUNCH<br />
13.30-15.30<br />
JS-06<br />
Czech NeuroPsychopharmacological<br />
Society (CNPS)<br />
From models of schizophrenia<br />
to clinical outcome: A<br />
psychopharmacological perspective<br />
PS-21<br />
Treatment approaches to<br />
comorbidities of ADHD<br />
15.30-16.00 COFFEE BREAK<br />
16.00-18.00<br />
JS-07<br />
Canadian College of<br />
Neuropsychopharmacology<br />
Advances in psychotropic drug<br />
development: Promising novel targets<br />
and agents for psychiatric disorders<br />
PS-22<br />
How to fight with bipolar disorder?<br />
From guidelines to clinical<br />
practice: Myths and realities<br />
18.00-18.30 COFFEE BREAK<br />
18.30-20.30<br />
WS-02<br />
Residency and fellowship training<br />
and short-term research / clinical<br />
possibilities in psychiatry in USA<br />
Tahir Tellioğlu, USA<br />
Alican Dalkılıç, USA<br />
PS-18<br />
Chronobiotics and<br />
chronotherapeutics in psychiatry<br />
PS-20<br />
Controversial topics in eating<br />
disorders<br />
PS-23<br />
Individualized medicine:<br />
Focus on pharmacogenetics<br />
KC-05<br />
EMDR course<br />
Serdar Güner, The Netherlands<br />
TIME HALL A<br />
09.00-10.30<br />
COURSE and WORKSHOP<br />
KC-01<br />
Biostatistics - Basic<br />
part 3<br />
Selim Kılıç, Türkiye<br />
PS-24<br />
Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety<br />
10.30-11.00 COFFEE BREAK<br />
11.00-12.00 CLOSING and AWARDS CEREMONY<br />
KC-02<br />
Biostatistics -<br />
Intermediate part 3<br />
Cengiz Han Açıkel, Türkiye
13.30<br />
15.00-16.00<br />
17.30-19.30<br />
17.30-19.30<br />
17.30-19.30<br />
Arriving to hotel - registration<br />
OPENING CONFERENCE<br />
NOVEMBER 23, 2011 WEDNESDAY<br />
Chairperson: M. Kemal Sayar, Türkiye<br />
16.30 - 17.00 COFFEE BREAK<br />
PS-01: Epigenetics or genetics: Gene-environment interactions over the life - span<br />
PS-02: Behavioral addictions and treatments: Review of recent data<br />
PS-03: Painful syndromes in psychiatry and their managements<br />
SCIENTIFIC PROGRAM<br />
HALL A<br />
Evolution of human brain functions: Identifying Claude Robert Cloninger, USA<br />
psychobiological targets for promoting well-being<br />
Co-chairs: Neşe Kocabaşoğlu, Türkiye - Alan Leslie Hudson, Canada<br />
From genes to epigenetics: Etiopathogenic mechanisms of diseases Ahmet Korkmaz, Türkiye<br />
Psychiatric disorders: Genes or childhood traumas? Ümit Başar Semiz, Türkiye<br />
ADHD: Genetics and /or acquired? Özgür Öner, Türkiye<br />
Psychosis: Genes and /or addictive subtances? Ali Doruk, Türkiye<br />
Alzheimer’s dementia: Genes and /or life-style? Engin Eker, Türkiye<br />
Alzheimer’s disease, genes and biomarkers Işın Baral Kulaksızoğlu, Türkiye<br />
Co-chairs: Bekir Aydın Levent - Lütfullah Beşiroğlu, Türkiye<br />
Co-chairs: Abdülkadir Çevik - Erol Göka, Türkiye<br />
HALL B<br />
Internet addiction Lut Tamam, Türkiye<br />
Shopping addiction Levent Sevinçok, Türkiye<br />
Pathological gambling Ömer Şenormancı, Türkiye<br />
From Don Juanism and nymphomania to hypersexual disorders Sultan Doğan, Türkiye<br />
Trichotillomania Ramazan Konkan, Türkiye<br />
Is binge eating a type of addiction? Fulya Maner, Türkiye<br />
HALL C<br />
Personality characteristics of pain in psychiatric disorders Mehmet Ak, Türkiye<br />
At the pain junction fibromyalgia syndrome and depression M. Kemal Sayar, Türkiye<br />
Alexithymia and painful syndromes Hüseyin Güleç, Türkiye<br />
Differences of SSRI and SNRI antidepressants of painful Abdurrahman Altğndağ, Türkiye<br />
syndromes treatments in psychiatry<br />
Hypnotherapy for painful syndromes in psychiatry M. Kerem Doksat, Türkiye
09.00-10.30<br />
11.00-12.30<br />
13.30-14.30<br />
14.30-16.00<br />
16.30-18.00<br />
18.30-20.30<br />
NOVEMBER 24, 2011 THURSDAY<br />
SCIENTIFIC PROGRAM<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
HALL A<br />
KL-01: Treatment of opioid dependence during pregnancy Peter R. Martin, USA<br />
Chairperson: Nazan Aydın, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
MD-01: Antidepressants are not associated with suicide risk<br />
Moderator : Serdar Dursun, Canada<br />
Proponent : Nesrin Dilbaz, Türkiye<br />
Opponent : Hakan Türkçapar, Türkiye<br />
12.30 - 13.30 LUNCH<br />
SATELLITE SYMPOSIUM<br />
MD-02: Antidepressants are useful in treatment of depression<br />
Moderator : M. Zihni Sungur, Türkiye<br />
Proponent : Ian Anderson, UK<br />
Opponent : Irving Kirsch, UK / USA<br />
16.00 - 16.30 COFFEE BREAK<br />
KL-02: Benzylpiperazine; a major contaminant of ecstasy, induces Alan Leslie Hudson, Canada<br />
marked changes in rat brain neurochemistry and behavior<br />
Chairperson: İlhan Yargıç, Türkiye<br />
18.00 - 18.30 COFFEE BREAK<br />
JS-02: Malaysian Psychiatric Association<br />
Malaysian perspective of substance dependence<br />
Co-chairs: Mohamed Husain Habil, Malaysia - Haluk Savaş, Türkiye<br />
Drug problems and harm reduction approach in Malaysia Mohamed Husain Habil, Malaysia<br />
National methadone maintenance therapy program (MMTP): Hazli Zakaria, Malaysia<br />
An update of five pilot projects in Malaysia<br />
Spiritually enhanced drug addiction rehabilitation (SEDAR) program: Rusdi Abd Rashid, Malaysia<br />
The innovative ways to upscale MMTP in Malaysia<br />
National MMTP: Paving the way towards liaison with the community Umi Adzlin Silim, Malaysia
09.00-10.30 PS-04: Adult attention - deficit hyperactivity disorder (ADHD) and comorbidity<br />
Co-chairs: Alan Leslie Hudson, Canada - Nesrin Dilbaz, Türkiye<br />
ADHD and prognosis Yasemen Işık Taner, Türkiye<br />
ADHD in adults: Impulsivity components and links with aggression Yankı Yazgan, Türkiye<br />
ADHD and substance use Cengiz Tuğlu, Türkiye<br />
ADHD and mood disorders in children Rasim Somer Diler, USA<br />
ADHD and psychotic disorders Cengiz Başoğlu, Türkiye<br />
Academic and occupational problems in ADHD Mücahit Öztürk, Türkiye<br />
11.00-12.30 PS-06: Neuroimaging in psychopharmacology: An update<br />
16.30-18.00<br />
10.30 - 11.00 COFFEE BREAK<br />
Co-chairs: Peter Martin, USA - Ali Saffet Gönül, Türkiye<br />
Neuroimaging studies in dementia, psychiatric disorders, drug discovery and more... Devrim Ünay, Türkiye<br />
Imaging of the serotonergic system in depression and anxiety Murad Atmaca, Türkiye<br />
Can psychiatric disorders be predicted by neuroimaging studies? Ali Saffet Gönül, Türkiye<br />
What is the real meaning of ventricular enlargement in schizophrenia? Buğçe Vedin, Türkiye<br />
From two dimensions to the third dimension<br />
12.30 - 13.30 LUNCH<br />
16.00 - 16.30 COFFEE BREAK<br />
NOVEMBER 24, 2011 THURSDAY<br />
JS-01: International Association for Cognitive Psychotherapy (IACP)<br />
Advances and problems in Cognitive Behavior Therapy (CBT)<br />
Co-chairs: M. Zihni Sungur, Türkiye - Stefan Hofmann, USA<br />
18.30-20.30 PS-07: The rationale of antipsychotic combinations in schizophrenia: Epidemiological and clinical evidences<br />
Co-chairs: Pavel Mohr, Czech Republic - İsmail Ak, Türkiye<br />
SCIENTIFIC PROGRAM<br />
HALL B<br />
Recent advances in the treatment of anxiety disorders Stefan Hofmann, USA<br />
Recent advances in translating science into practice: Collaborative Nikolaos Kazantzis, Australia<br />
empiricism and engagement with homework assignments<br />
As an evidence based approach CBT: Alarms in the treatment and M. Zihni Sungur, Türkiye<br />
application mistakes<br />
18.00 - 18.30 COFFEE BREAK<br />
Comorbidity vs co-occurrence in schizophrenia Özcan Uzun, Türkiye<br />
What are the scientific bases of the use of atypical antipsychotics? Ender Taner, Türkiye<br />
Pharmacogenetics and antipsychotic combinations Filiz Karadağ, Türkiye<br />
Is there any connection between depression and schizophrenia? Abdullah Akpınar, Türkiye<br />
Between extrapyramidal and metabolic side effects of antipsychotics: What can we do? Erdal Işık, Türkiye<br />
Other side effects of antipsychotics: What can we do? H. Murat Emül, Türkiye
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
HALL C<br />
09.00-10.30 PS-05: Brain mapping, TMS, NVS, biofeedback and deep brain stimulation in treatment of psychiatric disorders<br />
Co-chairs: Ercan Abay, Türkiye<br />
Brain mapping and computerized EEG treatment and biofeedback Mert Savrun, Türkiye<br />
of psychiatric disorders<br />
Transcranial Magnetic Stimulation (TMS) as a treatment for depression Ayhan Algül, Türkiye<br />
What is the best method of targeting TMS for depression? Novel rTMS Nevzat Tarhan, Türkiye<br />
depression treatment protocols<br />
What does transcranial magnetic stimulation (TMS) promise in Bahadır Bakım, Türkiye<br />
psychiatric disorders other than depression? Future perspectives<br />
Deep brain stimulation as an alternative treatment for Mehmet Aydın, Türkiye<br />
neuropsychiatric disorders<br />
Nervus Vagus Stimulation (NVS) in depression treatment Sadiye Visal Buturak, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
11.00-12.30 POSTER SESSIONS<br />
14.30-16.00 ORAL SESSIONS<br />
Co-chairs: Haluk Savaş - Ayhan Algül, Türkiye<br />
12.30 - 13.30 LUNCH<br />
Co-chairs: Ali Saffet Gönül - Yasin Bez, Türkiye<br />
16.00 - 16.30 COFFEE BREAK<br />
18.00 - 18.30 COFFEE BREAK<br />
NOVEMBER 24, 2011 THURSDAY<br />
18.30-20.30 PS-08: Advances in complementary alternative psychotropic drugs: Fish oil (omega-3 fatty acids),<br />
vitamine B12, folate ve other add-on therapies in psychiatric disorders<br />
Co-chairs: Manickam Thirunavukarasu, India - Mesut Çetin, Türkiye<br />
SCIENTIFIC PROGRAM<br />
What are the mechanisms of omega-3 fatty acids, vitamine B12, Cemal Kaya, Türkiye<br />
folate and other add-on therapies in psychiatric disorders?<br />
Omega-3 fatty acids in ADHD treatment İbrahim Durukan, Türkiye<br />
Are omega-3 fatty acids useful in maintenance treatments? Armağan Samancı, Türkiye<br />
Is fish oil promising in treating depression during pregnancy and lactation? Evrim Özkorumak, Türkiye<br />
Can St. John’s Wort be an alternative treatment of depression? Çiçek Hocaoğlu, Türkiye<br />
Complementary medicine alternatives in other psychiatric disorders Bülent Bahçeci, Türkiye<br />
(sleep, pain, etc.)
20.30-22.30 KC-01: Biostatistics - Basic part 1<br />
Selim Kılıç, Türkiye<br />
20.30-22.30 KC-02: Biostatistics - Intermediate part 1<br />
Cengiz Han Açıkel, Türkiye<br />
20.30-22.30 KC-04: Mindfulness and acceptance based therapies<br />
Kültegin Ögel, Türkiye<br />
15.00-19.00 THERAUPATIC ALLIENCE EDUCATION PROGRAM<br />
Hakan Türkçapar<br />
Sponsored by<br />
NOVEMBER 24, 2011 THURSDAY<br />
COURSES<br />
HALL D<br />
HALL E<br />
HALL C<br />
KC-01 & KC-02 Course participants should bring NOTEBOOK or NETBOOK with them.<br />
KC-01 & KC-02 Course registration is limited to 15 people for each and early application is recommended to register.<br />
There is no limit to the number of participants for courses other than KC-01 and KC-02 courses which are limited with 15<br />
participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro<br />
THERAUPATIC ALLIENCE EDUCATION PROGRAM<br />
Theraupatic Allience Education Program is limited to 40 people. Early application is recommended to register.
09.00-10.30<br />
11.00-12.30<br />
13.30-14.30<br />
16.30-18.00<br />
NOVEMBER 25, 2011 FRIDAY<br />
SCIENTIFIC PROGRAM<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
HALL A<br />
KL-03: Unipolar versus bipolar depression in children: What do Rasim Somer Diler, USA<br />
we know about the etiology, diagnosis, and treatment?<br />
Chairperson: Tümer Türkbay, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
MD-03: Antidepressants are useful in the treatment of bipolar disorders<br />
Moderator : Haluk Savaş, Türkiye<br />
Proponent : Selçuk Kırlı, Türkiye<br />
Opponent : Kaan Kora, Türkiye<br />
12.30 - 13.30 LUNCH<br />
SATELLITE SYMPOSIUM<br />
14.30-16.00 PS-13: Hormones and psychiatric disorders<br />
Co-chairs: Constantin Soldatos, Greece - İbrahim Balcıoğlu, Türkiye<br />
The hypothalamic - pituitary - adrenal axis Ertuğrul Eşel, Türkiye<br />
Thyroid axis Tayfun Turan, Türkiye<br />
Effects of oxytocin on the social behavior Nuray Atasoy, Türkiye<br />
Insulin Mesut Çetin, Türkiye<br />
Sex steroids Erdem Deveci, Türkiye<br />
Melatonin Müfit Uğur, Türkiye<br />
16.00 - 16.30 COFFEE BREAK<br />
KL-04: Transcultural psychiatry (a comparison of USA - Türkiye Alican Dalkılıç, USA<br />
and sample cases)<br />
Chairperson: Erol Göka, Türkiye<br />
18.00 - 18.30 COFFEE BREAK<br />
18.30-20.30 JS-04: The International Union of Basic and Clinical Pharmacology (IUPHAR)<br />
Pharmacogenomics of psychoactive drugs<br />
Co-chairs: Ingolf Cascorbi, Germany - Feyza Arıcıoğlu, Türkiye<br />
Role of polymorphic drug transporters in treatment resistant depression Tanja Brueckl, Germany<br />
Relationship between pharmacogenetic traits and personality Adrián Llerena, Spain<br />
Genetic causes of hypersensitivity to antipsychotics - the clozapine story Ingolf Cascorbi, Germany
09.00-10.30 PS-09: From preclinical studies to clinical practice in anxiety disorders<br />
Co-chairs: Hayriye Elbi - Raşit Tükel, Türkiye<br />
Behavioral models in anxiety disorders Hüseyin Günay, Türkiye<br />
Pharmacological models in anxiety disorders M. Murat Demet, Türkiye<br />
Genetic models in anxiety disorders Nurper Erberk Özen, Türkiye<br />
New drug molecules in pre-clinical applications of anxiety disorders Raşit Tükel, Türkiye<br />
The frequency of anxiety disorders in general hospitals Hayriye Elbi, Türkiye<br />
Pharmacotherapy vs psychotherapy in anxiety disorders? Şebnem Pırıldar, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
11.00-12.30 PS-11: Psychotropic drug treatments during pregnancy and lactation<br />
Co-chairs: Medaim Yanık - Nihat Alpay, Türkiye<br />
Schizophrenia Bülent Kayahan, Türkiye<br />
Bipolar disorders Fisun Akdeniz, Türkiye<br />
OCD Servet Ebrinç, Türkiye<br />
Depression Gökay Alpak, Türkiye<br />
Substance dependency Zehra Arıkan, Türkiye<br />
Panic disorder Faruk Uğuz, Türkiye<br />
12.30 - 13.30 LUNCH<br />
NOVEMBER 25, 2011 FRIDAY<br />
SCIENTIFIC PROGRAM<br />
14.30-16.00 PS-14: Clinical course of psychiatric disorders associated with trauma and treatment issues<br />
HALL B<br />
Co-chairs: Nahit Özmenler - Ümit Başar Semiz, Türkiye<br />
Trauma and psychotic disorders Selma Bozkurt Zincir, Türkiye<br />
Trauma and mood disorders Medine Yazıcı Güleç, Türkiye<br />
Trauma and anxiety disorders Esin Evren Kılıçaslan, Türkiye<br />
Trauma and personality disorders Barbaros Özdemir, Türkiye<br />
Trauma and dependencies Taner Öznur, Türkiye<br />
Trauma and sexual dysfunctions Murat Erdem, Türkiye<br />
16.00 - 16.30 COFFEE BREAK<br />
16.30-18.00 JS-03: Hellenic Society for the Advancement of Psychiatry and Related Sciences<br />
Disorders of sleep and wakefulness and their pharmacological management<br />
Co-chairs: Constantin Soldatos, Greece - Sunar Birsöz, Türkiye<br />
Insomnia and the effects of hypnotics on sleep Constantin Soldatos, Greece<br />
Hypersomnias and the effects of vigilance - promoting compounds Antigone Papavasiliou, Greece<br />
Depression and the effect of antidepressants on sleep Thomas Paparrigopoulos, Greece<br />
18.00 - 18.30 COFFEE BREAK
NOVEMBER 25, 2011 FRIDAY<br />
18.30-20.30 PS-16: Marijuana; from mellow to madness<br />
Co-chairs: Mohamed Husain Habil, Malaysia - Zehra Arıkan, Türkiye<br />
SCIENTIFIC PROGRAM<br />
What is prevalence of cannabis dependence in Türkiye? Hakan Coşkunol, Türkiye<br />
The effect of cannabis use on cognitive functions Cüneyt Evren, Türkiye<br />
The differences of marijuana psychosis from other substance induced psychoses Mükerrem Güven, Türkiye<br />
Pharmacological treatment of cannabis psychosis Ömer Geçici, Türkiye<br />
Selective serotonin reuptake inhibitors (SSRIs) in the treatment of cannabis dependence Musa Tosun, Türkiye<br />
Pharmacological drug treatment of substance-induced psychosis, Osman Vırıt, Türkiye<br />
drug interactions, and considerations<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
HALL B
09.00-10.30 PS-10: Will glutamatergic modulators be a target for the future therapy of depression?<br />
Co-chairs: Cyril Höschl, Czech Republic - Glen Baker, Canada<br />
HALL C<br />
Treatment with traditional antidepressants and related problems Ayşegül YIldız, Türkiye<br />
Glutamatergic system and its importance in the neurobiology of depression Feyza Arıcıoğlu, Türkiye<br />
Glutamatergic system and genetic markers associated with Hasan Herken, Türkiye<br />
antidepressant treatment<br />
Ketamine and other glutamatergic modulators as an antidepressant Serdar Dursun, Canada<br />
Do atypical antipsychotics have any glutamatergic effect? Kemal Yazıcı, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
11.00-12.30 PS-12: Vitamin and mineral supplementation in treatment of childhood psychiatric disorders<br />
Co-chairs: Tümer Türkbay - Özgür Öner, Türkiye<br />
Iron supplementation Ayhan Bilgiç, Türkiye<br />
Zinc supplementation Ebru Kültür Çengel, Türkiye<br />
Calcium and Vitamin D supplementation Ömer Faruk Akça, Türkiye<br />
Cholesterol and Omega 3 fatty acids supplementation Sabri Hergüner, Türkiye<br />
Vitamin B 12 and folate supplementation Burak Doğangün, Türkiye<br />
Antioxidant vitamin supplementation Betül Mazlum, Türkiye<br />
12.30 - 13.30 LUNCH<br />
16.00 - 16.30 COFFEE BREAK<br />
16.30-18.00 PS-15: Depression and pain<br />
Chairperson: Selçuk Kırlı, Türkiye<br />
Epidemiology of pain in depression Saygın Eker, Türkiye<br />
Clinical characteristics and mechanism of pain in depression Selçuk Kırlı, Türkiye<br />
Interaction of pain and depression in terms of clinical characteristics Yusuf Sivrioğlu, Türkiye<br />
and mechanism<br />
Impact of pain on treatment in depression Cengiz Akkaya, Türkiye<br />
18.00 - 18.30 COFFEE BREAK<br />
NOVEMBER 25, 2011 FRIDAY<br />
18.30-20.30 PS-17: Overcoming treatment resistance: An update<br />
Co-chairs: Orhan Doğan- Sefa Saygılı, Türkiye<br />
SCIENTIFIC PROGRAM<br />
Treatment resistant psychiatric disorders and comorbidities Tunç Alkın, Türkiye<br />
Treatment resistant psychiatric disorders and trauma history M. Akif Ersoy, Türkiye<br />
Strategies in treatment resistant psychotic disorders M. Emin Ceylan, Türkiye<br />
Strategies in treatment resistant depression Selçuk Aslan, Türkiye<br />
Strategies in treatment resistant panic disorders Erhan Bayraktar, Türkiye<br />
Psychosocial interventions in resistance to treatment Mustafa Yıldız, Türkiye
14.30-16.00 KC-03: CBT in somatization disorders<br />
Axel Würz, UK<br />
20.30-22.30 WS-01: Management of panic disorder<br />
Serdar Güner, The Netherlands<br />
20.30-22.30 KC-01: Biostatistics - Basic part 2<br />
Selim Kılıç, Türkiye<br />
20.30-22.30 KC-02: Biostatistics - Intermediate part 2<br />
Cengiz Han Açıkel, Türkiye<br />
NOVEMBER 25, 2011 FRIDAY<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
COURSES<br />
HALL C<br />
HALL C<br />
HALL D<br />
HALL E<br />
KC-01 & KC-02 Course participants should bring NOTEBOOK or NETBOOK with them.<br />
KC-01 & KC-02 Course registration is limited to 15 people for each and early application is recommended to register.<br />
There is no limit to the number of participants for courses other than KC-01 and KC-02 courses which are limited with 15<br />
participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro
09.00-10.30 JS-05: Indian Psychiatric Society<br />
Current concept of obsessive compulsive disorder (OCD)<br />
Co-chairs: Manickam Thirunavukarasu, India - Numan Konuk, Türkiye<br />
Current understanding of the concept of obsessive compulsive disorder Manickam Thirunavukarasu, India<br />
Biological theories of obsessive compulsive disorder A. Shyam Sundar, India<br />
Psychopharmacological and somatic interventions in OCD Kandasamy Arun, India<br />
Psycho-social interventions in OCD Manickam Thirunavukarasu, India<br />
10.30 - 11.00 COFFEE BREAK<br />
13.30-15.30 JS-06: Czech NeuroPsychopharmacological Society (CNPS)<br />
From models of schizophrenia to clinical outcome: A psychopharmacological perspective<br />
Co-chairs: Cyril Höschl, Czech Republic - Özcan Uzun, Türkiye<br />
Basic concepts of schizophrenia: Experimental approaches Cyril Höschl, Czech Republic<br />
Prediction validity in animal models of schizophrenia Tomas Palenicek, Czech Republic<br />
The ins and outs of human model of schizophrenia Jiri Horacek, Czech Republic<br />
Safety first, efficacy second? Fear and needs of treatment in the Pavel Mohr, Czech Republic<br />
absence of controlled data<br />
15.30 - 16.00 COFFEE BREAK<br />
NOVEMBER 26, 2011 SATURDAY<br />
16.00-18.00 JS-07: Canadian College of Neuropsychopharmacology<br />
Advances in psychotropic drug development: Promising novel targets and<br />
agents for psychiatric disorders<br />
Co-chairs: Glen Baker, Canada - Mesut Çetin, Türkiye<br />
SCIENTIFIC PROGRAM<br />
HALL A<br />
11.00-12.30 KL-06: Early intervention in anxiety and depression: What we know, Joseph Zohar, Israel<br />
what we don’t know and what we should know?<br />
Chairperson: Oğuz Karamustafalıoğlu, Türkiye<br />
12.30 - 13.30 LUNCH<br />
Novel imidazoline compounds as potential new therapies Alan Leslie Hudson, Canada<br />
for psychiatric disorders<br />
Advances in antipsychotic targets and drug development Serdar Dursun, Canada<br />
Advances in antidepressant targets and drug development Glen Baker, Canada<br />
18.00 - 18.30 COFFEE BREAK
NOVEMBER 26, 2011 SATURDAY<br />
SCIENTIFIC PROGRAM<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
HALL B<br />
09.00-10.30 KL-05: Medical marijuana use in psychiatry Tahir Tellioğu, USA<br />
Chairperson: Ömer Geçici, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
11.00-12.30 PS-19: Are the effects of psychopharmacological and other therapeutic approaches<br />
neuroregenerative or neurodegenerative? Review of recent data<br />
Co-chairs: Rüstem Aşkın - A. Saffet Gönül, Türkiye<br />
What is the hippocampal neurogenesis? Çağdaş Eker, Türkiye<br />
Effects of psychotropics Ömer Aydemir, Türkiye<br />
Effects of ECT, TMS, and others Alpay Ateş, Türkiye<br />
Effects of psychotherapies Mine Özmen, Türkiye<br />
Effects of physical exercise Hakan Balıbey, Türkiye<br />
12.30 - 13.30 LUNCH<br />
13.30-15.30 PS-21: Treatment approaches to comorbidities of ADHD<br />
Co-chairs: Meral Berkem, Türkiye - Rasim Somer Diler, USA<br />
Treatment approaches to psychiatric comorbidities of ADHD in children Tümer Türkbay, Türkiye<br />
Treatment approaches to psychiatric comorbidities of ADHD in adolescents Bengi Semerci, Türkiye<br />
Treatment approaches to psychiatric comorbidities of ADHD in adults İlhan Yargıç, Türkiye<br />
Treating children with ADHD and comorbid neurological disorders Murat Yüce, Türkiye<br />
Drug interactions in medications for comorbidities of ADHD Osman Abalı, Türkiye<br />
15.30 - 16.00 COFFEE BREAK<br />
16.00-18.00 PS-22: How to fight with bipolar disorder? From guidelines to clinical practice: Myths and realities<br />
Co-chairs: Haluk Savaş - Erhan Kurt, Türkiye<br />
How the guidelines are prepared? Are they necessary? Yasin Bez, Türkiye<br />
How to use them? Their benefits and limitations?<br />
Manic episode: Treatment recommendations in guidelines and Numan Konuk, Türkiye<br />
clinical challenges / realities?<br />
Bipolar depression: Treatment recommendations in guidelines and Haluk Savaş, Türkiye<br />
clinical challenges / realities?<br />
Maintenance in bipolar disorder: Treatment recommendations in İbrahim Eren, Türkiye<br />
guidelines and clinical challenges / realities?<br />
Mixed episode in bipolar disorder: Treatment recommendations in Ahmet Ünal, Türkiye<br />
guidelines and clinical challenges / realities?<br />
Type II bipolar disorder: Treatment recommendations in guidelines and Cengiz Başoğlu, Türkiye<br />
clinical challenges / realities?<br />
18.00 - 18.30 COFFEE BREAK
NOVEMBER 26, 2011 SATURDAY<br />
09.00-10.30 PS-18: Chronobiotics and chronotherapeutics in psychiatry<br />
Co-chairs: Tunay Karlıdere - Ahmet Korkmaz, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
12.30 - 13.30 LUNCH<br />
15.30 - 16.00 COFFEE BREAK<br />
18.00 - 18.30 COFFEE BREAK<br />
SCIENTIFIC PROGRAM<br />
HALL C<br />
Phylogenetic aspects of biological rhythms and behavior Okan Çalıyurt, Türkiye<br />
Melatonin and mood Ahmet Korkmaz, Türkiye<br />
A general overview of chronotherapeutics Yavuz Selvi, Türkiye<br />
Psychotropic drugs affecting biological rhythms (chronobiotics) Elif Oral, Türkiye<br />
Bright light therapy use in treatment of depressions other than Mustafa Güleç, Türkiye<br />
seasonal affective disorder<br />
Sleep deprivation use in treatment of depressive disorders Adem Aydın, Türkiye<br />
11.00-12.30 PS-20: Controversial topics in eating disorders<br />
Co-chairs: Atila Erol, Türkiye - Alican Dalkılıç, USA<br />
Psychopharmacological treatments in eating disorders Alican Dalkılıç, USA<br />
Night eating syndrome Özlem Orhan, Türkiye<br />
Efficacy of psychotherapy in bulimia nervosa Başak Yücel, Türkiye<br />
Body image issues in eating disorders Erdal Vardar, Türkiye<br />
Obesity and impulsivity Bilge Burçak Annagür, Türkiye<br />
Comorbidities in eating disorders Atila Erol, Türkiye<br />
16.00-18.00 PS-23: Individualized medicine: Focus on pharmacogenetics<br />
Co-chairs: Rüstem Aşkın - Feyza Arıcıoğlu, Türkiye<br />
Genetics and drugs: From research to clinical studies Turkish perspective Cem Şengül, Türkiye<br />
Pharmacogenomic biomarkers and individualized medicine in psychiatry Yeşim Aydın Son, Türkiye<br />
What is the rationale of individualized medicine in psychiatry? Hasan Herken, Türkiye<br />
Pharmacogenetics: Management of side effects and drug Murat Kuloğlu, Türkiye<br />
interactions of antipsychotics<br />
Pharmacogenetics and how individualized medicine can be Çiğdem Aydemir, Türkiye<br />
applied to the practice of psychiatry?<br />
Pharmacogenetics: Side effects and drug interactions of Oğuz Karamustafalıoğlu, Türkiye<br />
antidepressants and their management
18.30-20.30 KC-01: Biostatistics - Basic part 3<br />
Selim Kılıç, Türkiye<br />
18.30-20.30 KC-02: Biostatistics - Intermediate part 3<br />
Cengiz Han Açıkel, Türkiye<br />
18.30-20.30 KC-05: EMDR course<br />
Serdar Güner, The Netherlands<br />
NOVEMBER 26, 2011 SATURDAY<br />
18.30-20.30 WS-02: Residency and fellowship training and short-term research / clinical observership<br />
possibilities in psychiatry in USA<br />
Tahir Tellioğlu, USA - Alican Dalkılıç, USA<br />
ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop<br />
COURSES<br />
HALL D<br />
HALL E<br />
HALL C<br />
HALL B<br />
KC-01 & KC-02 Course participants should bring NOTEBOOK or NETBOOK with them.<br />
KC-01 & KC-02 Course registration is limited to 15 people for each and early application is recommended to register.<br />
There is no limit to the number of participants for courses other than KC-01 and KC-02 courses which are limited with 15<br />
participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro
NOVEMBER 27, 2011 SUNDAY<br />
09.00-10.30 PS-24: Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety<br />
Co-chairs: Ali Çayköylü - Mecit Çalışkan, Türkiye<br />
SCIENTIFIC PROGRAM<br />
HALL A<br />
Psychotropics and other drugs: Sleep and road traffic accidents Mustafa Bilici, Türkiye<br />
Effects of psychotropics and other drugs on flight and flight safety Muzaffer Çetingüç, Türkiye<br />
Effects of psychotropics and other drugs on cognitive functions and Serhat Çıtak, Türkiye<br />
employee security<br />
Sexual side effects of psychotropic and other drugs Adnan Özçetin, Türkiye<br />
Their side effects of psychotropics and other drugs on quality of life Ömer Böke, Türkiye<br />
10.30 - 11.00 COFFEE BREAK<br />
11.00 - 12.00 CLOSING and AWARDS CEREMONY
Author(s)<br />
Abstracts of the Invited Speakers<br />
1 C. R. Cloninger<br />
2 P. R. Martin<br />
3 A. L. Hudson, N. Zepeda, A. Perreault<br />
M. Lalies, G. Baker<br />
4 R. S. Diler<br />
5 A. Dalkilic<br />
6 T. Tellioglu<br />
7 I. Anderson<br />
8 I. Kirsch<br />
9 S. Kırlı<br />
10 S. Hofmann<br />
11 N. Kazantzis<br />
12 M. Z. Sungur<br />
13 R. A. Rashid, A. K. B. A. Bakar,<br />
H. B. Zakaria, U. B. Adzlin, M. H. Habil<br />
14 T. Paparrigopoulos<br />
15 C. R. Soldatos, T. PaparrigopoulosI<br />
16 A. Papavasiliou<br />
17 T. Brueckl, M. Uhr<br />
18 A. Llerena<br />
19 I. Cascorbi<br />
20 M. Thirunavukarasu<br />
21 A. S. Sundar<br />
22 K. Arun<br />
23 M. Thirunavukarasu<br />
24 P. Mohr, D. Hnidek, D. Seifertova<br />
25 C. Höschl<br />
26 J. Horacek, V. B. Valesova,<br />
T. Palenicek, F. Spaniel, C. Höschl<br />
27 S. Dursun, G. B. Baker, M. Mackay<br />
28 G. B Baker, N. D Mitchell,<br />
J. M. Le Melledo, S. Dursun<br />
Tit le<br />
<strong>Contents</strong><br />
The evolution of human brain functions: Implications for psychobiological targets for wellbeing<br />
Opioid dependence during pregnancy: Balancing risk versus benefit<br />
l-Benzylpiperazine, a major contaminant of ecstasy, induces marked changes in rat brain<br />
neurochemistry and behaviour<br />
Unipolar versus bipolar depression in children: What do we know about the etiology,<br />
diagnosis, and treatment?<br />
Transcultural psychiatry: Practice and sample cases in USA and status in Turkiye<br />
Medical marijuana use in psychiatry<br />
Antidepressants are useful in the treatment of depression: the case for the motion<br />
Have clinically significant benefits of antidepressants been demonstrated?<br />
Antidepressants are useful in the treatment of bipolar disorders<br />
Recent advances in the treatment of anxiety disorders<br />
Translating science into practice, collaborative empiricism and engagement in homework<br />
assignments in cognitive behavior therapy<br />
CBT as an evidence based treatment approach: Warning signs in therapy and common<br />
mistakes in daily practice<br />
A harm minimization program against drug use and HIV problems in Malaysia<br />
Depression and the effect of antidepressants on sleep<br />
Insomnia and the effects of hypnotics on sleep<br />
Hypersomnias and the effects of vigilance-promoting compounds<br />
Role of polymorphic drug transporter in treatment-resistant depression<br />
Relationship between pharmacogenetics and personality traits: Relevance for suicide<br />
Genetic causes of hypersensitivity to antipsychotics – the clozapine story<br />
Current understanding of the concept of obsessive compulsive disorder<br />
Biological theories of obsessive compulsive disorder<br />
Psychopharmacological and somatic interventions for OCD<br />
Psycho-social interventions for OCD<br />
Safety first, efficacy second? Fear and the need for treatment in the absence of<br />
controlled data<br />
Basic concepts of schizophrenia: Experimental approaches<br />
The ins and outs of the human model of schizophrenia<br />
Recent advances in the neurochemistry of schizophrenia and potential targets for<br />
antipsychotic drug development<br />
Advances in antidepressant targets and drug development<br />
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Author(s)<br />
Abstracts of the Invited Speakers<br />
29 E. Eker<br />
30 S. Doğan<br />
31 Ö. Şenormancı<br />
32 F. Maner<br />
33 M. Ak<br />
34 A. Altındağ, G. Elboğa<br />
35 H. Güleç<br />
36 K. M. Doksat<br />
37 R. S. Diler<br />
38 M. Öztürk<br />
39 N. Tarhan, G. Hızlı, S. Aydın<br />
40 B. Bakım<br />
41 Ayhan Algül<br />
42 Ş. V. Buturak<br />
43 M. D. Aydın<br />
44 N. B. V. Özçelik<br />
45 D. Ünay<br />
46 F. Karadağ<br />
47 E. Taner<br />
48 E. Özkorumak<br />
49 Ç. Hocaoğlu<br />
50 B. Bahçeci<br />
51 İ. Durukan<br />
52 M. C. Kaya<br />
53 H. Elbi<br />
54 N. E. Özen<br />
55 H. Günay<br />
56 S. Dursun, G. Baker, N. Mitchell<br />
57 F. Arıcıoğlu<br />
58 F. Uğuz<br />
59 S. Ebrinç<br />
Tit le<br />
Alzheimer’s disease: Genes and/or life style<br />
From Don Juanism and nymphomania to hypersexual disorders<br />
Pathological gambling: review of recent data<br />
Is binge eating a type of addiction?<br />
Pain and personality<br />
<strong>Contents</strong><br />
The differences between SSRIs and SNRIs in the treatment of psychiatric pain syndromes<br />
How does alexithymia lead to painful syndromes?<br />
Hypnotherapy for painful syndromes in psychiatry<br />
ADHD and mood disorders in children<br />
Academic and occupational problems in ADHD<br />
Concomitant use of qEEG and rTMS in treatment of depressive disorder, new approaches<br />
What does transcranial magnetic stimulation (TMS) promise in psychiatric disorders other<br />
than depression? Future perspectives<br />
Transcranial magnetic stimulation (TMS) as a treatment for depression<br />
Vagus Nerve Stimulation (VNS) in depression treatment<br />
Neurophysical basis of neurostimulative psychosurgery: A historical review, new<br />
perspectives, and future insights<br />
What is the real meaning of ventricular enlargement in schizophrenia?<br />
Neuroimaging studies in dementia, psychiatric disorders, drug discovery, and more<br />
Pharmacogenetics and antipsychotic combinations<br />
Scientific bases of use of atypical antipsychotics<br />
Is fish oil promising in the treatment of depression during pregnancy and lactation?<br />
Can St. John’s Wort be an alternative treatment for depression?<br />
Complementary medicine alternatives for other psychiatric abnormalities<br />
(Like insomnia and pain)<br />
Essential fatty acids in ADHD treatment<br />
Mechanisms of fish oil (Omega-3 fatty acids), vitamin B12, folate and other add-on<br />
treatments in psychiatric disorders<br />
Medical disease and anxiety disorders<br />
Genetic models in anxiety disorders<br />
Anxiety models in experimental animals<br />
Ketamine and other glutamate modulators as potential antidepressants<br />
The glutamatergic system and its importance in the neurobiology of depression<br />
Pharmacotherapy of panic disorder during pregnancy and lactation<br />
Psychotropic drug treatment during pregnancy and lactation in obsessive compulsive disorder<br />
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Author(s)<br />
Abstracts of the Invited Speakers<br />
60 Ö. F. Akça<br />
61 S. E. Ç. Kültür<br />
62 A. Bilgiç<br />
63 B. Mazlum<br />
64 S. Hergüner<br />
65 M. Uğur<br />
66 N. Atasoy<br />
67 T. Turan<br />
68 E. Deveci<br />
69 M. Cetin<br />
70 M. Y. Güleç<br />
71 S. B. Zincir<br />
72 M. Erdem<br />
73 C. Akkaya<br />
74 S. Kırlı<br />
75 C. Evren<br />
76 M. Güven<br />
77 M. Tosun<br />
78 S. Aslan<br />
79 M. A. Ersoy<br />
80 M. Yıldız<br />
81 A. Aydın<br />
82 E. Oral<br />
83 Y. Selvi<br />
84 M. Güleç<br />
85 Ö. Aydemir<br />
86 M. Özmen<br />
87 H. Balıbey<br />
88 A. Erol<br />
89 A. Dalkilic<br />
90 B. B. Annagür<br />
91 B. Yücel<br />
Tit le<br />
<strong>Contents</strong><br />
Vitamin and mineral supplementation in treatment of childhood psychiatric disorders –<br />
Calcium and vitamin D supplementation<br />
Zinc supplementation in psychiatric disorders of children<br />
The impacts of iron deficiency on mental health in childhood<br />
Antioxidant vitamin supplementation therapies in child psychiatry<br />
Effectiveness of omega fatty acid supplementation for childhood psychiatric disorders<br />
Melatonin and human behaviour<br />
Effects of oxytocin on social behaviour<br />
Thyroid hormones and psychiatric disorders<br />
Sex steroids and psychiatric disorders<br />
Insulin and psychiatric disorders<br />
Trauma and mood disorders<br />
Trauma and psychotic disorders<br />
Relationship of sexual dysfunction with trauma<br />
Impact of pain on treatment in depression<br />
Clinical characteristics and mechanism of pain in depression<br />
Effect of cannabis use on cognitive functions<br />
The differences between marijuana psychosis and other substance induced psychoses<br />
Selective serotonin reuptake inhibitors in the treatement of cannabis dependence<br />
Treatment strategies for treatment resistant depression<br />
Treatment resistant psychiatric disorders and trauma history<br />
Pyshosocial approaches for treatment resistant symptoms in patients with schizophrenia<br />
The use of sleep deprivation in the treatment of depressive disorders<br />
Psychotropic drugs effecting biological rhythm (Chronobiotics)<br />
A general overview of chronotherapeutics<br />
Bright light therapy in treatment of depressive disorders other than seasonal affective disorder<br />
Is the effect of psychotropic drugs neurodegenerative or neuroprotective?<br />
Effect of psychotherapy on neurogenesis<br />
Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative<br />
or neurodegenerative? Review of recent data and effects of physical exercise<br />
Comorbidities in eating disorders<br />
Psychopharmacological treatments in eating disorders<br />
Obesity and impulsivity<br />
Efficacy of psychotherapy in bulimia nervosa<br />
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Author(s)<br />
Abstracts of the Invited Speakers<br />
92 T. Türkbay<br />
93 B. Semerci<br />
94 M. Yüce<br />
95 O. Abalı<br />
96 A. Ünal<br />
97 Y. Bez<br />
98 I. Eren<br />
99 C. Şengül<br />
100 Ç. Aydemir<br />
101 Y. Aydın Son<br />
102 M. Çetingüç<br />
103 A. Özçetin<br />
104 S. Kılıç<br />
105 A. Würz<br />
106 K. Ögel<br />
107 S. Güner<br />
108 S. Güner<br />
Abstracts of Oral Presentations<br />
1 C. Neale, A. Scholey, M. Hughes,<br />
P. Johnston<br />
2 C. B. Şengül, M. E. Erdal, C. Şengül,<br />
Ö. İ. Ay, M. Efe, M. E. Ay, H. Herken<br />
3 M. C. Pieri<br />
4 O. Erbas, S. Bora<br />
5 S. Abolghasemi, G. Mahmodi, M. Zafari<br />
6 M. M. Abtahi, H. Molavi, J. Moshtaghian,<br />
K. Askari<br />
7 J. Shafaie, S. Farjad<br />
8 M. Allahtavakoli, B. Jarrott<br />
9 F. Hashemian, M. S. Tabatabayi,<br />
A. Sharifi, M. Majd<br />
Tit le<br />
Treatment approaches to psychiatric comorbidities of ADHD in children<br />
Treatment approaches to psychiatric comorbidities of ADHD in adolescents<br />
Treatment of neurological co-morbid disorders in children with ADHD<br />
Drug interactions of medications for comorbidities of ADHD<br />
Treatment of mixed episodes of bipolar disorders in manuals. What are the recommendations?<br />
How are the guidelines prepared? Are they necessary? How to use them? Their benefits and<br />
limitations?<br />
Maintenance treatment in bipolar disorder: What do guidelines recommend?<br />
Genetics and drugs: From research to clinical studies Turkish perspective<br />
Pharmacogenetics and how individualized medicine can be applied to the practice of psychiatry<br />
Pharmacogenomics biomarkers and personalized medicine in psychiatry<br />
The effects of psychotropic and other drugs on flight and flight safety<br />
Sexual side effects of psychotropic and other drugs<br />
Basic Biostatistics<br />
<strong>Contents</strong><br />
CBT in somatization disorders<br />
Mindfulness and acceptance based therapies<br />
Eye movement desensitization and reprocessing method [EMDR] Specifically designed for<br />
Turkish patient population in the Netherlands<br />
Alternative CBT method of panic disorder treatment for Turkish patients<br />
Bacopa monniera: Current trends and future directions<br />
Association of the DRD2 TaqIA, 5-HT1B A-161T, and CNR1 1359 G/A polymorphisms<br />
with alcohol dependence: A single center study in the Denizli Province of Turkey<br />
Treating psychotic substance abuse patients with opioid agonist therapy and the atypical<br />
antipsychotic olanzapine<br />
A comparison of the effects of typical and atypical antipsychotics on the basolateral<br />
amygdala of rats using deep brain EEG recordings<br />
The effect of cognitive-behavioral therapy in reducing the feeling of emotional<br />
pressure and blood sugar control in patients with type 2 diabetes<br />
Acute effects of nicotine on working and reference memory in rats using<br />
a 12-arm radial maze<br />
The relationship between personality characteristics and internet addiction in adolescents<br />
The sigma-1 receptor ligand, PRE-084, reduced infarct volume, neurological deficits,<br />
pro-inflammatory cytokines, and enhanced anti-inflammatory cytokines after embolic<br />
stroke in rats<br />
Comparison of the effects of bupropion and fluoxetine on reaction time in adults<br />
with major depressive disorder in a 4-week, single-blind study<br />
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Author(s)<br />
Abstracts of Oral Presentations<br />
10 O. Bigdeli, F. Hashemian, M. Shohrati,<br />
A. Mokri, M. Majd<br />
11 M. Altın, L. Alev, K. Özbek, D. Hobbs,<br />
J. Karagianis, T. Treuer, J. Raskin<br />
12 L. Alev, M. Altın, K. Özbek, D. Sheehan,<br />
A. Meyers, J. Ahl, A. Prakash,<br />
T. M. M. Oakes<br />
13 Z. Kechrid, M. Hamdikene<br />
14 G. R. Kheirabadi, M. Salehi,<br />
M. R. Maracy, M. Ranjkesh<br />
15 Serwa Mohamadzadeh Ashna<br />
16 O. Erbas, V. Evren, S. Bora,<br />
G. O. Peker<br />
17 O. Erbas<br />
Poster Presentation<br />
1 S. Korkmaz, M. Kuloglu, S. Saglam,<br />
M. Atmaca<br />
2 R. Konkan, E. Aydın, O. Güçlü,<br />
Ö. Şenormancı, M. Z. Sungur<br />
3 M. Zafari, A. Aghamohammadi<br />
4 H. Balibey, A. Balikci<br />
5 R. N. Yuksel, Z. E. Kaya, N. Dilbaz<br />
6 J. S. Ahn, J. Shin, K. C. Park, S. Min,<br />
M. H. Kim<br />
7 H. Yaci, E. K. Koca, Y. Uz, A. Demir,<br />
A. A. Ozşahin, F. M. Domac<br />
8 F. Canan, U. Aydınoglu, G. Sinani<br />
9 Ç. H. Yeloglu, H. Guveli, K. Sarp,<br />
B. Bahceci, C. Hocaoglu<br />
10 E. O. Sonmez, N. Kaya<br />
11 M. Ak, E. Sinici, O. Maden, A. Bozkurt,<br />
A. Ozsahin<br />
12 E. Valzdorf<br />
13 M. Nachnani, S. Beatson<br />
14 E. Valzdorf<br />
15 S. Karayılan, A. Erol<br />
Tit le<br />
<strong>Contents</strong><br />
A placebo-controlled double-blind add-on study of Ginseng in opioid withdrawal syndrome<br />
An in vitro analysis of disintegration times of different formulations of orally disintegrating<br />
olanzapine<br />
Effect of duloxetine on functional outcomes in patients with major depressive disorder<br />
Effect of vitamin D on zinc status, carbohydrate metabolism, and activities of some<br />
enzymes in alloxan-diabetic rats fed on a zinc deficient diet<br />
Gabapentin in the treatment of opioid withdrawal<br />
The role of transcranial magnetic stimulation in cognitive processes and treatment of<br />
psychiatric disorders<br />
Oxytocin inhibition of pentylenetetrazole-induced convulsions and its identification by<br />
behavioral measurement and thalamic EEG in the rats<br />
The effects of metoprolol and diltiazem in the prolonged QTc interval caused by<br />
ziprasidone injection in rats<br />
Visual hallucinations induced by bupropion: A case report<br />
Clinical features of patients with panic disorder in outpatient clinics of a psychiatric training<br />
and research hospital<br />
Effect of calcium in treatment of premenstrual syndrome<br />
Eye movement desensitization and reprocessing (EMDR) treatment in a patient with<br />
post-traumatic stress disorder: A case report<br />
Cabergoline induced manic episode: A case report<br />
Substance use and eating patterns of female adolescent students<br />
Neuroleptic malignant syndrome: A case report<br />
Treatment of clozapine induced obsessive compulsive behavior in a schizophrenic patient<br />
with valproic acid augmentation: A case report<br />
Treatment of bipolar disorder in adolescents: A case report<br />
Leukopenia and neutropenia due to venlafaxine use: A case report<br />
EMDR treatment for a sexual rape victim: A case report<br />
Influence of family and education factors on the inclination to commit crimes in<br />
Soviet times and today<br />
Survey of referral pathways to a crisis team<br />
Fluanxol and haloperidol efficacy evaluation in treatment of schizophrenic patients<br />
Anorexia nervosa and cannabis abuse: A case report<br />
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Author(s)<br />
Poster Presentation<br />
16 A. Yucel, M. Gulec, A. Aydin<br />
17 M. López, P. Dorado, A. Ortega,<br />
E. P. Lledó, N. Monroy, E. Machín,<br />
M. E. Alonso, A. Llerena<br />
18 P. Dorado, E. P. Lledó, E. Machín,<br />
A. Llerena, E. Terán, L. Beltrán<br />
19 S. E. Herizchi, I. T. Piri, I. T. Asvadi,<br />
Z. T. Sanaat, M. T. Golchin,<br />
R. T. Shabanloui<br />
20 O. Erbas, S. Bora, S. Demirgoren,<br />
G. Peker<br />
21 F. Maner, O. Hisim, O. Sahmelikoglu,<br />
O. C. Girit, A. Ermis, M. E. Ceylan<br />
22 Ö. Ç. Girit, F. Maner, E. Kılınç,<br />
D. İpekçioğlu, M. E. Ceylan<br />
23 M. Zafari, A. Aghamohammady<br />
24 M. G. Ayhan, F. Uguz, N. Kaya<br />
25 M. Altın, L. Alev, T. M. Durell,<br />
L. A. Adler, D. W. Williams, A. Deldar,<br />
J. J. Mcgough, P. E. Glaser, R. L. Rubin,<br />
E. S. Sarkis, T. A. Pigott, B. K. Boardman<br />
26 R. M. Alowesie<br />
27 R. Konkan, E. Aydın, O. Güçlü,<br />
Ö. Şenormancı, M. Z. Sungur<br />
28 N. R. N. Jaafar, N. Mislan, A. Baharudin,<br />
N. Ibrahim, S. A. Aziz, H. Sidi<br />
29 B. Tıkır, E. Göka, M. Ç. Aydemir,<br />
S. Duran<br />
30 E. A. Sünbül, M. Sünbül, F. F. Cengiz<br />
31 S. Hergüner, A. Hergüner<br />
32 J. S. Choi, H. W. Lee, J. Y. Lee,<br />
H. Y. Jung<br />
33 S. Kesebir, B. Baykaran, B. Toprak,<br />
A. E. Tezcan<br />
34 K. Chichinadze, T. Domianidze,<br />
T. Matitaishvili, I. Labadze,<br />
A. Lazarashvili, M. Khananashvili<br />
35 R. R. Hegazy, H. F. Zaki, O. A. Sharaf,<br />
I. E. Ismail, S. A. Kenawy<br />
36 M. İ. Atagün, Ü. Altınok, Ö. D. Balaban,<br />
Z. Atagün, L. R. Alpkan, K. Öneş<br />
Tit le<br />
<strong>Contents</strong><br />
Fluoxetine-induced thrombocytopenia: A case report<br />
Interethnic differences in UGT1A4 genetic polymorphisms in Mexican and Spanish<br />
populations<br />
Influence of CYP2C9 genetic polymorphism on losartan oxidation in an Ecuadorian<br />
population<br />
Efficacy of progressive muscle relaxation training on anxiety, depression and quality of life<br />
in cancer patients under chemotherapy<br />
Anxiety reducing effects of oxytocin on the basolateral amygdala by using an<br />
electrophysiological method<br />
Genital mutilation in a patient with schizophrenia: A case report<br />
Hoarding and mood disorder: A case report<br />
Effect of fish oil on treatment of premenstrual syndrome<br />
Improvement of risperidone-induced hyperprolactinemia with the addition of aripiprazole:<br />
Case report<br />
Atomoxetine for the treatment of ADHD in young adults with an assessment of associated<br />
functional outcomes<br />
Role of psychopharmacological intervention in cognitive and psychological recovery in<br />
hemorrhagic brain injury<br />
Obsessive beliefs in patients with panic disorder<br />
Erectile dysfunction in patients on methadone maintenance therapy in Malaysia<br />
Cerebellar contusion presenting with pure psychiatric symptoms and cerebellar cognitive<br />
affective syndrome: A case report<br />
Self-perception and anger with chest pain without cardiac etiology<br />
Mirtazapine treatment for weight loss and insomnia associated with methylphenidate:<br />
A chart review depression and somatic symptoms<br />
Rapid-onset hyponatremia induced by duloxetine in a middle-aged male with<br />
depression and somatic symptoms<br />
Gender specific metabolic adverse effects in bipolar patients: A comparison between lithium,<br />
quetiapine and olanzapine<br />
New model of psychogenic stress-induced depression and antioxidant system of rat brain<br />
Effects of strawberry leaf and celery seed extracts in terlipressin-induced chronic<br />
hyponatremia in rats<br />
Post traumatic stress disorder in patients with spinal cord injury and relevant factors<br />
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Author(s)<br />
Poster Presentation<br />
37 S. Kesebir, F. Akdeniz, A. Demir,<br />
M. Bilici<br />
38 S. Ö. Kavzoğlu, A. G. Hariri<br />
39 F. Canan, G. Sinani, Ü. Aydınoğlu<br />
40 Ö. Şenormancı, O. G. Güçlü, R. Konkan,<br />
Y. Altunkaynak, G. Şenormancı<br />
41 M. Kazemi, S. Karimi, H. Hasankhani,<br />
S. Kazemi<br />
42 S. S. A. Hashmi, A. A. A. Sabri,<br />
N. M. A. Felati<br />
43 A. Ansari, T. Negahban, A. R. Sayyadi<br />
44 A. Aydın, P. G. Özdemir, Y. Selvi, F. Uğuz<br />
45 F. Canan, Ü. Aydınoğlu, G. Sinani<br />
46 Y. Yang, J. Kim, B. Kim, M. Shin, S. Cho<br />
47 F. Jan, V. Kennedy<br />
48 K. Ögel, G. Karadayı, Z. Karaman,<br />
H. A. Arıcan, N. Kaya, U. Karaman,<br />
A. M. Altuğ<br />
49 K. Ögel, C. Koç, B. Karalar, A. Başabak,<br />
A. Aksoy, M. İşmen, R. Yeroham<br />
50 K. Ögel, A. Başabak, C. Koç, A. Aksoy,<br />
G. Karadayı<br />
51 S. Ulusoy, İ. Alnıak, K. F. Yavuz, T. Kara<br />
52 C. Neale, S. Benson, C. Stough, A. Scholey<br />
53 N. Sarp, A. A. Çoban, K. Ögel<br />
54 F. Yousefi, S. Mohamadzadeh<br />
55 K. Ögel, F. Karadağ, C. Evren,<br />
D. T. Gürol<br />
56 M. A. Abnavi, A. Javadpour,<br />
S. Mohamadzadeh<br />
57 A. A. Nasiripour1, G. Mahmodi,<br />
M. Zafari<br />
58 N. A. Kumsar, A. Erol<br />
59 H. A. Döm, M. A. Döke, Y. Y. Tuncel,<br />
G. Üstünkar, Y. A. Son<br />
Tit le<br />
<strong>Contents</strong><br />
A comparison before and after using lamotrigine in long term continued treatment: the effect<br />
of blood levels<br />
ICAM, VCAM and E-selectin levels in first episode schizophrenic patients<br />
Body dysmorphic disorder incidentally treated with bupropion<br />
Tardive akathisia with aripiprazole: A case report<br />
Comparing mental disorders between divorced couples and normal couples in a city of Iran<br />
Suicide rate in Oman in the period between January 2000 and December 2010<br />
The effect of the recitation of the Quran on depressed patients in the psychiatry department<br />
of Moradi hospital in Rafsanjan (IRAN)<br />
Dissociative symptoms associated with piracetam use: a case report<br />
Reversible normoprolactinemic galactorrhea induced by fluoxetine<br />
Influence of polymorphism of the norepinephrine transporter gene (SLC6A2) and alpha-2<br />
adrenergic receptor gene (ADRA2A) on regional cerebral blood flow in a Korean ADHD<br />
sample: a preliminary study<br />
Do we need specialist clinics to monitor metabolic side effects on chronic bipolar patients<br />
in Treatment? – Audit of management of bipolar disorder against NICE guidelines in South<br />
Staffordshire NHS Trust, UK<br />
Assessment of risk of absenteeism in elemantary school students<br />
Effectiveness of an addiction treatment program called SAMBA: A pilot study<br />
Psychometric properties of different forms of the Addiction Profile Index (BAPI)<br />
Aripiprazole treatment for the choreoathetoid movements and psychotic symptoms of<br />
Huntington’s disease: A case report<br />
Acute effects of Bacopa monnieri on mood in healthy young adults<br />
Anxiety and depressive symptom levels among adolescents with risk taking behaviour<br />
The relationship between mental health and academic achievement among Kordestan high<br />
school students<br />
Does the profile of addiction change according to the type of the substance used?<br />
Death anxiety among terminally ill inpatients<br />
The effective features of access to medical care in Iran<br />
Smoking behaviour during the course of paroxetine treatment: A case report<br />
Development of a SNP genotyping panel and a medical decision support algorithm to predict<br />
drug response in schizophrenia<br />
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Author(s)<br />
Poster Presentation<br />
60 Barış Yılbaş, Murat Gönen<br />
61 B. E. Cumurcu, R. Karlıdağ, Ş. Kartalcı,<br />
I. G. Gül, S. Demir, B. Yeşil<br />
62 U. M. Aksoy, Ş. G. Aksoy, F. Maner<br />
63 B. Soyer, J. Kenar, K. S. Karataş<br />
64 A. A. Bilgin, B. Çam<br />
65 Y. Taner, H. A. Taner<br />
66 H. Toğul<br />
67 H. Ünübol, B. Ünübol, J. Güler, A. Ünal<br />
68 İ. İnanlı, İ. Eren, T. Etli<br />
69 F. Büyükşahin, J. Güler, B. Ünübol,<br />
H. Ünübol, A. Ünal<br />
70 H. Balıbey, T. Türker, Z. Perdeci1,<br />
N. Bayar, M. B. Evren<br />
71 A. Aghamohammadi, M. Zafari<br />
72 T. Kuru, M. E. Karadere, S. Çelenk,<br />
B. Demirel, K. F. Yavuz<br />
73 Y. Yılmaz, Ö. Yanartaş, İ. Saygılı,<br />
Ü. B. Semiz<br />
74 Ö. Yanartaş, Y. Yılmaz, İ. Saygılı,<br />
S. B. Zincir, Ü. B. Semiz<br />
75 F. Arıcıoğlu, T. Utkan<br />
76 F. F. Cengiz, E. A. Sünbül<br />
77 A. A. Budaklı, M. A. Ateş, A. Algül<br />
78 F. Amani, A. Shaker<br />
79 K. S. Karataş, J. Güler, Ö. B. Topçuoğlu,<br />
E. D. Bostancı, B. Soyer<br />
80 S. Gümrü, E. Yarcı, Ö. Şehirli, Y. Yazır,<br />
T. Utkan, F. Arıcıoğlu<br />
81 M. C. Kaya, Y. Bez, S. Selek,<br />
H. A. Savaş, H. Çelik, H. Herken<br />
82 E. Mutlu, M. E. Ceylan, A. Aydın<br />
83 M. Ak, A. Bolu, S. Akarsu, D. Sezlev,<br />
T. Yanık, Ö. Uzun, F. Özgen, A. Özşahin<br />
84 R. Konkan, Ö. Şenormancı, O. Güçlü,<br />
E. Aydın, Mehmet Z. Sungur<br />
Tit le<br />
<strong>Contents</strong><br />
Basal ganglial hemorrhage induced mania<br />
Evaluation of cognitive functions in euthymic bipolar patients using mono- and multi- drug<br />
treatments<br />
Adult ADHD symptoms in cannabis dependence and the importance of comorbidity<br />
in Adult ADHD<br />
Ganser syndrome as a dissociative disorder: A case report<br />
Escitalopram induced galacthorrea: Phenomenon presentation<br />
Amisulpride use in treatment of Tourette’s disorder<br />
Lithium associated glossodynia syndrome: A case report<br />
Two cases of affective disorder due to immunosuppresive treatment that followed renal<br />
transplantation<br />
Varenicline induced psychotic disorders: A case report<br />
Affective disorders and catatonia: Report of two cases<br />
The relationship of incarceration, past suicide attempts, depression, anxiety and attention<br />
deficit hyperactivity disorder in cases of anti-social personality disorder<br />
Relation between unintended pregnancy and post-partum blues<br />
Comparison of antipsychotic prescribing in the treatment of schizophrenia between the years<br />
of 2004-2009<br />
Valproate-induced hyperammonemic encephalopathy: A case report<br />
Two cases of tardive dyskinesia associated with the use of paliperidone ER and their<br />
management<br />
Effects of agmatine in rats with chronic unpredictable mild stress<br />
A case of obsessive compulsive disorder with psychotic features that suffered from sexual<br />
trauma<br />
Priapism associated with zuclopenthixol treatment: A case report<br />
Prescribing patterns and inappropriate use of medications in patients referred to doctors in<br />
Ardabil City of Iran<br />
Bipolar affective disorder and normal pressure hydrocephaly: A case report<br />
Agmatine attenuats cognitive impairment and oxidative damage following chronic<br />
unpredictable mild stress: A behavioral, biochemical, and histological study<br />
Ceruloplasmin levels before and after treatment in patients with depression:<br />
A case-control study<br />
Foetality in schizophrenia<br />
Metabolic changes in the acute phase with olanzapine treatment<br />
Do cultural factors effect clinical manifestations of OCD? Clinical features of<br />
a Turkish sample<br />
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Author(s)<br />
Poster Presentation<br />
85 C. Evren, S. Çelik, R. Aksoy, T. Çetin,<br />
M. Ülkü, S. Yiğiter, E. Mutlu<br />
86 C. Evren, S. Çelik, R. Aksoy, T. Çetin,<br />
S. Yiğiter, M. Ülkü, E. Mutlu<br />
87 M. Ak, C. Yükselir, A. Bozkurt,<br />
M. Erdem, A. Özşahin<br />
88 A. Bolu, S. Akarsu, C. Çelik,<br />
B. Özdemir, K. N. Özmenler<br />
89 O. Durmaz, M. A. Ateş, M. Çetin,<br />
S. Ebrinç, C. Başoğlu, A. Algül<br />
90 R. Tükel, H. Gürvit, B. Özata,<br />
B. A. Ertekin, E. Ertekin, B. Baran,<br />
Ş. A. Kalem, N. Öztürk, G. S. Direskeneli<br />
91 S. G. Kabak, M. B. Baykaran, S. B. Zincir<br />
92 R. Konkan, M. Bayrak, O. Güçlü,<br />
Ö. Şenormancı, M. Z. Sungur<br />
93 A. Aydın, M. E. Ceylan, E. M.,<br />
A. F. Maner<br />
94 P. G. Özdemir, A. Aydın, M. Güleç,<br />
E. Füsün A. Çim<br />
95 F. Karadağ, H. Herken, B. Kaptanoğlu,<br />
Y. Enli, Ö. Kalkancı, C. B. Şengül,<br />
H. A. Alaçam<br />
96 N. A. Kumsar, A. Erol<br />
97 E. Valzdorf<br />
98 S. Barlak, A. Ateş, C. Başoğlu, S. Ebrinç<br />
99 N. A. Kumsar, A. Erol<br />
100 Ö. Ö. Sarıkaya, D. G. Öyekçin<br />
101 F. Hashemian, M. Majd, S. M. Hosseini,<br />
A. Sharifi, M. V. S. Panahi, O. Bigdeli<br />
102 S. Karimi, M. Kazemi, H. Hasankhani,<br />
S. Kazemi<br />
103 Y. Yılmaz, Ö.Yanartaş, İ. Saygılı,<br />
A. G. Hariri<br />
104 P. Dorado, H. Trejo, E. Alonso,<br />
E. P. Lledó, A. Llerena, M. López<br />
105 P. Dorado, E. L. Torres, E. M. P. Lledó,<br />
J. M. Antón, A. Llerena<br />
106 M. López, E. P. Lledó, H. Trejo,<br />
P. Dorado, J. Guerrero, M. E. Alonso,<br />
A. Llerena<br />
107 A. Karahan, A. Tiryaki, B. İskender,<br />
E. Özkorumak<br />
Tit le<br />
<strong>Contents</strong><br />
Reliability and validity of Turkish version the Brief Fear of Negative Evaluation Scale II<br />
(BFNE-II) among male patients with alcohol dependency<br />
Reliability and validity of Turkish versions of the Social Phobia Scale and Social Interaction<br />
Anxiety Scale among male patients with alcohol dependency<br />
ECT in treatment of pathological gambling: A case report<br />
Venlafaxine-mirtazapine combination in the treatment of post traumatic stress disorder<br />
Efficacy and 3-month follow-up of repetitive transcranial magnetic stimulation (rTMS) in<br />
treatment resistant depression: Three cases<br />
The effects of brain-derived neurotrophic factor Val66Met polymorphism on executive<br />
functioning in patients with obsessive-compulsive disorder<br />
Diagnostic confusion about OCD and schizophrenia: A case report<br />
Is vaginismus a specific phobia?<br />
Are personality traits helpful to predict psychosis?<br />
Switching to fluoxetine due to sertraline-induced urinary incontinence: A case report<br />
The relationship between the serum bilirubin levels and metabolic syndrome<br />
in schizophrenia patients<br />
Olanzapine abuse: A case report<br />
Various reasons for self-destructive acts and objects used to commit them in 1991<br />
Topiramate induced acute psychotic disorder<br />
Glass-aating behaviour with radiological findings: A pica case<br />
The use of bupropion in treatment Kleptomania’s: Two cases<br />
A randomized, double-blind, placebo-controlled trial of celecoxib augmentation of sertraline<br />
in the treatment of a drug-naïve women with major depression<br />
To compare marital conflicts, between divorced and normal couples in Sirjan of Iran<br />
Adult primary enuresis nocturna: A case report<br />
Major depressive disorder and the 5-HTTLPR in Spanish and Mexican populations<br />
Phenytoin toxicity in a pediatric epileptic patient and CYP2C9, CYP2C19, and ABCB1<br />
genetic polymorphisms<br />
Influence of CYP2D6 genetic polymorphism on fluoxetine and amitriptyline<br />
clinical response<br />
Evaluation of insight and functional recovery in patients with schizophrenia<br />
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Author(s)<br />
Poster Presentation<br />
108 O. Özdemir, Y. Selvi, H. Özkol,<br />
Y. Tülüce, L. Beşiroğlu<br />
109 C. Neale, A. Scholey, M. Hughes,<br />
P. Johnston<br />
110 S. Özdemir, F. A. Özdemir<br />
111 M. Güleç, Y. Selvi, Ü. Aydınoğlu<br />
112 S. B. Zincir, Ü. B. Semiz, A. Yenel,<br />
E. Başoğlu, M. Bilici, C. Tulay<br />
113 S. B. Zincir, Ü. B. Semiz, A. Demir,<br />
Y. Yılmaz, S. G. Kabak<br />
114 S. B. Zincir, A. Yenel, S. Ç. Parlak,<br />
G. Şimşek, A. Bayrak, D. Bilge,<br />
Ü. B. Semiz, M. Bilici<br />
115 M. Akbıyık, O. Karamustafalıoğlu<br />
116 M. Özten, A. Erol<br />
117 S. Karayılan, A. Erol<br />
118 M. Özten, A. Erol<br />
119 K. S. Karataş, J. Güler, A. Hariri<br />
120 B. Çam, H. Kurt<br />
121 H. Özer, A. Erol<br />
122 O. Kadıoğlu, G. Üstünkar, Y. A. Son<br />
123 A. Büyükkınacı, D. Ö. Can, G. Silsüpür<br />
124 Y. Şimşek, G. E. Sarıdoğan, E. Şahan,<br />
M. Nebioğlu, C. Cerit, M. Çalışkan<br />
125 O. Yılmaz, M. A. Ateş, G. Meral,<br />
C. Başoğlu, A. Algül, S. Ebrinç, M. Çetin<br />
126 E. Özkorumak, H. Hıdıroğlu, A. Tiryaki,<br />
İ. Ak<br />
127 M. Güleç, E. Oral, E. F. Aydın<br />
128 T. Kara, A. Çiftçi<br />
129 H. A. Altaiar<br />
Tit le<br />
<strong>Contents</strong><br />
Comparison of superoxide dismutase, glutathione peroxidase, and adenosine deaminase<br />
activities between respiratory and nocturnal subtypes of patients with panic disorder<br />
The neural and cognitive effects of Bacopa Monniera: An fMRI study<br />
Methlyphenidate induced thrombocytopenia in a pediatric patient with ADHD and stuttering<br />
Use of mirtazapine and olanzapine in treatment of major depressive disorder with psychotic<br />
features developed during pregnancy: A case report<br />
Effects of group musical therapy on inpatients with schizophrenia: A preliminary study<br />
Clinical correlations of childhood trauma and dissociation in a sample of female inpatients<br />
diagnosed with schizophrenia spectrum disorders and severe nonpsychotic disorders: the<br />
preliminary data<br />
Comparison of neurocognitive skills between generalized anxiety disorder and premenstrual<br />
dysphoric disorder patients: A controlled study<br />
Evaluation of olfactory function and olfactory bulb volume in major depressive disorder<br />
Fluoxetine induced hypomanic shift in a bulimic patient: A case report<br />
Schizophrenia and Mega Cisterna Magna: A case report<br />
Congenital hypogonadism and comorbid anorexia nervosa in a male patient: A case report<br />
Review of diagnosis and treatment of pregnant psychiatric patients in a state hospital<br />
Peripheral edema associated with mirtazapine: Presentation of a case<br />
Abuse of tianeptine: A case report<br />
GWAS with AHP based SNP prioritization approach to identify SNP biomarkers for<br />
Alzheimer’s disease<br />
A case report of a relapse in a major depression patient with valsartan/hydrochlorothiazide<br />
Monosymptomatic hypochondriacal psychosis: A case report<br />
Amisulpride in the treatment of treatment resistant tic disorder: A case report<br />
Evaluation of patients with obstructive sleep apnea syndrome referred to the sleep disorders<br />
unit of a university hospital<br />
Clozapine use in idiopathic tardive dystonia and paranoid schizophrenia comorbidity:<br />
A case report<br />
The clinical use of Buprenorphine-Naloxone in the opioid-dependent patient with Hepatitis C<br />
The use of z hypnotics in the management of insomnia in forensic psychiatric<br />
units in Oxford, England<br />
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Turkish Association for Psychopharmacology<br />
4th International<br />
Congress on Psychopharmacology<br />
“Innovations and continuity in psychiatry &<br />
psychopharmacology: better care for better health”<br />
November 23-27, 2011<br />
Antalya, Turkey<br />
www.psychopharmacology2011.org<br />
ABSTRACTS OF THE INVITED SPEAKERS
Abstracts of the Invited Speakers<br />
OPENING CONFERENCE<br />
The evolution of human brain functions: Implications for psychobiological targets for well-being<br />
Claude Robert Cloninger<br />
Washington University, St. Louis, MO, USA<br />
E-mail: crcloninger44@gmail.com<br />
The natural building blocks of human personality are described based on the evolution of human brain functions (Cloninger, 2009;<br />
Cloninger, 2011). The phylogeny of human beings is traced from early vertebrates through mammals. The functional capacities that<br />
emerge along this lineage of ancestors are described. Comparative neuroanatomy is reviewed to identify the brain structures and<br />
networks that emerged coincident with the emergent brain functions.<br />
Neocortical development in mammals proceeded in 5 major transitions from early mammals to early primates, monkeys and apes, early<br />
humans, and modern Homo sapiens. These transitions provide the foundation for human self-awareness related to sexuality, materiality,<br />
emotionality, intellectual communication, and spirituality respectively.<br />
The evolution of functions in humans is compared to the psychobiological model of temperament and character previously described on<br />
the basis of individual differences in learning and genetic variation in human beings. The psychobiological model of personality provides<br />
a natural and thorough description of both the evolution and the development of personality in human beings.<br />
These evolutionary findings are related to clinical approaches to assessment and treatment of children and adults. Identification of the<br />
causal processes underlying well-being and ill-being is helpful in improving assessment and treatment in comparison to the frequent<br />
drop-out relapse rates obtained when diagnosis and treatment are based on symptoms, rather than their causes. Monitoring symptoms<br />
of illness and past lifestyle behavior has failed to promote change in well-being in a strong and consistent way in either individual care<br />
or public health. A clinician’s effectiveness in treatment depends substantially on his or her attitude toward, and understanding of, the<br />
patient as a person endowed with self-awareness and the will to direct his or her own future (Cloninger and Cloninger, 2011a).<br />
The causes of well-being operate as components of a virtuous circle of reciprocally interactive processes (Cloninger and Cloninger, 2011a)<br />
which evolved and develop in a stepwise manner. For example, emotions, cognitions, and actions have reciprocal interactions with one<br />
another. The induction of a positive mood by humor or kindness leads to a broadening of attention to be more inclusive and less defensive<br />
in thinking, which I have described as an outlook of unity (Cloninger, 2004; Cohn et al., 2009; Fredrickson, 2004; Fredrickson and Losada,<br />
2005). In turn, an outlook of unity allows a person to cultivate greater self-acceptance, environmental mastery, and creativity, which in<br />
turn lead to greater health and happiness, thereby completing the self-reinforcing cycle.<br />
Positive emotional states can be induced by a variety of self-transcendent activities, such as acts of virtues, including cheerful humor,<br />
generosity, and humility (Cloninger and Cloninger, 2011b). Virtues interact with functional practices of well-being, including working in<br />
the service of others, letting go of fighting and worrying, and growing in awareness. In turn, virtues and self-regulatory functions interact<br />
with the body to promote human plasticity. Human beings probably show greater plasticity, and hence variability, than other animal<br />
species, which has allowed us to adapt to highly variable environmental conditions successfully.<br />
Key words: Cognition, emotionality, human characteristics, thinking, personality, character, health, happiness, wellness, well-being<br />
References:<br />
1. Cloninger, C.R., 2004. Feeling Good: The Science of Well-Being. Oxford University Press, New York.<br />
2. Cloninger, C.R., 2009. The evolution of human brain functions: the functional structure of human consciousness. Australian and New Zealand Journal of Psychiatry<br />
43, 994-1006.<br />
3. Cloninger, C.R., 2011. The Phylogenesis of Human Personality: Identifying the Precursors of Cooperation, Altruism, and Well-Being. In: Sussman, R.W. and Cloninger,<br />
C.R. (Eds.), The Origins of Cooperation and Altruism. Springer, New York, pp. 63-110.<br />
4. Cloninger, C.R., Cloninger, K.M., 2011a. Development of instruments and evaluative procedures on contributors to Illness and health. International Journal of<br />
Person-centered Medicine 1, in press.<br />
5. Cloninger, C.R., Cloninger, K.M., 2011b. Person-centered Therapeutics. International Journal of Person-centered Medicine 1, in press.<br />
6. Cloninger, C.R., Zohar, A.H., 2011. Personality and the perception of health and happiness. J Affect Disord 128, 24-32.<br />
7. Cloninger, C.R., Zohar, A.H., Cloninger, K.M., 2010. Promotion of well-being in person-centered mental health care. Focus 8, 165-179.<br />
8. Cohn, M.A., Fredrickson, B.L., Brown, S.L., Mikels, J.A., Conway, A.M., 2009. Happiness unpacked: positive emotions increase life satisfaction by building resilience. Emotion 9, 361-368.<br />
9. Fredrickson, B.L., 2004. The broaden-and-build theory of positive emotions. Philos Trans R Soc Lond B Biol Sci 359, 1367-1378.<br />
10. Fredrickson, B.L., Losada, M.F., 2005. Positive affect and the complex dynamics of human flourishing. Am Psychol 60, 678-686.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S34<br />
S34 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
LECTURES<br />
[KL-01]<br />
Opioid dependence during pregnancy: Balancing risk versus benefit<br />
Peter Robert Martin<br />
Departments of Psychiatry and Pharmacology, Vanderbilt University, Nashville, Tennessee, USA<br />
E-mail: peter.martin@vanderbilt.edu<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Public health consequences of opioid dependence during pregnancy can only be inferred as increasing proportions of opioid-dependent<br />
women are addicted to non-medically prescribed analgesics and receive obstetrical care without being identified as addicted or treated.<br />
Because treatment recommendations for management of opioid dependence in pregnancy have primarily derived from studies in heroindependent<br />
pregnant women, there is a need to characterize and compare the clinical courses and complications of injection drug use<br />
(IDU) and non-medically prescribed opioids. Intrauterine overdose or withdrawal and the neonatal abstinence syndrome (NAS) may occur<br />
regardless of the route of opioid administration; whereas other obstetrical complications are likely consequences of poor prenatal care/selfneglect<br />
typical for IDU. Methadone maintenance compared to active IDU is associated with improved prenatal care, increased fetal growth,<br />
reduced fetal mortality, decreased risk of HIV infection, decreased risk of pre-eclampsia, decreased NAS and reduced foster care placement;<br />
however, significant NAS is still observed in >50% of these births. Benefits of methadone maintenance during pregnancy for addiction to nonmedically<br />
prescribed opioid analgesics may be attributed to support, structure, and prenatal obstetrical oversight compared to the stressful<br />
and chaotic lifestyle of active addiction. While methadone has been the standard of care for >40 years, the Schedule III (methadone is Schedule<br />
II) partial opioid agonist buprenorphine merits examination in pregnancy because it has been found highly effective for treatment of opioid<br />
dependence, is associated with less severe withdrawal and is available in the U.S. under less severe restrictions than methadone. In the MOTHER<br />
study, maternal and neonatal outcomes of treatment with buprenorphine or methadone throughout pregnancy were compared in pregnant<br />
opioid-dependent women, in an international multi-center randomized, controlled, double-blind/double-dummy clinical trial (Jones et al.,<br />
N Engl J Med 2010;363:2320-31). Although comparable numbers of methadone-exposed (57%) and buprenorphine-exposed (47%) babies<br />
required treatment for NAS, buprenorphine-exposed neonates required 89% less morphine to treat NAS; spent 43% less time in the hospital;<br />
and spent 58% less time in the hospital being medicated for NAS. The safety of opioid maintenance treatment during pregnancy must be<br />
judged in the context of comprehensive services (other than the administered medication per se) provided to addicted women by treatment<br />
programs. Buprenorphine is not inferior to methadone but may be preferable in terms of certain fetal outcome measures. Further research is<br />
needed to implement safe buprenorphine induction procedures in pregnant women, to balance reported teratogenic effects of opioids and<br />
benefits of opioid maintenance, and to determine the comparative safety and efficacy of methadone and buprenorphine for mother/fetus<br />
with co-occurring alcohol/benzodiazepine dependence or other psychiatric disorders and the psychoactive medications used to treat them.<br />
Key words: Opioid dependence, pregnancy, buprenorphine, methadone<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S35<br />
[KL-02]<br />
l-Benzylpiperazine, a major contaminant of ecstasy, induces marked changes in rat brain<br />
neurochemistry and behaviour<br />
Alan Leslie Hudson 1 , Nubia Zepeda 1 , Amanda Perreault 1 , Maggie Lalies 1 , Glen Baker 2<br />
1 Department of Pharmacology, University of Alberta, Edmonton, Canada<br />
2 Department of Psychiatry, University of Alberta, Edmonton, Canada<br />
E-mail: ahudson@pmcol.ualberta.ca<br />
Ecstasy [(±) -3-4-methylenedioxymethamphetamine, MDMA] is a widely abused drug which in overdose can lead to serotonin syndrome.<br />
The patient presents with agitation, tremors, and muscle spasms, followed by hyperthermia which can lead to fatal organ failure. Recently<br />
ecstasy tablets have been found to contain piperazines, particularly 1-benzylpiperazine (BZP). The purpose of cutting ecstasy with BZP is<br />
to enhance the psychostimulant effects of MDMA. BZP is also marketed as a “legal high” in some countries; therefore some ecstasy tablets<br />
contain solely BZP. BZP is the active metabolite of an antidepressant drug, trelibet, which failed in clinical trials. There has been little study<br />
on the pharmacological effects of combining BZP with MDMA so we have investigated the bioavailability, neurochemistry and behavioral<br />
S35
Abstracts of the Invited Speakers<br />
profile of these drugs administered alone or in combination in rats. We have used the technique of brain microdialysis in rat frontal cortex,<br />
to monitor extracellular levels of noradrenaline, dopamine and serotonin in response to peripheral administration of BZP and MDMA. We<br />
were also able to monitor the animals for evidence of rodent serotonin syndrome. BZP (10mg/kg, i.p.) was able to elevate extracellular<br />
levels of dopamine, noradrenaline and to a lesser extent, extracellular serotonin in rat frontal cortex. MDMA (3mg/kg, i.p.) potently<br />
elevated extracellular serotonin and noradrenaline and to a lesser extent extracellular dopamine in frontal cortex. These neurochemical<br />
effects lasted for at least 2 to 3 hours relative to saline treated control animals. Combined BZP and MDMA administration led to markedly<br />
elevated extracellular levels of all three monoamines indicating the effects of the drugs were additive. BZP (10mg/kg, i.p.) caused marked<br />
behavioral activation, for example, increased locomotor activity and rearing behavior, whereas MDMA (3mg/kg, i.p.) resulted in flat body<br />
posture and less rearing. Similar to MDMA (3mg/kg, i.p.), BZP increased grooming, forepaw treading, sniffing and head weaving relative<br />
to saline injected animals. We also investigated a 5-HT2A receptor antagonist, ketanserin (3mg/kg i.p.), to see if it could attenuate BZPinduced<br />
behaviors. Ketanserin alone had little effect on rat behavior but when co-administered with BZP, was able to decrease locomotion<br />
and rearing behavior. Interestingly, ketanserin had little effect on the increased sniffing and head weaving induced by BZP. At the doses<br />
of drugs used in this study hyperthermia was not apparent in any of the animals but we were able to measure blood and brain levels<br />
of BZP and MDMA hence we know bioavailability was not a problem. Overall, these results suggest that BZP and MDMA share certain<br />
psychopharmacological and neurochemical properties in the rat. Furthermore, combined administration of BZP with MDMA leads to a<br />
marked elevation of extracellular levels of all three monoamines in the frontal cortex rather than just serotonin which, if translated into<br />
the clinical setting, may explain the agitation and sympathomimetic toxic syndrome reported in some patients. All animal studies were<br />
conducted in accordance with the Canadian Council on Animal Care Guidelines and Policies with approval from the Animal Care and Use<br />
Committee in Health Sciences for the University of Alberta. This work is supported with a grant from Canadian Institute of Health Sciences.<br />
Key words: Ecstasy, (±) -3-4-methylenedioxymethamphetamine, 1-benzylpiperazine, serotonin syndrome, rat behaviour, brain microdialysis<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S35-6<br />
[KL-03]<br />
Unipolar versus bipolar depression in children: What do we know about the etiology,<br />
diagnosis, and treatment?<br />
Rasim Somer Diler<br />
Department of Psychiatry, University of Pittsburgh, PA, US<br />
E-mail: dilerrs@yahoo.com<br />
Bipolar disorder (BP) is a familial and recurrent illness that significantly affects the child’s normal development. BP is often manifested by periods of<br />
depression during which the child has significant psychosocial problems and increased risk for suicide. However, most clinical studies have focused<br />
on the manic phase of the illness. The depressed phase of the illness in youth is less recognized and less often treated than mania. Moreover,<br />
depressed youth with BP are more likely to have more severe depression, greater suicidality, and higher rates of comorbidities and functional<br />
impairment relative to depressed youth with major depressive disorder (MDD or “unipolar depression”). However, it is difficult to clinically<br />
differentiate the symptoms of BP depression from those of MDD. This issue is very important because youth with BP depression may be treated<br />
with antidepressants that can precipitate an episode of mania or mixed BP symptoms. Also, it may take up to 10 years from the initial symptoms<br />
of depression until BP is diagnosed and appropriate treatment is prescribed. Thus, early identification of BP youth, especially during depression, is<br />
critical not only to improve the long-term prognosis of BP, but also to prevent inappropriate treatments for BP youth. As demonstrated recently in<br />
BP adults, improving the accuracy of early diagnosis of BP in youth may be achieved by identifying objective neural biomarkers at an early age that<br />
are specific to BP and not common to MDD. Treatment guidelines for BD in children and adolescents were recently developed, but the panel left out<br />
depression and agreed that there was insufficient evidence to develop a treatment algorithm for it. Several studies suggest that there are effective<br />
and well-tolerated treatment options (e.g., lithium, mood stabilizers, second-generation antipsychotics [SGA]) for manic or mixed episodes of BD<br />
in youth; however, there are no maintenance studies in depressed children and adolescents with BP and available data for depressive episodes<br />
in BP is limited to one small randomized and two open-label acute treatment studies in adolescents. Management of depression is very different<br />
in BP depression than in MDD; antidepressants are widely used in MDD, but may exacerbate or induce mania and suicide in depressed BP youth.<br />
Antidepressant monotherapy is therefore contraindicated for the treatment of BP depression, and studies in depressed BP adults show that<br />
combining antidepressants with mood stabilizers may also not be effective. In conclusion, early differential diagnosis and treatment of depression<br />
in youth is a key factor to enable youth to follow a normal developmental path and prevent an unrecoverable loss in their development.<br />
Key words: Child, bipolar, depression, neuroimaging<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S36<br />
S36 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
[KL-04]<br />
Transcultural psychiatry: Practice and sample cases in USA and status in Turkiye<br />
Alican Dalkilic<br />
Virginia Commonwealth University, Richmond, VA & SEH, Washington, DC, USA<br />
E-mail: E-mail: drdalkilic@gmail.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Culture refers to unique behavior patterns and lifestyle shared by a group of people that distinguish it from other groups. The views, beliefs, values, and<br />
attitudes of a group characterize their culture. Culture and people influence and interact with each other reciprocally (1). In clinical practice patient’s<br />
culture, physician’s culture, and medical culture play a significant role. Adequate and appropriate understanding of cultural dimensions is essential for<br />
culturally competent practice (1). Also the impact of culture in evaluation and treatment of children and adolescents is significant in psychiatric patients (2).<br />
Cultural competency is a requirement for medical licensure in most states the US. To prove clinical competency clinicians are required<br />
demonstrate cultural competency. Clinicians typically work in multicultural and multiethnic societies (1). Ongoing globalization and<br />
interconnection of economies and rapidly spreading new social media platforms will increase diversity in all communities, but especially<br />
in developing countries including Turkiye. Therefore cultural competency training should be incorporated into residency training and<br />
continuous medical education systems especially for mental health clinicians.<br />
Clinicians should be familiar with culturally relevant relations and interactions of their patients (1), in order to establish therapeutic alliance and<br />
provide competent care and therapy besides demonstrating cultural sensitivity, knowledge, and empathy. Also most psychotherapies are based<br />
on Euro-American values of individualistic and egocentric concept, which can be contrasted with more sociocentric, ecocentric, and cosmocentric<br />
views (3). This issue should be taken into consideration when treating patients from other cultures or subcultures in the US and Europe.<br />
In this presentation I will review transcultural psychiatry practice in the US, provide and discuss some cases and summarize the status in Turkiye.<br />
Key words: Transcultural psychiatry, Turkish American cases, transcultural psychiatry in USA<br />
References:<br />
1. Focus, winter 2006 Vol. IV. No. 1, 81-89. Introduction: Culture and Psychiatry. Tseng W-S, Streltzer J.<br />
2. Child Adolesc Psychiatr Clin N Am. 2010 Oct;19(4):661-80. Culture and development in children and youth. Pumariega AJ, Joshi SV.<br />
3. Transcult Psychiatry. 2007 Jun;44(2):232-57. Psychotherapy and the cultural concept of the person. Kirmayer LJ<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S37<br />
[KL-05]<br />
Medical marijuana use in psychiatry<br />
Tahir Tellioglu<br />
Brown University, Rhode Island Hospital Dept Psychiatry, Providence USA<br />
E-mail: TTellioglu@Lifespan.org<br />
Medical marijuana refers to the use of parts of the cannabis plant or synthetic forms of specific cannabinoids as a physician-recommended<br />
form of medicine. The cannabis plant has been known to have medicinal use as an analgesic, appetite stimulant, antiemetic, muscle<br />
relaxant and anticonvulsant agent. A number of clinical studies, some disputed, claim that cannabinoids present an interesting<br />
therapeutic potential as antiemetics, appetite stimulants in debilitating diseases (cancer and AIDS) and analgesics, and in the treatment<br />
of multiple sclerosis, spinal cord injuries, Tourette’s syndrome, epilepsy and glaucoma.<br />
Despite its illegality, patients have continued to obtain cannabis on the black market for self-medication for its self reported anti-anxiety<br />
or antidepressant effects. A survey of 3,000 patients in California from 1993-2000 revealed about 27% of individuals used it primarily for<br />
psychiatric conditions such as as an antidepressant or anxiolytic.<br />
Understanding the mechanisms of action of cannabinoids has revived therapeutic interest in these substances. However, clinical studies<br />
about the use of cannabis for psychiatric conditions are very limited. Further clinical trials, well-designed, carefully executed, and powered<br />
for efficacy, are essential to clearly define the role of cannabinoids in the treatment of psychiatric conditions.<br />
Key words: Medical marijuana, cannabis, psychiatric disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S37<br />
S37
Abstracts of the Invited Speakers<br />
DEBATES<br />
[MD-02]<br />
Antidepressants are useful in the treatment of depression: the case for the motion<br />
Ian Anderson<br />
Neuroscience and Psychiatry Unit, University of Manchester, UK<br />
E-mail: ian.anderson@manchester.ac.uk<br />
The group of drugs we call antidepressants have been available for nearly 60 years and are the first available physical treatment for<br />
depression that became accepted by the public and clinicians alike. However in the last decade, associated with the rise of evidencebased<br />
medicine and a concern about the medicalisation of distress, there has been a questioning and re-evaluation of their efficacy<br />
and place in the treatment of depression. This has occurred against the backdrop of increasing distrust of ‘Big Pharma’ and emphasis<br />
on psychological treatment approaches. I will be addressing some of the main challenges that have been put forward questioning the<br />
usefulness of antidepressants, ranging from the denial that depression is a disorder that can be treated by physical means, to the argument<br />
that there is no pharmacological or empirical evidence for a clinically useful benefit over psychologically-mediated placebo effects. To<br />
do this I will touch on recent developments in the understanding of how antidepressants might directly influence the processing by the<br />
brain of emotional material, consider the evidence that direct pharmacological effects are necessary to maintain the therapeutic effects of<br />
antidepressants and review the empirical evidence for clinically important efficacy from treatment trials in depression. I will conclude that<br />
while antidepressants are certainly not a panacea, denying their place in treating depression is based on prejudice rather than objective<br />
appraisal of the evidence.<br />
Key words: Depression, antidepressants, placebo, efficacy<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S38<br />
[MD-02]<br />
Have clinically significant benefits of antidepressants been demonstrated?<br />
Irving Kirsch<br />
Associate Director, Program in Placebo Studies (PiPS) and Lecturer in Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Professor Emeritus of<br />
Psychology, University of Hull & University of Connecticut<br />
E-mail: I.Kirsch@hull.ac.uk<br />
Despite their widespread use, clinically significant benefits of antidepressants have not been demonstrated for most of the patients to<br />
whom they are prescribed. Meta-analyses of complete data sets consistently show a drug-placebo difference in improvement on the<br />
Hamilton Rating Scale for Depression (HAMD) of approximately two points, which is well below the 3-point difference set by the National<br />
Institute for Health and Clinical Excellence (NICE) as a criterion of clinical significance (1).<br />
Drug placebo differences increase with increasing severity of depression, but reach clinical significance only for 10% of the patients to<br />
whom they are prescribed (2). Defenders of antidepressants claim that depression scores are inflated by researchers who are anxious to<br />
qualify patients for clinical trials. To the extent that this is true, it compromises the clinical trial data leading to drug approval, but even if<br />
these trials are discarded, the absence of negative evidence does not constitute positive evidence of effectiveness.<br />
Discontinuation studies show a relapse rate of approximately 50% when patients are switched to placebo. However, approximately<br />
half of the relapses may be due to prior administration of the active agent. In extension trials, in which responders are kept on<br />
placebo, the relapse rate is only 25% (3). These data suggest that antidepressants might induce a biological vulnerability to relapse.<br />
Consistent with this hypothesis, a meta-analysis of tryptophan depletion studies indicates that the risk of becoming depressed after<br />
acute lowering of serotonin levels is greatest between three and six months after discontinuation of an antidepressant (4). It is also<br />
consistent with the results of the STAR-D trial, which was designed to be more representative than typical clinical trials of what<br />
happens in clinical practice. Following successful treatment in the STAR-D trial, 93% of patients either relapsed or dropped out of the<br />
trial within a year (5). Taken together, these data suggest that in the long run, rather than helping depressed people, antidepressants<br />
may make them worse.<br />
S38 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
References:<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
1. Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT. Initial severity and antidepressant benefits: A meta-analysis of data submitted to<br />
the Food and Drug Administration. PLoS Medicine [serial on the Internet]. 2008; 5(2): Available from: http://medicine.plosjournals.org/perlserv/?request=getdocument&doi=10.1371/journal.pmed.0050045.<br />
2. Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J. Antidepressant Drug Effects and Depression Severity: A Patient-Level Metaanalysis.<br />
Journal of the American Medical Association2010;303(1):47-53.<br />
3. Andrews P, Kornstein S, Halberstadt L, Gardner C, Neale MC. Blue again: Perturbational effects of antidepressants suggest monoaminergic homeostasis in major<br />
depression. Frontiers in Psychology. [Original Research]. 2011;2.<br />
4. Ruhé HG, Mason NS, Schene AH. Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion<br />
studies. Molecular Psychiatry2007;12:331-59.<br />
5. Pigott HE, Leventhal AM, Alter GS, Boren JJ. Efficacy and Effectiveness of Antidepressants: Current Status of Research Psychotherapy and Psychosomatics2010;70:267-79.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S38-9<br />
[MD-03]<br />
Antidepressants are useful in the treatment of bipolar disorders<br />
Selçuk Kırlı<br />
Department of Psychiatry, Uludag University, Bursa, Turkey<br />
E-mail: kselcuk@uludag.edu.tr<br />
Using antidepressant drugs in Bipolar Depression (BD) has not been adequately considered or explored. This matter is indeed an area of<br />
ambiguity which should to be clarified as soon as possible due to the following facts concerning bipolar disorder:<br />
• It is repetitive and progresses relatively slowly<br />
• It tends to become chronic<br />
• It involves a high risk of suicide<br />
• It causes more disability than the other variations of the disease (1).<br />
Treatment manuals, expert views and practices do not fully agree with each other on the issue of whether or not it is appropriate to<br />
use antidepressant (AD) drugs to treat BD. There are also differences in the manuals of various countries although they have similar<br />
approaches. Americans and Canadians, in particular, strictly oppose the use of ADs in BD. They generally recommend using mood<br />
stabilizers (MSs) in treating less severe depressions, using ADs alongside these drugs only in severe depressions and discontinuing ADs as<br />
soon as possible. In Germany and some other countries, there is a long and firm tradition of using ADs as a first line treatment (2). Despite<br />
different approaches, it is a fact that the decision to use antidepressant drugs in BD is not easy.<br />
The difficulty might stem from a number of reasons including:<br />
• Studies supporting the effectiveness of ADs in BD are few in number and they are not sufficient to approve the use of ADs in this area.<br />
• Although the issue has not been supported by placebo-controlled studies, there is a common belief that ADs cause manic transitions and rapid cycles (3).<br />
The matters of debate that may clarify this issue can be summarized as follows (2):<br />
• Transition to mania and rapid cycling are significant phenomena in Bipolar Disorder (BD).<br />
• The issue of suicide is, in fact, of minimal importance in BD.<br />
• The efficacy of antidepressants in BD has not been supported by satisfactory evidence.<br />
• MSs having an AD effect in BD has been supported by satisfactory evidence.<br />
Here are some brief answers to the matters of debate:<br />
• Like ADs, MSs have also not been officially approved in the treatment of BD. It is worthwhile to discuss the new generation antipsychotics<br />
(NGAPs) which have been approved in this context.<br />
• The data on manic transition and rapid cycling are problematic for the use of tricyclics to a certain extent; the data obtained from modern<br />
antidepressants have largely removed this issue from being a special problem area. There are also other alternatives to diminish the risk (4).<br />
• The antidepressant effect is directed towards the syndrome, thus these drugs are also effective in BD, but there are no noteworthy<br />
positive data on this issue for MSs other than a slight benefit obtained from Lithium.<br />
• The issues of suicide and chronicity cause a greater risk than all other issues in terms of contribution to a bad result for BD.<br />
In view of these and similar benefit/risk comparisons, we can conclude that it is reasonable and necessary to use ADs as a single agent or<br />
in combination with MSs or NGAPs in the treatment of BD. This approach is already commonly applied in practice.<br />
Key words: Bipolar disorder, antidepressants, depression<br />
S39
Abstracts of the Invited Speakers<br />
References:<br />
1. Gijsman HJ, Geddes JR, Rendell JM, Nolen WA, Goodwinn GM: Antidepressant for bipolar depression: A systematic review of randomized, controlled trials. Am J<br />
Psychiatry 2004;161:1537-1547.<br />
2. Möller HJ, Grunze H: Have some guidelines fort he treatment of acute bipolar depression gone too far in the restriction of antidepressants? Eur Arch Psychiatry<br />
Clin Neurosci 2000;250:57-68.<br />
3. Sachs SG, Nierenberg AA, Calabrese JR, Ketter TA, Marangeli LB, Milowitz DJ, Miyahara MS, Bauer MS: Effectiveness of adjunctive antidepressant treatment for<br />
bipolar depression. N Eng J Med 2007;356:1711-1722.<br />
4. Ghaemi SN, Rosenquist KJ, Ko YJ, Baldassano CF, Kontos NJ, Baldessarini RJ: Antidepressant treatment in bipolar versus unipolar depression. Am J<br />
Psychiatry2004;161:163-165.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S39-40<br />
JOINT SYMPOSIA<br />
[JS-01]<br />
International Association for Cognitive Psychotherapy (IACP)<br />
Symposium title: Advances and problems in cognitive behavior therapy (CBT)<br />
Recent advances in the treatment of anxiety disorders<br />
Stefan Hofmann<br />
Department of Psychology, Boston University, Boston, USA<br />
E-mail: shofmann@bu.edu<br />
Cognitive behavioral therapy (CBT) is the first-line psychological treatment for anxiety disorders. Although effective, partial or nonresponse<br />
to treatment remains an all-too-common occurrence, with over half of patients failing to respond fully to first-line cognitive<br />
behavioral therapy. The same is true for pharmacological interventions for anxiety disorders. Combining CBT with conventional anxiolytic<br />
medication is typically not more effective than unimodal therapy for treating anxiety disorders. This presentation will examine strategies<br />
to augment and modify CBT to enhance its efficacy. Recently, the search for new strategies to augment CBT has turned to a unique model<br />
of combination therapy. Rather than using pharmacotherapy as an anxiolytic in its own right, it is used to augment the core learning<br />
processes of cognitive-behavior therapy and exposure procedures. Moreover, recent work in emotion research points to new intervention<br />
strategies for anxiety disorders, such as mindfulness-based therapies and meditation practices.<br />
The first half of this presentation will review the current literature on conventional and novel combination strategies. A particularly<br />
successful prototype of a novel augmentation strategy of CBT is the use of d-cycloserine (DCS), a partial agonist at the glycine recognition<br />
site of the glutametergic N-methyl-D-aspartate receptor, to facilitate extinction learning. The second half the presentation will review<br />
novel and adaptive emotion regulation strategies, including mindfulness and loving-kindness mediation.<br />
The efficacy of CBT for anxiety disorders can be enhanced by (1) augmenting the treatment with the cognitive enhancers such as DCS,<br />
and (2) modifying the intervention using novel emotion regulation strategies. The augmentation strategies are based on the fact that<br />
exposure-based treatments in humans partly rely on extinction to reduce the fear response in anxiety disorders. In fact, animal studies<br />
have consistently shown that DCS facilitates extinction learning. Similarly, recent human trials have shown that DCS enhances fear<br />
reduction during exposure therapy of some anxiety disorders. Positive findings so far have been reported in placebo-controlled trials for<br />
specific phobia, social anxiety disorder, panic disorder, and obsessive compulsive disorder. The strongest effects were observed in studies<br />
in which patients receive a small dose of DCS (50 mg) acutely 1 hour before the exposure trials with no more than 5 administrations<br />
weekly. The modification strategies of CBT have primarily focused on enhancing adaptive emotion regulation strategies, beyond<br />
traditional reappraisal strategies. Whereas cognitive reappraisal strategies are antecedent focused, these novel strategies are primarily<br />
emotion response focused. Although these strategies have only recently been studied as treatments for anxiety disorders, they are rooted<br />
in ancient Eastern and Buddhist practices. CBT is an evolving science that integrates traditional and modern approaches and is in line with<br />
modern emotion and neuroscience theories.<br />
Key words: Cognitive behavior therapy, anxiety disorders, combination drug therapy, NMDA, glutamate, mindfulness, meditation, emotion<br />
regulation<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S40<br />
S40 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Translating science into practice, collaborative empiricism and engagement<br />
in homework assignments in cognitive behavior therapy<br />
Nikolaos Kazantzis<br />
La Trobe University, Australia<br />
E-mail: Nikolaos@NikolaosKazantzis.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Cognitive-behavioral therapy is more efficacious when between-session ‘homework’ tasks are included. Although the evidence for the<br />
effectiveness of homework appears compelling, only limited research is available to guide day-to-day practice. Recently, the search for<br />
strategies to enhance homework compliance (or engagement) has centered on practitioner competence in developing collaborative and<br />
empirical therapeutic relationships. Rather than viewing practitioner competence as a “trait”, newer measures are better equipped to<br />
capture the fluctuations in competence from session-to-session, as well as the relationship between therapist competence and patient<br />
compliance, and their combined effects on positive treatment outcomes.<br />
This presentation will use meta-analytic methods to review the empirical data demonstrating the causal and correlational effects of<br />
CBT homework assignments in enhancing positive treatment outcomes. Positive results have been obtained in the treatment of major<br />
depressive disorder, social anxiety disorder, panic disorder, and generalized anxiety disorder. Data supporting the development of<br />
therapeutic relationships characterized by strong patient and therapist involvement in the therapeutic work (collaboration) of identifying<br />
and evaluating the patients’ belief system (empiricism) will also be covered. A recent study in the treatment of major depressive disorder<br />
suggests that therapist competence in following a compliance enhancement protocol, which focused on collaborative empiricism,<br />
enhanced treatment outcomes. In conclusion, the results of these studies suggest that patient engagement with homework assignments<br />
is an important determinant of positive CBT outcomes, but practitioner competence may enhance the effect when the patient-therapist<br />
relationship is characterized by collaborative empiricism.<br />
Key words: Cognitive behavior therapy; homework assignments; therapeutic relationship; treatment outcome<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S41<br />
CBT as an evidence based treatment approach: Warning signs in therapy and common<br />
mistakes in daily practice<br />
Mehmet Zihni Sungur<br />
Medical School of Marmara University, Dept. of Psychiatry, Istanbul, Tukey<br />
E-mail: mzsungur@superonline.com<br />
The remarkable results obtained from integration of cognitive and behavioral therapies and the simplicity and straightforward<br />
approaches of the treatment modality have attracted many therapists to practice cognitive-behavioral psychotherapy today.<br />
Unfortunately a considerable number of these therapists adhere to guidelines of a textbook-kind of therapy without formal training and<br />
adequate supervision, and therefore suggest standard package-type treatments with little or no attempt to develop individually tailored<br />
programmes. There are some crucial points that clinicians need to consider during the practice of CBT to increase positive treatment<br />
outcomes. This presentation will focus on significant points that should be taken into account during the daily practice of CBT, discuss<br />
common mistakes made in daily practice and the reasons why psychotherapy is devalued during delivery of psychological services, and<br />
suggest alternative ways to improve the efficiency of CBT for public care.<br />
Key words: Cognitive behavioral therapy, evidence based treatment, treatment principles and pitfalls<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S41<br />
S41
Abstracts of the Invited Speakers<br />
[JS-02]<br />
Malaysian Psychiatric Association<br />
Symposium title: Malaysian perspective of substance dependence<br />
A harm minimization program against drug use and HIV problems in Malaysia<br />
Rusdi Abd. Rashid 1 , Abdul Kadir Bin Abu Bakar 2 , Hazli Bin Zakaria 3 , Umi Binti Adzlin 4 , Mohammad Hussain Habil 5<br />
1University of Malaya Centre for Addiction Sciences(UMCAS), Kuala Lumpur, Malaysia<br />
2Hospital Permai, Johor Bharu, Malaysia<br />
3Dept. of Psychiatry, Hospital Universiti Kebangsaan Malaysia,Kuala Lumpur, Malaysia<br />
4Dept. of Psychiatry, Kajang Hospital, Selangor, Malaysia<br />
5Dept of Psychological Medicine,Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia<br />
E-mail: rusdirashid@gmail.com<br />
This symposium highlights the drug use and HIV situations in Malaysia from the perspective of the development of a harm minimization<br />
program, methadone assisted therapy for opiate dependents, and the world’s first integrated Islamic psychospiritual intervention with<br />
methadone treatment in a mosque setting.<br />
The speakers will present four topics that related to the drug problems in Malaysia. The first speaker will talk about harm minimization<br />
and the current drugs and HIV situations in Malaysia. The second speaker will highlight the harm reduction services available emphasizing<br />
pharmacotherapy options available in Malaysia, the challenges and future directions. The third speaker will focus on psychosocial<br />
intervention in particular an innovative psychospiritual intervention called the Spiritual Enhancement of Drug Addiction Rehabilitation<br />
(SEDAR) program in the Malaysian Ar-Rahman mosque. The fourth speaker will discuss Assisted Medication Therapy (AST) from an Islamic<br />
perspective.<br />
Harm minimization approaches in Malaysia are promising. However, the program needs large scale implementation and new strategies<br />
in order to make an impact on HIV/AIDS prevalence.<br />
New and larger platforms and more aggressive promotions are required to implement more harm minimization programs in the<br />
community.<br />
Key words: Addiction, harm minimization, HIV/AIDS, psychospiritual interventions<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S42<br />
[JS-03]<br />
Hellenic Society for the Advancement of Psychiatry and Related Sciences<br />
Symposium title: Disorders of sleep and wakefulness and their pharmacological management<br />
Depression and the effect of antidepressants on sleep<br />
Thomas Paparrigopoulos<br />
Athens University Medical School, 1st Department of Psychiatry, Athens, Greece<br />
E-mail: tpaparrig@med.uoa.gr<br />
Sleep mechanisms and the pathophysiology of depression are closely interrelated. Monoaminergic and cholinergic neurotransmission<br />
are heavily involved in both. Therefore, it is not surprising that depression is almost invariably associated with sleep abnormalities.<br />
Several hypotheses have been advanced to explain their occurrence. One suggests that an increased pressure of REM sleep might be<br />
responsible. Another proposes that a deficiency in the mechanism responsible for non-REM sleep, as explained by the two-process<br />
model of sleep regulation, may be implicated. Finally, a third hypothesis suggests that an imbalance between the monoaminergic and<br />
cholinergic systems in the central nervous system (CNS) could be responsible for the pathophysiology of depression and the observed<br />
sleep aberrations.<br />
In principle, most antidepressants increase synaptic levels of norepinephrine, serotonin, and dopamine; yet they may also act on<br />
muscarinic and histamine (H1) receptors. These effects purportedly underlie their principal therapeutic mode of action, as well as their<br />
potential mechanism of altering sleep architecture. In this line of thought it has been proposed that central to the therapeutic effect<br />
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Abstracts of the Invited Speakers<br />
of the majority of antidepressants is the observed strong and sustained suppression of REM sleep, without overlooking other factors<br />
involved in the mechanisms underlying treatment response. Moreover, tryptophan depletion and studies of selective serotonin reutake<br />
inhibitors (SSRIs) in sleep have shown that increases in serotonin levels could mediate the effect on REM sleep, which is often observed<br />
during antidepressant treatment. However, changes in non-REM sleep and sleep maintenance may be mediated through the action of<br />
other neurotransmitter systems.<br />
Although each antidepressant drug affects sleep architecture differently, there are some common features that characterize the various<br />
types of antidepressants. Thus, the majority of antidepressant drugs suppress REM sleep. Some, however, with little or no noradrenergic<br />
or serotoninergic reuptake inhibition, such as amineptine, tianeptine, nefazodone, trazodone, bupropion, and trimipramine, do not<br />
have clear-cut REM suppressant effects. Sleep continuity and total sleep time are improved with sedative medications, such as most<br />
tricyclic antidepressants (TCAs) and several antidepressants with 5-HT2c receptor antagonist properties, such as mianserin, mirtazapine,<br />
nefazodone, and trazodone. On the other hand, most (SSRIs) and clomipramine, show evidence early in treatment of stimulating effects,<br />
thereby reducing total sleep time and sleep efficiency, and promote wakefulness. However, these effects are fairly short-lived and there<br />
are few significant differences among drugs after a few weeks of treatment.<br />
In conclusion, the majority of antidepressant drugs suppress REM sleep and increase REM latency, although this is not always the case. As<br />
far as sleep efficiency and total sleep time are concerned, antidepressants can be distinguished as either sedative or energizing agents.<br />
This individualized profiling of antidepressants provides a diversity of therapeutic options in terms of the management of concomitant<br />
sleep disturbances in depression.<br />
Key words: Depression, antidepressants, medication, sleep<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S42-3<br />
Insomnia and the effects of hypnotics on sleep<br />
Constantin R. Soldatos, Thomas Paparrigopoulos<br />
Athens University Medical School<br />
E-mail: egslelabath@hol.gr<br />
Insomnia is conceived as the subjective complaint of reduced sleep quantity and/or quality and affects a significant proportion of<br />
the general population. Approximately 10% of the population worldwide meet the full ICD-10 criteria for chronic insomnia. Insomnia<br />
is the outcome of the interplay of many environmental, biological, and psychological factors; consequently, its treatment should not<br />
only focus on ameliorating sleeplessness but should also address all those predisposing, precipitating and perpetuating factors that<br />
cause and maintain insomnia. Insomniacs need an integrative individualized management, which includes sleep hygiene measures,<br />
psychotherapeutic techniques, and the utilization of sleep-promoting drugs. The focus of treatment should be nighttime symptoms, the<br />
feeling of non-restorative sleep, and impaired daytime functioning as well.<br />
Benzodiazepine or benzodiazepine-like hypnotics (z-drugs) are still considered as the drugs of choice for the treatment of insomnia.<br />
However, due to their abuse potential, their pharmacological properties, and their widespread use (there are estimates that one of<br />
every four adults in developed countries takes sleeping aids at some time point during the year), it is highly recommended that the<br />
use of hypnotic drugs is restricted to the initial period of treatment mostly as adjuncts to other psychotherapeutic measures. Both<br />
types of hypnotics focus primarily on the inhibitory neurotransmitter GABA through binding to GABAA receptors; however, other<br />
neurotransmitter systems, such as the serotoninergic and histaminergic, are also involved in the regulation of sleep-wakefulness and<br />
may be targeted by other compounds. The non-benzodiazepine drugs are generally preferred as a result of their improved binding<br />
selectivity and pharmacokinetic profile. However, their potential adverse effects, such as amnestic symptoms, next day residual<br />
sedation, and abuse potential, indicate the need for novel pharmacotherapies. In this line, agents acting on the melatonergic system<br />
and circadian mechanisms have been developed and approved for the treatment of insomnia (melatonin and the melatonin receptor<br />
agonist, ramelteon). Furthermore, a variety of other compounds targeting several neuroreceptors (i.e., GABAA agonism, melatonergic<br />
MT1/MT2 agonism, 5-HT2A antagonism, orexin receptor OX1/OX2 antagonism) are under investigation and may be added in the<br />
psychopharmacological armamentarium in the near future.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S43<br />
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Abstracts of the Invited Speakers<br />
Hypersomnias and the effects of vigilance-promoting compounds<br />
Antigone Papavasiliou<br />
Department of Neurology, Pendeli Children’s Hospital<br />
E-mail: theon@otenet.gr<br />
Hypersomnia is characterized by a propensity to fall asleep in situations when one is expected to be awake and alert. It may present with<br />
prolonged sleep episodes coupled with excessive daytime sleepiness (EDS) and frequent napping. It is described in narcolepsy, a neurological<br />
disorder characterized by EDS occurring with or without cataplexy; in idiopathic hypersomnia, also of central origin, characterized by EDS<br />
and episodes of prolonged nocturnal sleep; in recurrent hypersomnias, rare disorders manifesting with recurrent episodes of more or<br />
less continuous sleep (average duration of 1 week), recurring at highly variable intervals (one to several months), such as, Kleine–Levin<br />
syndrome and menstrual-related hypersomnia. Chronic sleep loss and/or poor sleep quality may be underlying reasons for EDS; these occur<br />
in numerous sleep disorders, such as obstructive sleep apnea (OSA) and in psychiatric disorders, particularly depression. Approximately<br />
80% of depressive states are associated with insomnia; patients do not necessarily have a higher propensity to fall asleep in daytime but<br />
report subjective sleepiness that differs from the EDS encountered in narcolepsy and OSA. There are also hypersomnias attributable to other<br />
medical conditions, drugs, or substances, as well as behaviorally induced hypersomnia caused by insufficient time to sleep.<br />
Transition between sleep and wakefulness is simply described as oscillations between two opponent processes, one promoting sleep,<br />
another promoting wakefulness. The complex neurobiological mechanisms and the neurotransmitters and neuromodulators underlying<br />
these processes, including noradrenergic, serotonergic, cholinergic, adenosinergic, and histaminergic systems and more recently, the<br />
hypocretin/orexin and dopamine systems, have been established. The mechanisms of action of some vigilance-promoting agents are as<br />
follows: psychostimulants act through enhanced dopamine action (amphetamines, methylphenidate) or acetylcholine action (caffeine);<br />
modafinil may act through enhanced central histamine, hypocretin, and possibly dopamine action; γ -hydroxybutyrate (GHB), acts on GABA<br />
and GHB receptors. EDS in narcolepsy is traditionally treated with psychostimulants; these are rarely effective in idiopathic hypersomnia,<br />
although this was not examined through randomized controlled trials. Modafinil, a first-line wakefulness-promoting medication, is a<br />
useful alternative to psychostimulants for EDS in narcolepsy (Level I evidence). It may be effective for EDS due to idiopathic hypersomnia<br />
(one Level IV study and expert consensus). It is not associated with rebound hypersomnolence, cardiovascular problems, or abuse<br />
potential, as may be seen with amphetamines. Modafinil alleviates sleepiness and fatigue in shift work disorders, residual sleepiness in<br />
treated sleep apnea syndrome, multiple sclerosis, Parkinson’s disease and depression. It is promising as an alternative to psychostimulants<br />
for excessive fatigue associated with medical and psychiatric disorders and as an augmentation medication for treatment-resistant<br />
depression. Due to rare serious complications (allergic and psychiatric), the EMA concluded that its benefit/risk balance was positive for<br />
narcolepsy but negative for other sleep disorders and neurological diseases, including idiopathic hypersomnia. The FDA has approved it<br />
for EDS in narcolepsy, shift work sleep disorder, and OSA. In narcolepsy, GHB at bedtime reduces nocturnal awakenings, increases stage<br />
3 and 4 sleep, and consolidates REM sleep periods; these effects coincide with improvement in daytime symptoms, including cataplexy.<br />
Key words: Vigilance-promoting agents, hypersomnia, psychostimulants, modafinil, γ -hydroxybutyrate<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S44<br />
[JS-04]<br />
The International Union of Basic and Clinical Pharmacology (IUPHAR)<br />
Symposium title: Pharmacogenomics of psychoactive drugs<br />
Role of polymorphic drug transporter in treatment-resistant depression<br />
Tanja Brueckl, M. Uhr<br />
Max Planck Institute of Psychiatry, Germany<br />
E-mail: brueckl@mpipsykl.mpg.de<br />
To be effective antidepressants and other centrally acting drugs have to penetrate the blood-brain barrier. Transport proteins such as<br />
p-glycoprotein that are located at the BBB do not only transport toxic substances but also many drugs back into the blood. In preclinical<br />
animal models and a study examining more than 400 patients, the relationship between polymorphisms in the ABCB1 gene coding<br />
for p-glycoprotein and the clinical efficacy of antidepressants could be demonstrated. With respect to those antidepressants that are<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
substrates of p-glycoprotein there is a significant statistical relationship between polymorphism and remission rate after 4 to 6 weeks.<br />
Clinically, genetic analysis of ABCB1 polymorphisms may be used to predict how likely it is that a patient will respond to therapy with<br />
antidepressants or other centrally acting drugs. This in turn will help to select the right drug and/or dosage (Neuron 2008, 57:203-209).<br />
Further data from a preliminary pilot study suggest that the treatment of depression could be optimized by a routine application of<br />
an ABCB1 gene test. Patients carrying the less favourable ABCB1 genotype with respect to the clinical efficacy of antidepressants may<br />
especially benefit from a dosage increase.<br />
P-glycoprotein in the membrane of vascular cells causes centrally acting drugs such as citalopram, paroxetine, venlafaxine and others to be<br />
transported from the brain back to the vascular lumen. If the protein is missing or if its function is impaired, more drugs pass from the blood into<br />
the brain. Depending on changes (polymorphisms) in the ABCB1 gene, p-glycoprotein allows varying amounts of a drug to pass into the CNS.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S44-5<br />
Relationship between pharmacogenetics and personality traits: Relevance for suicide<br />
Adrián Llerena<br />
International Union of Basic and Clinical Pharmacology (IUPHAR), Extremadura University Hospital<br />
E-mail: allerena@unex.es<br />
CYP2D6 genetic polymorphism is related to variability of the enzyme’s hydroxylation capacity. Subjects carrying zero CYP2D6 active<br />
genes are classified as Poor Metabolizers (PMs). The rest are Extensive Metabolizers (EMs) with one or two active genes, including a group<br />
of Ultra-rapid Metabolizers (UMs) with more than two active alleles. UMs have a hydroxylation capacity more than 100 times higher than<br />
PMs. The frequency of PMs and UMs in Spain is 7-10% and 4.9%, respectively (Llerena et al., 2009).<br />
A higher frequency of UMs has been found among individuals who committed suicide vs. those who died from natural causes (Zackrisson<br />
et al, 2010). One explanation for this relationship could be treatment failure with antidepressant drugs metabolized by CYP2D6<br />
(fluoxetine, paroxetine, fluvoxamine, venlafaxine, citalopram, etc.) (Llerena et al., 2004; Llerena et al., 2009) widely used to prevent suicide<br />
or to treat mood disorders. A complementary explanation could be via the implication of the polymorphic CYP2D6 in the endogenous<br />
metabolism. Since we found an association between this drug metabolizing enzyme and psychological functioning, CYP2D6 has been<br />
associated with behavioral and clinical risk factors such as personality and vulnerability to psychopathology (Llerena et al., 1993; Llerena<br />
et al., 2007; Gonzalez et al., 2008; Peñas-Lledó et al., 2009, Peñas-LLedó et al., 2010). These two hypotheses could explain the relationship<br />
found between CYP2D6 and suicide (Peñas-LLedón et al 2011, in press)<br />
The biotransformation of several antidepressants and antipsychotic drugs is mainly determined by genetic factors mediating the<br />
CYP2D6 gene polymorphism. Additionally, the potential interaction between CYP2D6 and endogenous metabolism must be taken into<br />
consideration due to its potential implication for personality traits (LLerena et al 1993; Gonzalez et al 2008) and functioning, such as:<br />
neurocognition (Peñas-Lledó et al 2009) and psychopathology, eating disorders (Peñas-LLedó et al., 2010) and suicide (Peñas-Lledó et al.,<br />
2011). In summary, the pharmacogenetics of CYP2D6 may be a useful tool to predict unexpected side-effects, interactions, or therapeutic<br />
failures of many relevant drugs and may explain the interethnic differences oberserved in the response to psychotropic drugs, but also<br />
vulnerability to psychopathology including suicide.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S45<br />
Genetic causes of hypersensitivity to antipsychotics – the clozapine story<br />
Ingolf Cascorbi<br />
Institute of Experimental and Clinical Pharmacology, University of Kiel, Germany<br />
E-mail: cascorbi@pharmakologie.uni-kiel.de<br />
Clozapine is considered to be the most efficacious drug to treat schizophrenia, but despite these benefits, clozapine prescriptions<br />
comprise only 2-10% of the total antipsychotic market for schizophrenia in the United States. It was introduced on the market in 1971 but<br />
was withdrawn in 1975 after reports of clozapine-induced agranulocytosis (CIA) in Finland. Due to its high efficacy in treatment-resistant<br />
schizophrenia, it was reapproved in 1990 by the FDA and health authorities in most other countries; however, regular hematological<br />
S45
Abstracts of the Invited Speakers<br />
monitoring was required. The implementation of this monitoring system has successfully reduced the incidence of CIA from 1.3% to 0.4%.<br />
Currently 239 cases of agranulocytosis are registered at the FDA adverse drug reaction data bank.<br />
There have been certain attempts to predict agranulocytosis by genetic association studies in particular in the NADPH myeloperoxidase<br />
complex (1) and FC-gamma receptors (2). We could identify an association to the polymorphic myeloperoxidase, responsible for oxidative<br />
reaction in neutrophils. More recently, confirmatory studies in two independent cohorts of 33 and 49 CIA cases and 54 and 78 controls<br />
indicated that markers in the HLA system are highly significantly associated with the risk of CIA. HLA-DQB1 6672G>C was associated with<br />
CIA conferring an odds ratio of 16.9 (3). Currently a large consortium led by Duke University has aimed to collect a large sample of well<br />
defined cases of CIA in order to allow genome-wide association studies.<br />
Key words: Clozapine, agranulocytosis, NADPH-oxidase, myeloperoxidase, HLA-system, genetic association<br />
References:<br />
1. Mosyagin I, Cascorbi I, Schaub R, Krüger T, Dettling M. Drug-induced agranulocytosis: impact of different fcgamma receptor polymorphisms? J Clin<br />
Psychopharmacol. 2005;25:435-40.<br />
2. Mosyagin I, Dettling M, Roots I, Mueller-Oerlinghausen B, Cascorbi I.. Impact of myeloperoxidase and NADPH-oxidase polymorphisms in drug-induced<br />
agranulocytosis. J Clin Psychopharmacol. 2004;24:613-7.<br />
3. Athanasiou MC, Dettling M, Cascorbi I, Mosyagin I, Salisbury BA, Pierz KA, Zou W, Whalen H, Malhotra AK, Lencz T, Gerson SL, Kane JM, Reed CR. Candidate gene<br />
analysis identifies a polymorphism in HLA-DQB1 associated with clozapine-induced agranulocytosis. J Clin Psychiatry. 2011;72:458-63.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S45-6<br />
[JS-05]<br />
Indian Psychiatric Society<br />
Symposium title: Current concept of obsessive compulsive disorder (OCD)<br />
Current understanding of the concept of obsessive compulsive disorder<br />
Manickam Thirunavukarasu<br />
Professor & Head, Department of Psychiatry, SRM MC & RC, Kattankulathur, 603203, India<br />
E-mail: arasueshwar@gmail.com<br />
Obsessive-compulsive disorder (OCD) is a relatively common disorder, occurring in around 2-3% of general population. In the past<br />
century, the understanding of the disorder has improved and has been clearly delineated as a valid nosological entity. The heterogeneity<br />
of the disorder has been explained based on various phenotypic subtypes. Factor analytic studies have provided consistent evidence that<br />
distinct obsessive-compulsive symptom dimensions exist, including obsessions/checking, contamination/washing, symmetry/ordering,<br />
and hoarding. It has been hypothesized that each symptom dimension may be underpinned by a distinctive set of bio-behavioral<br />
mechanisms. There has been a good deal of interest recently in the disorders characterised by similar phenomenology and psychobiology<br />
called obsessive compulsive spectrum disorder (OCSD). These include tic disorder, body dysmorphic disorder, impulse control and eating<br />
disorders. In view of all these changes in understanding and newer conceptualisation, OC(S)D might find a separate place for itself in the<br />
DSM V and ICD 11, rather than being classified under anxiety / neurotic spectrum disorders.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S46<br />
Biological theories of obsessive compulsive disorder<br />
A. Shyam Sundar<br />
Assistant Professor, Department of Psychiatry, SRM Medical College Hospital and Research Centre, Kattankulathur, 603203, India<br />
E-mail: a.shyamsundar@gmail.com<br />
Although the pathophysiology of OCD is still far from resolved, the existence of a biological basis for OCD has been clearly established.<br />
Twin, family, segregation and linkage studies have demonstrated that genetic factors contribute to the pathogenesis of OCD. There<br />
S46 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
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Abstracts of the Invited Speakers<br />
is a general consensus that fronto-striato-thalamo-cortical dysfunction is the neuronal basis of obsessive-compulsive disorder. The<br />
differential response of OCD to clomipramine and SSRIs, compared to other antidepressants, has led to the primacy of the serotonin (5HT)<br />
hypothesis of OCD. Currently serotonin has also been implicated in the pathophysiology of other OC spectrum disorders. However, several<br />
lines of research suggest that the dopamine system, with which 5HT interacts, may play a major role in the expression of OC symptoms.<br />
Recent genetic and neurochemical studies also implicate glutamate in the pathophysiology of OCD. The recognition of PANDAS (Pediatric<br />
autoimmune neuropsychiatric disorders associated with streptococcal infection) has increased the interest in the possibility of an<br />
immune-mediated pathophysiology of obsessive-compulsive disorder. In this presentation, these recent advances in biological models<br />
of OCD will be discussed.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S46-7<br />
Psychopharmacological and somatic interventions for OCD<br />
Kandasamy Arun<br />
Assistant professor, Department of Psychiatry, SRM Medical College & Research Center, Kattankulathur, 603203, India<br />
E-mail: arunnimhans05@gmail.com<br />
OCD was initially thought to be unresponsive to treatment but subsequently, a range of effective treatments has been developed on the<br />
basis of two approaches, pharmacological and psychosocial. Pharmacological agents such as Selective Serotonin Reuptake Inhibitors<br />
(SSRIs) and clomipramine have changed the face of OCD management. Around 50–60 % of patients showed remission after treatment. In<br />
treatment resistant cases, augmenting agents like clonazepam, risperidone and buspirone are used. Intravenous clomipramine is another<br />
option. Other strategies which are currently under study include riluzole and other drugs which act on the glutaminergic system, opioid<br />
agonists and inositol augmentation. Immunomodulatory therapies have also been studied especially in PANDAS. Development of newer<br />
somatic methods of treatment like repetitive trans-cranial stimulation (rTMS) and Deep Brain Stimulation (DBS) are promising in targeting<br />
the fronto-striato-pallido-thalamo-cortical circuits for treatment resistant OCD. Although controversial, stereotactic and gamma knife<br />
assisted neurosurgical procedures such as cingulotomy and anterior capsulotomy are also possible treatments for resistant cases.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S47<br />
Psycho-social interventions for OCD<br />
Manickam Thirunavukarasu<br />
Professor & Head, Department of Psychiatry, SRM MC & RC, Kattankulathur, 603203, India<br />
E-mail: arasueshwar@gmail.com<br />
We will review recent advances in the psychological treatments for obsessive compulsive disorder. In the early 20th century, psychological<br />
treatment for OCD consisted largely of psychodynamic psychotherapy. The general consensus of that era was that OCD was an<br />
unmanageable condition with a poor prognosis. Starting from the 1950s, laboratory studies on extinction of conditioned responses<br />
followed by clinical research led to the formulation of Exposure and Response Prevention (ERP) for OCD.We have developed a model<br />
combining ERP and CBT. This behavioral approach currently is the first-line intervention for adult obsessive-compulsive disorder. Recently<br />
predominantly cognitive approaches have been evaluated to overcome the shortcomings of ERP. Methodologically rigorous controlled<br />
trials have suggested that the benefits from CBT exceed those from placebo and attention-control conditions and have similar or greater<br />
efficacy than serotonergic monotherapy. The clinical predictors for response to CBT include symptom severity, symptom subtype, severe<br />
depression, the presence of comorbid personality disorders, family dysfunction and the therapeutic alliance. Combination treatment with<br />
pharmacotherapy has generally revealed promising results. Nevertheless, more studies are still needed in certain areas. We will explain in<br />
detail how we practice in our patients and the results.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S47<br />
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Abstracts of the Invited Speakers<br />
[JS-06]<br />
Czech NeuroPsychopharmacological Society (CNPS)<br />
Symposium title: From models of schizophrenia to clinical outcome: A psychopharmacological perspective<br />
Safety first, efficacy second? Fear and the need for treatment in the absence of controlled data<br />
Pavel Mohr, David Hnidek, Dagmar Seifertova<br />
Prague Psychiatric Center, Czech Republic<br />
E-mail: mohr@pcp.lf3.cuni.cz<br />
In clinical practice, physicians are routinely asked to make decisions about whether to initiate or continue antidepressant treatment in<br />
a situation where no safety data are available. Pregnancy and breast-feeding can serve as an example, where controlled clinical trials<br />
provide little guidance. Females of fertile age are rarely included in the early phases of clinical testing, indeed, Phase IIb and III trials have<br />
a standard provision to use a reliable method of contraception. Pregnancy during a drug trial is considered as a ‘serious adverse event’<br />
with subsequent study discontinuation. The reasons are not just ethical and legal but also marketing, including the drug manufacturers’<br />
fear of having their products associated with potentially grave side effects, such as malformations. Drug treatment in pregnancy and<br />
lactation thus pose a highly relevant clinical problem that cannot be addressed in controlled trials. Excessive concerns of negative<br />
consequences could erroneously result in a generalized recommendation to not get pregnant or to abort an existing pregnancy. However,<br />
the fetus may already have been exposed to drugs early in the first trimester during frequently unplanned pregnancies; in addition, recent<br />
epidemiological data indicate increasing consumption of psychotropics, including antidepressants, by pregnant women. Psychiatrists<br />
have to weigh the known risks of treatment discontinuation versus the potential risks for the fetus and infant. They should also consider<br />
whether alternative non-pharmacological interventions (psychotherapy, ECT, rTMS) are accessible or effective. The only available safety<br />
data on antidepressants come from animal studies, epidemiological trials, drug registries, case series, anecdotal case vignettes and clinical<br />
observations.<br />
Moreover, published findings have to be viewed with caution and interpreted correctly. For example, recent data suggested an increased<br />
teratogenic risk for the antidepressant paroxetine. While it is true that a meta-analysis confirmed an increased relative incidence of<br />
malformations, the absolute risk was raised from 3% to 4% for all congenital malformations and from 1% to 2% for cardiac malformations.<br />
In 2005 the Prague Psychiatric Center established a specialized consultation outpatient center for pharmacotherapy in pregnancy and<br />
breastfeeding. The center provides services and information on safety and treatment recommendations directly to patients, their treating<br />
psychiatrists and other physicians as well. The database consists of patients records, data on their illness, treatment and pregnancy<br />
outcome. Currently, a prospective study for the longitudinal follow-up of offspring exposed in utero to psychotropics has been designed.<br />
The focus is on their developmental milestones, physical health, neuropsychological performance and general well-being.<br />
Key words: Psychotropic drugs, pregnancy, lactation, drug safety, psychiatric disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S48<br />
Basic concepts of schizophrenia: Experimental approaches<br />
Cyril Höschl 1<br />
1Prague psychiatric centre, Centre of neuropsychiatric studies,<br />
3rd Medical faculty, Charles University, Prague, Czech Rep.<br />
E-mail: hoschl@pcp.lf3.cuni.cz<br />
One of the crucial questions in the study of schizophrenia is, whether the diagnosis of the disease represents one entity or a group of<br />
disorders (“Gruppe der Schizophrenien”). Nancy Andreasen suggests the term “lathomenology” for a bottleneck on the pathogenetic way<br />
from various possible etiological factors to diverse phenomenological expressions (symptoms) (Arch Gen Psych 1999;56:781-787). In the<br />
background of this common denominator, there is an anatomical and functional disruption in neuronal connectivity and communication,<br />
which can be a consequence of incomplete or erroneous neuron formation, migration, synaptogenesis or pruning during ontogenesis.<br />
Also apoptosis and activity dependent changes might play a role in this development. This all can happen from conception to early<br />
adulthood and can lead to the impairment in fundamental cognitive functions. This leads to the development of clinical symptoms,<br />
either positive or negative. Schizophrenia can be regarded as a “disconnection” or “information processing disorder”. There are many<br />
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Abstracts of the Invited Speakers<br />
neural circuits, where the clinical impact of the disconnection or misconnection is worthy of study. One of them is the fronto-thalamocerebellar<br />
circuit with the special role of the cerebellum not only in the synchronization of motor processes, but also in the coordination<br />
of motor-cognitive sequences. The disconnection of these circuits leads to “cognitive dysmetria”. Mezo-cortical pathways also represent<br />
a crucial pathogenetic point. Dopaminergic fibers from the ventral tegmental area to the pre-frontal cortex are under serotonergic<br />
inhibition via 5-HT2 receptors. This configuration can help in the understanding of the dual mode of action of novel antipsychotic agents,<br />
which are effective in both positive (hyperdopaminergic state in mezo-limbic areas) and negative (hypodopaminergic state in prefrontal<br />
cortex) symptoms. Disconnection can play a role also in circuits involved in executive functions (fronto-parieto-temporo-cingulate).<br />
On the neurochemical level, many imbalances in information processing can be explained by the framework of Carlsson’s scheme of<br />
psychotogenic pathways. The crucial mechanism involves striato-thalamic GABA-ergic control of gating, which is under glutamatergic<br />
control from cortex. The scheme can also explain the amphetamine model of psychosis, the dopamine hypothesis of schizophrenia, the<br />
glutamatergic model of schizophrenia and the psychotogenic effects of hallucinogens (LSD), atropine, phencyclidine etc. Our own study<br />
on the role of serotonin regulation of psychotogenic pathways will be reported (Bubeníková et al., The effect of tryptophan depletion on<br />
the action of haloperidol in MK-801 treated rats. Eur J Pharmacol, 2004; 502, 1-2:109-116).<br />
The background of disconnection may involve gene-environment interaction including early neuroinfection (inflammatory process).<br />
The classical antipsychotic drugs exert primarily antidopaminergic properties, which are responsible also for their side-effects such<br />
as hyperprolactinemia and extrapyramidal syndrome. Nevertheless, psychotogenic pathways in the brain involve several different<br />
mechanisms, which could serve as targets of antipsychotic modalities, e.g., facilitation of glutamatergic neurotransmission, blockade of<br />
serotonin 5-HT2A receptors, expression of BDNF and bcl2, inhibition of GSK-3β phosphorylation and thus apoptosis etc.<br />
Key words: Schizophrenia, glutamate, dopamine, serotonin, information processing disorder, gating<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S48-9<br />
The ins and outs of the human model of schizophrenia<br />
Jiri Horacek 1 , Vera Bubenikova Valesova 1 , Tomas Palenicek 1 , Filip Spaniel 2 , Cyril Höschl 1<br />
1Prague Psychiatric Center, Prague, Czech Rep.<br />
2 rd 3 Medical Faculty of Charles University, Prague, Czech Rep.<br />
E-mail: horacek@pcp.lf3.cuni.cz<br />
The experimental models of schizophrenia are based on morphological, biochemical and genetic findings in the clinical population. These<br />
models serve as an important tool for the research of etiology and pathophysiology, and for testing novel potential treatment methods.<br />
The experimental models of schizophrenia are divided into neurodevelopmental, pharmacological and genetic. Only the pharmacological<br />
model is useful in humans.<br />
An important role of the glutamatergic neurotransmitter system in the pathogenesis of schizophrenia has been supported by findings<br />
on various levels from molecular interactions up to the structural layout of the neuronal network in the human brain. The research of<br />
the glutamatergic system in schizophrenia has advanced with the use of non-competitive antagonists of glutamate NMDA receptors<br />
(phencyclidine, ketamine, and dizocilpine). These compounds change both human and animal behavior and induce schizophrenia-like<br />
manifestations in the field of different neurobiological modalities and markers.<br />
The models based on both acute and chronic administration of non-competitive antagonists of glutamate NMDA receptors in humans<br />
and rats show phenomenological validity and are suitable for searching for new substances with antipsychotic effects. In particular, the<br />
human model of schizophrenia based on infusion of ketamine exerts high face validity in term of induction both positive and negative<br />
symptoms, and characteristic cognitive, electrophysiological (qEEG) and metabolic (PET) changes.<br />
Nevertheless, the pathophysiology of schizophrenia remains unexplained. In the light of the neurodevelopmental model of schizophrenia<br />
based on the early administration of NMDA receptor antagonists, it seems that increased cellular destruction by apoptosis or changes<br />
in function of glutamatergic NMDA receptors in the early development of the central nervous system are decisive for subsequent<br />
development of psychosis, which often does not manifest itself until adulthood. Chronic administration of NMDA (not applicable<br />
in humans) antagonists initializes a number of adaptation mechanisms, which correlate with findings obtained in patients with<br />
schizophrenia; therefore, this animal model is necessary for research into the pathophysiology of this disease.<br />
This work was supported by project 1M0517 from the MEYS Czech Republic<br />
Key words: Schizophrenia, models, NMDA receptors, ketamine, glutamate, neurodevelopment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S49<br />
S49
Abstracts of the Invited Speakers<br />
[JS-07]<br />
Canadian College of Neuropsychopharmacology<br />
Symposium title: Advances in psychotropic drug development: Promising novel targets and agents for psychiatric disorders<br />
Recent advances in the neurochemistry of schizophrenia and potential targets for<br />
antipsychotic drug development<br />
Serdar Dursun, Glen Baker, Marnie Mackay<br />
Neurochemical Research Unit, University of Alberta, Edmonton, Canada<br />
E-mail: Dursun@ualberta.ca<br />
The dopamine hypothesis of schizophrenia has been a major influence for many years in stimulating research in schizophrenia<br />
and in assisting in the development of antipsychotic drugs. However, it has become obvious that other neurotransmitters and/or<br />
neuromodulators must also be involved. The antipsychotic drugs currently available are far from ideal and there is an urgent need to<br />
continue to search for new targets for potential antipsychotics.<br />
Much of the recent research on non-dopaminergic systems has focused on the amino acids glutamate and GABA, with the bulk of<br />
the results suggesting hypofunction of both in schizophrenia. Glutamate does not pass the blood-brain barrier readily and studies<br />
conducted to develop drugs that act at one or more of its multiple receptors have not, to our knowledge, yet produced potential new<br />
effective antipsychotics. Two other amino acids, glycine and D-serine, co-agonists at the NMDA glutamate receptor, have received<br />
considerable attention, and administration of these amino acids, usually in conjunction with currently available antipsychotics, have<br />
been reported in some studies to result in improvement of some symptoms of schizophrenia. However, these amino acids have to<br />
be administered in relatively high doses which may result in side effects such as peripheral neuropathies. There is now a great deal of<br />
interest in testing drugs that inhibit their uptake by neurons and/or glial cells (astrocytes and activated microglia), thus making increased<br />
levels of these amino acids available to interact with the NMDA receptor or, particularly in the case of D-serine, altering metabolism<br />
of the amino acid. This research also emphasizes the importance of glial cells. Microglia are also involved in immune responses and<br />
when activated release a number of proinflammatory cytokines that can result in some behavioural, cognitive, and neuroendocrine<br />
changes characteristic of schizophrenia. It is also of interest that there is now research indicating that there may be a dysfunction of<br />
oligodendrocytes and myelination problems in schizophrenia. Another exciting area of research with regard to schizophrenia is in<br />
the study of neuroactive steroids, rapid acting steroids which can act as positive or negative allosteric modulators at several types of<br />
neurotransmitter receptors, most notably GABA-A receptors and NMDA receptors. Plasma levels of several of these steroids are altered<br />
in a number of psychiatric disorders, including schizophrenia and some clinical studies suggest that pregnenolone may be a useful<br />
adjunctive agent in schizophrenia. Brain levels of some of these steroids have also been reported to be altered in laboratory animals<br />
following administration of currently available antipsychotics.<br />
In addition to the compounds mentioned above, potential interventions which may be added to the usual antipsychotic treatments<br />
include lamotrigine and minocycline. Furthermore, modulation of the nitric oxide pathway continues to gain considerable interest as a<br />
possible therapeutic target in the treatment of schizophrenia. We will report the results of an RCT double-blind crossover study on the<br />
addition of L-arginine, the precursor amino acid for nitric oxide, to usual treatment with antipsychotics in schizophrenic patients.<br />
Key words: Schizophrenia, antipsychotic development, glutamate, nitric oxide, D-serine, glycine, glia, neuroactive steroids<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S50<br />
Advances in antidepressant targets and drug development<br />
Glen B. Baker, Nicholas D. Mitchell, Jean Michel Le Melledo, Serdar Dursun<br />
Department of Psychiatry, University of Alberta, Edmonton, AB, Canada<br />
E-mail: glen.baker@ualberta.ca<br />
The biogenic amine hypothesis of depression, which suggests that depression is the result of a functional deficiency of noradrenaline<br />
(NA) and/or serotonin (5-hydroxytryptamine, 5-HT) at certain synapses in the brain, has had a major influence on research into the<br />
neurochemistry of depression for over fifty years, and most of the antidepressants currently available have an effect on one or both of<br />
these biogenic amines. However, it was obvious early on that other neurotransmitters or neuromodulators must also be involved, and the<br />
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Abstracts of the Invited Speakers<br />
search continues for other targets that may give clues for the development of future antidepressant drugs that are effective in a greater<br />
number of depressed patients, are faster acting and have an improved side effect profile over those currently available. Some of those<br />
targets will be discussed in this overview.<br />
The amino acids γ-aminobutyric acid (GABA) and glutamate are major inhibitory and excitatory neurotransmitters, respectively in the<br />
brain, and a delicate balance between them must be maintained for normal brain function. Research on GABA at the animal model and<br />
clinical levels implies a GABAergic deficit in depression, and animal studies and the rapid antidepressant action of intravenous ketamine<br />
in human subjects suggest hyperglutamatergia in depression, although the results of some neuroimaging studies to date do not seem<br />
to support these ideas. In recent years, there has been a great deal of interest in the possible roles of neuroactive steroids (rapid acting<br />
neurosteroids which can act as positive or negative modulators of a number of neurotransmitter receptors, most notably GABA-A and<br />
NMDA glutamate receptors) in the etiology and pharmacotherapy of depression. Allopregnanolone has received particular attention<br />
in this regard. Several researchers have proposed that the hypothalamic-pituitary-adrenal (HPA) axis plays a central role in the etiology<br />
of depression and there has been considerable interest in corticotropin-releasing hormone (CRH) receptor antagonists as potential<br />
antidepressants. The peptide substance P acts on neurokinin 1 (NK1) receptors, and there is ongoing interest in NK1 receptor antagonists<br />
as potential antidepressants. The role of the immune system in depression has been the focus of considerable research and it has been<br />
proposed that excessive proinflammatory cytokines (which are released by activated microglia) may result in depressive symptoms; it<br />
is of interest that such cytokines can activate CRH release and reduce levels of 5-HT in the brain. Although there are some contradictory<br />
results, several studies suggest that antidepressants increase expression of cyclic AMP-regulated element-binding protein (CREB) and<br />
brain-derived neurotrophic factor (BDNF). Dysfunction of melatonin secretion in depression has been suggested and this may account,<br />
at least in part, for sleep disorders experienced by many depressed subjects. Agomelatine, a melatonin receptor agonist and 5-HT2C<br />
receptor antagonist, is now marketed as an antidepressant. The potential interactions of several of the targets mentioned above will be<br />
discussed.<br />
Acknowledgements: The authors are grateful to the Canadian Institutes of Health Research (CIHR), the Canada Research Chairs program<br />
and the University of Alberta for Funding.<br />
Key words: Antidepressants, biogenic amines, GABA, glutamate, HPA axis, CRH, substance P, neuroactive steroids, glia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S50-1<br />
SYMPOSIA<br />
[PS-01]<br />
Symposium Title: Epigenetics or genetics: Gene-environment interactions over the life - span<br />
Alzheimer’s disease: Genes and/or life style<br />
Engin Eker<br />
Istanbul University, Cerrahpaşa School of Medicine, Department of Psychiatry<br />
E-mail: enginekertr@yahoo.com<br />
A number of genetic risk factors have been identified, but only a small proportion of Alzheimer’s disease (AD) cases can be explained by<br />
specific gene mutations. Several genetic risk factors have been linked to AD. Mutations in APP, PS1, and PS2 genes have consistently been<br />
associated with early-onset familial Alzheimer’s disease (FAD). A majority of AD cases manifest as sporadic late onset form (LOAD) typically<br />
with onset above the age of 65 years. Most people who develop Alzheimer’s are diagnosed after age 80. More recently a large number<br />
of genes have been implicated as a risk to LOAD, but only a few of these associations have been replicated such as the gene encoding<br />
for the APOE4 allele or loci in the clusterin (CLU), phosphatidylinositol binding clathrin assembly protein (PICALM), and complement<br />
receptor1 (CR1).<br />
Most diseases of aging are influenced by gene-environment interactions. AD has both genetic and environmental risk factors. The genetic<br />
susceptibility influenced by genes like ApoE4 are factors to be aware of, but perhaps more important are the environmental risk factors.<br />
Environmental risk factors can act as triggers in the expression of gene potential. Numerous studies indicate that ApoE4 carriers may be<br />
more vulnerable to environmental factors.<br />
Recent studies have shown that dietary factors, such as exposure to a Mediterranean diet, fish and high omega-3 diets, cigarette<br />
smoking, head trauma, infections, systemic inflammation, and metal exposure can significantly alter an individual’s risk of developing<br />
AD. On the other hand psychosocial factors such as education, social network, leisure activities and physical activity, chronic stress, and<br />
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Abstracts of the Invited Speakers<br />
depression also seem to be connected to the risk of developing AD. There are some somatic factors that are under the direct influence of<br />
environmental exposures, such as blood pressure, obesity, diabetes mellitus, cardio- and cerebrovascular diseases, and hyperlipidemia,<br />
have additionally been implicated in AD etiology.<br />
Key words: Alzheimer’s disease, genes, environmental risk<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S51-2<br />
[PS-02]<br />
Symposium Title: Behavioral addictions and treatments: Review of recent data<br />
From Don Juanism and nymphomania to hypersexual disorders<br />
Sultan Doğan<br />
Namik Kemal University, School of Medicine, Department of Psychiatry<br />
E-mail: sultandogan@yahoo.com<br />
Hypersexual Disorder is proposed as a new psychiatric disorder for consideration in the sexual disorders section of the DSM-V. Historically,<br />
excessive sexual behaviors were clinically documented by diverse clinicians such as the 19th century Western European pioneer sexologists<br />
Richard von Krafft-Ebing (1840–1902), Havelock Ellis (1859–1939), and Magnus Hirshfeld (1868–1935). Benjamin Rush(1745–1813), a<br />
physician and founding father of the United States (Rush, 1746-1813) also studied the same subject. These clinicians and investigators<br />
described a frame of persistent socially deviant sexual behaviors as well as clinical examples of males and females whose nonparaphilic<br />
(i.e., normophilic) sexual appetite was excessive and maladaptive. The clinical examples of such appetitive behaviors described by these<br />
investigators were precursors to the 20th century characterization of protracted promiscuity as Don Juanism (Stoller, 1975) or satyriasis<br />
(Allen, 1969) in males and nymphomania (Ellis & Sagarin, 1965) in females. The DSM-II (American Psychiatric Association, 1968) recognized<br />
sexual deviations as personality disorders but there was no mention of excessive or maladaptive nonparaphilic sexual behavior disorders.<br />
By 1980, the DSM-III (American Psychiatric Association, 1980) classified paraphilic disorders as distinct pathologies (Psychosexual<br />
Disorders) and a residual diagnostic category, Psychosexual Disorder Not Otherwise Specified included ‘‘distress about a pattern of<br />
repeated sexual conquests with a succession of individuals who exist only as things to be used (Don Juanism and nymphomania)’’. In the<br />
DSM-IV (American Psychiatric Association, 1994) and its text revision, DSM-IV-TR (American Psychiatric Association, 2000), the original<br />
DSM-III characterization of these behaviors was reestablished. Sexual Disorders Not Otherwise Specified (302.9) included a condition<br />
characterized by: ‘‘distress about a pattern of repeated sexual relationships involving a succession of lovers who are experienced by<br />
the individual only as things to be used’’. Until recently, authors have used different terms for hypersexual disorders, such as “sexual<br />
addiction” (Carnes), “paraphilia-related disorders and non-paraphilic hypersexuality” (Kafka), “excessive sexual desire disorders” (Marshal),<br />
“problematic hypersexuality” (Finlayson) and “compulsive sexual bahavior” (Cooper and Coleman). These disorders were described as<br />
markedly increased expressions of culturally normative sexual desire (fantasies, urges, and behaviors) persisting for a minimum duration<br />
of 6 months and associated with clinically significant personal distress, impairment in reciprocal romantic relationships or other adverse<br />
psychosocial consequences. Thera are several form of hypersexual disorders such as compulsive masturbation, pornography dependence,<br />
telephone sex dependence, cybersex, severe sexual desire incompatibility, anonymous sex and multiple sexual partners (Coleman 1995,<br />
Carnes 2007, Kafka 2000, Kafka 2007, Cooper 2002, Cooper 2003).<br />
There are significant gaps in the current scientific knowledge base regarding the clinical course, developmental risk factors, family history,<br />
neurobiology, and neuropsychology of hypersexual disorder. As is true of so many psychiatric disorders, the comment that ‘‘more research<br />
is needed’’ is certainly applicable to these conditions. Although there are significant shortcomings in the state of our current empirical<br />
knowledge, there is little doubt that patients with such conditions commonly present to clinicians as well as to specialized treatment<br />
programs.<br />
Key words: Don Juanism, nymphomania, hypersexual disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S52<br />
S52 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Pathological gambling: review of recent data<br />
Ömer Şenormancı<br />
Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
E-mail: senorman_7@hotmail.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Gambling, which could also be defined as risking one’s chances for a possible outcome, is a cultural phenomenon as old as humanity. While<br />
gambling is a form of entertainment without any drawbacks for the great majority, pathological gambling develops in a small minority.<br />
The prevalence (0.2%- 5.3%) in the adult population is gradually increasing due to the ease of accessibility such as Internet gambling. This<br />
increase and the accessibility of gambling becoming easier, have led to some sociodemographic changes in the population who have<br />
trouble with gambling. Recent studies have shown pathological gambling to be higher in the psychiatric patient population compared<br />
to the normal population (with no assigned psychiatric diagnosis) and that it is necessary to be included as part of the questioning in a<br />
psychiatric evaluation.<br />
Some drugs once thought to be a new hope in the pharmacological treatment of pathological gambling, have been proven ineffective<br />
in recent randomized, double-blind, and placebo-controlled studies. Current studies are testing GABAergic and antiglutamatergic drugs,<br />
that are thought to be effective in chemical and behavioral addictions, in the treatment of pathological gambling.<br />
Two large meta-analysis studies have reported that non-pharmacological therapy approaches are more effective in the treatment<br />
of pathological gambling. Behavioral therapy, cognitive behavioral therapy and short, motivational, individualized approaches are<br />
demonstrated to be effective. Although it is suggested that behaviorial therapy + cognitive behavioral therapy and short, motivational,<br />
and individualized approaches are equally effective, combining the two may improve the efficacy of the treatment. This presentation aims<br />
to describe pathological gambling accompanied by contemporary information with respect to treatment.<br />
Key words: Pathological gambling, impulse control disorder, pharmacotherapy, psychotherapy<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S53<br />
Is binge eating a type of addiction?<br />
Fulya Maner<br />
Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
E-mail: fmaner@ttmail.com<br />
Binge eating is characterized by recurrent episodes of eating, in a discrete period of time, an amount of food that is much larger than most<br />
people would eat in a similar time period under similar circumstances. There is a sense of lack of control over eating during the episode.<br />
Eating is much more rapid than normal and one eats until feeling uncomfortably full. After overeating one feels disgusted, depressed or<br />
guilty. Binge eating disorder is included in eating disorders not elsewhere specified in the DSM-IV and is a symptom of bulimia nervosa<br />
and anorexia nervosa.<br />
Research has shown that patients with eating disorders have high rates of co-occuring substance use disorders. The substance of abuse<br />
and food appear to compete for sites in the brain and abstinence from substance use causes craving for the substance and also for food.<br />
Addictions involving food and substances share similar etiologies and behavioral symptoms. Individuals suffering from binge eating<br />
disorder are more likely to have first degree relatives with a substance abuse disorder. According to retrospective reports of patients,<br />
the initiation of disordered eating usually began before substance abuse. The general reward pathway includes the ventral tegmental<br />
area and basal forebrain. Substance abuse has been shown to change the neural processes around these connections. The mesolimbic<br />
dopamine system connects the ventral tegmental area to the basal forebrain and is critical for the self-administration of psychomotor<br />
stimulants. Dopamine deficiency has been suggested to be a common characteristic of individuals who are prone to substance or food<br />
addiction. Striatal dopamine receptor (DRD2) availability is significantly lower in obese individuals than in controls. Body mass index is<br />
shown to correlate inversely with measures of D2 receptors.<br />
Functional neuroimaging studies have revealed that pleasant smelling, looking, and tasting food has reinforcing characteristics similar<br />
to drugs of abuse. Many of the brain changes reported for hedonistic eating are also seen in various types of addiction. Overeating may<br />
have an acquired drive similar to drug addiction with respect to motivation and incentive craving. In both cases, the desire and continued<br />
satisfaction occur after early and repeated exposure to stimuli.<br />
Addictive behavior manifests itself in permanent preoccupation with food and eating, withdrawal symptoms, continuation of disturbed<br />
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Abstracts of the Invited Speakers<br />
eating behavior in spite of negative consequences, loss of control, and frequent relapse.<br />
Human and animal studies have demonstrated that in some brains the consumption of sugar-rich foods or drinks primes the release of<br />
euphoric endorphins and dopamine within the nucleus accumbens, in a manner similar to some drugs of abuse. The neurobiological<br />
pathways of drug and “sugar addiction” involve similar neural receptors, neurotransmitters, and hedonistic regions in the brain. Craving,<br />
tolerance, withdrawal, and sensitization have been documented in both human and animal studies. In addition, there appears to be cross<br />
sensitization between sugar addiction and narcotic dependence in some individuals There also appears to be some common genetic<br />
markers between alcohol dependence, bulimia, and obesity, such as the A1 allele gene and the dopamine 2 receptor gene.<br />
Key words: Binge eating, eating disorder, addiction<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S53-4<br />
[PS-03]<br />
Symposium Title: Painful syndromes in psychiatry and their managements<br />
Pain and personality<br />
Mehmet Ak<br />
Department of Psychiatry, Gulhane School of Medicine, Ankara, Turkey<br />
E-mail: drmehmetak@gmail.com<br />
There is a dynamic two-way interaction between pain and personality and the psychophysiology and anatomy of this relationship are<br />
not elucidated fully. Is there a specific personality type of pain or do some people perceive and express pain more than others? Probably<br />
there is no clear answer to this question. So far chronic pain has been shown to affect personality, as indicated by studies using Cloninger’s<br />
Temperament and Character Inventory. A relationship has been demonstrated between some personality traits and pain. In studies that<br />
reported the prevalence of personality disorders, associations with chronic pain vary between 31% to 81%. The most frequently identified<br />
personality trait is one with paranoid features.<br />
Today I will talk mainly about studies using Cloninger’s model, because Cloninger’s integrative psychobiological approach provides a<br />
flexible framework for both clinical assessment and treatment planning. The most significant and consistent result of these studies was<br />
elevated harm avoidance scores. Harm avoidance scores still remain high even after controlling for the effect of depression and anxiety.<br />
Thus this temperament dimension is possibly an important state and trait feature for development of psychosomatic illnesses. These<br />
findings also confirmed that serotonergic systems are involved in the process of psychosomatic organization. Cloninger described that<br />
people with chronic anxiety, avoid harm that is characterized by more pain, are difficult to calm, tire easily, and display specific signs<br />
based on specific anticipatory anxiety. Harm avoidance refers to an inherited tendency to block the behavior in the answers given to the<br />
blocking, non-rewarding, and punishment signals. High harm avoidance behavior is observed in the form of social withdrawal, becoming<br />
tired easily, staying away from strangers, fear of uncertainty, and being pessimistic that there would be some problems in a situation even<br />
when others do not worry.. These people are timid, passive, insecure, and pessimistic individuals.<br />
Looking at the size of the character, it is seen that low self-directedness scores are the most common finding. The original meaning of<br />
self-directedness is in accordance with choosing goals and values of the individual, optimization of the behavior to maintain a situation,<br />
editing capabilities, and being strong-willed.<br />
Individuals with low self-directedness do not expect to be able to control and positively influence an aversive situation and overcome<br />
obstacles. Self-directedness is closely related to the concept of self-efficacy. Self-efficacy is defined as the personal conviction that one<br />
can successfully show problem-solving behavior in a given situation. There is much evidence which suggests that low self-efficacy plays<br />
an important role in pain control, coping with disability, and treatment outcome. Our clinical experiences show that pain can sometimes<br />
be the symbol of help, sometimes the quest for attention, and other times problems that can not be expressed. Emotions that are not<br />
expressed can mean pain and unexpressed emotions can be the cause of pain for some people that do not heal. In order to understand<br />
and to treat these people, employing a holistic assessment and approach are very important.<br />
Key words: Character, pain, temperament<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S54<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
The differences between SSRIs and SNRIs in the treatment of psychiatric pain syndromes<br />
Abdurrahman Altındağ, Gülçin Elboğa<br />
Gaziantep University, Medical School, Department of Psychiatry, Gaziantep, Turkey<br />
E-mail: draltindag@yahoo.com, aaltindag@yahoo.com<br />
The occurrence of depression with physical symptoms and pain is common. On the other hand, comorbid depression is also common<br />
in chronic pain syndromes. Antidepressants are effective in the treatment of psychological and physical symptoms of depression and<br />
chronic pain symptoms of non-depressed patients.<br />
It is not well described how antidepressants relieve the pain. However, it is suggested that this effect is related to serotonin and<br />
noradrenaline. Analgesic effects of antidepressants are independent from their effects on the mood. Antidepressants which have effects<br />
on both serotonin and noradrenaline are more effective than those with effects on one of these neurotransmitters in the treatment of<br />
depression and comorbid pain syndromes. Tricylic antidepressants (TCAs) have serotoninergic and noradrenergic effects. Therefore, they<br />
are superior to monoaminergic antidepressants, such as SSRIs, with regard to analgesic and antidepressant effects. The usage of TCAs is<br />
limited because of their safety profile and side effects. SNRIs have similar analgesic effects to TCAs. On the other hand they have lower<br />
side effects and a better safety profile. Additionally, SNRIs are more effective than SSRIs in the treatment of physical pain syndromes. SNRIs<br />
have a similar safety profile to SSRIs and almost similar costs to the older agents.<br />
Better diagnosis and treatment of pain symptoms, which are strong indicator of depressive relapses, will provide better quality of life and<br />
productivity in patients with depressive disorders.<br />
Key words: SSRI, SNRI, pain<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S55<br />
How does alexithymia lead to painful syndromes?<br />
Hüseyin Güleç<br />
Erenkoy Psychiatry Hospital, Istanbul, Turkey<br />
E-mail: huseyingulec@yahoo.com<br />
Several studies have focussed on defining the network of brain structures involved in pain. Pain perception (sensory discriminative,<br />
affective/emotional, cognitive/evaluative) has been shown to depend on different areas of the brain. Modern neuroimaging methods<br />
have been used to determine whether different pain symptoms involve similar brain structures. These studies indicated that acute<br />
physiological pain and neuropathic pain have distinct although overlapping brain activation patterns, but that there is no unique pain<br />
matrix/allodynia network.<br />
Several contemporary neuroscientists and cognitive scientists make a similar distinction between emotions as bodily events and feelings<br />
as mental events and regard symbolization as an important element in the cognitive processing of emotions. Awareness of feelings,<br />
together with the thoughts, fantasies, and memories that they elicit, facilitates modulation of the emotional arousal induced by stressful<br />
events. Feelings are attributed to the symbolic representation in working memory of the activity of unconsciously operating subsymbolic<br />
systems that generate the brain states and bodily responses which comprise emotions. These representations become integrated with<br />
representations of past experiences and representations of the self. Attributing the feeling of specific basic emotions to ‘viscerosomatic<br />
self-representations’ in the lower levels of the brain, attributing reflective awareness and the capacity for experiencing higher-order<br />
feelings to linguistic symbolizations and an ability to think in perceptual images is important for the parsing and regulation of emotional<br />
states.<br />
According to Lumley alexithymia is associated with tonic physiological hyperarousal, certain types of unhealthy behavior, and a biased<br />
perception and reporting of somatic sensations and symptoms. Alexithymia probably influences illness behavior, but there is little<br />
support for the hypothesis that alexithymia leads to chronic organic disease. Alexithymia links with physical illness due to four possible<br />
pathways: a) alexithymia leads to organic disease through physiological or behavioral mechanisms, b) alexithymia leads to illness behavior<br />
through cognitive or social mechanisms, c) physical illness leads to alexithymia, and d) both alexithymia and physical illness result from<br />
sociocultural or biological factors. Research on the effects of emotional trauma resulted in the hypothesis that traumatic experiences in<br />
childhood or adult life may have adverse consequences for physical health. It has been shown that there is evidence of a correlational<br />
association between childhood trauma and somatization in adulthood, and several retrospective studies with very large samples have<br />
S55
Abstracts of the Invited Speakers<br />
demonstrated an association between childhood trauma and the development of somatic disease in adult life. An unanswered question<br />
is: what are the psychological/biological mechanisms that might render trauma in earlier years a risk factor for the development of disease<br />
later in life? The associations between alexithymia, somatization, dissociation and trauma, have led to the suggestion that dissociation<br />
acts as a defense against emotionally distressing memories that are associated with the traumatic avents. Attachment insecurity and<br />
associated deficits in affect development and affect regulation are linked not only to the experience of being raised by parents with<br />
impaired capacities for mentalization, but sometimes also to more severe developmental traumas. Dissociation within emotion schemas<br />
is initially an adaptive response to external danger arousal and is especially severe when the child experiences the parent as a threat, for<br />
then there is no safe place to be.<br />
Key words: Alexithymia, cognitive processing of emotions, trauma, attachment, mentalizing, somatization<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S55-6<br />
Hypnotherapy for painful syndromes in psychiatry<br />
Kerem M. Doksat<br />
MD, Professor of Psychiatry, POLIMED Psychiatric Center<br />
E-mail: doksat@tnn.net, doksatster@gmail.com, doksat@superonline.com<br />
Hypnosis is a misnomer first used by Scottish Surgeon James Braid for a phenomenon probably as ancient as mammalian history. After the<br />
Austrian Neuropsychiatrist Sigmund Freud has fouled hypnosis in order to glorify his own theory, especially American Psychiatrist Milton<br />
Hyland Erickson rebuilt the reputation of hypnosis (1).<br />
In 1846, James Esdaile successfully performed 345 major operations by using mesmeric method in India. English surgeon John Ellitson<br />
mentioned similar success in many operations in 1843. With the introduction of ether in 1846 and chloroform in 1847, the mesmeric<br />
method, which has already serious oppositions, was forgotten. Hypnosis may be used alone or in combination with other methods. Its<br />
use in cancer pain, especially during the terminal phase, may reduce the requirement for opioids, or even totally eliminate them. Hypnosis<br />
may help the patients to experience with their consciousness fully open and free from side-effects like grogginess of the opioids during<br />
last phase before their terminal coma. It can be used in burns and for pain free labor. In dentistry it can be used for analgesia, dentists’<br />
chair phobia, and getting rid of gag reflex. It is effective in 30 to 50 percent of phantom limb pain cases.<br />
Hypnosis is reported to be effective for the treatment of migraine and other headaches and in many other pain syndromes; I also have a lot<br />
of anecdotal evidence. The approach should be adjusted for the patient; the skill and experience of the hypnotist, his or her relationship<br />
with the patient and the patient’s personal characteristics and preferences must be adjusted according to all of these. Indeed, hypnotic<br />
procedures may help people who are not much hypnotizable. For example, in cases experiencing both pain and tension intensively, even<br />
induction of relaxation reduces pain and in many of the hypnotic procedures, relaxation is utilized. If the patients cooperate well and<br />
accepts the procedure seriously, even if they are not hypnotizable, they may practice the hypnotist’s relaxation suggestions with success<br />
while sitting or lying comfortably (2).<br />
The principal techniques are (2,3): 1) Direct suggestion, 2) Utterance of neurophysiological metaphors, 3) Glove anesthesia replacement<br />
technique, 4) Replacement pain symptom’s site or differentiating the pain symptom, 5) Dissociation by using the imagination, 6)<br />
Technique of different interpretation of pain, 7) Auto-hypnosis (self-hypnosis).<br />
As a summary, the effect of hypnosis on pain is mediated by two mechanisms:<br />
1) Muscle relaxation,<br />
2) Change in perception and cognitive distraction.<br />
Hypnotherapy can be effective in many painful syndromes if suitable patients are chosen. Group psychotherapy and hypnosis can be<br />
effective in the treatment of cancer patients’ pain (4).<br />
References:<br />
1. Doksat R. Tatbikatı ve Nazariyatı ile Hipnotizma. İstanbul: Kader Basımevi, 1962. 253-281.<br />
2. Doksat MK. Ağrı ve Psikiyatri. Bursa: Psikiyatri ve Sanat Yayın Evi, 2003. 165-172.<br />
3. Arred Barabasz, Johnn G Watkins Hypnotherapeutic Techniques 2E. New York: Brunner-Routledge. 2005. 219-239.<br />
4. Porter LS, Keefe FJ. Psychosocial issues in cancer pain. Curr Pain Headache Rep. 2011 Aug;15(4):263-70.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S56<br />
S56 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
[PS-04]<br />
Symposium Title: Adult attention - deficit hyperactivity disorder (ADHD) and comorbidity<br />
ADHD and mood disorders in children<br />
Rasim Somer Diler<br />
Department of Psychiatry, University of Pittsburgh, PA, US<br />
E-mail: dilerrs@yahoo.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Five to 40% of children and adolescents with attention deficit hyperactive disorder (ADHD) also have comorbid major depressive disorders<br />
(MDD). Moreover, youths with ADHD have up to a 4 times higher risk of developing depressive disorders than the general adolescent population.<br />
Comorbidity with MDD has been associated with elevated impairment and higher rates of hospitalization versus ADHD alone. However,<br />
depression in youths with ADHD may be more difficult to diagnose, given that some symptoms overlap between the two disorders. Moreover,<br />
many of the medications used to treat ADHD cause side effects resembling symptoms of MDD. Available studies suggest the particular<br />
importance of anhedonia, social withdrawal, psychomotor retardation, negative views of self and future, and suicidal thoughts as symptoms that<br />
distinguish MDD in youths who have ADHD. Despite ongoing controversy, the view that pediatric bipolar disorder (PBD) is rare or non-existent<br />
has been increasingly challenged not only by case reports but also by systematic research; however, a significant portion of bipolar youth,<br />
especially children, have high comorbidity with ADHD. Significant debate exists on whether early onset bipolar disorder is mistakenly attributed<br />
to attention deficit hyperactivity disorder (ADHD), or whether ADHD is frequently misdiagnosed as mania. Among pediatric-onset cases of<br />
bipolar disorder, comorbid ADHD is frequently seen, and there is strong evidence to suggest that this pattern has a familial and genetic basis.<br />
Differentiating bipolarity in children with ADHD is not an academic discussion but also a great concern because of the associated complication of<br />
the treatment of these disorders. It is suggested that manic symptoms should represent a distinct change from a child’s usual level of functioning<br />
(e.g., change or worsening of distractibility during a mood episode in children with ADHD). There are some symptoms that mainly occur in BD<br />
youth as compared to other disorders (e.g., ADHD) and may help to differentiate between BD and these disorders, such as clinically relevant<br />
euphoria, grandiosity, decreased need for sleep, hypersexuality (without history of sexual abuse or exposure to sex), and hallucinations. We need<br />
larger longitudinal studies to better understand the risks and resilience factors of developing BP in ADHD youth.<br />
Key words: ADHD, depression, bipolar, child<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S57<br />
Academic and occupational problems in ADHD<br />
Mücahit Öztürk<br />
PEDAM Psikiyatri Merkezi, İstanbul, Turkey<br />
E-mail: mozturkpdm@gmail.com<br />
Attention Deficit Hyperactivity Disorder (ADHD) is a syndrome of inattention, hyperactivity, impulsiveness and other deficits of<br />
executive functions. It’s now well known that ADHD often continues into adulthood (1, 2). ADHD is a chronic disorder which leads to a<br />
negative impact on functioning throughout the life cycle (3). Children with ADHD are at significant risk of multiple forms of adolescent<br />
maladjustment. Approximately up to 60% of childhood cases continue symptomatic into adulthood. In the remaining 40 percent<br />
symptoms may remit in early adulthood (4). The manifestation of ADHD changes over the course of life. In some cases the hyperactivity<br />
may disappear but decreased attention span and impulse control problems persist (5).<br />
Approximately 1 in 25 adults have ADHD, 90% of whom may be currently untreated, with a potentially negative impact on the lives of<br />
patients and their families (6). Significant legal, academic, social, and occupational problems have been observed in adults with ADHD (7).<br />
Follow up studies suggest that up to 33% of ADHD teens versus 1% to 9% of controls drop out high school. Children with ADHD are at<br />
risk of negative academic outcomes. ADHD and similar problems entail a risk of underachievement at school. The results indicate that<br />
students with ADHD underachieve in the school situation in relation to their optimal cognitive capacity (3).<br />
Adolescents with ADHD complete less education by 2-3 years and demonstrate lower occupational performance at the age of 25 years. Adults<br />
with ADHD may struggle with frequent job changes, frequent partner changes, higher rates of divorce, increased motor vehicle accidents,<br />
poor money management and higher rates of unwed pregnancy (8). Although their educational performance is lower than people without<br />
ADHD, their early employment histories don’t differ from those people with similar education (5). Adolescents with ADHD were more likely<br />
to smoke cigarettes and use illicit drugs. Their academic attainment was below age norms with more than one fourth repeating grades (9).<br />
S57
Abstracts of the Invited Speakers<br />
Studies show that effective treatment significantly improves quality of life (3). Severity of childhood ADHD and treatment significantly<br />
predict the persistence of ADHD into adulthood (5). As previously shown by some research for children and adolescents, stimulant<br />
medications alone did not eliminate the academic achievement deficit of ADHD undergraduates. ADHD patients who were treated with<br />
stimulants were significantly less likely to subsequently develop depressive and anxiety disorders and disruptive behavior and less likely to<br />
repeat a grade compared with participants with ADHD who were not treated. Adolescents with ADHD were also significantly more likely<br />
to be absent during the academic year, and they were over eight times more likely than adolescents without ADHD to drop out of high<br />
school. These findings demonstrate that children with ADHD continue to experience severe academic impairment into high school (10).<br />
Key words: Attention deficit hyperactivity, academic performance, occupation<br />
References:<br />
1. Barkley RA. Major life activity and health outcomes associated with attention-deficit / hyperactivity disorder. J. Clin Psychiatry 2002;63 12:10-15.<br />
2. Weiss G, Hechtman L. Hyperactive Children Grown Up: ADHD in Children, Adolescents, and Adults. New York, NY: Guilford Press; 1993<br />
3. Cheng K, Myers KM, Stubble DE. Attention deficit hyperactivity disorder Child and Adolescent Psychiatry The Essentials Lippincott Williams &Wilkins<br />
4. Biederman J, Mick E, Faraone SV. Age dependent decline of symptoms of attention deficit hyperactivity disorder: Impact of remission definition and symptoms<br />
type. Am J Psychiatry 2000 157:816-818<br />
5. Sadock BJ, Sadock VA. Textbook of Child and Adolescent Psychiatry. 2009 Lippincott Williams &Wilkins<br />
6. Culpaper L, Mattingly G. Challenges in Identifying and Managing Attention-Deficit/Hyperactivity Disorder in Adults in the Primary Care Setting: A Review of the<br />
Literature Prim Care Companion J Clin Psychiatry 2010 v. 12(6);<br />
7. McCann BS, Roy-Byrne P Attention-deficit/hyperactivity disorder and learning disabilities in adults. Semin Clin Neuropsychiatry. 2000 Jul;5(3):191-7.<br />
8. Spetie L, Arnold EL. Attention deficit hyperactivity disorder in Lewis Child and Adolescent Psychiatry A Comprehensive Textbook 2007 Lippincott Williams &Wilkins<br />
9. Lam AK, Ho TP Early adolescent outcome of attention-deficit hyperactivity disorder in a Chinese population: 5-year follow-up study. J Fam Pract. 2011 Jun;60(6):364-7.<br />
10. Kent KM, Pelham WE Jr, Molina BS, Sibley MH, Waschbusch DA, Yu J, Gnagy EM, Biswas A, Babinski DE, Karch KM.The academic experience of male high school<br />
students with ADHD.Pediatrics. 2009 Jul;124(1):71-8.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S57-8<br />
[PS-05]<br />
Symposium Title: Brain mapping, TMS, NVS, biofeedback and deep brain stimulation in treatment of psychiatric disorders<br />
Concomitant use of qEEG and rTMS in treatment of depressive disorder, new approaches<br />
Nevzat Tarhan, Gökben Hızlı, Serap Aydın<br />
Üsküdar University, Neuropsychiatry Istanbul Hospital, Istanbul, Turkey<br />
E-mail: ntarhan@uskudar.edu.tr, ntarhan@gmail.com<br />
Repetitive transcranial magnetic stimulation (rTMS) therapy has been approved for treatment of depression by the FDA in 2008, and was<br />
included in APA Guidelines as published in October, 2010 issue of American Journal of Psychiatry. Although its efficacy is not as high as<br />
the efficacy of ECT, rTMS is safer in the treatment of depression in older patients. Especially the absence of common treatment side effects<br />
of ECT, such as confusion and memory problems, makes rTMS treatment more valuable in patients with high side effect risk.<br />
This study was performed by the quantitative EEG (qEEG) monitoring before and after rTMS treatment. The aim was to examine the<br />
predictive value of qEEG as a biological indicator of response to rTMS treatment.<br />
In Neuropsychiatry Istanbul Hospital, between dates of 2006-2010, rTMS had been applied to 1283 patients with a diagnosis of treatmentresistant<br />
depressive disorder. The patients discontinued the psychotropic medications 12 hours before the qEEG monitoring. qEEG records were<br />
taken just before the first and the last rTMS sessions. HAM-D 17 was performed before and after 15-20 (mean was 18) sessions of rTMS treatment.<br />
The patients with a medical history of epilepsy were excluded. The cases with no history of seizures, but with suspicious epileptical<br />
abnormality in pre-treatment EEG were included with special medical caution. rTMS treatment was performed at left DLPFC, as 25 hz. and<br />
1000 pulse, one session on each day, a total of 15-20 sessions, with Magstim Rapid.<br />
From 1283 cases, one patient had epileptic seizure as an adverse effect. Due to contraction of facial muscles, one patient had a broken<br />
tooth. In 3 patients suffering from tinnitus occurred, but later tinnitus decreased significantly.<br />
The statistical analyses of the cases are ongoing. The initial results with remission and response rates will be presented. qEEG power<br />
spectrum changes and changes in the activation compared to normative data base in LORETA will be evaluated.<br />
Key words: Repetitive transcranial magnetic stimulation (rTMS) therapy, quantitative EEG, depression treatment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S58<br />
S58 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
What does transcranial magnetic stimulation (TMS) promise in psychiatric disorders other than<br />
depression? Future perspectives<br />
Bahadır Bakım<br />
Sisli Etfal Research and Teaching Hospital, Psychiatry Clinic, Istanbul, Turkey<br />
E-mail: bbakim@yahoo.com<br />
Up to 40% of OCD patients fail to respond satisfactorily to generally adequate treatment options, and 10% cannot be helped at all. Because OCD<br />
may be related to increased neural activity in prefrontal subcortical circuits, the inhibitory effect of rTMS was hypothesized to be beneficial in OCD<br />
treatment. rTMS has recently demonstrated remote effects, with left prefrontal stimulation inducing changes in cerebral perfusion in the bilateral<br />
anterior cingulate and orbitofrontal cortex. In conclusion, in open-label studies, high-frequency rTMS of the right and/or left DLPFC appears to<br />
be effective in reducing obsessive-compulsive symptoms. However, this could not be replicated in double-blind, sham-controlled studies. As the<br />
efficacy of rTMS is often time limited, the necessity of a second rTMS after several weeks should be investigated and functional MRI studies of rTMS<br />
in OCD are needed to clarify the specific stimulation region of rTMS. Otherwise, as the improvement of symptoms is often noted in sham settings,<br />
it would be interesting to investigate the neural underpinnings of the placebo effect caused by sham rTMS.<br />
Several initial studies on negative symptoms of schizophrenia have suggested that the condition seems to respond to high frequency (20 Hz, 10 Hz)<br />
repetitive transcranial magnetic stimulation (rTMS). Low frequency rTMS (
Abstracts of the Invited Speakers<br />
of patients with medication-refractory unipolar depression who have failed one good (but not more than one) pharmacological trial.<br />
Key words: Transcranial magnetic stimulation, depression, rTMS<br />
References:<br />
1. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimulation of human motor cortex. Lancet1985;1(8437):1106-7.<br />
2. Nivoli AM, Colom F, Murru A, Pacchiarotti I, Castro-Loli P, González-Pinto A, et al. New treatment guidelines for acute bipolar depression: A systematic review. J<br />
Affect Disord 2011; 129(1-3):14-26.<br />
3. Fitzgerald PB, Hoy K, McQueen S, Maller JJ, Herring S, Segrave R, et al. A Randomized Trial of rTMS Targeted with MRI Based Neuro-Navigation in Treatment-<br />
Resistant Depression. Neuropsychopharmacology 2009; 34(5):1255-62.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S59-60<br />
Vagus Nerve Stimulation (VNS) in depression treatment<br />
Şadiye Visal Buturak<br />
Department of Psychiatry, Kırıkkale University, Faculty of Medicine, Kırıkkale, Turkey<br />
E-mail: visalbuturak@hotmail.com<br />
Major Depressive Disorder (MDD) is a prevalent, chronic, recurrent and disabling disorder and it is predicted that MDD will be the second most common<br />
cause of incapacitating disease in 2020 (1). Although a broad range of effective treatments is available, a considerable proportion of patients do not<br />
respond adequately (2). Patients who have already experienced recurrent depressive episodes often relapse and do not achieve full remission despite<br />
treatment with conventional therapies (3). A need for the development of alternative treatments for treatment resistant depression (TRD) that are<br />
effective, have fewer side-effects or have longer-lasting antidepressant effects has been identified. Vagus nerve stimulation (VNS) therapy is a type of<br />
treatment where a small electrical pulse is administered through an implanted neurostimulator to a bipolar lead attached to the left vagus nerve (4).<br />
VNS was approved by the US Food and Drug Administration in 2005 for the adjunctive long-term treatment of chronic or recurrent depression for<br />
patients 18 years or older who are experiencing a major depressive episode (MDE) and have not had an adequate response to 4 or more adequate<br />
antidepressant treatments. The mechanism of action of VNS is not fully understood although emerging data suggest that VNS therapy modulates the<br />
function of neural structures implicated in depression and also influences monoaminergic neurotransmission (5). In a randomized sham-controlled<br />
trial, VNS only showed a response rate of 15.2% compared to 10% with sham treatment (p=0.251) during a 10 week trial (6). But most of the open-label<br />
studies about the short and long-term efficacy of the VNS in patients with TRD showed significant reductions in response and remission rates. Rush et<br />
al. examined the effect of VNS in adult outpatients with nonpsychotic, treatment-resistant major depressive or bipolar I or II (depressed phase) disorders.<br />
Response rates were 40% for the Hamilton Depression Rating Scale (HDRS) (7). In an open pilot study of VNS in outpatients with treatment-resistant<br />
MDEs the response rate was 30.5% for the primary HDRS (28) measure, after 10 weeks of VNS (p =.0057) (8). George et al. compared data from the 205<br />
patients who completed the 12-month naturalistic study that was done by Rush et al. (9) with a matched control group of 124 patients with TRD who<br />
received only treatment as usual (TAU). Response rates according to the HDRS (24) at 12 months were 27% for VNS+TAU and 13% for TAU (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
with the determination of disordered brain structures at the levels of neurons and neuronal populations in brain mapping by creating<br />
mathematical formulations and treatment. Psychosurgery aims to regain systematic and comprehensive brain functions via minimally<br />
invasive nondestructive neurosurgical applications. Psychosurgery is indicated for treatment-refractory major mental illnesses such as<br />
depression, obsessive compulsive disorder, schizophrenia and others. Neurostimulative methods are preferred to neuroablative methods.<br />
Neurons have highly complex morphological, electrophysiological, and biochemical properties as reflected in many psychomotor<br />
functions, continuation of mental homeostasis, repertoire of activity patterns and multiple signaling pathways. Morphologically,<br />
neurochemically and electrophysiologically heterogeneous neuron groups project to the cerebral cortex, deep brain structures, brain<br />
stem, spinal cord and autonomous ganglia. These highly complex ascending and descending pathways participate in different functions,<br />
including cognition, motivation, emotion, speech, calculation, memory and autonomic regulation.<br />
Disorders of neuronal populations can cause neuropsychiatric illnesses. Neurostimulative applications are the most useful treatment<br />
methods for intractable cases. However, in experimental studies, stem cells and teacher neurons specifically educated by computerised<br />
mediums have begun to be implantated into the brain for education and stimulation of dysfunctional neuron groups.<br />
Psychosurgery has been directed to neurocomputer interfacing technologies. Hybride neuroelectric devices, neuromimetic protheses,<br />
sonic and photonic multichip modules, biotic-abiotic neuromodulators, bio-robotics and reconfigurable neural nanodevices have shown<br />
promise for future excellent treatment strategies for mental illnesses.<br />
Key words: Psychosurgery, deep brain stimulation<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S60-1<br />
[PS-06]<br />
Symposium Title: Neuroimaging in psychopharmacology: An update<br />
What is the real meaning of ventricular enlargement in schizophrenia?<br />
Nazlı Buğçe Vedin Özçelik<br />
Department of Psychiatry, Ege University, Izmir, Turkey<br />
E-mail: bugcevedin@gmail.com<br />
Schizophrenia usually starts during adolescence or young adulthood but tends to persist throughout life. Even at the time that the<br />
concept of schizophrenia was first defined, it was thought to be a brain disease. Before the development of brain imaging techniques,<br />
post-mortem brain examinations were performed. It was reported that patients had frontal atrophy and less brain weight than the normal<br />
population. After the development of computed tomography and magnetic resonance imaging techniques, the number of the studies<br />
in this field increased.<br />
Structural MRI imaging studies indicated that brain abnormalities were present at the onset of the disease. One strong piece of evidence<br />
indicating that schizophrenia is a neurodevelopmental disorder derives from the fact that many types of brain abnormalities are present<br />
at the time of the first episode off illness. These include decreased cerebral size, decreased frontal and temporal lobe sizes, decreased<br />
thalamic size, decreases in gray matter and white matter volumes and enlargement of the ventricles. These findings support the likelihood<br />
that this illness arises because of aberrations in the complex neurodevelopmantal processes that modulate brain maturation during the<br />
adolescent and young adult period.<br />
Lateral ventricular enlargement is one of the most consistent findings in patients with schizophrenia. However whether progressive<br />
ventricular dilatation occurs during the course of the illness has been controversial. Some findings suggest that there is progressive<br />
ventricular enlargement with no significant effect of age of onset, duration of illness or age at the baseline scan. In some longitudinal<br />
studies there was evidence that negative symptoms have an association with increases in total CSF volume and in the ventricles as<br />
indicated by the ventricular–brain ratio. Patients who achieve longer periods of remission have less expansion of the CSF, although, some<br />
findings support the premise that there is a subgroup of patients with neuroprogression.<br />
Key words: Schizophrenia, magnetic resonance imaging, lateral ventricle<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S61<br />
S61
Abstracts of the Invited Speakers<br />
Neuroimaging studies in dementia, psychiatric disorders, drug discovery, and more<br />
Devrim Ünay<br />
Department of Electrical-Electronics Engineering, Bahcesehir University, Istanbul, Turkey<br />
E-mail: devrim.unay@bahcesehir.edu.tr<br />
The continuous progress achieved in medical imaging technology in the past decades has led to considerable improvement in patient<br />
care. In consequence of this progress, neuroimaging (imaging the structure or function of the brain) has gained an increasingly important<br />
role in research and clinical practice.<br />
Dementia, a psychiatric/mental disorder defined as progressive loss in cognitive skills such as learning, memory, orientation and<br />
language, is a devastating and irreversible brain syndrome. Due to its increasing prevalence (especially in aging populations), long<br />
duration, caregiver burden and high financial cost of care, dementia has emerged as one of our major public health problems affecting<br />
20% of those over 80 years of age. As a result there is an increasing demand for a more accurate and earlier diagnosis and the value of<br />
neuroimaging in improving the diagnostic process is becoming widely accepted.<br />
Neuroimaging assessments may aid in the diagnosis of neurodegeneration as opposed to healthy aging, improve differential diagnosis,<br />
assist in the prediction of conversion to dementia in individuals at a higher risk of developing the disorder, improve the tracking of disease<br />
progression and finally may serve as an outcome measure for assessing drug efficacy. Hence, in clinical settings the diagnosis of dementia<br />
is increasingly taken based on combined analysis of data such as the patient’s cognitive skills, demographic status, family history of<br />
dementia and neuroimaging findings (such as the degree and distribution of atrophy).<br />
In addition to the improvement in patient care, recent advances in neuroimaging technology also have increased the need for tools to<br />
analyze and interpret the growing amount of neuroimaging data acquired. Accordingly, various semi-/fully automatic tools for analysis<br />
and interpretation of such data are made available by research centers as well as medical imaging companies.<br />
In view of the above, this work aims to provide a non-exhaustive summary of neuroimaging studies in psychiatric disorders with special<br />
emphasis on dementia and drug discovery. State of the art studies employing both structural (CT, MRI, etc.) and functional (fMRI, PET,<br />
SPECT, etc.) neuroimaging techniques and their potential contribution to diagnostic research as well as to drug discovery will be discussed.<br />
The work will also include a brief introduction on the related advances and open questions from an image processing standpoint, and<br />
finally present our recent research effort on computer-based measurement of dementia-related neuroimaging findings as compared with<br />
experts’ visual assessments for improved disease understanding, diagnosis, prognosis, and therapy planning.<br />
Key words: Dementia, drug discovery, fMRI, MRI, neuroimaging, PET, psychiatric disorders, SPECT<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S62<br />
[PS-07]<br />
Symposium Title: The rationale of antipsychotic combinations in schizophrenia: Epidemiological and clinical evidences<br />
Pharmacogenetics and antipsychotic combinations<br />
Filiz Karadağ<br />
Pamukkale University Medical Faculty, Psychiatry Department, Denizli, Turkey<br />
E-mail: filizlal@yahoo.com<br />
Pharmacogenetic studies in schizophrenia aim to use genetic information as a guide to establish individualized treatment options and to<br />
optimize the effectiveness of treatment. The heterogeneity of response to antipsychotics results in polypharmacy along and combination<br />
therapy into clinical practice, which lead to an increase in drug-related side effects and non-adherence to treatment.<br />
Dopamine and serotonin systems may provide some of the genetic polymorphisms and have been proposed to predict the efficacity<br />
of antipsychotic drugs. Affecting the intensity of the D2 receptors in the striatum, the DRD2- 141C Ins/Del polymorphism has been<br />
associated with unresponsiveness to clozapine in treatment-resistant patients and a longer response time to olanzapine and risperidone<br />
in first-episode patients. The D3 receptor DRD3 Ser9Gly polymorphism has been associated with unresponsiveness to clozapine and good<br />
response to first generation antipsychotics.<br />
The 5-HT2A receptor gene HTR2A-A-1438G and T102C polymorphisms may cause lower promoter activities and decreased 2A receptor<br />
density in some brain regions. A-1438G G/G carriers have been found to be less likely to respond to clozapine, olanzapine, and aripiprazole.<br />
S62 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
The T102C SNP C/C genotype has been associated with no response to clozapine and good response to risperidone and aripiprazole.<br />
The long allele of the serotonin transporter gene has been reported to be associated with better response to antidepressants, but<br />
there are only a few studieson schizophrenic patients. The effectiveness of pharmacogenetics-based combination therapies in patients<br />
unresponsive to treatment has not been studied yet; the DRD2 and DRD3 genes may be candidates for study.<br />
Antipsychotic metabolism: The Met/Met genotype of the COMT gene causes a 3- to 4-fold lower enzyme activity. The met allele carriers<br />
were more likely to respond to clozapine, especially showing improvement in cognitive functions. This polymorphism, seems to deserve<br />
assessment of the effectiveness of combination therapies in dealing with cognitive symptoms.<br />
The CYP2D6 enzyme plays an important role in the metabolism of antipsychotic drugs. Individuals carrying duplicate or multiple<br />
copies of the CYP2D6 gene are known as ultrarapid metabolizers. In ultrarapid metabolizers, due to the decrease in therapeutic efficacy<br />
of antipsychotic drugs, a combination of drugs that are metabolized by the same cytochrome enzyme would not provide further<br />
improvement in drug response.<br />
Antipsychotic-induced side effects: The DRD2 A2 allele of SNP Taq1A, the DRD3 Ser9 Gly Gly allele genetic polymorphisms related to<br />
D2 and D3 receptors, the COMT Val allele and the CYP2D6 gene variants have been reported to be associated with an increased risk of<br />
tardive dyskinesia.<br />
CYP2D6 poor and intermediate metabolizers may be more sensitive to the extrapyramidal side effects of antipsychotics. The 5HT2C gene<br />
(759T SNP) and the leptin gene are the most studied polymorphisms for antipsychotic-induced weight gain. All of the aforementioned<br />
polymorphisms may have implications for choice of rational antipsychotic combinations.<br />
Pharmaco-genetics-based rational antipsychotic combinations may yield promising results for cytochrome enzyme and COMT genes<br />
and the genes associated with side effects in schizophrenia. However, this issue should be supported and confirmed by clinical<br />
pharmacogenetics studies.<br />
Key words: Pharmacogenetics, schizophrenia, antipsychotics, side effects, dopamine, serotonin, polymorphism<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S62-3<br />
Scientific bases of use of atypical antipsychotics<br />
Ender Taner<br />
Department of Psychiatry, Gazi University Faculty of Medicine, Ankara, Turkey<br />
E-mail: tanerender@yahoo.com<br />
The predominant hypothesis regarding the pathophysiology of schizophrenia is that it is associated with impaired dopamine<br />
neurotransmission. The mesolimbic pathway originates from the midbrain ventral tegmental area and innervates the ventral striatum<br />
(nucleus accumbens), olfactory tubercle, and parts of the limbic system. The mesocortical pathway, also originating from the midbrain<br />
ventral tegmental area, innervates areas of the frontal cortex and has been implicated in learning and memory. Overactivity of the<br />
mesolimbic pathway has been implicated in the development of the positive symptoms of schizophrenia. The negative and some cognitive<br />
symptoms have been associated with a reduction of dopamine activity in the mesocortical pathways together with a hypostimulation<br />
of dopamine receptors in the prefrontal cortex. There are 2 overall goals of treatment: (1) to reduce the activity of hyperactive pathways<br />
mediating psychosis and (2) to increase the activity of hypoactive pathways that seem to mediate negative and cognitive symptoms,<br />
while simultaneously preserving the activity of the pathways that regulate motor movement and prolactin secretion. There is also a<br />
putative interrelationship between N-methyl-D-aspartate (NMDA) hypofunction and dopamine (DA) dysregulation and these processes<br />
may be linked to the pathogenesis of schizophrenia. It has been postulated that NMDA hypofunction in the prefrontal cortex and its<br />
connections may result in a pattern of dopamine dysregulation. In the prefrontal area, this pattern consists of a dopamine deficit and<br />
a hypostimulation of D1 receptors that are linked to the appearance of negative symptoms and cognitive impairment. However, at the<br />
subcortical level, NMDA hypofunction results in dopamine excess, hyperstimulation of D2 receptors, and the appearance of positive<br />
symptoms. It has also been suggested that the prefrontal dopamine deficit and the subcortical dopamine excess feed back, in turn, to the<br />
NMDA circuitry. In addition there is evidence that the deficit in cortical dopamine may also be linked to the generation of a subcortical<br />
dopamine excess. There is a complex modulation of dopamine by different serotonergic receptor systems as well as by nicotinic receptors.<br />
These may be additional sites for effects of antipsychotics. This conference tries to underline the current possible scientific basis for the<br />
use of atypical antipsychotics.<br />
Key words: Atypical antipsychotics, schizophrenia, mechanism of action, scientific basis<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S63<br />
S63
Abstracts of the Invited Speakers<br />
Is fish oil promising in the treatment of depression during pregnancy and lactation?<br />
Evrim Özkorumak<br />
Karadeniz Technical University, Psychiatry Department, Trabzon, Turkey<br />
E-mail: evrimozkorumak@yahoo.com<br />
Increasing concerns about neonatal syndromes following antidepressant use in the late phase of pregnancy(1) have caused more<br />
hesitation about their use. Although inadequate data about in utero exposure of antidepressants may present risks, the risks of untreated<br />
maternal depression must be considered as well. One candidate as an antidepressant is fish oil, in light of its omega-3 constituent.<br />
Omega-3 fatty acids are long-chain, polyunsaturated fatty acids found in plant and marine sources and helpful in treating various medical<br />
conditions (2). Omega-3 fatty acids may prove to be efficacious in a number of psychiatric disorders. Evidence suggests that omega-3<br />
fatty acids may have beneficial effects in mood disorders, including bothmajor depression and bipolar disorder, schizophrenia and<br />
dementia. Furthermore, omega-3 fatty acids may prove to be a safe and efficacious treatment for psychiatric disorders during pregnancy<br />
and breastfeeding (2).<br />
Major depressive disorder (MDD) is prevalent among women of childbearing age. Approximately 15% of women experience an episode<br />
of perinatal depression (PND), antenatally and/or postnatally (3). Because there are increasing concerns about possible adverse effects<br />
of antidepressant medication use during pregnancy and in breastfeeding mothers (4), it is important to investigate possible alternative<br />
treatments. Main dietary risk factors of postnatal depression are low riboflavin, low folate, low docosahexaenoic acid, low eicosapantaenoic<br />
acid, low calcium, low magnesium and low zinc. Oil-rich fish are a rich source of n-3 fatty acids, in particular eicosapentaenoic acid (EPA)<br />
and docosahexaenoic acid (DHA) (5). Evidence indicates that these fatty acids may be involved in the synthesis and regulation of brain<br />
neurotransmitters (dopamine, monoamine and serotonin), which are thought to be reduced in cases with depressive symptoms (6). More<br />
specifically, it is thought that high concentrations of DHA located in non-myelin cell membranes of the central nervous system may help<br />
support synaptic transmissions (7). Different human studies were identified investigating dietary and/or supplemental sources of n-3<br />
in relation to the development of postnatal depression. Only two of these trials were randomised controlled trials (8,9). Among others,<br />
three studies support the theory that dietary and supplemental sources of n-3 are associated with fewer postnatal depression symptoms<br />
(8,10,11) and five studies contest this theory (12,13,14).<br />
Key words: Omega-3 fatty acids, depression, perinatal depression<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S64<br />
[PS-08]<br />
Symposium Title: Advances in complementary alternative psychotropic drugs: Fish oil (omega-3 fatty acids), vitamine B12, folate<br />
ve other add-on therapies in psychiatric disorders<br />
Can St. John’s Wort be an alternative treatment for depression?<br />
Çiçek Hocaoğlu<br />
Rize University, Medical School, Department of Psychiatry, Rize, Turkey<br />
E-mail: chocaoglu@superonline.com<br />
The herb St. John’s Wort (Hypericum perforatum) has been used for centuries to treat a variety of medical illnesses. In certain areas of<br />
Europe, St. John’s Wort has been a commonly prescribed treatment for depression. In some countries extracts of the plant Hypericum<br />
perforatum L. (popularly called St. John’s Wort) are widely used for treating patients with depressive symptoms. Extracts of the plant<br />
Hypericum perforatum have been used in folk medicine for a long time for a range of indications including depressive disorders. Some<br />
researchers believe that specific chemical constituents of St. John’s Wort produce changes in depression in a manner similar to that of<br />
antidepressant medications, yet this hypothesis is problematic. In addition, studies that support the efficacy of St. John’s Wwort in patients<br />
with mild-to-moderate depression have limitations that may affect the accuracy of their conclusions. Studies measuring the effect of St.<br />
John’s Wort in major depression have reported conflicting results and need to be reexamined. In patients who meet the criteria for major<br />
depression, several recent placebo-controlled trials suggest that the tested hypericum extracts have minimal beneficial effects while<br />
other trials suggest that hypericum and standard antidepressants have similar beneficial effects. Preliminary data suggest that hypericum<br />
extract is effective in atypical depression based on the reported outcome of an 8-week double-blind, placebo-controlled, randomized<br />
S64 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
trial (positive results in patients with vegetative features of atypical depression, i.e. hyperphagia or hypersomnia). The study supports the<br />
beneficial effect of St. John’s Wort in depression with atypical features and the validity of the definition of atypical depression on the basis<br />
of reversed vegetative signs.<br />
Consequently, St. John’s Wort is considered by some to be an alternative to conventional therapies but, clinicians need to know whether<br />
it is an effective and safe treatment for different levels of severity of depression. Current evidence does not support its use and because<br />
of potential drug interactions, St. John’s Wort is not a benign treatment.<br />
Key words: St. John’s Wort, depression<br />
References:<br />
1. Shelton RC. St John’s wort (Hypericum perforatum) in major depression. J Clin Psychiatry. 2009;70 Suppl 5:23-7.<br />
2. Mannel M, Kuhn U, Schmidt U, Ploch M, Murck H.St. John’s wort extract LI160 for the treatment of depression with atypical features - a double-blind, randomized,<br />
and placebo-controlled trial. J Psychiatr Res. 2010 Sep;44(12):760-7. Epub 2010 Feb 23.<br />
3. Kasper S, Gastpar M, Müller WE, Volz HP, Dienel A, Kieser M, Möller HJ. Efficacy of St. John’s wort extract WS 5570 in acute treatment of mild depression: a reanalysis<br />
of data from controlled clinical trials. Eur Arch Psychiatry Clin Neurosci. 2008 Feb;258(1):59-63. Epub 2007 Dec 14.<br />
4. Trautmann-Sponsel RD, Dienel A. Safety of Hypericum extract in mildly to moderately depressed outpatients: a review based on data from three randomized,<br />
placebo-controlled trials. Affect Disord. 2004 Oct 15;82(2):303-7.<br />
5. Linde K, Mulrow CD, Berner M, Egger M. St John’s wort for depression. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD000448.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S64-5<br />
Complementary medicine alternatives for other psychiatric abnormalities<br />
(Like insomnia and pain)<br />
Bülent Bahçeci<br />
Department of Psychiatry, Rize Üniversity, Rize,Turkey<br />
E-mail: bulentbahceci@hotmail.com<br />
Complementary and alternative medicine have been used for the treatment of a variety of diseases for a long time. Since the applications<br />
of these two branches of medicine have been increasingly spreading globally and have been accompanied by inadequate scientific<br />
studies in the literature, the NIH has established the National Centre for Complementary and Alternative Medicine (NCCAM). The aims of<br />
the centre are to investigate the safety/reliability and efficacy of complementary and alternative medicine applications, and to integrate<br />
those that are scientifically proven to be effective into conventional therapies. All health protection and medical applications/practices<br />
outside of conventional medicine are referred to as complementary and alternative medicine (CAM).<br />
CAM applications are becoming widespread in Turkey, as well, and are sought by 34-77% of sufferers as the first choice for therapy.<br />
Recently CAM, which has found applications in a wide range of areas, has also been used for psychiatric diseases. The use of CAM in the<br />
treatment of chronic pain, eating and sleeping abnormalities, alcohol and substance addiction, Alzheimer’s disease and delirium has<br />
yielded contradictory results in the national and international literature. Therefore, it has been reported that CAM methods require further<br />
evidence-based studies.<br />
Taking into consideration the widespread use and popularity of CAM, it is evident that these methods must be investigated further for<br />
their side effects, dosages, indications, interactions with other drugs, and standardisations. In addition, the regulations concerning their<br />
use must be redrawn and physicians must follow the relevant literature in order to prevent possible harm to their patients before initiating<br />
CAM treatments.<br />
Key words: Complementary and alternative medicine, psychiatry, education<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S65<br />
S65
Abstracts of the Invited Speakers<br />
Essential fatty acids in ADHD treatment<br />
İbrahim Durukan<br />
Deparment of Child and Adolescent Psychiatry, Gülhane Military Medical School, Ankara, Turkey<br />
E-mail: idurukan2003@yahoo.com<br />
Attention deficit hyperactivity disorder (ADHD) is characterized by problems with attention, hyperactivity and impulsivity. These problems<br />
often severely affect families, relationships and school performance. Although stimulants and atomoxetine are efficacious in many<br />
children, these medications can have side effects such as insomnia, decreased appetite, irritability and impaired growth. The etiology<br />
of ADHD is generally accepted to be complex and multifactorial. Little progress has been made in elucidating predisposing biological<br />
factors. Related contributory factors for ADHD etiology are diet, nutrition and particular abnormalities in the metabolism of the longchain<br />
polyunsaturated fatty acids (LCPUFAs).<br />
Essential fatty acids (EFAs) as a complementary or alternative treatment for ADHD have been used as both a primary and an adjunctive<br />
treatment in many countries. Humans are unable to synthesize linoleic acid (an omega-6 fatty acid), and a-linolenic acid (ALA), an omega-<br />
3 fatty acid. The main dietary sources of linoleic acid and ALA are vegetable oils and their seeds.<br />
Both omega-3 and omega-6 LCPUFAs have critical importance for normal brain development and function. Large amounts of both omega-<br />
6 and omega-3 LCPUFAs are deposited in the central nervous system during fetal life. During infancy, dietary intake of both omega-3 and<br />
omega-6 LCPUFAs continues to be essential for neuronal development. LCPUFAs and their derivates work as facilitators of dopamine,<br />
serotonin and norepinephrine release, as regulators of gene transcription, as modulators of Na+ -K+ ATPase channel function and as the<br />
precursors of pro-inflammatory and anti-inflammatory molecular families. The most abundant LCPUFA in the brain is DHA from the omega-<br />
3 series, which is concentrated at nerve cell synapses and is important for neural cell signalling and neurotransmitter processes.<br />
There is increasing evidence that omega-3 LCPUFAs play a part in many neurodevelopmental and psychiatric disorders. ADHD, dyslexia,<br />
developmental coordination disorder and autistic spectrum disorder are suggested to be related to the omega-6/omega-3 spectrum of<br />
disturbances. Several studies of LCPUFA supplementation in children with ADHD symptoms have been conducted. Open-label EFA trials<br />
in ADHD demonstrate that ADHD symptoms are responsive to EFA supplementation. Despite successful open-label trials, randomized<br />
controlled trials of EFA in ADHD have generally been unsuccessful in demonstrating treatment effects and some of them even displayed<br />
better results for the placebo group. There are three studies with partial positive results but these studies represent a small minority and<br />
two of them have several methodological limitations.<br />
The side effects of EFA are generally related to the gastrointestinal system and usually include diarrhea, nausea, fishy aftertaste, belching<br />
and indigestion. These side effects seem to be mild, transient and infrequent, and also appear in the placebo groups.<br />
Current findings from randomized clinical trials of EFA in children with ADHD are not promising. Most randomized trials have clearly<br />
demonstrated lack of superiority compared to placebo. Moreover, the studies that showed positive findings did not use children properly<br />
diagnosed with ADHD and none of them demonstrated clinical improvement in more than one setting. This delineation does not support<br />
the use of EFA supplements as a treatment for children with ADHD. Future studies should be planned to consider methodological issues<br />
such as proper ADHD diagnosis, blinded controls, adequate sample size and behavioral assessment in more than one setting.<br />
Key words: ADHD, essential fatty acids<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S66<br />
Mechanisms of fish oil (Omega-3 fatty acids), vitamin B12, folate and other add-on treatments<br />
in psychiatric disorders<br />
Mehmet Cemal Kaya<br />
Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey<br />
E-mail: mcemalkaya@yahoo.com<br />
The need for new treatments has led several investigators to examine the potential role of omega-3 fatty acids, found in marine and plant<br />
sources, in the treatment of psychiatric disorders. Omega-3 fatty acids are associated with normal brain development, neuronal plasticity,<br />
and function (1). Cell biology and molecular studies suggest that omega-3 fatty acids modulate membrane fluidity and dopaminergic<br />
and serotonergic neurotransmission (2). It has been observed that omega-3 fatty acids have effects on the phospholipid cell membrane<br />
and the secondary messenger system similar to mood stabilizing drugs like lithium (3). It has been also demonstrated by recent studies<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
that add-on treatments with omega-3 fatty acids in mood disorders significantly improved the symptoms. Another way to investigate the<br />
effects of omega-3 fatty acids is by estimating the regional brain concentrations of various metabolites with proton magnetic resonance<br />
spectroscopy (PMRS). In a study that used this method in a population with first-episode psychosis, improvement of the negative<br />
symptoms of the patients were observed parallel to the increase in glutathione availability and modulation of the glutamine/glutamate<br />
cycle with ethyl-eicosapenthaenoic acid augmentation treatment (4). Post-mortem polyunsaturated fatty acid concentrations in the<br />
prefrontal areas of antipsychotic-naive schizophrenia patients were found to be lower than those of schizophrenia patients treated with<br />
atypical antipsychotics. Additionally, in an animal study, increases in the omega-3 fatty acid concentration in erythrocytes and prefrontal<br />
cortex were observed after long-term treatment with risperidone.<br />
One of the earliest reports about the possible psychiatric effects of vitamin B12 deficiency belongs to Langdon in 1905. Vitamin B12<br />
together with folate are essential for conversion of homocysteine to methionine and synthesis of adenosyl-methionine. S-adenosylmethionine<br />
is responsible for methylation in the metabolism of neurotransmitters (5). There are various studies that showed associations<br />
of depression, dementia and schizophrenia with deficiencies of folate and vitamin B12. Some studies have focussed on folate rather<br />
than vitamin B12 and have suggested a stronger role for folate in depression. Independent from serum levels of folate and vitamin<br />
B12, augmention with these vitamins may be beneficial to patients who have predominantly cognitive symptoms, who are resistant to<br />
treatment, pregnantor use lithium (6).<br />
Consequently, augmentation with omega-3 fatty acids, folate and vitamin B12 may have some clinical benefits in the treatment of some<br />
psychiatric disorders. However, mechanisms of their actions still need to be further elucidated.<br />
Key words: Omega-3 fatty acids, vitamin B12, folate, psychiatric disorders<br />
References:<br />
1. Bazan NG. Lipid signaling in neural plasticity, brain repair, and neuroprotection. Mol Neurobiol 2005; 32: 89–103<br />
2. Yao JK, Leonard S, Reddy R. Altered glutathione redox state in schizophrenia. Dis Markers 2006; 22: 83–93<br />
3. Frangou S, Lewis M, Wollard J, Simmons A. Preliminary in vivo evidence of increased N-acetyl-aspartate following eicosapentanoic acid treatment in patients with<br />
bipolar disorder. J Psychopharmacol 2007; 21: 435-439<br />
4. Berger GE, Wood SJ, Wellard RM, Proffitt TM, McConchie M, Amminger GP, Jackson GD, Velakoulis D, Pantelis C, McGorry PD. Ethyl-eicosapentaenoic acid in firstepisode<br />
psychosis. A 1H-MRS study. Neuropsychopharmacology 2008; 33: 2467-2473<br />
5. Bottiglieri T. Folate, vitamin B12, and neuropsychiatric disorders. Nutr Rev 1996; 54:382-390<br />
6. Lindeman RD, Romero LJ, Koehler KM, Liang HC, LaRue A, Baumgartner RN, Garry PJ. Serum vitamin B12, C and folate concentrations in the New Mexico elder<br />
health survey: Correlations with cognitive and affective functions. J Am Coll Nutr 2000; 19: 68-76<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S66-7<br />
[PS-09]<br />
Symposium Title: From preclinical studies to clinical practice in anxiety disorders<br />
Medical disease and anxiety disorders<br />
Hayriye Elbi<br />
Ege University, School of Medicine, Dept. of Psychiatry, İzmir, Turkey<br />
E-mail: hayriye.elbi@yahoo.com;hayriye@ege.edu.tr;hayriye.elbi@med.ege.edu.tr<br />
Chronic medical illness causes us to face our vulnerabilities and is a significant risk factor for the development of an anxiety disorder.<br />
The vulnerability could be associated with the stress of illness and coping with the limitations of illness. Anxiety disorders may also<br />
develop secondary to predisposing biological mechanisms (as in diabetes or thyroid disorders) or may be related to a patient’s specific<br />
medications.<br />
We need to explore the causes of an anxiety disorder and plan our treatment so that it will not interfere with the medical disease and its<br />
treatments. Drug interactions are very important in medical comorbidity cases. Every disorder comes with a new life style and necessity<br />
for new adaptations. The uncertainty and barriers to daily life worsen the situation. I will review the anxiety associated with medical<br />
diseases and the current treatments for it.<br />
Key words: Medical diseases, anxiety disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S67<br />
S67
Abstracts of the Invited Speakers<br />
Genetic models in anxiety disorders<br />
Nurper Erberk Özen<br />
Department of Psychiatry, Ufuk University, Ankara, Turkey<br />
E-mail: nerberk@superonline.com<br />
Animal models are key to our understanding of many human diseases and psychiatric disorders are no exception. Animal models have<br />
provided insight into the neurotransmitter systems and brain circuitry underlying psychiatric illnesses that have enabled the screening<br />
of potential psychiatric medications for efficacy and guided the search for new pharmacotherapies. However, modeling complex<br />
psychiatric disorders in animals presents distinct challenges. Modeling psychiatric disorders in animals is difficult due to the complexity<br />
of human thoughts, emotions, and behavior; the heterogeneity of many psychiatric disorders; and the requirement of self-reporting of<br />
internal state for diagnosis. According to the DSM-IV, most psychiatric diagnoses are made when a patient displays a certain number of<br />
diagnostic criteria. However, patients with the same diagnosis can differ significantly in specific symptoms, perhaps implying differences<br />
in the underlying etiology of their disorders and explaining the heterogeneity of response to pharmacotherapy. Many symptoms are<br />
identified by the patient’s report of internal state (e.g., obsessive obtrusive thoughts or ruminations). This leads to questions of how we<br />
can best model disorders in animals that are, by definition, both heterogeneous and dependent on report of internal state. Rather than<br />
attempting to model a psychiatric disorder in its entirety, most neuroscientists focus on individual aspects or dimensions of a disorder<br />
and use physical manifestations and measurable behaviors when modeling a particular aspect.<br />
Inferences from experiments with animal models have the potential to impact clinical practice; therefore, stringently validating such<br />
models is of utmost importance. The strengths and weaknesses of a model can be conceptualized with different types of validity.<br />
Three important types of validity are suggested as predictive, face, and construct validity. In the first one, the animal should display<br />
reduced anxiety when treated with anxiolytics (predictive validity). In the second type, the behavioral response of an animal model to<br />
a threatening stimulus should be comparable to the response known for humans (face validity). Finally, in the third type of validity, the<br />
mechanisms underlying anxiety as well as the psychological causes should be identical (construct validity). In the meantime there is no<br />
consensus about which type of validity is superior. Some authors argue that predictive validity is most essential but the others suggest<br />
that constructive validity is the most crucial. On the other hand, these three requirements are difficult to achieve in any animal model for<br />
each anxiety disorder. Moreover, in the related literature, the term“animal model of anxiety” is used for animals that are altered in their<br />
anxiety-related behavior, as well as for test assays conceptualized to assess anxiety-related behavior in animals.<br />
Key words: Anxiety disorders, genetic, rat, transgenic<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S68<br />
Anxiety models in experimental animals<br />
Hüseyin Günay<br />
Etimesgut Military Hospital, Psychiatry Clinic, Ankara, Turkey<br />
E-mail: huseyingunaydr@yahoo.com<br />
The basic measure in testing validity of an animal model is its prediction validity, which means making true assumptions for a disorder<br />
in humans. The necessary features of an animal model are analogy to a disorder in humans, objective testing, effective interventions in<br />
humans and the capability of retesting. Structural validity is the capability to retest of the target condition and first sight validity is the<br />
measurement of phenomenological similarity. First sight validity points to the surface similarity between the model and the disease and<br />
structural validity points to the underlying mechanisms. Anxiety models are mainly used in understanding causes and mechanisms and<br />
also determining drug effects. Anxiety in animals, which is similar to humans, can be developed with different environmental conditions.<br />
These situations can help to understand and intervene to treat anxiety. Three ways are used in the development of anxiety models: using<br />
a new environment, reward and punishment applications, and punishment procedures.<br />
Anxiety models using new environment:<br />
These are the methods for establishing and evaluating anxiety models in a new environment, such as elevated plus maze and derivers,<br />
elevated T-maze, open field, staircase test, social isolation, novelty suppressed feeding, social interaction, holeboard, predatory odor,<br />
operant conflict tests for reward-punishment applications and experiments with punishment procedures such as defensive burying,<br />
passive avoidance, foot shock, hot plate and four plate tests.<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
The purpose of this study is to show the usefulness of the tests in the literature and to compare the advantages and disadvantages in<br />
terms of structural validity and first sight validity.<br />
Key words: Anxiety, anxiety models<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S68-9<br />
[PS-10]<br />
Symposium Title: Will glutamatergic modulators be a target for the future therapy of depression?<br />
Ketamine and other glutamate modulators as potential antidepressants<br />
Serdar Dursun, Glen Baker, Nick Mitchell<br />
Neurochemical Research Unit, University of Alberta, Edmonton, Canada<br />
E-mail: Dursun@ualberta.ca<br />
Depression is seen as a complex neuropsychiatric disorder affecting integrated pathways connecting discrete cortical, subcortical, and<br />
limbic regions and their associated neurotransmitter and molecular mediators. One episode of major depression is a strong predictor of<br />
future episodes, and more than 50% of individuals who have an episode of major depression experience a recurrence.<br />
Unfortunately, currently approved pharmacological treatments for depression require several weeks for onset of efficacy. Despite<br />
advances in the understanding of the psychopharmacology of depression and the introduction of several novel classes of antidepressants<br />
in the last 3-4 decades, patient response to any given pharmacological approach continues to be unsatisfactory.<br />
Although almost all of the prescription drugs currently available as antidepressants have effects on noradrenaline (NA) and/or<br />
5-hydroxytryptamine (5-HT), it is obvious that other factors are also important in the etiology and pharmacotherapy of depression and<br />
that the monoamines cannot be considered in isolation. Perhaps the most exciting system and that for which there is now substantial<br />
translational evidence for a role in depression is that involving glutamate. Ample evidence indicates that glutamate homeostasis and<br />
neurotransmission are disrupted in major depressive disorder but the nature of these disruptions and the mechanisms by which they<br />
contribute to the syndrome are unclear. Likewise, the specific effects of existing antidepressants on glutamate are unclear, as is the<br />
potential of drugs directly targeting glutamatergic neurotransmission to act as novel antidepressant medications. However, these are<br />
areas of active research and some exciting results have been obtained.<br />
This presentation will review the current knowledge of the contribution of the N-methyl-D-aspartate (NMDA) receptor, one of the several<br />
types of glutamate receptors, to depression and its treatment. Several lines of evidence, in humans and in animal models, support<br />
the contention that neurotransmission via the NMDA receptor is dysregulated in depression. Drugs targeting the NMDA receptor as<br />
antagonists have shown antidepressant properties in both clinical and preclinical studies. Nevertheless, other effects of such medications,<br />
including both cognitive side effects and their psychotomimetic properties, complicate such an application and represent a challenge to<br />
the development of clinically useful agents.<br />
There is a recent hypothesis that the therapeutic effects of monoaminergic antidepressants and the NMDA receptor antagonist ketamine<br />
may be mediated by increased alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-to-NMDA glutamate receptor activity<br />
in critical neuronal circuits. It has been hypothesized that ketamine directly mediates this receptor activity, whereas monoaminergic<br />
antidepressants work indirectly and gradually; this may explain, in part, the lag of onset of clinical improvement of several weeks that<br />
is observed with traditional antidepressants. Ketamine (intravenous) is the first medication reported to produce rapid, relatively longlasting<br />
antidepressant efficacy. Although the precise antidepressant mechanisms of action of ketamine remain unclear, there is preclinical<br />
evidence to suggest that both AMPA and NMDA receptor subtypes are involved. In terms of neuroanatomical sites of action, it has been<br />
shown that the subgenual cingulate cortex (Sg CG) is overactive in depression while the dorsal frontal regions and posterior cingulate are<br />
underactive and that successful treatment normalizes the pattern. There is also evidence from functional magnetic resonance imaging<br />
(fMRI), which has demonstrated that the effect of ketamine resembles the pattern of normalisation after successful antidepressant<br />
treatment, i.e., in healthy volunteers there is decreased orbitofrontal cortex (OFC)–Sg CG blood oxygen level-dependent (BOLD) signal<br />
response and increased BOLD signal response in the dorsolateral prefrontal cortex (PFC) (Brodmann area 8) and the posterior cingulate<br />
region. These findings suggest that an overactive Sg CG may be the dysfunctional organising region in depression.<br />
Key words: Ketamine, rapid antidepressant efficacy, glutamate, NMDA receptor<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S69<br />
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The glutamatergic system and its importance in the neurobiology of depression<br />
Feyza Arıcıoğlu<br />
Department of Pharmacology, Marmara University, Istanbul, Turkey<br />
E-mail: feyza.aricioglu@gmail.com<br />
Recent advances in research on depression have confirmed that it is common, recurrent and disabling mental disorder affecting millions<br />
of individuals worldwide. Current medications for the treatment of depression have limited efficacy and delayed onset of therapeutic<br />
action. Existing antidepressants used to treat these disorders are insufficient for many. Patients continue to have low remission rates,<br />
delayed onset of action, residual subsyndromal symptoms, and relapses. New therapeutic agents able to exert faster and more sustained<br />
antidepressant effects are urgently needed to treat these disorders. Multiple lines of evidence suggest that inflammation and glutamate<br />
dysfunction contribute to the pathophysiology of depression. Excess levels of inflammatory mediators occur in a subgroup of depressed<br />
patients. Patients with depression have been found to exhibit increased blood inflammatory biomarkers, including inflammatory cytokines,<br />
which have been shown to be involved in depression. Activation of inflammatory pathways is believed to contribute to a confluence of<br />
decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of<br />
glial elements, consistent with findings that characterize depressive disorders. Neurotrophic factors such as brain-derived neurotrophic<br />
factor (BDNF) are involved in the pathogenesis of mood disorders and in the action of at least some drugs. It has been shown that serum<br />
BDNF levels are decreased in patients with depressive disorder and antidepressant treatment induces BDNF expression. In this context,<br />
the glutamatergic system has been implicated in the pathophysiology of depression in unique clinical and neurobiological ways. The data<br />
from depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood<br />
and increase treatment response to conventional antidepressant medication. The past decade of efforts to find improved treatment for<br />
depression has been dominated by genome-driven programs of rational drug discovery directed toward highly selective ligands for<br />
nonmonoaminergic agents. To date, the monoaminergic systems (serotonin, norepinephrine, and dopamine) have received the most<br />
attention in the neurobiology of depression, and all classes of antidepressants target these monoaminergic systems. Accumulating<br />
evidence suggests that the glutamatergic system plays an important role in the neurobiology and treatment of depression. Many<br />
reports have highlighted alterations in glutamate signaling as well as changes in the expression of AMPA or NMDA receptor subunits<br />
in depression. In parallel, there is growing interest in the non-competitive NMDA receptor antagonist, ketamine, which produces a<br />
rapid and sustained antidepressant response in patients with treatment-resistant depression. Importantly, such effects of ketamine are<br />
seen at subpsychomimetic doses of the drug. Moreover, ketamine produces a profound reduction in suicidality. Based on findings with<br />
ketamine, there is interest in developing subtype-selective NMDA antagonists, particularly those that act through allosteric mechanisms.<br />
A final glutamatergic strategy for treating depression may be through modulating metabotropic (G protein-coupled) glutamate (mGlu)<br />
receptors. During the last 10 years, several selective mGlu receptor competitive antagonists and potentiators have been discovered.<br />
Selective mGlu receptor antagonists are among the most promising agents under development for the treatment of depression. Overall,<br />
this system holds considerable promise for developing the next generation of therapeutics for the treatment of depression.<br />
Key words: Glutamate, depression, cytokines, neurotrophic factors, NMDA, mGLU receptors<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S70<br />
[PS-11]<br />
Symposium Title: Psychotropic drug treatments during pregnancy and lactation<br />
Pharmacotherapy of panic disorder during pregnancy and lactation<br />
Faruk Uğuz<br />
Selcuk University, Meram Faculty of Medicine, Department of Psychiatry<br />
E-mail: farukuguz@gmail.com;farukuguz@hotmail.com<br />
Panic disorder is one of important psychiatric problems during pregnancy and lactation. The prevalence rate of this disorder has been<br />
reported to be 0.4%-4.0% in the perinatal period. In addition, the perinatal period may affect the onset or course of panic disorder.<br />
Although pharmacotherapy of panic disorder is well known, data on treatment of this disorder during pregnancy and lactation are very<br />
limited. It is difficult to decide about pharmacotherapy of panic disorder during the perinatal period, particularly during pregnancy,<br />
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Abstracts of the Invited Speakers<br />
because both effective pharmacological agents and untreated maternal anxiety seem to be associated with several negative outcomes<br />
on the course of pregnancy and the fetus. Despite the absence of practical guidelines for pharmacological management of panic disorder<br />
during pregnancy and lactation, some general points about pharmacological treatment include the following: (1) Pharmacotherapy<br />
should be preferred when the potential impact of untreated maternal panic disorder is higher than the impact of the pharmacological<br />
agent on the fetus or new mother. (2) The patient and relatives should be informed about the benefits and risks of pharmacological<br />
treatment or nontreatment of the current maternal psychiatric picture and written informed consent forms should be obtained. (3)<br />
Selective serotonin reuptake inhibitors except paroxetine and low dose imipramine may be preferred during pregnancy. (4) Sertraline,<br />
paroxetine, orlow doses of imipramine or clomipramine appear to be appropriate pharmacological agents during the lactation period.<br />
Key words: Panic disorder, pregnancy, lactation<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S70-1<br />
Psychotropic drug treatment during pregnancy and lactation in obsessive compulsive disorder<br />
Servet Ebrinç<br />
GATA Haydarpasa Training Hospital, Clinic of Psychiatry, Istanbul, Turkey<br />
E-mail: sebrinc1@gmail.com<br />
According to recent studies, obsessive compulsive disorder(OCD) is one of the leading cause of disability and the prevalence of OCD is<br />
found to be 0.2-3.5% in pregnancy and 2.7-9% in the postpartum period.<br />
The efficacy and tolerability of SSRIs and SNRIs in the treatment of OCD are well-determined in many double-blind randomized controlled<br />
trials. Despite the fact that it is well known that OCD patients may benefit from antiobsessional therapy during pregnancy and the<br />
postpartum period, very little data are available about the efficacy of the treatment and no evidence suggests that patients would react<br />
differently to these drugs. Hence, OCD women who are pregnant and in the postpartum period might be treated using standardized<br />
treatment approaches.<br />
During pregnancy and the postpartum period, the treatment of OCD should clinically take the risks and benefits of several treatment<br />
modalities and the expectations of the patient into account. While cognitive-behavioral therapy (CBT) is the leading choice in nonpharmacological<br />
treatment of OCD, pharmacoterapy might be used if necessary.<br />
If CBT is inadequate and pharmacotherapy is needed, during pregnancy, fluoxetine, and during the lactation period, paroxetine, are<br />
proposed to be the first line treatments. Although evidence is limited, other SSRIs are acceptable as alternative treatment options.<br />
All of the antidepressant drugs are transferred to the nursing infant during breastfeeding. The American Academy of Pediatrics classifies<br />
psychotropic drugs as “drugs whose effects are unknown, but may be of concern.” The best way of determining the exposure to the drug is<br />
measuring the drug concentration in the plasma of the baby. Clinical evaluation is important to identify any side effects while monitoring the baby.<br />
There is no evidence indicating an increase in the rates of intrauterine death or malformation in the case of exposure to tricyclics or<br />
SSRIs. Whether exposure to SSRIs causes a decrease in birth weight or an increase in premature births is not certain and the evidence is<br />
controversial. Nonetheless, The Food and Drug Administration (FDA) has determined that first trimester exposure to paroxetine might<br />
cause an increase in the risk for congenital malformations particularly cardiac defects. Therefore, the FDA has changed paroxetine’s<br />
pregnancy category from C (risk can not be ruled out) to D (positive evidence of human fetal risk).<br />
A “withdrawal syndrome,” consisting of symptoms in the locomotor, central nervous, respiratory and gastrointestinal systems may occur<br />
in newborns exposed to SSRIs in the third trimester. Although monitoring is required in an exposed newborn, this syndrome is relatively<br />
mild, can be managed with supportive therapy and diminishes within 2 weeks. Some evidence points out an increase in the rates of<br />
persistent pulmonary hypertension in infants exposed to SSRIs during the third trimester. Before delivery, lowering the dosage of the<br />
mother’s drugs that might have been augmented due to the symptom severity of OCD, is recommended.<br />
Key words: lactation, obsessive-compulsive disorder (OCD), psychopharmacotherapy, pregnancy<br />
References:<br />
1. Clinical Management Guidelines for Obstetrician-Gynecologists Use of Psychiatric Medications During Pregnancy and Lactation. ACOG Practice Bulletin,<br />
(Reprinted with permission from Obstetrics & Gynecology 2008; 111:1001–1020)<br />
2. Brandes M, Soares CN, Cohen LS. Postpartum onset obsessive-compulsive disorder: diagnosis and management. Arch Womens Ment Health 2004; 7:99–110<br />
3. Use of Psychoactive Medication During Pregnancy and Possible Effects on the Fetus and Newborn Amerikan Academy of Pediatrics Committee on Drugs Pediatrics<br />
2000; 105; 880-887<br />
4. Koran LM, Hanna GL, Hollander E et al. Practice Guidline for theTreatment of Patients with Obsessive-Compulsive Disorder. Copyright 2010, American Psychiatric<br />
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Abstracts of the Invited Speakers<br />
Association.<br />
5. McGuinness M. OCD in the Perinatal Period: Is Postpartum OCD (ppOCD) a Distinct Subtype? A Review of the Literature. Behavioural and Cognitive Psychotherapy<br />
2011, 39, 285–310<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S71-2<br />
[PS-12]<br />
Symposium Title: Vitamin and mineral supplementation in treatment of childhood psychiatric disorders<br />
Vitamin and mineral supplementation in treatment of childhood psychiatric disorders – Calcium and<br />
vitamin D supplementation<br />
Ömer Faruk Akça<br />
Samsun Psychiatry Hospital, Child and Adolescent Psychiatry Clinic, Samsun, Turkey<br />
E-mail: dromerakca@gmail.com<br />
Vitamin D has significant roles in cell proliferation, the immune system and the nervous system as well as in bone development. Adult<br />
studies indicate that vitamin D deficiency may be related to some neurological and psychiatric disorders like Parkinson’s disease,<br />
Alzheimer’s disease and depression (1). Childhood studies on this subject are mainly related to the impact of vitamin D deficiency on the<br />
development of autism. Because vitamin D has an essential role in the development of the nervous system, some investigators suggest<br />
that vitamin D deficiency during pregnancy may contribute to the development of autism. Autism is stated to be more frequent in people<br />
with dark skin and people who live in countries at higher latitudes. Additionally, children of mothers who consume more vitamin D in<br />
pregnancy have better mental development and present with fewer autistic signs. This knowledge indicates that vitamin D may be a<br />
mediator in the emergence of autism for genetically vulnerable people (2). Autism frequency has increased in recent years and this increase<br />
has occurred at the same time as the suggestions on the avoidance of sunlight have arisen. This coincidence is claimed to be supportive<br />
of the autism-vitamin D hypothesis (2,3). This hypothesis suggests two possible mechanisms: 1) vitamin D deficiency during pregnancy<br />
may cause inappropriate development of the fetal brain and then autistic signs may emerge, 2) in light of the hypotheses that autism<br />
is an autoimmune disorder and vitamin D is important for immune system functions, it may be assumed that vitamin D deficiency may<br />
cause autistic signs in vulnerable individuals (4). Some studies have stated that autism is more frequent in children of winter pregnancies<br />
and people of higher latitude countries (4). Additionally, it is stated that autistic patients have the lowest vitamin D levels among all kinds<br />
of psychiatric disorders in a psychiatry inpatient clinic (5). In another recent study, autistic children have lower 25-hydroxy vitamin D,<br />
1,25-hydroxy vitamin D and calcium levels in comparison with healthy children (6). These findings are supportive of this hypothesis.<br />
According to this hypothesis, it can be estimated that children with rickets would have more autistic symptoms. There is no recent study<br />
on this assumption. However, in past studies it has been stated that these children had more mental disorders, which disappeared after<br />
treatment (7).<br />
On the other hand, because children with autism may have food selectivity, vitamin D and calcium deficiency may occur in these children<br />
more frequently. Some investigations were made on this subject and many of them found supportive findings (8,9).<br />
We may conclude that autism-vitamin D relationship needs to be investigated more with larger sample studies.<br />
Key words: Autism, vitamin D, calcium<br />
References:<br />
1. Kesby JP, Eyles DW, Burne TH, McGrath JJ. The effects of vitamin D on brain development and adult brain function. Mol Cell Endocrinol 2011; Article in press.<br />
2. Cannell JJ. Autism and Vitamin D. Med Hypotheses 2008; 70: 750-759<br />
3. Cannell JJ, Hollis BW. Use of Vitamin D in Clinical Practice. Altern Med Rev 2008; 13:6-20.<br />
4. Grant WB, Connie MS. Epidemiologic evidence supporting the role of maternal vitamin D deficiency as a risk factor for the development of infantile autism.<br />
Dermatoendocrinol 2009; 1:223-228.<br />
5. Humble MB, Gustafsson S, Bejerot S. Low serum levels of 25-hydroxyvitamin D (25-OHD) among psychiatric out-patients in Sweden: relations with season, age,<br />
ethnic origin and psychiatric diagnosis. J Steroid Biochem Mol Biol 2010;121:467-470.<br />
6. Meguid NA, Hashish AF, Anwar M, Sidhom G. Reduced Serum Levels of 25-Hydroxy and 1,25-Dihydroxy Vitamin D in Egyptian Children with Autis J Altern<br />
Complement Med 2010; 16:641-645.<br />
7. Cannell JJ. On the aetiology of autism. Acta Paediatr 2010; 99:1128–1130.<br />
8. Zimmer MH, Hart LC, Manning-Courtney P, Murray DS, Bing NM, Summer S. Food Variety as a Predictor of Nutritional Status Among Children with Autism. J Autism<br />
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Dev Disord. 2011 Article in press.<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
9. Emond A, Emmett P, Steer C, Golding J. Feeding Symptoms, Dietary Patterns, and Growth in Young Children With Autism Spectrum Disorders Pediatrics 2010;<br />
126:337-342.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S72-3<br />
Zinc supplementation in psychiatric disorders of children<br />
Sadriye Ebru Çengel Kültür<br />
Department of Child and Adolescent Psychiatry, Hacettepe University, Ankara, Turkey<br />
E-mail: ebru.kultur@gmail.com;ecengel@softhome.net<br />
Micronutrient supplementation is considered as a useful intervention in many cases. Zinc is one of these micronutrients and an essential cofactor<br />
for over 100 enzymes, both metalloenzymes and metal-enzyme complexes that are required in the metabolism of carbohydrates, fatty acids,<br />
proteins and nucleic acids. Zinc is considered as an essential element in neuronal development, synaptogenesis and synaptic transmission.<br />
In experimental animal studies, zinc deficiency during early brain development is mainly related with malformations. In humans,<br />
neuropsychological and neurobehavioral effects of zinc deficiency are largely studied in severely zinc deficient groups or cases exposed to<br />
deficiency during early developmental stages. In addition zinc supplementation studies mainly occur in the gestational period or infancy<br />
and use zinc doses higher than the protective dosage. Limited numbers of interventional trials have been performed to demonstrate<br />
the effects of zinc supplementation on behavioral, cognitive and neuropsychological functioning in school-aged children. Some of these<br />
studies showed no significant effects on average attention span and short-term memory. On the other hand some found improvement<br />
in neuropsychological performance and decrease in the number of children with clinically significant parents’ scores for attention deficit<br />
and hyperactivity. When searched for internalizing symptoms, no significant effect was revealed in parent-teacher rated scales.<br />
In clinical cases with attention deficit hyperactivity disorder (ADHD) and autism low serum zinc levels were reported. Zinc supplementation<br />
studies in ADHD cases showed significant improvement reported in parents’ and teachers’ ratings of hyperactivity, impulsivity and<br />
socialization scores. Furthermore, one study found that improvement was mainly in parent-teacher-rated inattentive symptoms in ADHD<br />
cases. In a placebo controlled study, zinc supplementation in addition to ADHD treatment revealed a 37% reduction in d-amphetamine<br />
dose compared to placebo, though no significant superiority of zinc supplementation for ADHD symptoms was observed.<br />
In conclusion, zinc supplementation studies suggest a special relationship to ADHD diagnosis. However it is not possible to establish<br />
either an etiological relation or an alternative treatment approach in ADHD.<br />
Key words: Zinc supplementation, ADHD<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S73<br />
The impacts of iron deficiency on mental health in childhood<br />
Ayhan Bilgiç<br />
Department of Child and Adolescent Psychiatry, Meram Faculty of Medicine, Selcuk University, Konya, Turkey<br />
E-mail: bilgicayhan@yahoo.com<br />
Numerous studies have found associations between iron deficiency (ID) and iron deficiency anemia (IDA) and poor cognitive and motor<br />
development in infancy and early childhood. In addition, it has been reported that there are associations between ID/IDA and some<br />
childhood neuropsychiatric disorders including attention deficit hyperactivity disorder, conduct disorders, autism spectrum disorders,<br />
restless leg syndrome, sleep disturbance and Tourette’s syndrome. Iron is required for proper function of some enzymes that are engaged<br />
in the myelinization process and in monoamine neurotransmitter synthesis. Therefore, it has been considered that these negative effects<br />
of ID and IDA are related to the vital roles of iron in the brain. Thus, authors have suggested that the presence of ID without anemia is<br />
sufficient for occurrence of functional disturbances, although exceptions exist. There are studies which considered that, especially early<br />
in life, the negative impacts of ID on psychomotor and neurological development do not seem to be reversible by iron supplementation<br />
and ID may cause permanent hazards in the brain. However, some studies have reported that iron supplementation resolved the effects<br />
of ID including cognitive and motor development problems in children and the development of psychiatric disorders. Despite there being<br />
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Abstracts of the Invited Speakers<br />
large amounts of data, the possible confounding effects of poor socioeconomic backgrounds prevent causal inferences. Even nowadays,<br />
it is still not clear whether poor development of iron-deficient children is related to poor social backgrounds or irreversible damage due<br />
to ID and if it is remediable with iron treatment.<br />
Key words: Iron deficiency, children, development, psychiatric disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S73-4<br />
Antioxidant vitamin supplementation therapies in child psychiatry<br />
Betül Mazlum<br />
İstanbul University, Institute of Experimental Medicine, Department of Neuroscience, İstanbul, Turkey<br />
E-mail: drbakkaloglu@yahoo.com<br />
Oxidative stress can be defined as an imbalance between pro-oxidant molecules produced by the body during metabolism and members<br />
of the antioxidant system, in favor of the former. Antioxidant defense mechanisms include antioxidant enzyme systems and molecules<br />
(vitamins, minerals, etc.) which have the ability to detoxify free oxygen radicals.<br />
The brain is highly vulnerable to oxidative stress since it has limited antioxidant capacity, high energy demand and high lipid content.<br />
Moreover, each brain region may have a genetically determined different vulnerability levels to oxidative stress.<br />
Oxidative stress, which is included in the pathogenesis of cancer, aging, cardiovascular and neurodegenerative disorders, is also<br />
considered for pathogenetic mechanisms underlying psychiatric disorders including schizophrenia, bipolar disorder, depression, autism<br />
and attention deficit hyperactivity disorder. There are accumulating data about increased oxidative stress particularly in childhood autism<br />
and therefore antioxidant therapies are considered as an alternative treatment option. In addition, vitamin and mineral supplementation<br />
are recommended to compensate low intake when children with autism have feeding problems. The data about the effects of antioxidant<br />
therapies in autism are restricted but promising. Since oxidative stress is a common finding in the pathogenesis of different disorders, it can<br />
be suggested that individual differences, including single nucleotide polymorphisms of the genes coding for members of the antioxidant<br />
defense system, might determine the vulnerability level to oxidative stress. Individual genetic differences might also be the determinant<br />
of the level of benefit from antioxidant vitamin therapies. Not only the factors related to the biochemistry of leading antioxidant vitamins<br />
(vitamin A, C and E) but also the disease and patient related differences might be acting on the response to supplementation with these<br />
vitamins. These two groups of factors might determine the details of supplementation therapies with antioxidant vitamins in the future:<br />
1) Factors related to the patient and the nature of the disease, i.e. the affected brain areas for a specific disorder, the vulnerability of these<br />
brain areas to oxidative stress, accompanying diseases and possible effects of antioxidant vitamin supplementation on the pathogenesis<br />
of these comorbid diseases; 2) Factors related to the biochemistry of the antioxidant vitamins in the body, i.e., polymorphisms of<br />
molecules mediating intestinal absorption and blood-brain transfer of vitamins, important effects of these vitamins on specific gene<br />
regulation and effects of vitamins on brain mechanisms.<br />
Antioxidant vitamin supplementation is a promising alternative therapy in psychiatry, but it should be kept in mind that these vitamins<br />
might also have undesirable results through their effects on other biological processes. This part of the panel will focus on the study<br />
results of antioxidant vitamin supplementation therapies in child psychiatry and molecular data about the genetic and biochemical<br />
processes of antioxidant vitamins in the body.<br />
Key words: Antioxidant vitamins, psychiatry<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S74<br />
Effectiveness of omega fatty acid supplementation for childhood psychiatric disorders<br />
Sabri Hergüner<br />
Selcuk University, Meram Faculty of Medicine, Department of Child and Adolescent Psychiatry, Konya, Turkey<br />
E-mail: herguners@yahoo.com<br />
Neuronal membranes are composed of phospholipids containing large amounts of polyunsaturated fatty acids (PUFA), especially the<br />
omega-3 and omega-6 acids. Because humans cannot manufacture these de novo, they are “essential” in the diet. Membrane stability is<br />
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essential for neuronal maturation as well as for advanced integrated central system activities including attention, alertness and motor<br />
coordination. PUFA are critically important for normal brain development and functioning. During fetal life, large amounts of PUFA are<br />
deposited in the central nervous system. During infancy, dietary intake of PUFA, both omega-3 and omega-6 acids, continues to be<br />
essential for neural development.<br />
PUFA are metabolized to prostaglandins and other eicosanoids, which modify many metabolic processes and immune functions. They<br />
moderate dopamine, serotonin and norepinephrine release, regulate gene transcription and Na-K-ATPase channel function. There is<br />
increasing evidence that omega acids play a part in many neurodevelopmental and psychiatric disorders including attention deficit<br />
hyperactivity, dyslexia, developmental coordination disorder and autism spectrum disorders.<br />
The focus of this speech will be on the effects of PUFA supplementation on pediatric neurodevelopmental disorders.<br />
Key words: Children, neurodevelopmental disorders, omega fatty acids<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S74-5<br />
[PS-13]<br />
Symposium Title: Hormones and psychiatric disorders<br />
Melatonin and human behaviour<br />
Müfit Uğur<br />
İstanbul Üniversitesi, Cerrahpaşa Tıp Fakültesi, Psikiyatri AD, Cerrahpaşa, İstanbul, Turkey<br />
E-mail: mugur52@hotmail.com<br />
Melatonin is secreted from the pineal gland and regulates the sleep wake cycle, core body temperature, ovulation, and sexual behavior<br />
in females, as well as immune and cardiovascular functions. It also has antioxidant, antiinflammatory, and glucose regulatory properties.<br />
Melatonin also changes behavior especially in depressed patients or patients who are prone to a psychiatric illness.<br />
External noradrenergic stimuli act on the suprachiasmatıc nuclei and control melatonin secretion, which in turn regulates autonomic<br />
functions and daily behaviors by acting as an endogenous synchronizer.<br />
Melatonin, which manages body core temperature, the sleep wake cycle, and gonadal sex steroids, also causes some behavioral problems<br />
in case of depression. In bipolar manic patients nocturnal melatonin is found to be higher than in depressed patients because of<br />
noradrenergic stimulation.<br />
Melatonin secretion and body core temperature are also closely related. Core body temperature is the lowest when the nocturnal melatonin<br />
secretion is high. By controlling core body temperature, melatonin also helps to regulate the body metabolism and glucose utilization.<br />
Ovulation in females is under the control of melatonin. When melatonin is the lowest nocturnally, which causes high core body<br />
temperature, it is time for ovulation in females. High core body temperature and low nocturnal melatonin secretion return to normal<br />
after the ovulation occurs. It also controls the secretion of sex steroids by its suppressive effect on the gonads. Nowadays some research<br />
is working on using it as an oral contraceptive agent.<br />
It also regulates immune functions by acting on T lymphocytes and help organisms to have a high defense against infections, supplying<br />
an anti-inflammatory effect and serving as an antitumor agent.<br />
Today it is used specifically for the treatment of sleep disorders such as:<br />
-Advanced sleep phase syndrome<br />
-Delayed sleep phase syndrome<br />
-Circadian rhythm disorders<br />
-Insomnia<br />
-Irregular sleep wake cycle<br />
-Jet-Lag<br />
-Seasonal affective disorders<br />
-REM related behavior disorders<br />
Key words: Melatonin<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S75<br />
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Abstracts of the Invited Speakers<br />
Effects of oxytocin on social behaviour<br />
Nuray Atasoy<br />
Zonguldak Karaelmas University, Faculty of Medicine, Psychiatry Department, Zonguldak, Turkey<br />
E-mail: nurayulus@yahoo.com<br />
Oxytocin (OXT) is traditionally viewed as a female hormone that is primarily associated with labor and it has a very special affect on<br />
mothering. In mothers it increases their attachment to their infant, promoting the feeling of love, and makes her infant more valuable<br />
to her. Oxytocin has been called the love and bonding hormone. Furthermore, oxytocin mediates attachment behavior over the course<br />
of development, with lower urinary concentrations of oxytocin found in maltreated children and in adult males with a history of early<br />
separation. Psychologically, oxytocin promotes a feeling of well being and tranquility. It also suppresses the fear that would normally<br />
cause a mother to back off from a threat. In humans, based on the animal literature, it has been postulated that beyond these peripheral<br />
actions, central OXT modulates cognition in the context of social interactions, thus promoting positive sociality.<br />
In particular, recent experiments have shown that OXT promotes trusting behavior, enhances facial emotion recognition and memory<br />
for positive social information, reduces social stress, improves social cognition in socially impaired individuals with autism, and alters<br />
dysfunctional cognition in social phobia.<br />
Functional imaging studies have just begun to elucidate the underlying neural correlates of these pro-social effects. A number of studies<br />
have provided evidence that the amygdala might be a key structure for the mediation of the social cognitive effects of OXT. Several studies<br />
have shown that a single dose of OXT reduced amygdala reactivity to pictures of aversive scenes and faces with negative valence.<br />
While studies of oxytocin and monogamous behavior in humans have not been conducted to date, one study found that in co-habiting<br />
couples, greater partner support is associated with higher plasma oxytocin in both men and women before and after a period of warm<br />
partner contact.<br />
The OXT system is a sexual dimorphic system. For example, OXT plasma levels tend to be higher in females and synthesis, as well as OXT<br />
receptor affinity, appears to be modulated by gonadal steroids such as estradiol and progesterone. It has been shown, in a study on<br />
prairie voles, that female parenting behavior is more dependent on OXT, whereas male parenting behavior is associated with vasopressin.<br />
Another study demonstrated that aggression is associated with OXT in females, but not in males. However, the hypothesis of homology<br />
between paternal and maternal behavior has not yet been adequately tested and it is possible that different neuroendocrine circuits could<br />
lead to the same behavior in males and females. Future studies should include both sexes to determine a possible sexual dimorphism in<br />
the neural effects of OXT, considering gonadal steroids and OXT receptor affinity.<br />
Key words: Oxytocin, social behaviour<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S76<br />
Thyroid hormones and psychiatric disorders<br />
Tayfun Turan<br />
Department of Psychiatry, Erciyes University, Kayseri, Turkey<br />
E-mail: mtturan@erciyes.edu.tr<br />
The role of the hypothalamic-pituitary-thyroid (HPT) axis in psychiatric symptoms and disorders has been stressed in many studies.<br />
Secretion of thyroid hormones is controlled by this axis. Hypothalamic thyrotropin releasing hormone (TRH) stimulates pituitary<br />
thytrotropin-stimulating hormone (TSH) and the latter controls the secretion of thyroid hormones. Serum thyroid hormones regulate the<br />
HPT axis by a negative feedback system. The main secretion of the thyroid gland is thyroxine (T4). T4 is converted into triiodothyronine (T3)<br />
in various tissues, especially in brain, by enzymes called “deiodinases”. Transthyretin, a hormone transporter, transports T4 into the brain (1).<br />
Thyroid hormones play a critical role in the developing and functioning of the brain (2). In this regard, it is suggested that interactions<br />
between thyroid hormones and neurotransmitter systems, especially serotonin (5-HT), norepinephrine (NE) and acetyl choline (Ach),<br />
probably contribute to the regulation of mood and behaviour (1). T3 enhances the effects of NE, 5-HT and γ-aminobutyric acid, which are<br />
thought to be involved in the etiology of some psychiatric conditions (3).<br />
In the literature there are many case reports and studies indicating probable relationships between clinical or subclinical thyroid diseases<br />
and psychiatric disorders. So far, many cases have been reported of hypothyrodism or hyperthyroidism associated with psychiatric<br />
disorders, including mania, depression, schizophreniform psychosis, paranoid psychosis, cognitive disturbances, delirium and anxiety<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
(4-9). One percent of thyrotoxic patients are suggested to have been first diagnosed with a psychiatric disease (5). Interestingly, it<br />
seems that both hyperthyroism and hypothyroidism could lead to mania, anxiety or schizophrenic symptoms. The underlying reason<br />
for the co-occurrence of thyroid diseases and psychiatric disorders is not yet known. However, in these cases, combined hormonal and<br />
psychotropic interventions may improve symptoms.<br />
Several studies have assessed HPT axis activity in various psychiatric disorders, especially mood disorders and anxiety disorders. Up<br />
to 45% of the euthyroid patients with major depression showed blunted TSH response to TRH stimulation (10). Moreover, thyroid<br />
hormones accelerate the antidepressant effect of tricyclic antidepressants (11). HPT axis alterations may play an important role in the<br />
pathophysiology of bipolar disorder, but this area has received much less attention than major depressive disorder. However, it seems<br />
that abnormalities of this axis are not uncommon among bipolar patients, especially among the rapid cycling subgroup. So far, thyroid<br />
dysfunctions such as hypothyroidism and exaggerated TSH response to TRH have been found in rapid cycling patients (12,13). In some<br />
bipolar patients, latent thyroid dysfunction becomes overt by lithium treatment. Moreover, it has been suggested in a recent study that<br />
bipolar disorder itself may cause increased thyroid volumes and decreased thyroid hormones as well as lithium treatment in patients (14).<br />
Few studies have investigated possible thyroid dysfunctions in psychotic patients. In a study, schizophrenic patients showed increased<br />
serum T4 levels, which normalized after antipsychotic treatment. Elevated serum T4 levels in schizophrenic patients may suggest an<br />
impairment of T4 metabolism in the brain (4).<br />
A few studies of panic disorder have demonstrated evidence of a blunted TSH response to TRH. A previous study showed higher TSH<br />
levels in non-medicated patients with severe panic attacks (7). Increased TSH levels seen in patients with panic disorder might be due to<br />
reduced intracerebral 5-HT concentrations (15).<br />
Eletroconvulsive therapy (ECT) itself may affect the HPT axis as do psychotropic drugs. In a previous study, elevated TSH levels were found<br />
following ECT in depressed patients. This response might contribute to the therapeutic effect of ECT (16).<br />
In conclusion, the HPT axis and thyroid hormones play an important role in the pathophysiology of many psychiatric disorders. However,<br />
further well-designed studies are needed to clarify the confusion in this field.<br />
Key words: Hypothalamic-pituitary-thyroid axis, thyroid hormones, psychiatric disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S76-7<br />
Sex steroids and psychiatric disorders<br />
Erdem Deveci<br />
Regional Training and Research Hospital, Department of Psychiatry, Erzurum, Turkey<br />
E-mail: erdemdeveci@gmail.com<br />
Sex steroids play very important roles in the development and function of the central nervous system and have long been known to<br />
exert powerful effects on brain differentiation, neural plasticity, central neurotransmission and behavior. Estrogens, progestins, and<br />
androgens are able to induce several effects in brain areas of the central nervous system, through binding with specific receptors (1).<br />
Sex steroid hormones act through genomic mechanisms, modulating synthesis, release and metabolism of many neuropeptides and<br />
neurotransmitters, and through non-genomic mechanisms, influencing electrical excitability, synaptic function, morphological features<br />
and neuron-glia interactions (2).<br />
Animal research has shown that estrogens, progesterone and testosterone are critically involved in myelination, forming the basis of white<br />
matter connectivity in the central nervous system. Animal studies have also provided evidence that estrogen modulates dopaminergic<br />
activity and affects dopamine related behaviors in animals in a variety of ways.<br />
Clinical observations suggest that sex steroids have potent effects on mood, mental state and cognitive functions. Data also suggest<br />
that estrogen has a pivotal role in modulating other neurotransmitter systems such as serotonergic and glutamatergic systems that<br />
have implications for schizophrenia and mood disorders (3,4). Sex steroid deficiency causes many neuroendocrine changes. At the<br />
hypothalamic level, estrogen withdrawal gives rise to vasomotor symptoms, eating behavior disorders, and altered blood pressure<br />
control. On the other hand, at the limbic level, the changes in serotoninergic, noradrenergic and opioidergic tones contribute to<br />
modifications in mood, behavior and nociception.<br />
Studies of testosterone concentrations in depression have yielded inconsistent results reporting low as well as high testosterone levels<br />
associated with depression (5). On the other hand anabolic steroid use has increased in prevalence in many countries over the past<br />
decade, and it can lead to aggression, depression, mania and psychosis, in addition to a range of physical complications which seem to<br />
be important in clinical practice (6).<br />
Key words: Depression, estrogen, mood disorders, progesterone, schizophrenia, testosterone<br />
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Abstracts of the Invited Speakers<br />
References:<br />
1. McEwen BS Steroid hormones are multifunctional messengers to the brain. Horm Res. 1992; 37(Suppl 3):1-10.<br />
2. Genazzani A.R. et al. Endocrinology of Menopausal Transition and Its Brain Implications CNS Spectr. 2005 Jun;10(6):449-57.<br />
3. Janice R, Stevens MD Schizophrenia: reproductive hormones and the brain. Am J Psychiatry 2002; 159:713-719.<br />
4. Seeman MV. The role of estrogen in schizophrenia. J Psychiatry Neurosci 1996; 21:123-125.<br />
5. Zarrouf FA, Artz S, Griffith J, Sirbu C, Kommor M. Testosterone and depression: systematic review and meta-analysis. J Psychiatr Pract 2009;15:289-305.<br />
6. Hall, R. C. W., Hall, R. C. W. & Chapman, M. J. Psychiatric complications of anabolic steroid use. Psychosomatics, 2005; 46- 285.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S77-8<br />
Insulin and psychiatric disorders<br />
Mesut Cetin<br />
Department of Psychiatry, GATA Haydarpasa Training Hospital, Uskudar, Istanbul, Turkey<br />
E-mail: mesutcetin@yahoo.com<br />
Insulin is a hormone central to regulating carbohydrate and fat metabolism in the body. Insulin also influences other body functions, such<br />
as enhancing acute thermoregulatory and glucoregulatory responses to food intake. It is also a neuropeptide transmitter and enhances<br />
learning and memory.<br />
Hypoglycemia is a lack of sufficient glucose and a scarcity of the sources of glucose, which can dramatically manifest itself with impaired<br />
functioning of the central nervous system and can cause dizziness, speech problems, and even loss of consciousness. While producing<br />
those symptoms, hypoglycemia also provokes a rapid increase in epinephrine secretion, which leads to tremulousness, lightheadedness,<br />
perspiration, anxiety, hunger, nausea, and tachycardia. These symptoms present like a panic attack, suggesting that if hypoglycemia does<br />
provoke anxiety attacks it may be through its action as a nonspecific stressor, perhaps by interacting with an underlying CNS disorder<br />
that predisposes to panic. The fear of hypoglycemia-induced bodily symptoms of arousal has been implicated in the pathogenesis of<br />
both spontaneously occurring and experimentally provoked panic attacks. The fear of bodily symptoms may be a characteristic of panic<br />
disorder and is hypothesized to predict state anxiety and panic frequency during experimentally induced peripheral arousal.<br />
Insulin resistance and metabolic syndrome (MS) have become worldwide problems. MS is a cluster of risk factors associated with<br />
increased risk of cardiovascular diseases and type 2 diabetes. Based on research data from 2004, 40% of adults in Turkey meet the criteria<br />
for diagnosis of metabolic syndrome. The use of certain medications, such as atypical antipsychotics, may increase insulin resistance and<br />
the risk of the metabolic syndrome.<br />
Key words: Insulin, panic disorder, insulin resistance, hypoglycemia, depression<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S78<br />
[PS-14]<br />
Symposium Title: Clinical course of psychiatric disorders associated with trauma and treatment issues<br />
Trauma and mood disorders<br />
Medine Yazıcı Güleç<br />
Erenkoy Mental Research and Training Hospital, Istanbul, Turkey<br />
E-mail: drmedineyazici@yahoo.com, medineyazici@hotmail.com<br />
There is increasing evidence for the role of adverse childhood experiences in the occurence of mood disorders (MD). A great number of<br />
studies have shown that there is a correlation between MD and parental indifference, neglect and sexual and physical abuse. Angst et<br />
al., in a 20-year longitudinal study, suggested that childhood family issues have a robust correlation with the chronicity of bipolar and<br />
unipolar MD, and adverse childhood experiences give rise to low self-esteem and anxious personality. The presence of childhood trauma<br />
(CT) has found to be associated with increases in rates of substance abuse, early age of onset, rapid cycling, and suicide. There is severe<br />
CT in half (49%) of bipolar MD patients.<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Individuals with CT have both an overall increased risk for depression and a substantially increased sensitivity to the depressogenic<br />
effects of stressful life events. The relation between CT and stressful life events is dose dependent and correlated with the intensity of the<br />
neuroticism. It has been shown that the severity of CT predicts an early age of onset and the number of life time depressive episodes,<br />
and that it is associated with more comorbidity. Increased rates of emotional CT, depressive symptoms and anxiety have been reported<br />
in treatment resistant group of patients.<br />
Childhood adverse life events are associated with various neuroendocrine and neuroanotomical changes. There is a 6 times larger ACTH<br />
response to stress in depressive female patients who reported CT. These patients also have an increased cortisol response and heart<br />
rate response to psychosocial stress. Women, who have reported CT but were not depressed, have exhibited normal cortisol responses,<br />
despite having increased an ACTH response. This can be interpreted as resilience against depression, an adrenal adaptation to central<br />
sensitization. It has been reported that decreased hippocampal volume (18%) in depression is related to CT and that the hippocampal<br />
volumes of depresssive patiens who did not report CT were equal to those of the control group. Repeated bursts of CRF in response to<br />
stress during development and increased cortisol reactivity over the course of time may contribute to smaller hippocampi after childhood<br />
trauma exposure, leading to further sensitization of the stress responses. These results would suggest that there are biologically distinct<br />
subtypes of depression as a function of childhood trauma.<br />
The effect of CT on predisposition to illness is associated with genotype. The s/s allele of the serotonin transporter gene, the gene<br />
polymorphism of BDNF and the CRF-1 gene have been shown to be related to vulnerability to trauma effects.<br />
CT is associated to decreased response to pharmacological treatment. Among chronically depressed patients with no history of early<br />
trauma, combination treatment was most effective in attaining remission compared to pharmacotherapy and psychotherapy. In contrast,<br />
in chronically depressed patients with early-life trauma, remission rates were significantly higher for psychotherapy alone versus<br />
pharmacotherapy. Combination treatment did not have any further advantage over psychotherapy alone. Improved effects of cognitive<br />
and behavioral therapies, group therapies and EMDR have been reported in various studies. Questioning about CT in MD patients seems<br />
to be important for treatment planning, assessment of risks and prophylactic interventions.<br />
Key words: Childhood trauma, mood disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S78-9<br />
Trauma and psychotic disorders<br />
Selma Bozkurt Zincir<br />
Erenkoy Mental Health and Diseases Training and Research Hospital, Istanbul, Turkey<br />
E-mail: sbozkurtzincir@yahoo.com<br />
In recent years, there has been a growing awareness of the importance of abuse or trauma in shaping the course of people’s lives. There<br />
is growing literature to indicate that trauma is also linked with more severe psychiatric disturbances, including symptoms indicative of<br />
psychosis in general and schizophrenia in particular. Several lines of evidence suggest an association between trauma and psychosis with<br />
a dose-response effect. First, studies have demonstrated a high incidence of trauma in the lifetimes of patients with psychosis. Abused<br />
patients are particularly likely to experience positive symptoms, such as paranoid ideation, thought insertion, visual hallucinations, ideas<br />
of reading someone else’s mind, ideas of reference, and hearing voices making comments. Secondly, it has been suggested that of all<br />
diagnostic categories, psychosis displays the strongest association with child abuse. Thirdly, according to some researchers childhood<br />
sexual abuse is the most powerful predictor of later psychiatric symptoms and disorders after controlling for significant demographic<br />
variables.<br />
It has been suggested that the experience of abuse may create a biological or psychological vulnerability for the development of<br />
psychotic symptoms, including sub-clinical psychotic experiences such as low-grade delusional ideation, suicidal thinking and isolated<br />
auditory hallucinations. Exposure to psychological trauma worsens the prognosis of expression of psychosis, in terms of greater likelihood<br />
of transition to a more severe psychotic state. According to recent cognitive models of psychosis early adverse experiences such as<br />
social marginalization, childhood loss or severe childhood trauma may create an enduring cognitive vulnerability characterized by less<br />
subjective control over these experiences, negative schematic models of the self and a world that facilitates external attributions. This<br />
tendency to externally attribute events may lie beneath paranoid ideation.<br />
Current ideas about biological consequences of early adversities lend even more credibility to the notion of an enduring psychological<br />
vulnerability. It has been suggested that adverse life events or significant losses might be able to mould the neurodevelopmental<br />
abnormalities that underlie sensitivity to stressors, if they occur early enough or are sufficiently severe. Thus abnormal neurodevelopmental<br />
processes may originate from traumatic events in childhood. Specifically, when exposure to stressors persists and heightened stress-<br />
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Abstracts of the Invited Speakers<br />
induced glucocorticoid release is chronic, permanent changes in the hypothalamic-pituitary-adrenal (HPA) axis may ensue. This may<br />
account for the dopaminergic abnormalities considered central to biological accounts of psychosis. Other researchers are also examining<br />
the role of dissociative processes, attachment styles, and trauma related cognitive biases to try to better understand precisely how<br />
childhood trauma can lead to psychosis later in life.<br />
Clinically it is imperative to routinely enquire about traumatic experiences to respond appropriately and to offer psychosocial treatments<br />
to those who report traumatic life events in the context of psychotic experiences.<br />
Key words: Trauma, psychotic disorders, schizophrenia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S79-80<br />
Relationship of sexual dysfunction with trauma<br />
Murat Erdem<br />
Gulhane Military Medical Faculty, Psychiatry Department, Ankara, Turkey<br />
E-mail: drmerdem@yahoo.com<br />
Exposure to sexual trauma in adulthood is perceived as helplessness and loss of control even if sexuality has been defined as a pleasant<br />
event before trauma. Feelings of guilt and shame occurring after trauma as well as secondary clinical pictures such as depression,<br />
post traumatic stress disorder, and alcoholism are major causes of sexual dysfunction. Also sexual abuse in childhood raises a sense of<br />
weakness and perception of inadequacy. These individuals are at risk of developing inappropriate sexual behaviors over time. Indulging<br />
in sexual behaviors and thoughts that are evaluate sexuality as a gift or privilege are precursors for these inappropriate behaviors. In<br />
addition, the stigmatization caused by feelings of shame and guilt in these children is another cause of sexual problems in the future.<br />
Childhood sexual trauma is associated with negative attitudes about sexuality, lack of sexual satisfaction, orgasmic failure, need for sexual<br />
therapy and low self-esteem about sexual attractiveness. Chronic pelvic pain is a significant clinical entity which causes sexual dysfunction<br />
in many ways. In studies, the rate of traumatic childhood sexual experiences was found to be over 60% in these patients (N. Leithner,<br />
2006). The difference between patients with chronic pelvic pain and a healthy control group was found to be even greater in terms of the<br />
increasing violence of sexual trauma. In a study of 63 patients with chronic pelvic pain, a history of sexual trauma was identified in 64.5%<br />
of cases and deficiencies in sexual function were found to be associated with the level of depression in these patients (ME Randolph,<br />
2006).<br />
There are several studies that show that physical and sexual trauma plays a role in the etiology of vaginismus. In a study comparing the<br />
childhood and adolescent sexual traumas of patients with vaginismus and dyspareunia and control groups -(each group consisting of<br />
29 patients) childhood sexual trauma was found to be twice as high as the control group in the vaginismus group (Reissing ED, 2003).<br />
In the literature there are case reports suggesting that EMDR is effective in cases of vaginismus resulting from childhood sexual trauma.<br />
In studies evaluating the relationship between childhood sexual traumas and a specific sexual dysfunction, aand in studies examining<br />
sexual functioning in general, a strong relationship has been found between these two situations. Structural vulnerability and the severity<br />
of sexual trauma were also reported to affect this relationship. While childhood sexual trauma is associated with sexual stimulation<br />
disorder, orgasmic disorder, vaginismus, dyspareunia and emotional problems about sexuality (sexual guilt, sexual anxiety etc.) in most<br />
individuals, high-risk sexual behaviors, characterized by extreme preoccupation with sexuality and uncontrolled sexual relationships, are<br />
seen in fewer individuals.<br />
Sexual childhood trauma in men is being reported, recognized and treated less frequently than the actual prevalence. Sexual dysfunction<br />
in these individuals was reported to be seen at least five times more than people who have not been exposed to a trauma. In a study of<br />
1793 individuals, exposure to sexual trauma before age 16 has been reported at more than 1/3 of women and about 1/6 of men. In both<br />
sexes, especially in women, an association between the presence of childhood sexual trauma and sexual dysfunction has been identified<br />
(Najma JM, 2005). Leonard et al. found that problems associated with orgasm are the most frequent sexual problems seen in individuals<br />
who were exposed to a childhood sexual trauma (2008).<br />
Key words: Trauma, sexual dysfunction<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S80<br />
S80 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
[PS-15]<br />
Symposium Title: Depression and pain<br />
Impact of pain on treatment in depression<br />
Cengiz Akkaya<br />
Departments of Psychiatry, Uludag University, Bursa, Turkey<br />
E-mail: cakkaya@uludag.edu.tr<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Major depressive disorder (MDD) is a chronic, disabling condition with a wide range of symptoms, including core mood symptoms of<br />
depression and anxiety, cognitive and behavioral deficits, and somatic/physical disturbances. Approximately two-thirds of patients with<br />
depression experience physical pain symptoms (e.g. headache, neck and back pain, abdominal pain, diffuse musculoskeletal pain). Pain<br />
as a symptom of depression, often has a negative impact upon other depressive symptoms (for example, it may induce or exacerbate<br />
low energy, sleep disturbance, and anxiety), adherence to medication, and obtaining adequate therapy. Therefore, pain influences both<br />
the course of depressive illness and the treatment outcome. Also the severity of pain is found to be a strong predictor of poor response<br />
and health-related quality of life. Impairments in social and occupational functioning may increase when depression and pain coexist.<br />
Patients who fail to achieve remission after antidepressant therapy are more likely to suffer residual pain and other physical symptoms<br />
compared with remitted patients.<br />
The close relationship between pain and depression, and the growing evidence of a connection between treatment outcomes in these<br />
conditions, suggests that maximal patient benefit may result from treatments which effectively address both emotional and physical<br />
symptom domains. Therefore, treatments that address both depression and pain are highly desirable. Neurobiological evidence suggests<br />
that mood and chronic pain are connected via serotonin and noradrenaline neurotransmitter pathways. Serotonin and norepinephrine<br />
play a key modulating role in pain mechanisms in the central nervous system. Serotonin modulates both descending inhibitory and<br />
facilitatory pathways and thus exerts both an antinociceptive and a pronociceptive effect. Noradrenaline, however, typically acts centrally<br />
in an antinociceptive manner, exerting its effects via a-2-adrenoreceptors in the descending antinociceptive pathways.<br />
Efficacy for treating pain is best established for tricyclic antidepressants. But through the last decade, antidepressant medications,<br />
particularly selective serotonin reuptake inhibitors (SSRIs) and selective serotonin and norepinephrine reuptake inhibitors (SNRIs), are<br />
widely used in the management of MDD. SSRIs are often favored in practice because of their tolerability and safety. However, their efficacy<br />
in pain is thought to be relatively weak. On the other hand the mechanism of SNRIs has been hypothesized to confer analgesic effects<br />
independent of antidepressant action. Evidence suggests that potentiation of both serotonin and norepinephrine is required for effective<br />
analgesia; drugs that inhibit only one of these systems (particularly serotonin) appear to have a limited effect. Whether antidepressants<br />
relieve pain through direct analgesic effects or indirectly through antidepressant action is still under discussion. There may be a close<br />
association between analgesic and antidepressant effects and pain relief may be secondary to mood improvement.<br />
Key words: Pain, depression, antidepressant<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S81<br />
Clinical characteristics and mechanism of pain in depression<br />
Selçuk Kırlı<br />
Department of Psychiatry, Uludag University, Bursa, Turkey<br />
E-mail: kselcuk@uludag.edu.tr<br />
Although there is a large amount of data indicating that depression and pain symptoms are closely interrelated, they are not included in<br />
depression symptoms in the classification systems. Even so, new developments in neuroscience have carried the data on this interrelation<br />
and co-occurrence beyond the epidemiological dimension to the awareness of a common underlying mechanism (1,2).<br />
Although such a co-occurrence and the mechanisms that influence it are being discussed more and more, pain symptoms still cannot<br />
be well assessed or monitored and they are usually described by terms such as ‘medically unexplainable’, ‘functional’ or ‘psychosomatic’.<br />
The following statements may be made about the clinical characteristics of the symptoms (1):<br />
• They do not conform to the anatomic localizations which would help explain their causes.<br />
• They may vary in severity and location.<br />
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Abstracts of the Invited Speakers<br />
• Pain symptoms occur in 1/5 – 1/3 of patients with depression. These ratios are approximately 4 times higher than the ratios of those<br />
with no depression. The ratios in the literature about pain symptoms in patients with depression are approximately 65% on average (3).<br />
• Chronic pain is a significant individual risk factor for suicide and self-injury.<br />
• Chronic pain results in increases in treatment costs and a poorer outcome.<br />
• The presence of pain as a residual symptom is the strongest predictor of recurrence.<br />
It should be kept in mind that chronic pain, which is considered as being ‘functional’ in terms of the mechanisms involved in having pain<br />
during depression, is medically unexpected, self-generated and associated with vulnerability to pain. Therefore, central factors should<br />
play a leading role in experiencing it (4). Living with pain causes negative emotions, but beyond that, continuous pain is a physical<br />
symptom of depression. A neurobiological explanation of experiencing these two situations concurrently is not all that difficult when the<br />
broadness and diversity of the mechanisms involved in experiencing depression are taken into consideration (5).<br />
The mechanisms involved in this co-occurrence may be summarized as follows:<br />
• The connection between the emotional and somatic (e.g. pain) symptoms of depression is probably set up through the HPA axis. This<br />
system plays an important function in vulnerability to stress.<br />
• The changes that emerge in the transfer of NA and 5HT in the CNS are of critical significance in terms of both depression and chronic<br />
pain pathophysiology (6). Monoamines regulate both mood symptoms and sensations of pain.<br />
• Pain stimuli are carried from the periphery to the CNS by primary afferent fibers and are regulated by stimulating glutamate and<br />
suppressor GABA.<br />
• The sub-cortical areas involved are the hypothalamus, periaqueductal gray matter, raphe dorsalis and locus coeruleus. These areas are<br />
also regulated by 5HT and NA.<br />
• Cortical processing of a pain sensation is carried out in the relevant areas of the cortex.<br />
In conclusion, it is obvious that common pathophysiological processes underlie the co-occurrence of depression and somatic pain<br />
symptoms seen in this picture and it is important to take such pain symptoms into consideration in a comprehensive treatment approach.<br />
Key words: Pain, depression, clinical characteristics<br />
References:<br />
1. Peveler R, Katona C, Wessley S, Dowrick C: Painfull symptoms in depression: under-recognized and under treatment. British J Psychiatry 2006;188:202-203.<br />
2. Von Knorring L, Ekselius L: Idiopatic pain and depression. Quality of Life Research 1994;3:557-568.<br />
3. Bair MJ, Robinson RL, Katon W, Kroenke K: Depression and pain comorbidity. A literatüre rewiev. Arch Gen Psychiatry 2003;163:2433-2445.<br />
4. Mohr P, Bitter I, Svestka J, Seifritz E, Karamustafalıoğlu O, Koponen H, Sartorius N: Management of depression in the presence of pain symptoms. Psychiatria<br />
Danubina 2010;22:4-13.<br />
5. Nemeroff CB, Vale WW: The neurobiology of depression: inroads to treatment and new drug discovery. J Clin Psychiatry 2005;66 (suppl. 7):5-13.<br />
6. Wise TN, Fishbain DA, Holder-Perkins V: Painfull physical symptoms in depression: a clinical challenge. Pain Med 2007;8 (suppl. 2):75-82.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S81-2<br />
[PS-16]<br />
Symposium Title: Marijuana; from mellow to madness<br />
Effect of cannabis use on cognitive functions<br />
Cüneyt Evren<br />
Bakirköy Training and Research Hospital for Psychiatry, Neurology, and Neurosurgery AMATEM, İstanbul, Turkey<br />
E-mail: cuneytevren@yahoo.com<br />
If we look at the data of recent years, probation admissions to AMATEM Istanbul, which are mostly related to cannabis use, have increased<br />
significantly; the number of first admissions/number of control admissions for 2008, 2009 and 2010 are 2318/24261, 3759/31862 and<br />
5639/30959, respectively. As for other psychoactive substances, the negative effects of cannabis use on cognitive functions are well<br />
known. Some cannabis-related cognitive function deficits improve after cessation of cannabis use, but growing evidence also suggests<br />
that other deficits persist after cannabis is discontinued and may hinder an individual’s ability to make the best use of behavioral<br />
therapies, putting him or her at greater risk for relapse of cannabis use (1).<br />
Cannabis seems to continue to exert impairing effects in executive functions even after 3 weeks of abstinence and beyond. Although<br />
basic attentional and working memory abilities are largely restored, most enduring and detectable deficits are seen in decision-making,<br />
S82 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
concept formation, and planning. Those subjects reporting chronic, heavy cannabis use show the most enduring deficits (2). One can<br />
suggest that some of these impairments are not completely reversible upon cessation of cannabis use and moreover may interfere with<br />
the treatment of cannabis addiction. Therefore, targeting cognitive impairment associated with chronic cannabis use may be a promising<br />
novel strategy for the treatment of cannabis addiction (3).<br />
While acute administration of cannabis to patients with schizophrenia exacerbates symptoms and cognitive impairments and may have<br />
enduring effects, cannabis has also been found to have some beneficial effects on cognition, at least in certain subgroups of patients (4).<br />
Cannabis using patients had better attention and executive functions than non-cannabis using patients at baseline and after one year of<br />
treatment in a representative sample of first-episode schizophrenia patients. Cannabis using patients appear to comprise a subgroup of<br />
patients with better premorbid adjustment and premorbid frontal cognitive functions (5).<br />
Thus, while cannabis use is traditionally associated with cognitive impairment, the relationship is more complex in the case of schizophrenia.<br />
Key words: Cannabis, cognitive functions<br />
References:<br />
1. Blume AW, Marlatt GA. The role of executive cognitive functions in changing substance use: what we know and what we need to know. Ann Behav Med 2009;<br />
37:117-25.<br />
2. Crean RD, Tapert SF, Minassian A, Macdonald K, Crane NA, Mason BJ. Effects of chronic, heavy cannabis use on executive functions. J Addict Med 2011; 5:9-15.<br />
3. Sofuoglu M, Sugarman DE, Carroll KM. Cognitive function as an emerging treatment target for marijuana addiction. Exp Clin Psychopharmacol 2010; 18:109-19.<br />
4. Yücel M, Bora E, Lubman DI, Solowij N, Brewer WJ, Cotton SM, Conus P, Takagi MJ, Fornito A, Wood SJ, McGorry PD, Pantelis C. The impact of cannabis use on<br />
cognitive functioning in patients with schizophrenia: a meta-analysis of existing findings and new data in a first-episode sample. Schizophr Bull 2010 (In press)<br />
5. Rodríguez-Sánchez JM, Ayesa-Arriola R, Mata I, Moreno-Calle T, Perez-Iglesias R, González-Blanch C, Periañez JA, Vazquez-Barquero JL, Crespo-Facorro B. Cannabis<br />
use and cognitive functioning in first-episode schizophrenia patients. Schizophr Res 2010;124:142-51.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S82-3<br />
The differences between marijuana psychosis and other substance induced psychoses<br />
Mükerrem Güven<br />
Akdeniz University Research and Practice Center for Alcohol and Substance Addiction, Antalya,Turkey<br />
E-mail: mguven@akdeniz.edu.tr<br />
Psychosis may be observed in intoxication from cannabis, alcohol, opiates, inhalants, stimulants, amphetamines, hallucinogens,<br />
phencyclidine, anxiolytics, sedatives and hypnotics. The condition of psychosis may also occur due to abstinence from alcohol, anxiolytics,<br />
sedatives, and hypnotics (1). Although mostly alcohol-dependent psychotic disorders are reported, the cannabis-psychosis relationship<br />
arouses more interest among researchers. Hypomania and agitation are more frequently noted in cannabis users compared with users<br />
receiving other substances. The symptoms of cannabis-psychosis usually disappear with a decrease in cannabis use, but the true nature<br />
of perception (flashbacks) hallucinations may be re-lived. As distinct from psychosis depending on other substances, evidence regarding<br />
the relationship between cannabis usage and the first attack of schizophrenia is increasing (2). There are long-term clinical follow-up<br />
studies to distinguish the acute toxic psychosis revealed in cannabis users from psychoses similar to schizophrenia, and also some<br />
studies conducted on the assumption that “cannabis psychosis” is distinct from other psychoses caused by other substances. Auditory<br />
hallucinations and emotional blunting are reported less commonly in cannabis psychosis compared to non-substance dependent<br />
psychoses. In a study investigating cannabis-induced psychoses, no significant relationship was determined between usage and the onset<br />
age of receiving cannabis; however, it has been put forth that a relation exists between cannabis use, the length of addiction and the quality<br />
and amount of cannabis received (3). Capsi et al. have reported that the risk for cannabis-induced psychosis is high in people carrying<br />
the valine-158 allele of the catechol-O-methyltransferase (COMT) gene (2005). Abuse substances affect different neurotransmitters in the<br />
central nervous system (4). Positive psychotic symptoms such as paranoid delusions and hallucinations are observed in half of cocaine<br />
addicts. As the period of cocaine use increases, negative symptoms and paranoid psychosis can be recorded. Stimulants such as cocaine<br />
and amphetamine can reveal psychosis by increasing dopaminergic activity in the central nervous system (CNS). Cannabinoid-1 (CB-1)<br />
receptors are responsible for the effects of cannabis in the CNS. In the lateral putamen, pallidum and substantia nigra, CB-1 receptors<br />
are determined to be present in a high degree. Many neurotransmitter systems taking part in the etiology of schizophrenia, especially<br />
glutamatergic and dopaminergic systems, are affected by activation of the CB-1 receptor (5). Effects of substances on neurotransmission<br />
should be better investigated to understand how substance-induced psychotic disorder develops.<br />
Key words: Addiction, cannabis, psychosis, substance abuse<br />
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Abstracts of the Invited Speakers<br />
References:<br />
1. American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: APA.<br />
2. Van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol 2002;15:319-327.<br />
3. Makkos Z, Fejes L, Inczedy-Farkas G, Kassai-Farkas A, Faludi G, Lazary J. Clinical characteristics of cannabis-induced schizophrenia spectrum disorder.<br />
Neuropsychopharmacol Hung. 2011 Sep;13(3):127-38.<br />
4. Caspi A, Moffitt TE, Cannon M, McClay J, Murray R, Harrington H, Taylor A, Arseneault L, Williams B, Braithwaite A, Poulton R, Craig IW. Moderation of the effect of<br />
adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O methyltransferase gene: longitudinal evidence of a gene X<br />
environment interaction. Biol Psychiatry 2005; 15;57(10):1117-7.<br />
5. Müller-Vahl KR, Emrich HM. Cannabis and schizophrenia: towards a cannabinoid hypothesis of schizophrenia. Expert Rev Neurother. 2008 Jul;8(7):1037-48. Review.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S83-4<br />
Selective serotonin reuptake inhibitors in the treatement of cannabis dependence<br />
Musa Tosun<br />
Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey<br />
E-mail: musatosun@hotmail.com<br />
Treatment of cannabis dependence should aim cannabis abstinence and psychosocial support as in general dependency treatment<br />
approach.<br />
The cannabis detoxification of the patient might be achieved by treatment interventions in hospital setting or following up the patient<br />
closely in outpatient setting. In outpatient setting, the regular urinalyses and close monitoring of the patient must be carried out. The<br />
metabolites of the cannabinoids could be detected in urinalysis from 3 days up to 4 weeks following the last use.<br />
Individual, family, and group psychotherapies might be beneficial while supporting the patient. Education is the most important element<br />
for both “abstinence” and “support programs,” as the motivation to quit and not to restart is primarily due to education on the effects and<br />
harmful consequences of cannabis abuse. Tranquilizer drugs might be efficient in short term withdrawal symptoms that might be seen<br />
in cannabis abusers or addicts.<br />
Selective serotonin reuptake inhibitors (SSRIs) as other antidepressant agents may be used in the treatment of depressive patients, who<br />
use cannabis as a self treatment for depression, and in co-morbid depression of cannabis use disorders or in depressive symptoms caused<br />
by cannabis abuse. In addition, SSRIs might also be used in the treatment of cannabis-induced anxiety disorders.<br />
There is growing interest in the use of antidepressants in cannabis abuse because of highly reported depression rates during the<br />
treatment of cannabis abuse or after the cessation. Nevertheless, there is a dearth of knowledge about the treatment of cannabis abuse<br />
with SSRIs. In a double blind placebo controlled study, fluoxetine has been reported to decrease the frequency of cannabis use in alcoholic<br />
patients with depression.<br />
References:<br />
1. Cornelius JR Salloum IM, Haskett RF, Ehler JG, Jarrett PJ, Thase ME, Perel JM. Fluoxetine versus placebo for the marijuana use of depressed alcoholics. Addict Behav.<br />
1999 Jan-Feb;24(1):111-4.<br />
2. Hall W. & Degenhardt L. : Cannabis-Related Disorders. in Kaplan & Sadock’s Comprehensive Textbook of Psychiatry 8th ed. Lippincott Williams & Wilkins,<br />
Philadelphia, 2005. Vol. I: 1211-1220<br />
3. Tosun M. : Alkol ve Diğer Maddeler ile İlişkili Bozukluklar. İ.Ü.Cer.Paş.Tıp Fak. Yayınları, Rektörlük Yay.No: 4215, Fak.Yay.No. 229, İstanbul, 2000 : 96-100.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S84<br />
S84 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
[PS-17]<br />
Symposium Title: Overcoming treatment resistance: An update<br />
Treatment strategies for treatment resistant depression<br />
Selçuk Aslan<br />
Gazi University, Medical School, Psychiatry Department, Ankara, Turkey<br />
E-mail: saslan@gazi.edu.tr<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Depression is a disorder with heterogenic etiology and variable clinical features. Response to the treatment is defined as a 50% reduction<br />
in admission symptoms. Recent studies with large numbers of patients have revealed that acute phase treatment should last for 6 weeks,<br />
including at least 4 weeks with effective dosages. Approximately 60% of patients have a response to the first antidepressant treatment.<br />
The remainder, 40% of patients, either has a partial response or they are non-responders (Fava 1996).<br />
At the end of 6 weeks with optimum treatment dosing, if symptoms have not reduced by 20-25%, patients are described as nonresponders<br />
and drug treatment should be switched to another type of antidepressant medication. Patients, who do not respond to<br />
trials of adequate dosages and periods of two or more different classes of antidepressant treatments, are considered as treatmentresistant<br />
depression (TRD). If there is a partial response to antidepressant treatment, waiting for couple of weeks is the rational approach.<br />
The patients who have high depression scores at the initial evaluation have relatively higher degrees of partial or non-response to<br />
antidepressant medications. These cases are more likely to have comorbid axis 1 and axis 3 physical disorders. An 8-12 week period of<br />
effective antidepressant treatment should be applied in these cases. Thase and Rush, proposed 5-stage-model for the description of TRD<br />
(1997). Later in the STAR D study, Rush et al. developed sequences of treatment alternatives for relieving depression (Rush et al. 2003).<br />
On the other hand, increasing drug dosages results in more side effects and adverse reactions. Some patients may be low metabolizers<br />
and higher doses may result in significant side effects. Also fast metabolizer patients may respond to higher doses of medications. Efficacy<br />
of atypical antipsychotics, stimulants, pindolol, lithium, and lamotrigine have been tested for augmentation in ongoing treatment for TRD<br />
in clinical trials (Caravalho et al 2009). In severe cases with no response or partial response to treatment, inpatient treatment should be<br />
considered.<br />
Non-responders or partial responders can be treated with electro convulsive therapy with anesthesia or non-responders can be treated<br />
with rTMS (Paul et al 2006). Selected non-responsive cases may be treated with more invasive techniques such as deep brain stimulation<br />
or vagus nerve stimulation. Biological predictors should be identified to irecognize patients who will not respond to two adequate trials<br />
of different antidepressant.<br />
In addition, psychotherapeutic interventions during the treatment period, such as observing and revealing automatic thoughts,<br />
assumptions, and basic beliefs and depressive schemas, should be evaluated and behavioral and cognitive interventions can be applied.<br />
Activity scheduling and participating in regular exercise might also be helpful to some degree.<br />
Key words: Depression, treatment resistant depression<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S85<br />
Treatment resistant psychiatric disorders and trauma history<br />
Mehmet Akif Ersoy<br />
Ege University School of Medicine, Department of Psychiatry, Izmir, Turkey<br />
E-mail: akifersoy@gmail.com<br />
Although many clinicians depending on their experience will agree that childhood trauma history will cause treatment resistance<br />
regardless of the diagnosis, studies investigating this issue directly are scarce. During our search of literature we have found publications<br />
on the relationship between childhood trauma and treatment resistance in a few disorders such as obsessive compulsive disorder (OCD),<br />
major depression, and bipolar affective disorder. One study reported that 82% of OCD cases had a history of childhood trauma. In this<br />
study 39% of the cases met the criteria for post traumatic stress disorder (PTSD) and half of those who had a history of trauma met the<br />
PTSD criteria. It is noticeable that those who had major depression or borderline personality disorder, in addition to OCD, had a higher<br />
risk of having comorbid PTSD. Treatment resistant OCD cases should be screened for PTSD and having comorbid major depression and/<br />
or borderline personality disorder helps to predict PTSD and may help to determine the severity of the illness.<br />
S85
Abstracts of the Invited Speakers<br />
An indirect approach is looking for comorbidity of trauma related disorders in treatment resistant cases. One study has pointed out that<br />
OCD cases with comorbid PTSD have worse treatment outcomes. A meta-analysis study has revealed that childhood trauma not only<br />
effects lifetime risk of major depression, it also negatively effects severity of clinical parameters and results of treatment. This particular<br />
study, which included 16 epidemiological studies (23544 cases), showed that childhood abuse is related to recurrent and persistent<br />
depressive episodes. Another meta-analysis of 10 clinical studies with a total of 3098 cases, found that childhood abuse is related to<br />
absence of remission and absence of treatment response in depression.<br />
In bipolar disorder, those who have had childhood trauma, had earlier onset of illness, more severe current symptoms of mania or<br />
depression and more frequent episodes of depression. Half of adult bipolar disorder patients were found to have severe childhood trauma.<br />
In patients with early childhood trauma such as early loss of parents and physical or sexual abuse or neglect, psychotherapy alone had<br />
favorable results compared to monotherapy of antidepressants, while interestingly combination of psychotherapy and pharmacotherapy<br />
was slightly more effective than psychotherapy alone. Researchers have stressed that psychotherapy must be included in the treatment<br />
of chronic depression patients with childhood trauma.<br />
Studies which directly investigate the relationship of treatment resistance and childhood trauma are scarce. Some comorbid conditions,<br />
such as personality disorders, that complicate treatment of depression are known to be related to childhood trauma.<br />
As a result, we can with great confidence state that childhood trauma is related to treatment resistance in most psychiatric conditions.<br />
Especially in cases of treatment resistance, childhood trauma should be investigated and appropriate treatment modalities should be<br />
added to the treatment regime.<br />
Key words: Treatment resistance, childhood trauma<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S85-6<br />
Pyshosocial approaches for treatment resistant symptoms in patients with schizophrenia<br />
Mustafa Yıldız<br />
Kocaeli University School of Medicine, Department of Psychiatry, Kocaeli, Turkey<br />
E-mail: myildiz60@yahoo.com<br />
One of the main goals in the treatment of schizophrenia is to increase psychosocial functioning and to provide a satisfying life for patients<br />
with schizophrenia who have persistent symptoms although all treatment efforts, including ECT, had been performed. Whatever the<br />
clinical conditions of the patients are, they have a right to live in dignity in their community like other people. The emphasis in psychiatric<br />
rehabilitation approaches is on enhancing psychosocial functioning and quality of life of patients. Increasing the functioning of patients<br />
depends on controlling symptoms as much as possible and preventing exacerbations. Patients should learn and practice coping skills<br />
(humming or singing, reading aloud, thinking “stop”, listening to the radio, watching TV, doing favorite hobbies, telling the voices to go<br />
away, doing physical exercise, going to movies etc.) for their persistent symptoms. Sometimes it may be necessary to use behavioral<br />
techniques; for example, a patient showing 20 aggressive behaviors due to command hallucinations a week, showed on aggressive<br />
behavior a month after applying a behavior modification program. Patients should be placed in a program, in which their healthy<br />
aspects can be developed and keep them in continuing daily activities, so that they become empowered. All these results can take place<br />
by collaboration and coordination of different services. Being provided a safe environment, getting positive feedback, participating in<br />
occupational activities and working in a less stimulating milieu are also important for patients.<br />
It could be possible for patients to live a more satisfying and more normal life by integrating treatment and rehabilitation services. The<br />
elements of integrated approaches are: patients’ participation in treatment and the maintenance of treatment, development of treatment<br />
alliances, teaching illness management, using cognitive behavioral treatment methods, modifying new resources to attain personal<br />
goals, accommodating community resources, establishing relationships with psychosocial clubs, involving families in the treatment, and<br />
providing personal support services (case management), supported employment, supported residence, and peer supports.<br />
Key words: Schizophrenia, persistent symptoms, functioning, rehabilitation<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S86<br />
S86 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
[PS-18]<br />
Symposium Title: Chronobiotics and chronotherapeutics in psychiatry<br />
The use of sleep deprivation in the treatment of depressive disorders<br />
Adem Aydın<br />
Department of Psychiatry, Yuzuncu Yıl University, Van, Turkey<br />
E-mail: adem.dr@gmail.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Sleep deprivation has been used for exploring functions of sleep among healthy individuals and for treating patients suffering from<br />
depressive symptoms. Sleep deprivation is a rapid, effective and brief therapeutic alternative. Two types of sleep deprivation applications<br />
have been implemented; one is deprivation of sleep for whole night and the other is partial deprivation of sleep in the second part of<br />
the night. Although various hypotheses have been developed pertaining to the treatment potential of sleep deprivation in depression,<br />
the mechanisms underlying the process are still obscure (1). Early systematic research conducted by Pflug and Tolle proposed that<br />
patients characterized by endogenous depressive symptoms receptive to sleep deprivation have deficits in their circadian systems and<br />
sleep deprivation aids at ameliorating the dysregulation in the biological rhythm (2). Sleep deprivation and REM sleep deprivation act<br />
like antidepressants and some antidepressants have suppressing effects on REM sleep. Hence the role of REM sleep on the development<br />
of depression has received more attention. The reduction of REM latency and REM intensity are prominent features in patients with<br />
depression. Sleep deprivation reverses these two effects (3).<br />
The psychological response to sleep deprivation seems to occur regardless of diagnostic category such as endogenous-reactive,<br />
psychotic, nonpsychotic, unipolar, bipolar, schizoaffective, or seasonal (4). Merely diurnal variation (soothing of affect is typical in patients<br />
with depression in the later hours of daytime) and chronobiological differences are substantial in the psychological response to sleep<br />
deprivation (5).<br />
About 50-60 percent of patients with depression are prone to reflect antidepressant influences after one-night of sleep deprivation<br />
therapy. Deceleration in symptom severity as well as amelioration in suicidal thoughts occurs. The temporary antidepressant influence of<br />
the initial application does not predict inadequacy of further applications. If applications of sleep deprivation are continued one or two<br />
times per week, it has been claimed that it is likely to provide effective prophylaxis (6).<br />
Although sleep deprivation provides a rapid psychological response and a potent influence, its application is not prominent in major<br />
depression. Sleep deprivation can be qualified as an awkward method, because the application requires constant monitoring and to<br />
ensure wakefulness of patients as well as carrying a relapse risk in fiesta. The most prominent advantage of sleep deprivation compared<br />
to other medications and ECT is that it causes rapid and apparent improvement in affect. Therefore the pros and cons of sleep deprivation<br />
should be taken into account in treatment planning.<br />
Key words: Depression, sleep deprivation, treatment<br />
References:<br />
1. Rechtschaffen A. Current perspectives on the function of sleep. Perspect Biol Med 1998;41:359-390.<br />
2. Pflug B, Tolle R. Disturbance of the 24 hour rhythm in endogenous depression and treatment of endogenous depression by sleep deprivation. Int<br />
Pharmacopsychiatry 1971;6:187-196.<br />
3. Giedke H, Schwarzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev 2002;6:361–377.<br />
4. Wirz-Justice A. Biological rhythm disturbances in mood disorders. Int Clin Psychopharmacol 2006;21:11-5.<br />
5. Selvi Y, Gulec M, Agargun MY, Besiroglu L. Mood changes after sleep deprivation in morningness–eveningness chronotypes in healthy individuals. J Sleep Res<br />
2007;16:241–4.<br />
6. Hemmeter UM, Hemmeter-Spernal J, Krieg JC. Sleep deprivation in depression. Expert Rev Neurother 2010;10(7):1101-15.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S87<br />
S87
Abstracts of the Invited Speakers<br />
Psychotropic drugs effecting biological rhythm (Chronobiotics)<br />
Elif Oral<br />
Department of Psychiatry, Faculty of Medicine, Atatürk University, Erzurum, Turkey<br />
E-mail: oralelif@yahoo.com<br />
Biological clocks such as circadian, ultradian, and infradian rhythms have their own organizations, independently from environmental<br />
conditions. Although there is biological sustainability, psychiatric disorders and also psychotropic medications have important effects<br />
on the synchronization of biological clocks. Various biological mediators such as glutamate, γ aminobutyric acid, histamine, dopamine,<br />
acetylcholine, serotonin and their receptor systems take on the mediation of inner clocks via psychotropic drugs.<br />
Histaminergic activity is highly increased during wakefulness. H1 antagonists, generally increase Slow-Wave Sleep and stage 2 sleep<br />
and reduce rapid eye movement sleep. Diphenhydramine can cause subjective sedation and decreased sleep latency with no effect<br />
on memory or learning processes. The long elimination half-lives of these drugs can result in next-day sedation and impairment of<br />
psychomotor and cognitive function the next morning.<br />
Benzodiazepines shorten sleep-onset latency, increase total sleep time and stage 2 sleep, and suppress rapid eye movement sleep and<br />
slow-wave sleep. The risk of rebound insomnia is greatest with rapid elimination of benzodiazepines.<br />
About 65% of major depressive disorder patients report sleep complaints. Based on polysomnography studies, sleep architecture is<br />
estimated to be disturbed in up to 90% of depressed patients. Except desipramine, all TCAs block H1 and α1 receptors to varying degrees.<br />
As a general rule, the noradrenergic TCAs (e.g. desipramine, protriptyline) are considered ‘activating’. These agents have a tendency to<br />
increase sleep-onset latency as well as to decrease total sleep time, associated with an increase in wake time after sleep onset. Paroxetine<br />
and fluoxetine clearly suppress REM sleep, both among healthy volunteers and depressed patients. Compared to other SSRIs, citalopram<br />
may be less activating and therefore less likely to disrupt sleep continuity.<br />
Lithium and valproate have many acute, subacute, and chronic effects on systems, at the cellular and molecular levels. Lithium treatment<br />
modifies circadian rhythms in humans and in most animals, primarily by lengthening the period of the cycle.<br />
Most of the sleep-promoting effects of antipsychotic drugs have been related to their potency to antagonize α adrenergic, histaminergic,<br />
or cholinergic neurotransmission. Among classical antipsychotics, drugs having these properties, such as phenothiazines and<br />
thioxanthenes, are clearly sedative and promote sleep. Among atypical antipsychotics, drugs having this pharmacodynamics profile are<br />
olanzapine, clozapine, and quetiapine. Clozapine and olanzapine increase total sleep time and sleep efficiency and have no clear-cut<br />
effect on REM sleep.<br />
Key words: Psychotropic drugs, biological rhythm<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S88<br />
A general overview of chronotherapeutics<br />
Yavuz Selvi<br />
Department of Psychiatry, Yuzuncu Yil University, Van, Turkey<br />
E-mail: dryavuzselvi@yahoo.com<br />
The sleep-wake cycle occurs because of the two independent but additive processes, homeostatic sleep and circadian processes. Circadian<br />
rhythms play a significant role in regulating daily behavioral rhythms, cortisol and melatonin secretions, body temperature, sleep/wake<br />
cycle, alertness and performance levels. Disrupted synchronization of circadian rhythms impairs cognition, behavior and mood with<br />
deterioration of sleep-wake cycle and social rhythms. Some clinical and neurobiological findings suggest circadian dysregulation in<br />
depressive patients. Diurnal variation of mood, early morning awakening, phase advance for body temperature, cortisol, latency of the<br />
first phase of REM sleep for several other hormones and monoamines or their metabolites and sleep disturbances are core features of<br />
depression that have linked depression with circadian rhythm function (1,2).<br />
Clinical and neurobiological findings have promoted the idea that the restoration of circadian rhythm could have an antidepressant effect.<br />
The term, chronotherapeutics, refers to biologically-based, non-pharmaceutical and clinical interventions that act on disrupted biological<br />
rhythms in order to achieve therapeutic effects in the treatment of psychiatric conditions (3). Delayed therapeutic effects, tolerability,<br />
side effects, and drug–drug interactions of pharmacotherapeutic agents, as well as pregnancy and the postpartum period, prevent<br />
antidepressant use and promote chronotherapeutic interventions.<br />
S88 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Chronotherapeutics are applied effectively in endogenous, reactive, unipolar, bipolar, schizoaffective depression, depression in the<br />
elderly, secondary depression, depression in pregnancy and postpartum depression. The target of chronotherapeutic interventions, as<br />
in antidepressant drug treatments, is to modulate the same neurotransmitter systems (5-HT, NA, DA), the same brain structures, and the<br />
same clinical symptoms and findings more rapidly and with fewer side effects. These interventions include wake therapy (the use of<br />
prolonged periods of wakefulness; partial or total sleep deprivation), shifting of sleep time (sleep phase advance therapy; stepwise shift<br />
forward of the sleep-wake cycle to the early evening); bright light therapy in correct time and sufficient dose, and dark or rest therapy for<br />
bipolar mania and rapid cycling patients. When the therapeutic effects are transient, different chronotherapeutic interventions can be<br />
combined to maximize antidepressant response and prevent relapse. Psychiatrists should consider chronotherapeutic interventions as<br />
strong and safe treatment approaches (3,4).<br />
Key words: Biological rhythm, chronotherapeutics, mood, sleep, sleep deprivation<br />
References:<br />
1. Lack LC, Wright HR. Chronobiology of sleep in humans. Cell Mol Life Sci. 2007; 64(10):1205-15.<br />
2. Selvi Y, Besiroglu L, Aydin A. Chronobiology and Mood Disorders. Current Approaches in Psychiatry 2011; 3(3):368-386.<br />
3. Benedetti F, Barbini B, Colombo C. Smeraldi E. Chronotherapeutics in a psychiatric ward. Sleep Med Rev. 2007;11(6):509-22.<br />
4. Hajak G, Landgrebe M. Time and depression: when the internal clock does not work. Medicographia. 2010;32:146-151.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S88-9<br />
Bright light therapy in treatment of depressive disorders other than seasonal affective disorder<br />
Mustafa Güleç<br />
Department of Psychiatry, Ataturk University, Erzurum, Turkey<br />
E-mail: mustafagulec78@yahoo.com<br />
Studies of light therapy for non-seasonal depression have a history at least as long as studies of seasonal affective disorder (SAD), but<br />
on the whole the results have been less clear-cut (Tuunainen et al., 2005). The APA work group found, within its selection, positive<br />
evidence for efficacy except when light therapy and medication were combined (Golden et al., 2005). Studies completed by the time<br />
of the present congress clearly would have reversed that conclusion (Benedetti et al., 2003; Martiny, 2004; Terman, 2006). The strategy<br />
has been recommended by the Committee on Chronotherapeutics of the International Society for Affective Disorders (Wirz-Justice et<br />
al., 2005) and in an international response (Wirz-Justice et al., 2004) to a review of new antidepressants that overlooked light therapy,<br />
published in Science (Wirz-Justice et al., 2004). A difficulty with most non-seasonal studies has been their inability to confront the early<br />
hypothesis that light therapy is specifically tuned to patients with SAD as a countermeasure to long winter nights. Seasonality lies on a<br />
continuous dimension from noticeable (but not disturbing) to mildly, moderately and severely disturbing (Terman, 1988). SAD falls into<br />
the latter category, with major depressive episodes restricted to winter. In a far larger number of cases, recurrent or chronic depressions<br />
are exacerbated in winter but can occur at any time of year. Such patients provide moderate global seasonality scores (Rosenthal et al.,<br />
1987) in comparison to higher scores for SAD. Thus, patients with non-seasonal depressions can still show seasonality, which might be<br />
the key to their response to light therapy. Subsequent to the aforementioned inconclusive meta-analysis of light therapy for non-seasonal<br />
depression (Tuunainen et al., 2005), some researchers conducted an investigation to clarify this issue with a patient sample in which<br />
depression was chronic and without any seasonal modulation (Goel et al., 2005). Under morning light therapy, the proportion of subjects<br />
with depression rating scale improvement of 50% or more was 0.60 vs. 0.10 for the low-output negative air ionizer placebo. Moreover,<br />
there are also very recent reports claiming that bright light therapy alone is effective in some patient groups with non-seasonal major<br />
depression (Kripke, 2011a; Kripke, 2011b; Martiny, 2011). Now, we can begin to surmise that light therapy for seasonal and non-seasonal<br />
depression is equally effective. Perhaps the patients with non-seasonal depression are light deprived at any time of year, and this situation<br />
results in exacerbation of circadian rhythm phase delay, given the absence of the critical early morning light signal that synchronizes the<br />
internal clock to local time. Such delay may be depressogenic regardless of the season. However, the growing concern about medication<br />
side effects would seem to fit well for our old-new alternative (Terman, 2007).<br />
Key words: Seasonal affective disorder, non-seasonal affective disorder, depression, treatment, bright light<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S89<br />
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Abstracts of the Invited Speakers<br />
[PS-19]<br />
Symposium Title: Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or<br />
neurodegenerative? Review of recent data<br />
Is the effect of psychotropic drugs neurodegenerative or neuroprotective?<br />
Ömer Aydemir<br />
Department of Psychiatry, Celal Bayar University, Manisa, Turkey<br />
E-mail: soaydemir@hotmail.com<br />
Various stress experiences affect gene expression of neurotrophic/growth factors in the hippocampus. Among the neurotrophic factors,<br />
brain-derived neurotrophic factor (BDNF) has the most prominent role. With the stress producing effects of early life traumas, the level<br />
of BDNF decreases and susceptibility to depression develops. Recurrent and insufficiently treated depressive episodes have further<br />
impact on decreased BDNF and increase neuronal atrophy. Decreased level of BDNF in patients with major depressive disorder has been<br />
demonstrated in many studies and BDNF levels increase after antidepressant treatment, along with symptom recovery, in comparison<br />
to those seen in healthy control subjects. This increase cannot be achieved in patients that do not respond to antidepressant treatment.<br />
The neuroprotective effect of antidepressants are mediated by mitogen activated protein kinases/extracellular regulated kinases (MAPK/<br />
ERK) and wingless/glycogen synthase kinases (Wnt/GSK). In a meta-analysis, 23 studies were evaluated and data for 1504 patients were<br />
subjected to statistical analysis. The effect size was calculated as 0.62 (95% confidence interval: 0.36-0.88). As a result of meta-regression,<br />
the change in the level of serum BDNF after antidepressant treatment was independent of the change in depressive symptomatology,<br />
duration of treatment, and history of antidepressant use. As clinical improvement obtained with antidepressant treatment persists, the<br />
level of serum BDNF remains unchanged.<br />
Beside antidepressants, mood stabilizers, especially lithium have been studied with respect to neuroplasticity. Neuroprotective effects of<br />
mood stabilizers are mediated by increasing transcriptional activity of (cAMP response element binding protein) CREB, inhibiting GSK-3B<br />
and increasing the expression of BDNF. In studies both with lithium and valproate, increased cerebral grey matter volume was reported.<br />
In lithium studies increases in left anterior cingulate volume, right anterior cingulate volume, hippocampal volume and amygdala volume,<br />
and in valproate studies an increase in left anterior cingulate volume were found. Both mood stabilizers are associated with increased<br />
hippocampal N-acetyl aspartate level.<br />
Antipsychotic drugs do not have a group effect. While haloperidol does not have any effect on phosphorilated ERK (pERK), olanzapine<br />
increases it. Haloperidol also decreases the level of BDNF and is suggested to have neurotoxic effects. Among the other antipsychotics,<br />
clozapine, quetiapine and risperidone prevent cell death. It has been demonstrated that clozapine and quetiapine increase the level of<br />
BDNF. Quetiapine is suggested to increase proliferation of mature neurons, although there is no evidence that clozapine and olanzapine<br />
have the same effect.<br />
Key words: Psychotropic drugs, neuroplasticity, neurodegeneration, neuroprotective effect<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S90<br />
Effect of psychotherapy on neurogenesis<br />
Mine Özmen<br />
Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey<br />
E-mail: drmineozmen@yahoo.com<br />
Adverse life experiences in childhood are considered to be associated with emotional and cognitive development as well as brain<br />
structure and functions. It is suggested that they might reduce neurogenesis, which in turn may cause memory, learning, functional<br />
stress response disturbances. It is known that hippocampal neurogenesis is affected by stress, hormones, aging, environment and activity.<br />
Exposure to acute or chronic stress may result in suppression of one or more phases of neurogenesis. In animal studies, reduction of<br />
neurogenesis in the caudal part of the hippocampus was shown after maternal separation of 3-weeks old rats. Although it was reported<br />
that the suppression was reversible after appropriate time and treatment in some studies, some other writers suggest that early life stress<br />
in the first 2 weeks can cause irreversible reduction in neurogenesis. Besides, there is an argument that neurogenesis can not increase by<br />
learning in the animals which were exposed to prenatal stress. One suggested reason for this lifetime persistency of reduced neurogenesis<br />
is that stress occurring in early childhood coincides with the development of dentate gyrus. It has been shown that corticosteroids<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
inhibit neurogenesis in the hippocampus, subventricular zone and olfactory epithelium and this inhibition can remit by pharmacological<br />
treatments. There are case reports and studies with limited cases, which suggest that effective psychotherapy can reduce symptoms and<br />
this reduction can change the in the hypothalamic-pituitary axis. It may be hypothesized that in an effective psychotherapy process,<br />
coping with stress, new relationship experiences and learning can increase neurogenesis and this may be one of the mechanisms of<br />
effectiveness of psychotherapy. This hypothesis should be tested with animal and human studies in which neurobiology; psychiatry and<br />
neuroscience disciplines can interact and work together.<br />
References:<br />
1. Korosi A et al. Early-life stress mediated modulation of adult neurogenesis and behavior. Behav Brain Res. (2011) doi:10.1016/j.bbr.2011.07.037<br />
2. McEven BS. Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling. Ann NY Acad Sci 2010 Sep;1204 Suppl:E38-59.<br />
3. Miranda Olffa, Giel-Jan de Vriesa, Yener Guzelcana, Johanna Assiesc, Berthold P.R. Gersons. Changes in cortisol and DHEA plasma levels after psychotherapy for<br />
PTSD. Psychoneuroendocrinology (2007) 32, 619–626<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S90-1<br />
Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or<br />
neurodegenerative? Review of recent data and effects of physical exercise<br />
Hakan Balıbey<br />
Ankara Military Hospital, Psychiatry Clinic, Ankara, Turkey<br />
E-mail: hbalibey@gmail.com<br />
Research in humans and animals has shown that exercise improves mood and cognition. Physical activity has been consistently shown<br />
to be associated with improved physical health, life satisfaction, cognitive functioning, and psychological well-being. Conversely, physical<br />
inactivity appears to be associated with the development of psychological disorders.<br />
Physical activity also causes a robust increase in neurogenesis in the dentate gyrus of the hippocampus, an important brain area<br />
for learning and memory. The results of epidemiological studies (cross-sectional, prospective and retrospective) support a positive<br />
relationship between cognition and physical activities. They include supramolecular mechanisms (e.g. neurogenesis, synaptogenesis,<br />
and angiogenesis) which, are in turn controlled by molecular mechanisms, such as brain-derived neurotrophic factor (BDNF), insulin-like<br />
growth factor (IGF-1), hormones and second messengers.<br />
An active lifestyle might prevent or delay loss of cognitive function with aging or neurodegenerative disease. Exercise could involve<br />
common cellular pathways important for neurogenesis, cell survival, synaptic plasticity and vascular function. Optimal maintenance of<br />
brain health might depend on exercise. The beneficial effects of exercise are likely to be mediated in part by hippocampal neurogenesis.<br />
Further investigation into the functional significance of neurogenesis, by designing behavioral tasks that are specific for the dentate gyrus,<br />
will help to determine the relative contribution of the new cells.<br />
Exercise influences brain vasculature. In particular, physical activity increases the proliferation of brain endothelial cells and angiogenesis<br />
throughout the brain. Growth factors such as insulin-like growth factor (IGF) and vascular endothelial growth factor (VEGF) play an<br />
important role in the angiogenic and neurogenic effects of exercise on the brain. The neurotrophin BDNF is considered to be the most<br />
important factor upregulated by physical activity because it has an important role in synaptic plasticity and cell genesis, growth and<br />
survival. Interestingly, there is a positive interaction between BDNF expression and serotonin. Serotonin receptor activation enhances<br />
BDNF expression in hippocampal cells, BDNF is recognized to be a key protein modulating brain plasticity and it is distributed widely<br />
throughout the brain. In humans, serum BDNF concentrations rise after exercise.<br />
The involvement of such pathways, particularly in the hippocampus, may in turn lead to an improvement in cognitive function,<br />
enhancement of psychological well-being, and a decrease in the risks of Alzheimer’s disease (AD) and dementia as well as decreases in<br />
symptoms of depression and anxiety. While intense exercise (as observed in conditions such as “excessive exercise” and “overtraining<br />
syndrome”) leads to a lessening of anxiety, these mood variations are more related to the construct of depression than to the construct<br />
of anxiety.<br />
Physiological effects of exercise and the benefits of exercise on psychiatric disorders will be discussed in the light of current literature in<br />
this presentation.<br />
Key words: Physical activity, exercise, BDNF, hippocampal neurogenesis, neuroregeneration, neurodegeneration, synaptic plasticity, cognition,<br />
mood<br />
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Abstracts of the Invited Speakers<br />
References:<br />
1. Lista I, Sorrentino G. Biological mechanisms of physical activity in preventing cognitive decline. Cell Mol Neurobiol. 2010;30(4):493-503.<br />
2. van Praag H. Exercise and the brain: something to chew on. Trends Neurosci 2009;32(5 ):283–90.<br />
3. Little Exercise, Big Effects: Reversing Aging and Infection-Induced Memory Deficits, and Underlying Processes. Barrientos R. M., Frank M.G, Crysdale N.Y, Chapman<br />
T.R, Ahrendsen J.T at all. The Journal of Neuroscience, 2011; 31(32):11578 –86.<br />
4. Christofoletti G, Oliani M.M, Bucken L.T, Gobbi S, Beinotti F, Stella F. Physical activity attenuates neuropsychiatric disturbances and caregiver burden in patients<br />
with dementia. Clinics (Sao Paulo). 2011; 66(4): 613–8.<br />
5. Ma Q. Beneficial effects of moderate voluntary physical exercise and its biological mechanisms on brain health. Neurosci Bull. 2008;24(4):265-70.<br />
6. van Praag H. Neurogenesis and exercise: past and future directions. Neuromolecular Med. 2008;10(2):128-40.<br />
7. Ang. ET, Tai YK, Lo SQ, Seet R, Soong TW.Neurodegenerative Diseases: Exercising Toward Neurogenesis and Neuroregeneration. Front Aging Neurosci. 2010; 2: 25.<br />
8. Tomporowski P. D., Lambourne K., Okumura M. S. Physical activity interventions and children’s mental function: an introduction and overview. Prev Med. 2011;<br />
52(Suppl 1): S3–S9.<br />
9. Fadillioglu E., Kaya B., Uz E., Emre M.H., Ünal S. Effects of Moderate Exercise on Mild Depressive Mood, Antioxidants and Lipid Peroxidation. Bull Clin<br />
Psychopharmacol 2000; 10(4):194-200.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S91-2<br />
[PS-20]<br />
Symposium Title: Controversial topics in eating disorders<br />
Comorbidities in eating disorders<br />
Atila Erol<br />
Sakarya University, School of Medicine, Department of Psychiatry, Sakarya, Turkey<br />
E-mail: erolatila@gmail.com<br />
Patients with eating disorders exhibit high rates of psychiatric comorbidity and the number of comorbid psychiatric disorders is high.<br />
The treatment of co-occurring psychiatric problems in eating disordered patients is essential for good clinical management and the<br />
outcome of treatments. Higher rates of comorbidity often mean greater severity, treatment resistance and poor outcomes in eating<br />
disorders. The most prevalent Axis I disorders seem to be mood and anxiety disorders, alcohol and substance abuse, and bipolar disorder.<br />
Axis II disorders are also common. At least 80% of anorexia nervosa (AN) or bulimia nervosa (BN) patients have at least one additional<br />
psychiatric disorder over their lifetime. Mood disorders are very common among patients with AN. Major depressive disorder occurs in<br />
50-70% of AN patients. Bulimic patients have 52-75% affective disorder, with 63% having major depression. Lifetime prevalence rates of<br />
major depression in BN are 50-65%.<br />
Among study samples with restricting and binging /purging anorexia nervosa, prevalence rates of any anxiety disorder are found to be<br />
between 24% and 71%, respectively. Among patients with BN prevalence rates for any anxiety disorder, social phobia, generalised anxiety<br />
disoder (GAD) or panic disorder are reported to be 36%, 17%, 12% and 10% respectively. The approximate rates of any anxiety disorder in<br />
BN are reported to be between 57 and 75 %.<br />
Thirty-five percent of restricting AN patients have obsessive compulsive disorder (OCD) and binging/purging AN patients have 44% OCD.<br />
BN patients have comorbid OCD 40% of the time. Lifetime prevalence rates of substance abuse in AN ranged from 12% to 18% and in<br />
BN the rates ranged from 30% to 70%. The results of clinical studies indicate that patients with BPD have higher rates of eating disorders<br />
compared with the general population. Rates of lifetime BPD in eating disorders patients are variable but higher than rates of BPD in the<br />
general population. Among eating disorder patients post-traumatic stress disorder rates were found between 8% to 11%.<br />
Key words: Eating disorders, anorexia, bulimia, comorbidity<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S92<br />
S92 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Psychopharmacological treatments in eating disorders<br />
Alican Dalkilic<br />
St. Elizabeths Hospital, Washington, DC 20032, USA<br />
E-mail: drdalkilic@gmail.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Pharmacological treatment options have limited evidence of benefit in treatment of eating disorders, yet a comprehensive psychiatric<br />
evaluation besides a physical exam and basic screening tests (complete blood count (CBC), basic metabolic panel, Mg, P, thyroid<br />
stimulating hormone (TSH), lipid panel, pregnancy test, urine analysis (UA), urine drug screen (UDS), ECG, and Dexa scan) should be<br />
conducted. Establishing a therapeutic alliance with empathy, positive regard, reassurance, and support (1) sets up the foundation for a<br />
successful treatment process. The patient’s safety should be evaluated with particular attention paid to suicidal ideation, plans, intentions,<br />
history of attempts and impulsive or compulsive self-harm behaviors. After assessing eating disorder symptoms, signs, and behaviors and<br />
the general medical condition of the patient a decision about treatment site (specialized inpatient unit, residential treatment or partial<br />
hospital program, intensive outpatient, or outpatient care) can be made. In eating disorders in general, but especially in adolescences with<br />
eating disorders, inclusion of the family and primary support group in the treatment process is essential.<br />
The treatment options and goals in eating disorders include nutritional rehabilitation, psychosocial interventions, medications, and other<br />
somatic treatments. Nutritional rehabilitation aims to restore weight, normalize eating patterns, achieve normal perception of hunger<br />
and satiety cues, and correct biological and psychological problems caused by malnutrition (1). Psychosocial interventions include<br />
individual and group based cognitive behavioral and interpersonal therapies, acceptance and mindfulness therapies, and psychodynamic<br />
approaches, as well as nutritional counseling, dialectical behavioral therapy (DBT), and family therapies. There are more therapies with<br />
specific names such as mealtime support and multifamily group therapy, but they use similar approaches to the previously mentioned<br />
ones.<br />
Although there is clinical evidence about use of antidepressants in treatment of eating disorders (especially SSRIs, calcium, vitamin D,<br />
and zinc and limited data about benzodiazepines, mood stabilizers, and atypical antipsychotics), so far only fluoxetine is approved for the<br />
treatment of bulimia nervosa by the Federal Drug Administration (FDA) 1,2). Sertraline has been found to be effective in a randomized<br />
and controlled trial, as well. Medications have not been proven to be more effective than psychosocial interventions in treatment of eating<br />
disorders so far. Some studies have found the combination of CBT with medication to be more effective. Topiramate has been found to<br />
be effective in some small controlled trials especially in reducing binging behavior, but due to potential side effects is should be reserved<br />
as a secondary medication (1,3). Topiramate or zonisamide are prescribed to target binging behavior and also for weight reducing effects<br />
in patients who may benefit from weight loss. Bright light therapy is another intervention demonstrated to decrease binge frequency in<br />
several controlled trials (1).<br />
Although clinicians are advised to use caution when prescribing medications to eating disorder patients due to potentially dangerous<br />
medical co-morbidities, some medications should be avoided or used only as last resorts. Bupropion is contraindicated in bulimia due to<br />
a heightened seizure risk (1,3). Medications that increase the risk of arrhythmia or prolong the QTc interval should be avoided or if they are<br />
used, adverse events should be monitored closely. Sibutramine was taken off the market in USA in 2010 due to cardiac adverse events. In<br />
addition, medications with a narrow therapeutic range such as lithium should be avoided. Benzodiazepines, especially the ones with high<br />
addiction potential, should not be used in patients with addiction risk. In clinical practice many eating disorder patients end up being on<br />
multiple medications due to high rates of co-morbidity with anxiety and mood disorders, substance abuse and dependence conditions,<br />
trauma related disorders, and personality disorders. Beside reviewing pharmacological treatment options in eating disorders we will also<br />
discuss the management of cases with co-morbid conditions.<br />
Key words: Eating disorders, pharmacology, pharmacotherapy, treatment, pharmacological treatment<br />
References:<br />
1. American Psychiatric Association Practice Guidelines for the Treatment of Psychiatric Disorders Compendium. American Psychiatric Association 2006 1,612<br />
pages ISBN 978-0-89042-385-1.<br />
2. Pharmacotherapy of eating disorders. Jackson CW, Cates M, Lorenz R. Nutr Clin Pract. 2010 Apr;25(2):143-59. Review.<br />
3. Psychopharmacology of eating disorders in children and adolescents. Golden NH, Attia E. Pediatr Clin North Am. 2011 Feb;58(1):121-38, xi. Review.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S93<br />
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Abstracts of the Invited Speakers<br />
Obesity and impulsivity<br />
Bilge Burçak Annagür<br />
Department of Psychiatry, Selcuk University, Selcuklu Medical School, Konya, Turkey<br />
E-mail: bilgeannagur@yahoo.com<br />
Obesity is not inlcuded in eating disorders characterized by the DSM-IV classification of the American Psychiatry Association. Current<br />
clinical diagnosis depends on body mass index (BMI). Although it was not evaluated among eating disorders, it presents psychological<br />
characteristics seen commonly in eating disorders. Characteristics related with eating disorders such as low self-esteem, body<br />
dissatisfaction, perfectionistic attitudes, impulsivity and disinhibition have also been observed in obese patients (1,2). Obese patients are<br />
divided into two subgroups, with or without binge eating disorder (BED). Body weights of subjects with binge eating disorder are related<br />
to their overeating and psychopathologies, especially depression, are more frequent compared to the other group.<br />
Aggressiveness and anger are involved in significant psychopathological characteristics common in patients with eating disorders (3).<br />
Some researchers suggested that impaired eating behavior is related to low self-esteem and high self-directed hostility. Problems about<br />
revealing their anger were detected among these individuals. Besides, problems in controlling the expression of anger, accompanying<br />
impulsive explosive behaviors are also present (4).<br />
The current status of obesity treatment is not satisfactory. Some treated individuals regain the lost weight in a short time (5). Many<br />
researchers are investigating approaches to keep off the lost weight with treatment strategies to lose weight. In previous reports, it has<br />
been demonstrated that most obese individuals returned back to their basal BMIs or to higher values within 1-5 years (6). Nowadays, the<br />
question is ‘What is the difference between the ones who keeps off the weight they lose and those who do not?’. Impulsivity is the possible<br />
predictor of relapse in obesity treatment (5). Obese subjects are suggested to be more impulsive than lean ones. Impulsive characteristics<br />
are higher in obese patients with BED (7). Impulsive people appear to have no control over their behaviors on eating and they have more<br />
interest in food with higher calories. Impulsivity is also considered as a predicting factor among patients who quit treatment. In a survey<br />
among the children between the ages of 8-12 years in the Netherlands, impulsivity was measured by behavior and the results of treatment<br />
were evaluated. As a result, it was demonstrated that impulsive children lose less weight compared to the others. It was also concluded<br />
that impulsive children are more prone to eating delicious foods; therefore more attention should be given to their dietary control (5).<br />
Another issue supporting the relationship between obesity and impulsivity is the occurrence of obesity in children with attention deficiency<br />
and hyperactivity disorder (ADHD) (8). ADHD was detected in most of the children (58%) who were receiving obesity treatment. Also, the<br />
BMI of children with ADHD was higher than the control group (9). In addition, there is evidence for decreased levels of D2 receptors in<br />
the striatum of obese subjects (10-13). With regard to the therapeutic implications, recent studies indicate that methylphenidate (MPH),<br />
a drug widely used for ADHD, reduced overall energy intake with a selective reduction in dietary fat (14,15). Dopamine (DA) exerts<br />
neuromodulatory influences over behavior and cognition via the fronto-striato-cerebellar circuitry and pharmacotherapy is thought to<br />
target these systems to ameliorate problems with impulsivity, inattention and hyperactivity. To explain the comorbidity of ADHD and<br />
obesity, it has been hypothesized that a predisposition to glucose starving and obesity is due to inadequate dopaminergic activity in the<br />
reward center of the brain. Consumption of large quantities of carbohydrates (carbohydrate binging) stimulates production and usage of<br />
dopamine within the brain and it results in a kind of therapeutic effect (16,17).<br />
All this information should guide the planning of treatment. Specific cognitive behavioral approaches developed for the treatment of<br />
impulsive behavior could contribute much to the treatment of obesity(18).<br />
Key words: Eating disorders, impulsivity, obesity<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S94<br />
Efficacy of psychotherapy in bulimia nervosa<br />
Başak Yücel<br />
Department of Psychiatry, Istanbul University, Istanbul, Turkey<br />
E-mail: byucel@superonline.com, basakyucel@gmail.com<br />
The efficacy and importance of psychotherapy in bulimia nervosa have been examined in many studies recently. Most of the eating<br />
disorder experts acknowledge the notion that psychological interventions are the best available treatment for BN. Although different<br />
psychotherapeutic recommendations have been offered by NICE (National Institute for Health and Clinical Excellence) and APA (American<br />
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Abstracts of the Invited Speakers<br />
Psychiatric Association), several treatment approaches received strong endorsement for BN. Cognitive behavioral therapy (CBT) is<br />
recommended as an effective treatment for bulimic patients and considered the ‘treatment choice’ for BN and binge eating disorder (BED),<br />
it is also supported by strong evidence-based literature.<br />
With regard to the efficacy of CBT specifically in BN, in various studies CBT was associated with more improvements in bulimic and<br />
depressive symptoms of patients than symtoms of control patients in waiting-list and any other psychotherapy cases. In terms of general<br />
psychiatric symptoms, studies have not shown any difference between CBT and any other psychotherapy.<br />
Other psychotherapy choices have included interpersonal psychotherapy (IPT), dialectical behavior therapy, supportive and psychodynamic<br />
psychotherapy, and certain self-help approaches. Thus, in clinical practice there have been a number of evidence-supported treatments<br />
for BN patients.<br />
IPT is a psychological treatment for BN that has demonstrated long-term outcomes that are comparable to those for CBT. Currently,<br />
all controlled studies of IPT for BN have been comparison studies with CBT. Although there have been only few controlled trials of<br />
psychodynamic treatment of eating disorders, these reports yielded important findings in this field. Standard dialectical behavior therapy<br />
(DBT) has been adapted to address a variety of problematic behaviors associated with emotion dysregulation in bulimia nervosa and<br />
also DBT may be used in BN patients with comorbid borderline personality disorder. Beside these, the knowledge in the field of self-help<br />
treatments continues to develope.<br />
Key words: Bulimia nervosa, psychotherapy<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S94-5<br />
[PS-21]<br />
Symposium Title: Treatment approaches to comorbidities of ADHD<br />
Treatment approaches to psychiatric comorbidities of ADHD in children<br />
Tümer Türkbay<br />
GATA, Department of Child and Adolescent Psychiatry, Ankara, Turkey<br />
E-mail: tumerturkbay@yahoo.com;tturkbay@gata.edu.tr<br />
Attention-deficit hyperactivity disorder (ADHD) is highly comorbid with other psychiatric disorders. Each of the comorbid disorders<br />
modifies the overall clinical presentation and treatment response. Sometimes there can be more complex situations. For example,<br />
depressed children demonstrate diminished concentration and irritability and it may be difficult to differentiate from the cardinal<br />
symptoms of ADHD. Children with ADHD and comorbid disorders have poorer prognoses than those with ADHD alone.<br />
Both stimulant medications and atomoxetine markedly reduce symptoms of comorbid oppositional defiant disorder, which often requires<br />
adjunctive parent training and behavior management. Severely explosive anger may require the use of atypical antipsychotics. In conduct<br />
disorder, stimulant medications and atomoxetine also reduce aggressive behavior and antisocial acts. Atypical psychotics or mood<br />
stabilizers may be used for highly aggressive-explosive cases.<br />
The majority of children with comorbid ADHD/depression can be managed with a psycho stimulant. However, initial treatment with<br />
antidepressant drugs should be saved for treating children with more severe depression. Stimulants can exacerbate symptoms of anxiety<br />
disorders. Atomoxetine, SSRIs and behavioral therapies reduce anxiety symptoms.<br />
If tic disorders are mild or episodic, they usually require no treatment. Most ADHD/tic disorder patients will not demonstrate an<br />
exacerbation of their tics with stimulants. Nevertheless, if tics worsen with stimulant use, an antipsychotic or alpha agonist should be<br />
added to the psychostimulant.<br />
Key words: Attention deficit hyperactivity disorder, comorbidity, management<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S95<br />
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Abstracts of the Invited Speakers<br />
Treatment approaches to psychiatric comorbidities of ADHD in adolescents<br />
Bengi Semerci<br />
Institute, Istanbul, Turkey<br />
E-mail: bengisemerci@bengisemerci.com, info@bengisemercienstitusu.com<br />
Adolescences with ADHD, who suffer from social problems, are under risk of depression, anxiety, destructive conduct disorder, and drug<br />
addiction. If there are co-morbid disorders associated with ADHD, it makes the treatment difficult and causes some other complications.<br />
The fundamental treatment principles of the psychiatric co-morbidities of ADHD are also effective for adolescence period. However,<br />
especially, we should be careful about the conditions that have high prevalence during adolescence period and the conditions which<br />
affect prognosis in a negative way. These situations need to be assessed in diagnosis and treatment plan.<br />
Anxiety Disorders: Some researches indicate that a stimulant treatment has small effects on anxiety disorder. The treatment of ADHD<br />
without anxiety disorder gets more successful results. However, according to recent research, treatment is also effective on anxiety<br />
disorder.<br />
In general, considering the effect of CBT on the anxiety disorder treatment, it is suggested that CBT beside medication treatment is<br />
effective on ADHD having co morbidity with anxiety disorder. If there is co morbidity, it is suggested that the priority needs to be given<br />
to ADHD and that if the anxiety symptoms continue, another medication treatment should be considered.<br />
Mood Disorders: Depression is an important problem in adolescence period. The important point in treatment is to identify that if ADHD<br />
causes to depressive findings or major depression.<br />
If ADHD cooccurs with major depression, both of them need to be treated. The treatment may be done either by stimulants or atomoxetine<br />
or only by SSRIs or tricyclic anti depressants. The last option is to use the two methods both.<br />
When there is co-morbid depression and ADHD, the efficacy of antidepressants is lower than when it is depression alone. In clinical<br />
observation, depression findings in adolescence period should be assessed attentively. If there is major depression, the treatment should<br />
be carried out together with ADHD. Selective serotonin reuptake inhibitors (SSRI) may be used with stimulants.<br />
Conduct Disorders: If ADHD is not treated, it may possibly turn to conduct disorder. In many studies, the use of stimulants for the<br />
treatment of co-morbid ADHD and conduct disorder is investigated. The results of these studies show that stimulants are effective when<br />
the morbidities are both separate or together.<br />
However, if there are co-morbid ADHD and conduct disorder, the effectiveness of stimulants on aggression is lower. If there are co-morbid<br />
ADHD and aggression and if the typical ADHD treatment does not work, it may be useful to add atypical antipsychotics to the treatment. If<br />
ADHD is co-morbid with conduct disorder, working with adolescents, using behavioural approaches, supporting families and to providing<br />
them education about the problem may be helpful.<br />
If ADHD co occurs with drug addiction, both disorders should be treated. Stimulants can be used in a controlled way. However, due<br />
to addiction, prescribing stimulants may be cause legal problems. Atomoxetine and bupropion could be other options. Eventhough,<br />
antidepressants are effective in ADHD, their effectiveness in addiction is limited.<br />
Key words: ADHD, adolescence, co-morbidity, treatment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S96<br />
Treatment of neurological co-morbid disorders in children with ADHD<br />
Murat Yüce<br />
Department of Child and Adolescent Psychiatry, Ondokuz Mayıs University, Samsun, Turkey<br />
E-mail: muryuce@yahoo.com<br />
Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, and<br />
impulsive behaviors. ADHD is one of the most common childhood psychiatric disorders.<br />
Children with ADHD also have many comorbid disorders and psychiatric symptoms. ADHD may be accompanied with neurological<br />
disorders such as epilepsy, headache, and cerebral palsy. Neurological co-morbid conditions can lead to reduction in the level of function,<br />
adherence to treatment difficulty, increasing the price of healthcare and medical complications. Therefore, diagnosis and treatment of<br />
these neurological co-morbid problems with ADHD are important.<br />
ADHD is seen more commonly in children with epilepsy according to the normal population. Approximately 20% of children diagnosed<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
with epilepsy have ADHD as well. Some antiepileptic drugs are known to cause lethargy and impairment of attention. Barbiturates and<br />
benzodiazepines may worsen the symptoms of ADHD. It has been reported that some drugs such as tiagabin, zonisamide, and topiramate<br />
can cause cognitive slowing and concentration problems. Psychostimulants are frequently used in the treatment of ADHD. It has been<br />
reported that these medications do not severely effect epileptic seizures and may improve cognitive functions.<br />
In this presentation treatment approaches for children and adolescents with ADHD and co-morbid neurological disorders will be<br />
discussed.<br />
Key words: ADHD, children, neurological co-morbidity, treatment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S96-7<br />
Drug interactions of medications for comorbidities of ADHD<br />
Osman Abalı<br />
İstanbul Medical Faculty, Child and Adolescent Psychiatry, İstanbul, Turkey<br />
E-mail: osmanabal@hotmail.com<br />
ADHD is a very common psychiatric disorder in childhood. Children with ADHD have frequently another psychiatric disorder. Conduct<br />
disorder, learning disorder, addiction, and mood disorders are frequently seen in children with ADHD. It has been estimated that 23%-<br />
42% of youth receiving psychiatric drugs are receiving multiple drugs (1). Recently drug interactions have been emphasized in these<br />
patients. Stimulant drugs and atomoxetine, which is a non stimulant drug, are used in patients with ADHD. Interactions between these<br />
drugs and other psychotropic drugs are important for treatment quality. Drug interactions should be considered to prevent adverse<br />
effects and increase treatment quality. Possible drug interactions could impact on liver, intestine, or plasma. There are a lot of important<br />
risks due to drug interactions in patients with ADHD. Drug plasma levels can change due to CYP-P450 system interactions. It is estimated<br />
that approximately 7% of the population may be poor metabolizers, causing slow metabolism(2). Also inhibitors of the cytochrome P450<br />
can increase drug levels by several folds. Some drugs inhibit these systems very potently so that concentration of drug can reach very<br />
high levels. Important complications such as neuroleptic malignnant syndrome, serotonergic syndrome, and hallucinations can be seen<br />
during these interactions. Treatment strategies should be reviewed from this perspective. Possible drug interactions couldn’t be exactly<br />
predicted by the clinicians for every patient. But potential drug interactions should be considered for every patient. Drug interactions will<br />
be discussed at this presentation. The treatment strategies will be updated for long term good quality treatment based on the literature.<br />
Key words: ADHD, drug interactions, co-morbidity<br />
References:<br />
1. McIntyre RS, Jerrell JM. Polypharmacy in children and adolescents treated for major depressive disoerder: a claims database study. Journal of clinical<br />
psychiatry.2009;70(2):24-46.<br />
2. Barton J: Atomoxetin: a new pharmacotherapeutic approach in the managment of ADHD, Archives of disease in childhood 2005;1(90):26-29.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S97<br />
[PS-22]<br />
Symposium Title: How to fight with bipolar disorder? From guidelines to clinical practice: Myths and realities<br />
Treatment of mixed episodes of bipolar disorders in manuals. What are the recommendations?<br />
Ahmet Ünal<br />
Gaziantep University, Faculty of Medicine, Department of Psychiatry, Gaziantep, Turkey<br />
E-mail: drahmetunal@hotmail.com<br />
There are still clinical states with uncertainties in psychiatry in terms of diagnosis and treatment. Mixed states in bipolar disorders is one<br />
of these states. The Diagnostic and Statistical Manual of Mental Disorders – IV (DSM – IV) defines mixed states as a period in which manic<br />
and depressive diagnosis criteria prevail together. However, observing all depressive and manic symptoms together during the mixed<br />
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Abstracts of the Invited Speakers<br />
episode is not a common occurrence. The Cincinnati criterion has a more flexible approach in terms of diagnosis; a complete manic states<br />
together with at least three depression symptoms is enough to diagnose the case as mixed mania. There are studies that identify mixed<br />
mania as “a severe form related to mania,” “a transition period between manic and depressive episodes,” or “a separate emotional state.”<br />
15-20% of all manic episodes have characteristics that belong to the mixed mania. In comparison to a classic manic episode, the mixed<br />
mania has a more severe psychopathology. Episodes of dysphoria are observed more frequently, and it is frequently reported that<br />
dysphoria is an important part of mixed states. In comparison to a classic manic episode, the duration of hospitalization is longer, the<br />
number of attacks is higher, and the good periods are shorter during mixed episode. In addition, the psychotic characteristics and<br />
catatonic symptoms are more, and the rate of suicide is higher.<br />
The most important element of treating the mixed episode is making the right diagnosis. The basis used to determine the treatment<br />
method is the same as those recommended for treating manic episodes. Unfortunately, there are no comprehensive studies that address<br />
treating mixed mania. There are limited data related to the efficacy of medications on mixed mania or which medication is better than<br />
the other. In general, combining drugs and clinical experiments are required for the short-term and long-term treatment of mixed mania<br />
patients. According to the Turkish Psychiatric Association (TPA), the treatment for mixed episodes of bipolar disorder is as follows: The<br />
treatment starts with valproate, lithium is added if the decrease in symptoms is not >25% within 4-5 days; in the event that the degree of<br />
symptoms do not get better by 50% at the end of three weeks, an alternative is using an atypical antipsychotic and stopping the lithium-<br />
valproate combination by gradually reducing the amount given to the patient, or moving on to a lithium – carbamazepine combination,<br />
and if >50% progress is not reached at the end of Week 6, it is recommended that patients receive ECT.<br />
In comparison to classic manic episodes, the rate of response to mood stabilizers for mixed episodes is lower. Antidepressants should also<br />
not be used to treat symptoms of depression during this period. This situation proves the need for other treatment options. Olanzapine<br />
can be used effectively in acute and preventative treatment of mixed mania; however, its disadvantages are weight gain, diabetes, and<br />
metabolic syndrome risk. Ziprasidone has a high level of effectiveness that incorporated psychotic and mixed mania. There is evidence<br />
that risperidone is effective in treating manic episodes; however, the amount of information related to its efficacy in mixed episodes is<br />
limited. The number of studies about the efficacy of quetiapine on mixed episodes is also limited. The efficacy of aripiprazole on manic<br />
and mixed episodes is addressed by some studies.<br />
In conclusion, mixed states in bipolar disorder are common clinical reflections. Mood stabilizer treatment strategies are the form of<br />
treatment that gives the best results. Mood stabilizer and antipsychotics can be used in the form of monotherapy or combination. Among<br />
these mood stabilizers, valproate is the one that has been studied most and is the most recommended. Aripiprazole, ziprasidone, and<br />
olanzapine are the antipsychotics that should be utilized first and foremost.<br />
Key words: Bipolar disorder, mixed mania<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S97-8<br />
How are the guidelines prepared? Are they necessary? How to use them?<br />
Their benefits and limitations?<br />
Yasin Bez<br />
Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey<br />
E-mail: yasinbez@gmail.com<br />
Some important points when preparing guidelines are search strategies and methods to assess evidence and the criteria for rating the<br />
strenght of evidence and making a clinical recommendation. The development of treatment guidelines mostly aims to standardize<br />
treatment and to provide clinicians with algorithms, which would be able to carry research findings to everyday clinical practice, by<br />
organizing information from diverse sources into an easily accessible format (1). From this point of view, treatment guidelines may be useful<br />
to avoid non-evidence-based treatment decisions. Thus, their common use should be supported. On the other hand, they get quickly outof-date<br />
and may interfere with following the most recent treatment approaches. Besides, they may not fully apply to the everyday clinical<br />
setting. Besides the benefits and limitations of guidelines another important point is the adherence of the clinicians to these guidelines (1).<br />
Despite considerable efforts to develop them, adherence to the treatment guidelines for bipolar disorders are not enough yet. For<br />
example a study from United States demostrated adherence of 64.1% of the psychiatrists to the treatment guidelines (2). Another study<br />
conducted in France reported a 40% non-adherence rate to treatment guidelines of bipolar disorder among psychiatrists (3).<br />
Current and more detailed data about preparation, use, benefits, and limitations of treatment guidelines will be further discussed in this<br />
presentation.<br />
Key words: Bipolar disorders, guidelines<br />
S98 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
References:<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
1. Fountoulakis KN, Vieta E, Sanchez-Moreno J, Kaprinis SG, Goikolea JM, Kaprinis GS. Tretament guidelines for bipolar disorder: A critical review. J Affective Dis 2005;<br />
86: 1-10.<br />
2. Perlis RH. Use of treatment guidelines in clinical decision making in bipolar diorder: a pilot survey of clinicians. Curr Med Res Opin 2007; 23; 467-475.<br />
3. Samalin L, Guillaume S, Auclair C, Llorca PM. J Nerv Ment Dis 2011; 199: 239-243.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S98-9<br />
Maintenance treatment in bipolar disorder: What do guidelines recommend?<br />
Ibrahim Eren<br />
Konya Research and Training Hospital, Psychiatry Department, Konya, Turkey<br />
E-mail: drieren@yahoo.com<br />
Bipolar disorder is a serious mental illness presenting with exacerbations and remissions. Relapses should be minimized and that is<br />
achieved by preventive treatments. Developing easily applicable and reachable algorithms by incorporating data coming from various<br />
sources, implementing research findings in daily practice, and providing standardized treatment choices are all important. Many<br />
guidelines have been published for bipolar disorders so far.<br />
American Psychiatric Association (APA) Guidelines: This guidelines recommend preventive treatment after one manic episode. The<br />
main goals of treatment are to prevent relapse, resolve subclinical residual symptoms, and to decrease suicide risk. Lithium and valproate<br />
are primary agents, as they have the most evidence of efficacy. Their alternatives lamotrigine, carbamezapine, and oxscarbamezapine are<br />
secondary agents. In general continuation of preventive medications used during acute management is first choice during maintenance<br />
treatment. ECT can be used as a maintenance treatment. Antipsychotics should be discontinued if there is no persistent psychotic symptoms.<br />
Cognitive behavioral, interpersonal, and psychodynamic therapies can be used in addition to medications. Psychoeducation is reported<br />
to be beneficial. Keeping lithium levels between 0.8-1.0 mEg/L during maintenance phase were mentioned to be more effective. In this<br />
guideline generally accepted treatments were mentioned as non-definite recommendations.<br />
Texas Medication Algorithm: Acute phase doses should be continued at least 3 months. All patients are recommended to receive<br />
antimanic medications during maintenance phase, if necessary some can receive low dose antidepressants. Lifelong maintenance<br />
treatment is recomended if patients had 2 manic episodes or one manic episode with positive family history, or the acute episode was<br />
very severe. This group of authors think antimanic medications are the core of the treatment and they emphasize depression less. In<br />
addition they recommend ECT and tricyclics, which were demonsterated to be effective, in final stages due to side effects and patient<br />
preferences.<br />
Expert Opinion Series on Medication Treatment in Bipolar Disorder: They recommend continuation of treatment, which was effective<br />
in acute phase except in divalproex monotherapy and predominantly depressive cases. They suggest adding lithium in those cases.<br />
They recommend that antipsychotics should be stopped during maintenance phase, but some patients may need to continue taking<br />
antipsychotics. In that case, one of olanzapine, risperidone, or quetiapine can be chosen. Against manic episode risk they suggest to<br />
increase the dose of mood stabilizer, add another mood stabilizer, and try additional treatments afterwards. This algorithm has many<br />
structural features and is very detailed.<br />
British Psychopharmacology Association Guidelines: According to this guideline lithium is the first choice and second choice<br />
medications include valproate, olanzapine, carbamazepine, oxcarbazepine, and lamotrigine. Treatment resistant cases can be treated with<br />
medication combinations, clozapine, or ECT.<br />
World Federation of Biological Psychiatry Associations Biological Treatments in Bipolar Disorders: It is recommended to use<br />
combination of antidepressant and mood stabilizers after depressive episodes. After manic episodes lithium, anticonvulsants, or<br />
antipsyhotics are suggested. When first line treatments fail, trying combinations of first line agents is recommended. It seems to be<br />
the most balanced guideline published so far. While they avoid newly discovered treatments , they support use of antipsychotics and<br />
antidepressants with caution.<br />
Canmat: Once the patient becomes asymptomatic, it is suggested to discontinue all medications other than mood stabilizers and to<br />
continue maintenance treatment for 6-12 months after a single episode of illness. This guideline has similarities with APA guideline and<br />
recommends lifelong maintenance treatment in patients with recurrent episodes or positive family history.<br />
Australia and New Zealand Bipolar Disorder Treatment Algorithm: It suggests to avoid antidepressant use during maintenance phase<br />
after depressive episodes due to precipitating mania and rapid cycling, but recommends mood stabilizer and antidepressant use in cases<br />
with recurrent depressive episodes. The duration of treatment after first manic episode is 6 months and lithium, valproate, carbamazepine,<br />
S99
Abstracts of the Invited Speakers<br />
or lamotrigine are listed as recommended medications to prevent recurrent episodes.<br />
NICE Treatment Guidelines: They recommend at least 2 year of maintenance treatment after 1 episode. Long term preventive treatment<br />
should be considered in the following cases: One manic episode with prominent risk factors and negative results and bipolar II cases<br />
with significant functional loss, suicide risk, and frequent recurrent episodes. Lithium, olanzapine, or valproate can be used in long term<br />
maintenance treatment, but valproate should not be used in women with pregnancy potential.<br />
When monotherapy with one of those is not adequate, one of three can be added as a second agent or monotherapy can be tried with a<br />
different agent. Possible combinations are lithium-valproate, lithium-olanzapine, or valproate-olanzapine.<br />
Turkish Psychiatry Association Guidelines: Maintenance treatment is suggested in general after second episode, but it can be started in cases<br />
with risk factors. If a mood stabilizer was initiated during acute phase, it should be continued in maintenance phase, if not, then one should be<br />
started. When a mood stabilizer will be chosen for maintenance phase, it should be lithium. After second episode, whatever the type of episode<br />
was, the same mood stabilizer should be continued if there was one. When there is not adequate response and recurrence occurs a second<br />
mood stabilizer should be added. In cases using lithium as first mood stabilizer, valproate should be given priority as the second mood stabilizer.<br />
In conclusion, even there are similarities in many areas among guidelines, there are also different recommendations regarding treatment options.<br />
Those differences stem from complex clinical presentations of bipolar disorder and different cultural and traditional treatment approaches.<br />
Key words: Bipolar disorder, maintenance phase, guidelines<br />
References:<br />
1. Fountoulakis KN, Vieta E, Sanchez-Moreno J, Kaprinis SG, Goikolea JM, Kaprinis GS. Tretament guidelines for bipolar disorder: A critical review. J Affective Dis 2005;<br />
86: 1-10.<br />
2. Perlis RH. Use of treatment guidelines in clinical decision making in bipolar diorder: a pilot survey of clinicians. Curr Med Res Opin 2007; 23; 467-475.<br />
3. Samalin L, Guillaume S, Auclair C, Llorca PM. J Nerv Ment Dis 2011; 199: 239-243.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S99-100<br />
[PS-23]<br />
Symposium Title: Individualized medicine: Focus on pharmacogenetics<br />
Genetics and drugs: From research to clinical studies Turkish perspective<br />
Cem Şengül<br />
Pamukkale University, School of Medicine, Department of Psychiatry, Denizli, Turkey<br />
E-mail: acemsen@gmail.com<br />
Genetic studies in psychiatry are on the rise and they form an important portion of all psychiatric research in last years. The genetic studies<br />
in psychiatry vary from classical association and linkage studies to genome wide association, and copy number variant studies. Genetic<br />
studies were focusing on different dimensions of psychiatric conditions. First of all, associations of target genes with psychiatric disorders<br />
were investigated in majority of studies. Association of drugs and genetics were also studied in many research projects. Genetic drug<br />
association studies consist of studies with efficacy and frequency of side effects of drug on different genetic polymorphisms. Recently,<br />
μ-opiate receptor gene (OPRM1) Asn40Asp single-nucleotide polymorphism was found to be associated with naltrexone drug response in<br />
alcoholic patients. This finding was very important for revealing effect of genetics on drug response. Naltrexone was effective in aspartate<br />
(Asp) 40 allele carriers but drug was ineffective in homozygote asparagine (Asn) carriers. Different genetic polymorphisms of genes<br />
encoding enzymes and receptors that were related to dopaminergic, serotonergic and glutamatergic systems were also associated with<br />
antipsychotic and antidepressant drug response and side effects. For example 5-HT2C receptor 759C/T gene polymorphism was associated<br />
with antipsychotic induced weight gain and T102C polymorphism of 5HT2A receptor gene was associated with response to risperidone.<br />
Genome wide association and copy number variations are new genetic techniques revealing more detailed and reliable results. Studies<br />
using these techniques might be more useful for exploring interactions between drugs and genetics. Studies on association of genetics<br />
with psychiatric disorders were limited and there were only a few studies available on association of genetics with psychiatric drugs in<br />
Turkey. Financial problems and approval speed and requirements of ethics committees are important barriers for conducting studies on<br />
genetic drug interaction. Resolving these issues might increase interest of psychiatrists on this topic.<br />
Key words: Genetics, polymorphism, drug<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S100<br />
S100 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
Pharmacogenetics and how individualized medicine can be applied to the practice of psychiatry<br />
Çiğdem Aydemir<br />
Ankara Numune Research and Education Hospital, First Psychiatry Clinic, Ankara, Turkey<br />
E-mail: aydemircigdem@yahoo.com<br />
Choice of psychotropic agents is a critical problem during the follow up of mentally ill patients. Some of the patients experience remission,<br />
however significant proportions of the patients continue to suffer from psychiatric symptoms and side or adverse effects.<br />
Psychotropic drug efficiency may not occur until a considerable time after the initiation of the therapy after which the clinician can<br />
determine, whether the regimen is effective or not. During this period treated patients may experience continuous psychiatric symptoms,<br />
employment loss, social dysfunction, and medical morbidity.<br />
Efforts to identify the best possible drug regimen for the patients focused on many points, such as clinical variables, predictors of possible<br />
side effects, plasma and CSF neurotransmitter levels, metabolite levels, and brain imaging, but they have only limited success. Up to date<br />
in practice, drug selection is made based on clinical symptom profile and possible side effects of treatments.<br />
The pharmacogenetics of the psychotropic drugs is a possible way to decide the suitable drug for the patient. Pharmacogenetics is the<br />
study of genetically determined interindividual differences in response to pharmalogical agents. In this field there are genetically coded<br />
pharmacokinetics (genetically based differences that influence the bioavailability of a drug), pharmacodynamics (genetically based<br />
differences in the proteins at which a drug acts) of the drugs, and dynamics of their side effects.<br />
The renal clearance of drugs appears to be similar in age- and weight-matched healthy subjects with no defined genetic polymorphisms.<br />
Studies regarding the inheritance mostly account for the ability to eliminate drugs. The genetic differences in pharmacokinetics have<br />
proved that they may be applied to the most of the drugs metabolism. Genetic polymorphisms have been identified and defined for<br />
some drug transporters, primarily P-gp, and several hepatic enzymes important for the cellular transport and metabolism of many drugs<br />
used in psychopharmacology. Genetic polymorphism in a drug-metabolizing enzyme can result in subpopulations of people who may<br />
deviate from the population mean in their ability to metabolize substrates of the affected enzyme. People who are poor metabolizers<br />
constitute at least 1% of the population, but the majority of people are normal or rapid metabolizers, and some are identified as ultra rapid<br />
metabolizers. The practical implications of metabolic phenotyping are most meaningful when the metabolic pathways of therapeutically<br />
administered drugs are known and when drug concentration has been correlated to either therapeutic or toxic effects.<br />
Genetic differences in the receptors, on which the drugs act, are another important factor in predicting the effects and side effects. Findings<br />
in this field are scarce in comparison to pharmacokinetics studies however some research projects are in progress. After the results of these<br />
studies are obtained; different variables other than plasma concentration of the drug would be available in pharmacotherapy practice.<br />
There is a dramatic increase in the amount of availability of the genetic information in public since samples can be easily collected by<br />
peripheral blood collection or mucosal smearing. Progress in genetic-molecular technology made possible to conduct genetic research<br />
on individual genes or entire genomes. In the future by the help of pharmacogenetic approach clinicians will be able to understand the<br />
predictors of drug efficacy and side effects, as a result individualized medicine will be applied in the practice of psychiatry.<br />
Key words: Pharmacogenetics, psychiatry, treatment, individualized medicine<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S101<br />
Pharmacogenomics biomarkers and personalized medicine in psychiatry<br />
Yeşim Aydın Son<br />
Middle East Technical University, Informatics Institute Department of Health Informatics, 06800, Ankara, Turkey<br />
E-mail: yesim@metu.edu.tr<br />
Transformation of clinical medicine was one of the long term goals of the Human Genome Project, expected to impact the practice<br />
within 10-20 years after the announcement of first draft of human genome. As of 2011 we are just entering into this era and emerging<br />
applications of technologies based on genomic research is indicating that Human Genome Project will be able keep its promise.<br />
Translational and clinical research to develop new personalized medicine approaches are going strongly; identification of predictive and<br />
diagnostic biomarkers is accelerating with the help of high-throughput technologies, and molecular diagnostics and pharmacogenomics<br />
is one of the growing markets worldwide with the goal of early detection, prevention, and intervention of diseases and to predict drug<br />
efficacy to guide dosing and avoid adverse reactions.<br />
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Abstracts of the Invited Speakers<br />
Single Nucleotide Polymorphisms (SNPs) are the most common form of genomic variations and the main genetic reason behind<br />
individual phenotypic differences. Also SNP variations are suggested to be the underlying reason of many complex diseases, they are<br />
considered as a good candidate for personalized medicine and pharmacogenomics applications. Genome-Wide Association Studies<br />
(GWAS) of SNPs are among the promising approaches for the identification of disease causing variants. The high-dimension of the SNP<br />
genotyping data presents a challenge for the understanding of the genotype and its possible implications for the etiology of the diseases<br />
and also for the identification of the representative SNPs to design the follow up studies for the validation of the associations. One of<br />
the bioinformatics tools developed to overcome this challenge is METU-SNP (http://metu.edu.tr/~yesim/metu-snp.htm), which aims to<br />
fasten the identification of associations described through GWAS. Today through genomic research and meta-analysis of genotyping<br />
experiments we are able to reveal SNP biomarkers associated with disease and drug reactions. Next, translational research has to be<br />
conducted in order to develop genomic diagnostics to apply this information into practice in medical clinics. Design of diagnostic assays<br />
for the diagnosis and prediction of drug response in psychiatric disorders can especially guide the initial selection of antipsychotics or<br />
antidepressants based on the individual genomic information of the patients.<br />
Development of personalized medicine approaches and utilizing genomic diagnostic assays like the examples will be presented in this<br />
talk will eliminate or decrease the number of trial-and-errors in selection of right therapy and dosage for the right patient and will also<br />
minimize emergency visits due to side effects of the drugs. Also prescription of right medicine and therapy plan at the initial diagnosis<br />
will increase trust between the healthcare professionals and the patients, which in return expected to provide higher cooperation and<br />
adherance rates of patients to their therapy. Application of pharmacogenomics and personalized medicine approaches in clinical decision<br />
making is expected to decrease the cost of healthcare in psychiatry as in other disciplines, while offering higher quality healthcare..<br />
Key words: Personalized medicine, biomarkers, molecular diagnostics, pharmacogenomics, Single Nucleotide Polymorphisms (SNPs), METU-SNP,<br />
rational drug use<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S101-2<br />
[PS-24]<br />
Symposium Title: Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety<br />
The effects of psychotropic and other drugs on flight and flight safety<br />
Muzaffer Çetingüç<br />
Aviation and Space Medicine Center, Anadolu University, Eskisehir, Turkey<br />
E-mail: mcetinguc@hotmail.com<br />
There are data that the side effects of many prescription drugs impair the psychomotor and cognitive performance of patients; with<br />
psychotropic drugs having even more of these negative side effects. Particularly drugs like benzodiazepines, antipsychotics, barbiturates,<br />
trycyclic antidepressants, stimulants, narcotic analgesics, and antihistamines that affect the central nervous system top the list for risks of<br />
accidents, injuries, and cognitive impairments. Along with these, anticoagulants, chemotherapeutic agents, antidiarrheals, antiemetics,<br />
and steroids should not be allowed for pilots. It is debatable that SSRIs have a mild side effect profile. SSRIs and bupropion are given<br />
to military pilots up to 6 months after resolution of anxiety and depressive symptoms in Canada and Australia. But the civil aviation<br />
authorities did not grant any privileges to these drugs.<br />
The gold standard in aviation for a pilot to fly efficiently and safely is to be in good mental and physical health and not to be affected by<br />
any medication during flights. The regulations both international and national have clear rules that permanently or temporarily restrain<br />
pilots from flying activities in the case of any sickness or medication treatment. The rules stating that a sick person cannot function as<br />
a pilot in a plane or an air traffic controller in a tower are rational. However since the notion of being sick and the tasks during a flight<br />
spread over a wide range, local health authorities can issue “waivers” for special situations. For example pilots with conditions like type-2<br />
diabetes, asthma, rheumatoid arthritis, sarcoidosis, or melanoma cannot fly; but in certain forms of these conditions that are stabilized<br />
with treatment, that have not caused serious limitations, and that do not affect performance, the pilot may be allowed to fly. Atopic<br />
dermatitis that recover with application of pomades, allergic rhinitis that is treated with nasal sprays, asthma that is treated with steroid<br />
inhalers, type-2 diabetes that is controlled with metformin are examples of allowed conditions. The drugs that are assumed not to have<br />
any side effects that might affect flight safety are: Aspirin, paracetamol, most antibiotics, depot penicillins, gout and thyroid medication,<br />
antiacids, nasal decongestants, oral contraceptives, topical analgesics and steroids, nonsteroidal anti-inflammatory drugs, vitamins,<br />
metformin, modafinil, caffeine, etc. Clearly, the patients need to be monitored for the first few days of use considering these drugs may<br />
have idiosyncrasies.<br />
S102 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
It is a problem when pilots take drugs without consulting authorized doctors for fear of flight suspensions. Adding to that reasons like<br />
the cost of doctor’s visits, losing compensation for the duration of suspension, upsetting supervisors due to disrupted flight schedules<br />
may lead pilots to taking OTC drugs. What’s worse is that they can order DTC drugs over the internet based on unscientific news, articles,<br />
and ads. There are several herbal supplements available in the market today that contain suspicious ingredients that claim to treat pain,<br />
help flu like symptoms, reduce stress, aid sleep, improve sexual performance, reduce blood fat levels, help lose weight, prevent aging, or<br />
provide vitamins and minerals. Therefore the attempts of the pilots to treat themselves create risks and the unknown side effects of those<br />
preparations pose serious problems to flight safety.<br />
Key words: Psychotropic drugs, SSRI, flight safety, pilots<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S102-3<br />
Sexual side effects of psychotropic and other drugs<br />
Adnan Özçetin<br />
Department of Psychiatry, Duzce University, Duzce, Turkey<br />
E-mail: adozcetin@gmail.com;adozcetin@yahoo.com<br />
Sexual dysfunctions are revealed by different organic and/or psychogenic factors and proceed with the addition of psychogenic reasons<br />
to almost all organic reasons. The organic/psychogenic discrimination of etiologies is crucial in sexual dysfunctions. The most important<br />
and practical way of discrimination is systematic and detailed history. The diffuse type sexual dysfunction established in elderly people<br />
should be considered primarily based on organic reasons. Furthermore alcohol/narcotics, drug abuse, the existence of somatic or systemic<br />
diseases also strengthen the possibility of organic based sexual dysfunction. The drugs and ingredients causing significant sexual side<br />
effects include: Alcohol and narcotics, antihistaminics, decongestants, diuretics, chemotherapeutics, antiulcer drugs, antihypertensives,<br />
anticonvulsants, asthmatic drugs, cardiac drugs, psychotropic drugs (antipsychotics, antidepressants, mood stabilizers, anxiolytics,<br />
sedative hypnotics), and others.<br />
It is mostly difficult even impossible to learn about the sexual side effects of drugs by physicians. Previous studies have revealed that<br />
patients usually didn’t mention the sexual side effects of drugs to their physicians. Therefore the physicians should specifically ask<br />
about the sexual side effects of drugs beside the dosage, preferred effects, and other side effects. Besides, relationship between sexual<br />
dysfunction and other diagnosis and drugs used by the patient should be considered.<br />
There are major unfavorable results of sexual side effects including: Loss of adaptation to drug use, abandonment of drug therapy,<br />
deterioration of psychiatric or other diseases, continuation of sexual dysfunctions, and disruption of quality of life. Significant side effects<br />
exist during the medical treatment of psychiatric disorders. The mechanism of emergence of sexual dysfunction due to medication use<br />
is complicated. Sexual dysfunctions due to medications occur by the effects of medications on peripheral and central neurotransmission.<br />
Serotonin mostly reveals negative effects on sexual behavior. However, its effects can also be positive according to receptor subtype<br />
and localization. Higher prolactin levels cause sexual dysfunction. The increase in dopaminergic activity has positive effects on sexual<br />
desire. Antipsychotics, antidepressants, anxiolytics, and other psychotropic drugs mostly have negative effects on sexual desire and<br />
behavior. Psychotropic drugs like bupropion, mirtazapine, moclobemid, reboxetine, and tianeptin have little or no sexual side effects.<br />
Even dopaminergic drugs like bupropion have positive effects on sexual desire.<br />
Key words: Drug, sexual dysfunction, side effect<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S103<br />
S103
Abstracts of the Invited Speakers<br />
COURSES<br />
[KC-01]<br />
Basic Biostatistics<br />
Selim Kılıç<br />
Gulhane Military Medical School, Department of Epidemiology, Ankara, Turkey<br />
E-mail: drselimkilic@gmail.com, skilic@gata.edu.tr, drselimkilic@yahoo.com<br />
The aims of this course are to teach the basic statistical approach and terminology, to teach the use of the SPSS for Windows package<br />
program and its basic characteristics and principals, to perform the basic descriptive and analytical statistics by using SPSS for Windows<br />
package program and to interpret the results.<br />
At the end of the course, the participants will be able to perform descriptive statistics, select the appropriate statistical tests to compare<br />
differences between or within groups and be able to draw some graphics by using the SPSS for Windows package program in a datasheet<br />
which is composed by the course director.<br />
The participants, upon completion of this course, will be able to generate and test hypotheses, compose a datasheet iusing the SPSS for Windows<br />
program, enter data in the datasheet, transform the data to other forms, select the appropriate statistical test for comparison of groups and computation<br />
of basic statistics, interpret and write the results, interpret the p value and confidence interval, and draw some graphs by using the SPSS program.<br />
The participants will learn to calculate mean, median, mode, standard deviation, quartiles, frequency and percents as descriptive statistics.<br />
They will learn and differentiate categorical, ordinal, and continuous variables by studying examples. To compare categorical variables, the<br />
use of the chi-square test and interpretation of the results will be discussed. For continuous variables, the appropriate test will be determined<br />
with respect to group numbers, whether groups are dependent or independent and whether the variables are parametric or nonparametric.<br />
According to the existing conditions, the participants will decide when they should use the independent samples t test, ANOVA, paired samples<br />
t test, or repeated measures of ANOVA as parametric tests and Mann Whitney U, Kruskal Wallis, Wilcoxon ranked signs test, or Friedman test<br />
as a nonparametric tests. They will also use correlation analysis to determine the linear association between continuous and ordinal variables.<br />
By using the SPSS program, participants will compose bar and pie graphs for nominal and box plot graphs for continuous variables to<br />
demonstrate the results.<br />
Key words: descriptive statistics, p value, confidence interval<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S104<br />
[KC-03]<br />
CBT in somatization disorders<br />
Axel Würz<br />
Department of Psychiatry, Marmara University, Istanbul, Turkey<br />
E-mail: messageaxel@googlemail.com, niz2hear@gmx.net<br />
Despite a high prevalence of somatic symptoms without demonstrable organic cause in nearly every branch of medicine, understanding,<br />
classification and treatment of these disorders have posed a considerable challenge.<br />
As the DSM-V is in development, the proposed changes in comparison to the DSM-IV can be seen to reflect the current understanding of<br />
non-organic physical symptoms. It is likely that somatization disorder, hypochondriasis, undifferentiated somatoform disorder and pain<br />
disorder will be combined into a new category entitled “Complex Somatic Symptom Disorder” (CSSD) which emphasizes the symptoms<br />
plus the patients’ abnormal cognitive processes. The term “complex” is intended to indicate that the symptoms must be persistent and<br />
must include both somatic symptoms (criterion A) as well as dysfunctional cognitive processes (criterion B) for the diagnosis to be made.<br />
Cognitive processes such as dysfunctional attention focusing, symptom catastrophizing, and symptom expectation that may be included<br />
in criterion B also show the influence cognitive models have exercised in the understanding of these disorders.<br />
These cognitive processes have to be evaluated against the background of possible psychiatric comorbidities, current life stressors,<br />
possible past traumatic events and learning experiences that shaped emotion regulation in an unhelpful way. Contributing to the<br />
maintenance of symptoms and resulting from dysfunctional cognitions are behaviours such as imbalanced level of activity, avoidance<br />
and safety-seeking and reassurance-seeking behaviors.<br />
S104 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of the Invited Speakers<br />
In cognitive behavioural therapy (CBT) of these disorders all the factors maintaining and contributing to the disorder are possible targets<br />
for treatment. The first and possibly most important step is to develop, in cooperation with the patient, an alternative explanation of the<br />
patient’s symptoms other than the presence of an organic cause. During the course of treatment the patient can then collect evidence<br />
that supports the alternative explanation of symptoms.<br />
The techniques that can be employed within the framework of the cognitive-behavioral approach are aimed at addressing the underlying<br />
dysfunctional cognitive processes and behaviors. They may comprise cognitive restructuring, attention-training, behavioral experiments,<br />
exposure, activity planning, and emotional-regulation techniques.<br />
Conventionally, treatment can be conducted in individual and group sessions and usually comprises about 15 one-hour sessions. There is evidence<br />
showing that CBT is effective in decreasing symptom severity and overall distress. However, there are limited number of studies comparing<br />
different treatment modalities such as CBT and pharmacological interventions. Also it is not clear if combining CBT and pharmacological<br />
treatment increases effectiveness. In addition different forms of therapy such as computer-based treatment have been developed.<br />
The cognitive behavioral model has been influencing the current understanding of somatization and CBT has shown effectiveness in<br />
its treatment although further studies are welcomed. Even if a full course of CBT cannot be offered, e.g. in an outpatient setting, and<br />
pharmacological treatment is chosen, it appears promising to integrate at least certain parts of cognitive-behavioral treatment such<br />
as developing an alternative explanation for the patient’s symptoms and exploring the role of processes such as attention, avoidance,<br />
unbalanced activity levels and safety-seeking and reassurance-seeking behaviors.<br />
Key words: Somatization, CBT, somatoform, hypochondriasis, treatment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S104-5<br />
[KC-04]<br />
Mindfulness and acceptance based therapies<br />
Kültegin Ögel<br />
Acibadem University, Medical Faculty, Istanbul, Turkey<br />
E-mail: ogelk@ogelk.net<br />
Mindfulness has reached far beyond the disciplines where it originated and has become an evidence-based psychotherapy method. In<br />
particule, the application of mindfulness based therapies in addition to traditional methods for psychiatric disorders prevents relapses.<br />
Mindfulness is concentrating with the aim of focusing at the moment in a nonjudgmental way. Mindfulness means being conscious of<br />
the current experience and accepting it. In other words, mindfulness is a unique and receptive form of consciousness in which stimulants<br />
are not evaluated, not classified and not analyzed.<br />
Mindfulness and acceptance based therapies deal with the thought itself instead of the content of the thought. It may be said that they<br />
help cognitive restructuring in this way. Mindfulness and acceptance based therapies differ from cognitive behavioral therapies in that<br />
way and are accepted as third wave therapies.<br />
Acceptance should not be confused with submission and giving up. Acceptance directs the person to turn to the current experience<br />
(opening up) instead of running away from the experience (closing up). By this means, the person learns to be with and accept<br />
experiences that are pleasant, unpleasant, or neutral. The person develops the skill of being fair to his or her own experiences. Being aware<br />
of what is happenibg causes a willingness to let things that are pleasant or unpleasant happen just as they are.<br />
Mindfulness acceptance therapies involves; Mindfulness Based Stress Reduction (MBSR), Mindfulnnes Based Cognitive Therapy (MBCT),<br />
Acceptance and Commitment Therapy (ACT), and Dialectical Behavior Therapy (DBT).<br />
The common basic strategies that all these therapies use are:<br />
- Acceptance<br />
- Focusing at the moment<br />
- Cognitive defusion and decentering<br />
- Being nonjudgmental<br />
- Observing<br />
Adaptation of the different viewpoints that are offered by mindfulness and acceptance based therapies by therapists, who have understood<br />
them, is useful. However, understanding of the basic rationale of the therapy by all psychiatrists and psychologists is also useful.<br />
Key words: Mindfulness, acceptance, psychotherapy<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S105<br />
S105
Abstracts of the Invited Speakers<br />
[KC-05]<br />
Eye movement desensitization and reprocessing method [EMDR]<br />
Specifically designed for Turkish patient population in the Netherlands<br />
Serdar Güner<br />
Praktijk Voor Psychiatrie, The Netherlands<br />
E-mail: serdarmineguner@gmail.com<br />
Dr. Serdar Guner reports that those behaviorally troubled Dutch patients with Turkish origin have not necessarily been benefitted by those<br />
10-15 sessions of EMDR during their psychiatric evaluations necessitated by different conditions. The clinicians have reportedly been applying<br />
traditional EMDR methods first to be objectifying relaxation through imagination and later on processing the completion of catharsis during<br />
as well as after the said eye movements. The patients, however, have been reporting no benefits and even at times, worsened clinical<br />
conditions after the given session. Dr. Guner has finally extracted the facts centered on this failure relevant to the given patient population.<br />
Those Turkish-Dutch clients have not been acknowledged about the rationale relevant to which-treats-what phenomenon through the<br />
catharsis. Lacking of explanation centralized around acknowledgement along with a possible language barrier has been hindering the<br />
therapeutic process. This finding has eventually led him to develop a sister method specifically designed for this patient population. He<br />
has slowly but steadily, started informing his patients about shock, repression of the feelings during it, and the effect of those repressed<br />
emotions on the people in short as well as long term trajectories. He, later on, used metaphors in picturing the process through which<br />
the said repressed emotions would be surfaced by means of EMDR. One of the interesting demographics has been the cultural difference<br />
of this given patient population. Those Dutch clients with Turkish origins have not been motivated in processing anything if they had not<br />
understood what they were doing. While this, in fact, is also true with the people from the other cultures, Dutch-Turks appeared to be a bit<br />
more autonomous in directing themselves in comparison with the Western Europeans who have likely been more conformists with their<br />
clinicians even when they have not necessarily been understanding what and why they were doing in any recommended method.<br />
Dr. Guner reviews his methodology designed for this population during his presentation. Most of the work has been an “acknowledgement”<br />
in his following up with his patients. This variant method has been helping PTSD patients’ feeling relaxation even after first two sessions.<br />
Dr. Guner reports that about 150 of his patients have been very happy about the outcome of this EMDR variant.<br />
Key words: EMDR, PTSD, psychotherapy<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S106<br />
WORKSHOP<br />
[WS-01]<br />
Alternative CBT method of panic disorder treatment for Turkish patients<br />
Serdar Güner<br />
Praktijk Voor Psychiatrie, The Netherlands<br />
E-mail: serdarmineguner@gmail.com<br />
I have been working as a psychiatrist and psychotherapist in the Netherlands for more than 20 years during which I have diagnosed and<br />
treated many Turkish panic patients by the virtue of sharing the same language, culture, and other demographics of the native land,<br />
Turkish Republic. The most important factor that led me to develop a different approach than that of a classical cognitive behavioral<br />
therapy -- focusing on neuro-vegetative reactions, neutralizing them through psycho-education and home-work, generating an insight<br />
into catastophic thoughts while “living” and finally easing up the panic attacks -- was the given patients’ thinking of the methods as<br />
“ridicilous,” and not doing their homeworks or acting as if they completed them even they did not.<br />
The alternative method I devised was related to use a lot of metaphors corresponding to the patients’ lives, generating an insight into<br />
catastrophic thoughts while “understanding” their bodily dynamics, self-controlling neuro-vegetative reactions, and acknowledging<br />
“the mechanism of panic reaction.” Since it is relatively short, not necessitating homework, and easy to understand for the panic stricken<br />
patients, it promotes motivation leading to less relapses and even if relapses occur, achieving quicker and easier recovery.<br />
The method appears to be effective among the native Dutch patients, as well as immigrants.<br />
The presentation will be providing details of this newly applied successful panic treatment.<br />
Key words: CBT, panic disorder, psychotherapy<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S106<br />
S106 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Turkish Association for Psychopharmacology<br />
4th International<br />
Congress on Psychopharmacology<br />
“Innovations and continuity in psychiatry &<br />
psychopharmacology: better care for better health”<br />
November 23-27, 2011<br />
Antalya, Turkey<br />
www.psychopharmacology2011.org<br />
ABSTRACTS OF ORAL PRESENTATIONS
Abstracts of Oral Presentations<br />
[SO-01] Ref. No: 93<br />
Bacopa monniera: Current trends and future directions<br />
Chris Neale 1 , Andrew Scholey 1 , Matthew Hughes 1 , Patrick Johnston 2<br />
1 Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University of Technology, Melbourne, Australia<br />
2 Department of Psychology, University of York, York, England<br />
E-mail: chrisneale@swin.edu.au<br />
Objectives: Bacopa monniera (BM) is an Indian herb used for centuries as a memory tonic in Ayurvedic medicine. Preclinical research has<br />
shown that BM acts as an antioxidant, improves memory, and reduces amyloid plaque deposition in animal models of Alzheimer’s disease.<br />
Human studies suggest that BM provides a fairly robust benefit to performance on certain attention, working memory, and learning tasks.<br />
This talk will present a review of BM research through animal models to human clinical trials and what research is currently being undertaken on BM.<br />
Methods: Two studies will be discussed further to the review of BM:<br />
(1) An acute dose-ranging study of healthy young adults where participants were required to complete a multi-tasking framework (MTF)<br />
and mood scales at baseline, 1 hr and 3 hrs post dose. The dosage was 300 or 600mg of BM or a matched placebo.<br />
(2) The study utilized a double blind, placebo controlled crossover design where all participants completed a 90 day course of both<br />
Bacopa (300mg daily) and placebo during the study. The participants were aged between 40 and 65 years and in good health. The<br />
interventions were separated by a 120 day washout period. The scans were undertaken on a 3T Siemens TRIO magnet before and after<br />
each 90 day intervention where participants would complete two runs of the task per scan visit.<br />
Results: (1) There was a significant, dose-dependent effect of treatment on ratings of alertness favouring the 600 mg treatment at both<br />
post-dose assessment times. There was a trend for dose-related effects on performance of the MTF, in particular for the Stroop task where<br />
there was an advantage for the 300 mg dose.<br />
(2) The data collection is still ongoing. The baseline data show a bilateral increase in BOLD activation in the precentral gyrus and precuneus<br />
with activation extending to the left inferior frontal gyrus (n=7, p=.005) when compared with controls using a task greater than baseline mask.<br />
Conclusions: The conclusions are speculative at this point for both studies, one being still in the data collection stage, one being<br />
underpowered. However, the methodologies and the future directions of these studies will be discussed.<br />
Key words: Bacopa monniera, human cognition, fMRI, nutraceuticals<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S108<br />
[SO-02] Ref. No: 143<br />
Association of the DRD2 TaqIA, 5-HT1B A-161T, and CNR1 1359 G/A polymorphisms<br />
with alcohol dependence: A single center study in the Denizli Province of Turkey<br />
Ceyhan Balcı Şengül 1 , Mehmet Emin Erdal 3 , Cem Şengül 2 , Özlem İzci Ay 3 , Muharrem Efe 2 , Mustafa Ertan Ay 3 , Hasan Herken 2<br />
1 Psychiatry Clinic, Denizli State Hospital, Denizli, Turkey<br />
2 Department of Psychiatry Pamukkale School of Medicine; Denizli,Turkey. 3 Department of Genetics Mersin School of Medicine, Mersin, Turkey<br />
E-mail: acemsen@gmail.com<br />
Background: Alcohol dependence is associated with genetic variants of alcohol-metabolizing enzymes and genes related to the<br />
dopaminergic, gamma-aminobutyric acidergic, glutamatergic, opioid, cholinergic, and serotonergic systems. Genetic variations in the<br />
endogenous cannabinoid system are also involved in alcohol dependence.<br />
Objective: The present study was aimed at evaluating the association between three polymorphisms, DRD2 TaqIA, 5-HT1B A-161T and<br />
CNR1 1359 G/A (rs1049353), and alcohol dependence.<br />
Methods: One hundred and twenty three patients, who were admitted to the Alcohol and Substance Abuse Center of Denizli State Hospital<br />
and diagnosed with alcohol dependence according to the DSM-IV criteria, and 125 healthy volunteers were included in the study.<br />
Results: Of the three polymorphisms investigated, 5-HT1B A-161T was the only one found to be associated with alcohol dependence.<br />
Conclusion: The 5-HT1B receptor A-161T polymorphism might be a promising marker for alcohol dependence; however, future studies<br />
are needed to clarify these findings.<br />
Key words: Alcohol dependence, DRD2 TaqIA, 5-HT1B A-161T, CNR1 1359 G/A, polymorphism<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S108<br />
S108 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of Oral Presentations<br />
[SO-03] Ref. No: 102<br />
Treating psychotic substance abuse patients with opioid agonist therapy and<br />
the atypical antipsychotic olanzapine<br />
Maria Chiara Pieri 1<br />
1 Department of Drug Addiction, Bologna Est, Italy<br />
E-mail: chiara.pieri@ausl.bologna.it<br />
Objectives: The aims of the study were: 1. To evaluate the efficacy of olanzapine in patients on methadone maintenance treatment; 2. To<br />
explore the time-course variation of cravings and weight at baseline and every 2 months for the first 6 months and then every 6 months until<br />
the end of the study (30 months). 3. To compare the severity of the symptoms between patients on methadone and patients on buprenorphine.<br />
Methods: The patients were enrolled from the Outpatient Addiction Unit in Bologna, Italy. All patients gave written informed consent. We<br />
randomized 32 patients to treatment with methadone and 13 to treatment with buprenorphine. Based on inclusion and exclusion criteria,<br />
36 patients were included in the study and they were divided into three treatment groups.<br />
At the baseline and follow-up sessions the following rating scales were administered: The Minnesota Multiphasic Personality Inventory-2<br />
(MMPI-2), the SCID-II (to identify and determine DSM-IV Axis II disorders i.e. personality disorders), Bech-Rafaelsen Mania and Melancholia<br />
Scales (BRMAS, BRMES; Bech et al. 1988, to cover severity of manic and depressive symptoms, respectively), and a VAS (Visual Analogic<br />
Scale, to quantify craving for drugs).<br />
Also the body weight of the participants was registered and followed.<br />
Results: After six months, no significant difference was found among the three subgroups, even though the olanzapine+methadone<br />
group achieved better and quicker results and sustained them for longer periods. There was no significant difference at baseline and at<br />
the end of the study in all patients.<br />
Total and partial BRMES and BRMAS scores did not significantly change during the follow-up period (6 th -30 th month), eventhough the<br />
curve displayed a downward trend. The VAS total scores were significantly lower both at the 6th and 30th month (p
Abstracts of Oral Presentations<br />
Materials & Methods: The experiments performed in this study were carried out according to the rules in the Guide for the Care and Use<br />
of Laboratory Animals adopted by the National Institutes of Health (U.S.A) and received Ege University Animal Ethics Committee’s consent.<br />
(Approval number: 2010-081)<br />
In this study, 9 Sprague-Dawley (450-500 g) adult male rats (16-20 weeks old) were used. The rats were maintained under controlled<br />
environmental conditions throughout the study: 21-25 °C ambient temperature, 12:12 light-dark cycle (light from 7:00-19:00h), and<br />
Standard laboratory food and tap water available ad libitum. Under anesthesia, a small hole was drilled. Then by using the bregma as a<br />
reference for the stereotaxic method (coordinates Anteroposterior: - 2.8 mm, Lateral: + 4.8 mm, Ventral: - 8.5 mm) (Paxinos Rat Brain), an<br />
exterior insulated bipolar EEG electrode was placed in the basolateral amygdala.<br />
The electrodes were fixed by using a dental acrylic (numerous alloys are used in the making of dental restorations). Rats were anesthetized<br />
by using ketamine (40 mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP).<br />
Three days after the electrode was fixed, spontaneous amygdala EEG records were taken from the rats by injecting saline, when they<br />
were awake and in their own box. Subsequently at 7 days intervals (5 times more than the half life of the drugs), olanzapine 1 mg/kg,<br />
haloperidol 1 mg/kg, chlorpromazine 5 mg/kg or ziprasidone 1 mg/kg doses were IP administered. Before each drug injection amygdalar<br />
EEG records were taken to observe the baseline rhythm of the amygdala. These drug doses were chosen after consideration of the<br />
hypermetobolism of rats.<br />
EEG recording was started 30 minutes after drug injection and each rat was recorded for 20 minutes. Signals were amplified by 10,000<br />
times and filtered within a range of 1-60 Hz. System records were taken by a Biopac MP30 amplifier system and evaluated with FFT (Fast<br />
Fourier Transform) and PSA (Power Spectral Analyses) methods. During this process Delta 1-4 Hz, Theta 4-8 Hz, alpha 8-12 Hz and beta<br />
12-20 Hz waves in the EEG are accepted as the ratio of percentage in PSA (Power Spectral Analyses) methods. We confirmed electrode<br />
locations histologically following euthanisation.<br />
Results: According to the data obtained, the perceptibly dominant frequency in amygdala spontaneous activity was founded to be 1-4<br />
Hz (Delta).<br />
When we compared the EEG records in the 1-4 Hz (Delta) band of the groups which were given typical and atypical antipsychotic drugs to<br />
the control group given isotonic saline, there was significant (p < 0.005) inhibition. On the other hand in the 4-8 Hz (Theta) and the 8-12<br />
Hz (Alpha) (Figure 4) bands, a significant (p < 0.005) increase was observed.<br />
When the EEG records of the group which was given atypical antipsychotics were compared to the typical antipsychotic administered<br />
groups, in the 1-4 Hz band a significant increase (p< 0.05) and in the 4-8 Hz and 8-12 Hz bands significant inhibition (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of Oral Presentations<br />
[SO-05] Ref. No: 142<br />
The effect of cognitive-behavioral therapy in reducing the feeling of emotional<br />
pressure and blood sugar control in patients with type 2 diabetes<br />
Shahnam Abolghasemi 1 , Ghahraman Mahmodi 2 , Mandana Zafari 2<br />
1 Department of Medicine, Islamic Azad university,Tonekabon, Iran<br />
2 Department of Medicine, Islamic Azad university, Sari, Iran<br />
E-mail: ghahraman48@yahoo.com<br />
Objective: The results of some studies show that diabetes patients experience some psychological problems, such as depression, stress, selfnegative<br />
labeling, and lack of self confidence. In this study, we investigated the effect of cognitive-behavioral therapy (CBT) in reducing the<br />
feeling of emotional pressure and blood sugar control in type 2 diabetes patients, who were referred to the Tonekabon Society of Diabetes.<br />
Methods: This feeling was measured by using Marghan’s Measure for Feeling of Emotional Pressure. In addition, the blood sugar levels<br />
of all patients were tested and recorded. The 24 patients, who had the highest emotional pressure scores, were selected and randomly<br />
divided into two groups, each consisting of 12 patients. They were provided CBT.<br />
After the end of CBT, they were tested again. The collected data were tested by SPSS software, 10th edition and ANCOVA covariance<br />
statistical test.<br />
Results & Conclusions: There were some meaningful differences between the pre-and post-test levels of emotional pressure. The results<br />
of the blood sugar test also indicated a reduction in the level of blood sugar and normalization of blood sugar control in some patients<br />
with diabetes type 2.<br />
Key words: Stress, blood sugar, lack of self confidence, CBT<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S111<br />
[SO-06] Ref. No: 110<br />
Acute effects of nicotine on working and reference memory in rats using<br />
a 12-arm radial maze<br />
Mahsa Movahed Abtahi 1 , Hosein Molavi 1 , Jamal Moshtaghian 2 , Karim Askari 1<br />
1 University of Isfahan, Faculty of Education and Psychology, Department of Psychology<br />
2 University of Isfahan, Faculty of Science, Department of Biology<br />
E-mail: m.movahedabtahi@gmail.com<br />
Objectives: It has been shown that nicotine plays a significant role in improvement of memory. Based on this finding, nicotinic drugs are<br />
being developed for possible use as co-treatments for cognitive impairment in some kinds of mental disorders. However, past studies<br />
have mostly emphasized working memory function following acute administration of nicotine and the few studies concerned with<br />
reference memory have shown no significant effects. As the 8-Arm Radial Maze, which has been used in most of the studies in this field,<br />
provides a lower task difficulty, the present article aims to replicate previous studies with a specific emphasis on reference memory using<br />
a 12-Arm Radial Maze which provides a higher level of cognitive task demands.<br />
Methods: Three groups of male Wistar rats were used. The rats were subcutaneously injected with three doses of nicotine 20 min prior<br />
to the start of each trial on the Radial- Arm Maze. The first group was injected with 0.1 mg/kg nicotine solution, the second group was<br />
injected with 0.4 mg/kg , and the third group was the control which received saline.<br />
The spatial memory of the rats was tested on a 12-Arm Radial Maze. The arm choices were recorded when the rat had placed all of its<br />
paws beyond the threshold at the proximal end of the arm. Each session of the testing continued until the rat ate all 6 baits or until the<br />
maximum time of 6 minutes was over. There was at least 24 hours between drug injections during which time the rats were not tested.<br />
Results: The results of repeated analysis of variance showed a significant difference in working memory errors among the three groups,<br />
but there was no significant difference in reference memory errors between the groups. An inverted U-shaped dose-effect curve was seen<br />
for reference memory which showed that nicotine first results in increased reference memory errors and then, perhaps because of the<br />
effect of training, the number of errors decreased.<br />
Conclusions: The current study suggests a negative correlation between acute consumption of nicotine and long-term spatial<br />
performance on a 12-Arm Radial Maze, which contradicts the former assumption on an 8-Arm Radial Maze. This finding also emphasizes<br />
the different mechanisms underlying working and reference memory that should be considered in pharmacotherapeutic interventions<br />
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Abstracts of Oral Presentations<br />
with nicotinic drugs and other drugs for memory impairments in various mental disorders.<br />
Key words: Nicotine, reference memory, learning, radial-arm maze<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S111-2<br />
[SO-07] Ref. No: 243<br />
The relationship between personality characteristics and internet addiction in adolescents<br />
Jalal Shafaie 1 , Sharooz Farjad 2<br />
1 Shafa jalal,Young Researchers Club, Islamic Azad University, Ardabil<br />
2 Farjad Sharooz, Department of Educational Managment, Islamshar Branch, Islamic Azad University, Tehran<br />
E-mail: jalal.shafa@gmail.com<br />
Introduction: Personality has been identified as a significant factor in internet addiction. The purpose of the present research was to<br />
investigate the role of personality factors in the prediction of internet addiction in adolescents.<br />
Materials-Methods: The research subjects consisted of 261 (146 females, 115 males) adolescents from the city of Ardabil. They were<br />
selected by using the random clustering method. The data of the Young Internet addiction (IAT) test and the NEO-FFI Personality<br />
Inventory were used together. The data were analyzed by Pearson’s correlation coefficient and multivariate regression analysis.<br />
Results: The result of the Pearson correlation coefficients showed that there were significant relationships in adolescent girls between<br />
neuroticism (r=0.42, P
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of Oral Presentations<br />
[SO-09] Ref. No: 254<br />
Comparison of the effects of bupropion and fluoxetine on reaction time in adults<br />
with major depressive disorder in a 4-week, single-blind study<br />
Farshad Hashemian, Marjan Sadat Tabatabayi, Ali Sharifi, Marzieh Majd<br />
Department of Clinical Pharmacy, Islamic Azad University, Pharmaceutical Sciences Branch,Tehran, Iran<br />
E-mail: hashemian.f@iaups.ac.ir<br />
Objectives: Some studies have shown that adults diagnosed with major depression have longer reaction time compared to the<br />
healthy population. Longer reaction time may result in educational and occupational impairment and increased risk of fatal driving<br />
incidents. Consequently, any impact on reaction time induced by drug therapy may have either positive or negative effects on treatment<br />
outcome and quality of life of patients. Bupropion is an effective antidepressant, which clearly acts via different mechanisms than other<br />
antidepressants. Its mechanism of action is thought to be dopamine and/or norepinephrine reuptake inhibition with negligible effects<br />
on serotonin.<br />
While bupropion is considered an antidepressant with minimal effects on alertness and cognitive function, the present study was<br />
designed to evaluate the effects of bupropion on reaction time in comparison with fluoxetine, in adult patients with major depressive<br />
disorder.<br />
Methods: A total of 30 patients who met the DSM-IV criteria for major depression were recruited for this study. Patients were randomly<br />
assigned to receive either bupropion (200 mg/day) or fluoxetine (20 mg /day) for 4 weeks. Reaction time was assessed at baseline, 2 and 4<br />
weeks of treatment using validated computer-generated tasks and keyboard tapping tests in which the data was collected and analyzed<br />
for auditory and visual stimuli. In addition, the participants were assessed using the Hamilton depression rating scale at baseline, 2 and 4<br />
weeks of treatment. The number of correct responses, omissions, and substitution errors for each stimulus were calculated.<br />
Results: No significant differences were observed between the groups regarding demographic characteristics and Hamilton depression<br />
score at baseline.<br />
In both groups, the number of correct responses to the visual stimuli increased significantly after 4 weeks of treatment (P
Abstracts of Oral Presentations<br />
patients treated with methadone.<br />
Methods: A total of 36 male opioid-dependent patients, aged between 18 and 50 years who met the DSM-IV criteria for opioid dependence,<br />
were randomly assigned into two groups of 18 members, to receive either ginseng (two 250 mg capsules daily) or placebo for the first 15<br />
days of detoxification. All patients were treated with a Methadone Maintenance Treatment (MMT) protocol. Opioid withdrawal syndrome<br />
severity was measured by the Clinical Opioid Withdrawal Scale (COWS) on days 0, 1, 7, 10, and 15. In addition, the required daily methadone<br />
dosage was recorded and compared between the groups. This trial was registered in the Iranian Registry of Clinical trials (IRCT) under ID of<br />
IRCT201009063106N4 and was approved by the Ethics Committee of Azad University (approval number: 4115).<br />
Results: Patients in the two treatment groups did not differ significantly in socio-demographic and clinical variables at the baseline.<br />
As expected, a statistically significant decrease in the COWS total score and symptoms was observed from the first day to the end of the<br />
study in both treatment groups.<br />
As shown in figure 1, the required daily methadone dosage was lower in the ginseng group from day 5 to the end of the study (P
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of Oral Presentations<br />
Conclusions: The in vitro disintegration test is a proxy for the disintegration process in a patient’s mouth. Differences found in the<br />
formulation and manufacturing processes of ODO products may be associated with different disintegration times, which may potentially<br />
impact their use in clinical practice.<br />
Key words: In vitro analysis, orally disintegrating olanzapine<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S114-5<br />
[SO-12] Ref. No: 118<br />
Effect of duloxetine on functional outcomes in patients with major depressive disorder<br />
Levent Alev 1 , Murat Altın 1 , Kübra Özbek 1 , David Sheehan 2 , Adam Meyers 3 , Jonna Ahl 4 , Apruva Prakash 3 , Tina Marie Myers Oakes 4<br />
1Eli Lilly Turkey,<br />
2University of South Florida College of Medicine, Tampa, USA<br />
3Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, USA<br />
4Lilly, Indianapolis, USA<br />
E-mail: alev_levent@lilly.com<br />
Objective: Patients with major depressive disorder (MDD) often have a reduced ability to function socially, maintain and enjoy<br />
relationships and work. The aim of this analysis was to investigate the efficacy of duloxetine vs. placebo on improvement in functioning<br />
after 8 weeks of treatment.<br />
Methods: This was a pooled analysis of data from two separate 9-month studies conducted under the same protocol in patients with<br />
MDD (DSM-IV-TR) to examine the efficacy of duloxetine 60 mg/day (n = 518) vs. placebo (n = 258) on impairment in functioning. Pooling<br />
the data from these studies was specified a priori in the protocol to allow for increased power to detect differences between duloxetine<br />
and placebo on secondary and exploratory objectives. The measures included in this analysis were: the Hamilton Depression Rating Scale<br />
(HAMD) Item 7 (Work / Activities), the Sheehan Disability Scale (SDS), the Social Adaptation Self-evaluation Scale (SASS) to assess social<br />
behavior, the Massachusetts General Hospital Cognitive and Physical Functioning Questionnaire (CPFQ) and the Profile of Mood States<br />
-brief form (BPOMS) subscales Vigor / Activity (VA) and Fatigue / Inertia (FI) used as surrogate measures of function. Mean changes from<br />
baseline were analyzed by using a mixed-effects model repeated measures approach (MMRM). An analysis of covariance (ANCOVA) using<br />
a last observation carried forward (LOCF) approach was conducted as a sensitivity analysis. The endpoint for this analysis was at week 8.<br />
Results: At baseline, patients had moderately severe levels of SDS global functional impairment scores (18.3±6.9). At the endpoint,<br />
there was significant improvement from baseline (MMRM) with duloxetine treatment on the HAMD Work / Activities (p
Abstracts of Oral Presentations<br />
adequate diet (AZ containing 5.4 mg zinc/100g). The second group was given a zinc deficient diet (ZD containing 0.12 mg zinc/100g),<br />
and the third group received a zinc deficient diet and was treated orally with vitamin D (12.5µg/kg) (ZD + VD). Body weight gain was<br />
recorded regularly during the experimental period. After three weeks, the animals were sacrificed and blood glucose, serum cholesterol,<br />
serum triglycerides, serum total protein, serum urea, serum zinc, liver zinc, kidney zinc, pancreatic zinc, femur zinc, liver glutathione<br />
concentrations, serum glutamic oxalic transaminase (GOT), serum glutamic pyruvic transaminase (GPT) and serum alkaline phosphatase<br />
activities were determined.<br />
Results: The body weight gain of the zinc deficient diabetic animals at the end of three weeks of dietary manipulation was significantly<br />
lower than that of the zinc adequate diabetic animals. The zinc deficient diet significantly increased the blood glucose, serum cholesterol,<br />
serum triglycerides, and serum urea of the zinc deficient diabetic rats as compared to their counterparts fed on an adequate zinc diet.<br />
Meanwhile serum zinc, femur zinc, pancreatic zinc, liver zinc, kidney zinc, serum total protein, and liver glutathione levels were diminished.<br />
The consumption of a zinc deficient diet led also to an increase in GOT and GPT and a decrease of serum alkaline phosphatase activities.<br />
However, vitamin D treatment ameliorated all of the previous physiological and biochemical parameters.<br />
Conclusion: In conclusion, this study demonstrated that vitamin D reduced the severity of diabetes development caused by zinc<br />
deficiency. In other words, vitamin D probably increased zinc absorption which led to insulin synthesis and secretion and improvement<br />
of insulin activity.<br />
Key words: Zinc deficiency, diabetic rats, alloxan, vitamin D, GOT, GPT, alkaline phosphatase<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S115-6<br />
[SO-14] Ref. No: 152<br />
Gabapentin in the treatment of opioid withdrawal<br />
Gholam Reza Kheirabadi, Mehrdad Salehi, Mohammad Reza Maracy, Mansor Ranjkesh<br />
Isfahan University of Medical Sciences, Iran<br />
E-mail: kheirabadi@bsrc.mui.ac.ir<br />
Objectives: To evaluate the efficacy of gabapentin (1600 mg/day) as an adjunct to methadone-assisted detoxification (MAD) in the<br />
treatment of opioid withdrawal symptoms.<br />
Methods: Design: A 3-week open label study (as the second phase) following a double blind placebo controlled study with 900mg/day of<br />
gabapentin (as the first phase of this study). Setting: A specialized outpatient clinic for the treatment of patients with addictive disorders.<br />
Participants: Twenty-seven opiate addicts, who met the DSM-IV-TR criteria for opioid dependency, randomly selected among outpatients<br />
referred to our clinic. Intervention: The subjects received adjunctive treatment with gabapentin (1600 mg/day) in addition to MAD for<br />
three weeks. Measurements: The Subjective Opiate Withdrawal Scale (SOWS) with a total score of 0 to 64 was administered at six timepoints<br />
during the study.<br />
Results: The total SOWS score was significantly decreased after the intervention. Compared with our previous trial, an almost significant<br />
difference was observed in total SOWS scores between groups treated with gabapentin 1600 mg/day and 900 mg/day at the end of the<br />
intervention period (p = 0.06). Gabapentin at a dose of 1600 mg/day was significantly superior to a dose of 900 mg/day in decreasing the<br />
severity of coldness, diarrhea, dysphoria, yawning, and muscle tension.<br />
Conclusion: Add-on gabapentin at a dose of 1600 mg/day may be effective in reducing some of the withdrawal symptoms in opiate<br />
addicts undergoing methadone-assisted detoxification.<br />
Key words: Opium dependence, opioid withdrawal, gabapentin<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S116<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of Oral Presentations<br />
[SO-15] Ref. No: 103<br />
The role of transcranial magnetic stimulation in cognitive processes and treatment<br />
of psychiatric disorders<br />
Serwa Mohamadzadeh Ashna<br />
Young Researchers Center, Islamic Azad University, Sanandaj Branch, Sanandaj, I.R. Iran<br />
E-mail: srwa.mohamadzade@gmail.com<br />
Background and Objectives: Transcranial magnetic stimulation (TMS) is a neurostimulation and neuromodulation technique, based on<br />
the principle of electromagnetic induction of an electric field in the brain. This field can be of sufficient magnitude and density to depolarize<br />
neurons. When TMS pulses are applied repetitively they can modulate cortical excitability, increasing or decreasing it depending on the<br />
parameters of stimulation, even beyond the duration of the train of stimulation. This effect has behavioral consequences and therapeutic<br />
potential. Due to its easy use and relatively minor side effects, transcranial magnetic stimulation is now widely used in neurosciences and<br />
medicine. The main areas of transcranial magnetic stimulation application are:<br />
1) the investigation of cortical and spinal excitability,<br />
2) the investigation of neuronal plasticity,<br />
3) the investigation of neuronal connectivity,<br />
4) functional mapping, and<br />
5) the treatment of some neurological and psychiatric disorders.<br />
Transcranial magnetic stimulation alone or in combination with other noninvasive neuroimaging (PET – positron emission topography,<br />
MRI – magnetic resonance imaging) and neurofunctional (EEG – electroencephalography, ERP – event-related potentials, FMRI – functional<br />
magnetic resonance imaging) methods allows the conduction of research on brain functions. Thus, transcranial magnetic stimulation is<br />
suitable as a diagnostic tool in neurological and neuropsychiatric brain investigations.<br />
Method: The method of research in this paper was a review of the literature regarding publications that applied TMS for treatment and<br />
investigation goals. A total of 104 relevant papers were identified and reviewed and the results are presented here.<br />
Results: TMS is, through inducement of an electrical field, a useful instrument to visualize regional activities in response to stimulation.<br />
The mechanism of effect of TMS is through inducing the depolarization of neurons that in turn activates other neurons and produces<br />
behavioral and cognitive outcomes, depending on the stimulated area and its function. For example some of the observable TMS-induced<br />
effects are: phosphene by stimulating the occipital cortex, interrupting working memory and speech processes by stimulating the<br />
frontal lobe, or improving verbal memory in major depressive disorder through modulating effects on the dopamine system. TMS, unlike<br />
electroconvulsive therapy (ECT), does not have any substantial cognitive side effects. TMS has effects on neurochemical and synaptic<br />
processes in neurons. There are reports in the literature that depression, mania, schizophrenia, pain disorder, hallucinations, catatonia,<br />
post traumatic stress disorder, obsessive compulsive disorder, Parkinson’s disease, epilepsy, neuronal plasticity studies, tick disorders,<br />
migraine and dystonia are improved by TMS procedures.<br />
Conclusions: Current published studies and meta-analyses have evaluated the efficacy of rTMS, given in treatment paradigms that were<br />
almost certainly suboptimal (e.g. duration of two weeks), and found that TMS is a safe and tolerable intervention. These findings raise the<br />
possibility of using TMS as a therapeutic device in psychiatric disorders and neuroscience research.<br />
This study summarizes the mechanisms of effect, advantages, and side effects of TMS and reviews studies of the efficacy of transcranial<br />
magnetic stimulation on psychiatric disorders.<br />
Key words: Transcranial magnetic stimulation (TMS), neuromodulation, electromagnetic induction<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S117<br />
[SO-16] Ref. No: 112<br />
Oxytocin inhibition of pentylenetetrazole-induced convulsions and its identification<br />
by behavioral measurement and thalamic EEG in the rats<br />
Oytun Erbas, Vedat Evren, Saylav Bora, Gonul O. Peker<br />
Department of Physiology, Ege University, School of Medicine, Izmir, Turkey<br />
E-mail: oytun.erbas@ege.edu.tr<br />
Objective: In this study, our aim was to reveal the possible anticonvulsant effects of oxytocin (OX) in high doses, as oxytocin has inhibitory<br />
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Abstracts of Oral Presentations<br />
effects in brain. In addition, these effects were correlated with thalamic EEG recordings. To create the convulsions, pentilentetrazol (PTZ)<br />
was used.<br />
Materials-Methods: In this study sixty 8-12 weeks old Sprague-Dawley adult male rats, which were separated into 10 groups (n=6), were<br />
used. In the first through the fifth groups 10, 20, 40, 80, and 120 U/kg OX was injected intraperitoneally (i.p) in order. In the sixth group<br />
(control), saline was injected.<br />
Five minutes after of each injection of OX, 70 mg/kg i.p. PTZ was injected into the all rats and seizures were induced.<br />
We evaluated the seizure behaviors with the Racine Convulsion Scale and we determined the threshold seizure dose of PTZ, around 35<br />
mg/kg, and the suppressive dose of OX, around 80 and 120 U/kg.<br />
The rats, which were placed in a Plexiglas cage, were evaluated according to the severity of convulsions from 0 to stage 5.<br />
The scale of convulsions was: (0):Normal,(1):Frozen,(2):Nodding,(3):Superficial clonic movements,(4): Bilateral clonus in front extremities<br />
(piano play)(5):generalized tonic clonic seizures and falling sideways.<br />
To show the anticonvulsant effects of oxytocin using the EEG, the seventh through the tenth groups were used. Under anesthesia a small<br />
hole was drilled. Then by taking the bregma as a reference using the stereotaxic method (coordinates AP:-3.6 mm, L:+2.8 mm, V:-5.0 mm)<br />
(Paxinos Rat Brain), an exterior insulated bipolar EEG electrode was placed in the left thalamic nucleus. In the seventh group thalamic EEG<br />
records were taken after only saline injection.<br />
The rats in the eighth and ninth groups were injected intraperitoneally (ip) with 80 and 120 U/kg OX , respectively. In the tenth group<br />
(control), just saline was injected. Five minutes after each OX injection, 35 mg/kg i.p. PTZ was injected into the all rats.<br />
EEG recordings were taken for 20 minutes. The signals were amplified by 10,000 times and filtered with a range of 1-60 Hz. System records<br />
were taken by a Biopac MP30 amplifier system and evaluated with the FFT (Fast Fourier Transform) and PSA (Power Spectral Analyses)<br />
methods. During this process Delta 1-4 Hz, Theta 4-8 Hz, alpha 8-12 Hz and beta 12-20 Hz waves in the EEG are accepted as the ratio of<br />
percentage in PSA methods. We affirmed the electrode location histologically following euthanisation.<br />
RESULTS: We observed that oxytocin has a powerful anticonvulsant effect, which appears at 40 U/Kg (Stage 3.14±0.69 ) and 80 U/kg (Stage<br />
3.0±0.57) doses moderately and which shows the maximum effect at 120 U/kg (Stage 1.57±0.53) doses (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Abstracts of Oral Presentations<br />
mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP)), an ECG was taken in derivation (D) I and the normal QTc interval was determined. To<br />
calculate the QTc interval, Bazett’s formula was used.<br />
The rats were divided into 3 groups (n=6). For the first group, 3 mg/kg ziprasidone and saline, for the second group, 3 mg/kg ziprasidone<br />
and 1 mg/kg metoprolol and for the third group, 3 mg/kg ziprasidone and 2 mg/kg diltiazem were administered intraperitoneally.<br />
Two hours later, under anesthesia, the QTc interval was calculated by taking the ECG in derivation I.<br />
Results: In the first group of rats, given ziprasidone and saline the QTc interval (0.161±0.01 s) was significantly (p
Turkish Association for Psychopharmacology<br />
4th International<br />
Congress on Psychopharmacology<br />
“Innovations and continuity in psychiatry &<br />
psychopharmacology: better care for better health”<br />
November 23-27, 2011<br />
Antalya, Turkey<br />
www.psychopharmacology2011.org<br />
POSTER PRESENTATIONS
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-001] Ref. No: 133<br />
Visual hallucinations induced by bupropion: A case report<br />
Sevda Korkmaz 1 , Murat Kuloglu 2 , Sadullah Saglam 3 , Murad Atmaca 2<br />
1 Department of Psychiatry, 3 Department of Neurology, Psychiatric Hospital<br />
2 Department of Psychiatry Firat University School of Medicine, Elazig-Turkey<br />
E-mail: skorkmaz23@hotmail.com<br />
Bupropion is an antidepressant, which inhibits reuptake of norepinephrine and dopamine. It is a relatively reliable antidepressant in terms<br />
of side effects and also is used in the treatment of nicotine deprivation (1, 2). Most frequent side effects are insomnia, dry mouth, and<br />
headache (3). Here we present a case who developed visual hallucinations during bupropion treatment.<br />
Case: F.Y: A 51 year old woman was admitted to the outpatient clinic with complaints of hump, horror, and seeing spider images. Visual<br />
hallucinations, anxiety, irritability, insomnia, and anhedonia were noted on psychiatric examination. Except for the visual hallucinations,<br />
there was no other perception abnormality nor other psychotic symptoms. History: she reported to a psychiatrist with complaints<br />
of joylessness, weakness, fatigue, and anhedonia. She was diagnosed with major depressive disorder and subsequently was put on<br />
bupropion 150mg/day. After a week, the dosage of bupropion was increased to 300mg/day. On the first day of the bupropion dose<br />
increase to 300 mg/day, spider images developed in both of her eyes and in the following days these images increasingly continued. The<br />
images lasted for days and scared the patient, ruined her sleep pattern, and increased her anxiety. The patient saw an ophthalmologist<br />
with these complaints and at the medical examination there was no evidence of an organic or pathological disorder. Her blood pressure<br />
was under control with treatment. The patient had been treated with escitalopram and duloxetine 6 years ago with a diagnosis of<br />
depressive disorder, but the patient specified that she had not had any visual complaints. There were not any relevant symptoms at<br />
that time and patient was not describing any clear stress factors. The family history was unremarkable. The patient did not have such<br />
complaints as dizziness, tinnitus, or paraesthesia and there was not any pathological finding at the neurological examination. Also there<br />
were no abnormal findings in the blood tests, urinalysis, and MR imaging. The Beck depression, Beck anxiety, and SCL-90 scales showed<br />
high levels of anxiety and moderate depression. After the assessment of all these data, suspicion was focused on the bupropion as the<br />
main cause of the spider images (visual hallucinations). The patient did not accept hospitalization, thus she was followed up periodically.<br />
First the dosage of bupropion was decreased to 150 mg and bupropion treatment was stopped completely in a few days. Alprazolam 0.5<br />
mg/day treatment was started to decrease the patient’s anxiety. Paroxetine 10 mg/ day was started and increased to 30 mg/day in two<br />
weeks. Following the discontinuation of the bupropion, the visual hallucinations disappeared in a few days. The patient came for controls<br />
monthly and at the end of the 6th month the symptoms of depression and anxiety had decreased considerably.<br />
Comment: Bupropion has become a popular antidepressant in the treatment of depressive disorders in Turkey and is preferred frequently<br />
because of its relatively low incidence of side effects. Nevertheless every kind of side effects including psychotic symptoms that appear<br />
during treatment should be assessed carefully.<br />
Key words: Bupropion, hallucination, antidepressant<br />
References:<br />
1. Ascher JA, Cle JO, Colin JN, et al. Bupropion: A review of its mechanism of antideressant activity. J Clin Psychiatry 1995;56:395-401.<br />
2. Englisch S, Inta D, Eer A, Zink M (2010) Bupropion for depression in schizophrenia. Clin Neuropharmacol; 33(5): 257-259.<br />
3. Hurt RD, Sachs DPL, Glover ED, Offord KP, Johnston JA, Dale LC, et al. A comparison of sustained release bupropion and placebo. N Engl J Med 1997;337:1195-1202.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S121<br />
[PP-002] Ref. No: 139<br />
Clinical features of patients with panic disorder in outpatient clinics of a psychiatric<br />
training and research hospital<br />
Ramazan Konkan 1 , Erkan Aydın 1 , Oya Güçlü 1 , Ömer Şenormancı 1 , Mehmet Z. Sungur 2<br />
1 MD, Psychiatrist in Deparment of Psychiatry in Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, Istanbul Turkey<br />
2 MD, Proffessor in Deparment of Psychiatry, Marmara University School of Medicine, Istanbul Turkey<br />
E-mail: ramazankonkan@gmail.com<br />
Objective: Panic disorder is a disorder characterized by recurrent unexpected panic attacks where the patient may exhibit avoidance<br />
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Poster Presentations<br />
behavior by experiencing anticipatory anxiety for further attacks. According to the DSM-IV-TR, panic disorders are divided into two types:<br />
with and without agoraphobia. Agoraphobia is an anxiety disorder in which there are repeated attacks of intense fear and anxiety, and<br />
a fear of being in places where escape might be difficult, or where help might not be available, and it results in obvious avoidance of<br />
feared places and situations. Panic attack is characterized by intense anxiety that occurs unexpectedly and spontaneously, accompanied<br />
by somatic and cognitive symptoms. A marked deterioration can be observed in patients’ functions, particularly due to the anticipatory<br />
anxiety and avoidance behaviors (1,2). The cognitive rationale of panic disorder is linked to a catastrophic interpretation of bodily<br />
sensations. Negative and anxiety-related processes of thought such as heart attack, cerebral hemorrhage, and loss of control are effective<br />
in the origin of panic attacks due to a catastrophic interpretation (3). The objective of our study was to identify clinical characteristics<br />
involved in the onset and maintenance of this disorder in patients who presented to a training and research hospital.<br />
Method: The study included 101 consecutive patients with panic disorder who presented to the clinics at the Bakirköy Hospital for<br />
Mental and Neurological Disorders, met the inclusion criteria, volunteered to participate in the study, and provided informed consent.<br />
The diagnosis was made by two psychiatrists, who were not involved in the study. The diagnosis was confirmed using the Structured<br />
Clinical Interview Form for the DSM-IV Axis I Disorders (SCID-I). The patients filled in a sociodemographic form, which examined clinical<br />
characteristics of the disease in detail, including the identifiable life events triggering the disease and the environmental conditions where<br />
the attacks developed, taking the SCID-I clinical interview guide into consideration.<br />
Results: The mean age of participants was 36.73 ± 9.42 years (min: 19, max: 58 years). The mean age of onset was 29.94 ± 9.17 years,<br />
and the mean duration of disease was 6.73 ± 7.65 years. The sociodemographic characteristics of the participants are outlined in Table 1.<br />
Distribution of the complaints listed in accordance with the DSM-IV-TR panic disorder criteria by their incidence is provided in Table 2 (only<br />
the first 3 criteria among the DSM-IV-TR panic disorder criteria were included in the assessments). The clinical characteristics of patients<br />
specific to panic disorder are shown in Table 3.<br />
Discussion: Understanding the clinical characteristics specific to panic disorder, which have a significant impact on the functioning<br />
of a person due to escape, avoidance, and safety seeking behaviors as a result of a catastrophic interpretation of bodily sensations, is<br />
important in conceptualization and therapeutic interventions of the disorder.<br />
In the present study, the population was not well reflected in terms of gender as participants were consecutively enrolled from the clinics<br />
of a training and research hospital. It was a single-center study, and Axis I and II comorbidities were not evaluated. We believe that further<br />
studies eliminating such limitations would be beneficial.<br />
Key words: Panic disorder, panic symptoms, avoiding behavior<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S121-2<br />
[PP-003] Ref. No: 141<br />
Effect of calcium in treatment of premenstrual syndrome<br />
Mandana Zafari, Azar Aghamohammadi<br />
Department of Midwifery Group, Islamic Azad University, Sari Branch, Sari, Iran<br />
E-mail: mandanazafari@iausari.ac.ir<br />
Purpose: The occurrence of menses is a natural and biological event, which is experienced by half of the human race for about 30 years of<br />
life. This natural phenomenon is often surrounded by vagary, delusions, and negative views, and for some women menses means disorder,<br />
wound or mental and physical impurity. This feeling is matched with premenstrual stress and its destructive complications overshadow<br />
the lives of these women. This syndrome as an unsolvable problem lasting during a significant portion of human life and causes family<br />
problems, misbehaviour with children, problems at work, or absences from work. All of these consequences have caused the public media<br />
to pay much attention to this syndrome in recent years. The purpose of this study was to determine the effect of calcium in the treatment<br />
of premenstrual syndrome.<br />
Method: This study was done using a semi-experimental method, among all of medical students at the Medical School of Mazandaran,<br />
who filled in the questionnaire to diagnose this syndrome (Rosignol Bonlender Questionnaire) during a period of 3 months. This<br />
questionnaire included demographic information, entrance and omission criteria, check paper, and a symptom list of Rosignol Bolender.<br />
A total of 200 girls who suffered from the moderate or severe form of this syndrome were selected randomly and divided in two groups.<br />
The first group (100 girls) took 100 mg /day of calcium for 7 days at the end of their cycle and the second group (100 girls) took placebo<br />
for 7 days at the end of their cycle. The duration of the treatment was 3 months. After the treatment, the severity of physical and mental<br />
symptoms was compared. Also the comparison after the intervention was done in two groups.<br />
Results: Based on the independent sample test, these two groups were homogeneous with respect to age (p = 0.233, based on<br />
independent sample test ), education level (p = 0.328, based on x2 tests , length of menstrual cycle (p = 0.245), based on independent<br />
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Poster Presentations<br />
sample test ), severity of physical symptoms before intervention (p = 0.141), severity of mental symptoms before the intervention (p =<br />
0.132), severity of physical and mental symptoms altogether before the intervention (p = 0.144). In the first group there was a meaningful<br />
difference between the severity of physical (p= 0.000), mental (p= 0.000) and physical & mental symptoms combined (p= 0.000 ) between<br />
before and after the intervention measurements. The reduction in severity of physical, mental, and physical and mental symptoms<br />
altogether after the intervention were meaningful between the two groups (p= 0.000).<br />
Conclusion: Based on our results calcium may improve the symptoms of premenstrual syndrome.<br />
Key words: Premenstrual syndrome, calcium, placebo, physical symptoms, mental symptoms<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S122-3<br />
[PP-004] Ref. No: 203<br />
Eye movement desensitization and reprocessing (EMDR) treatment in a patient<br />
with post-traumatic stress disorder: A case report<br />
Hakan Balibey 1 , Adem Balikci 2<br />
1 Department of Psychiatry Ankara Military Hospital, Ankara, Turkey<br />
2 Department of Psychiatry Samsun Military Hospital, Samsun, Turkey<br />
E-mail: hbalibey@gmail.com<br />
Post-traumatic stress disorder (PTSD) is a psychiatric disorder that is characterized by autonomic, dysphoric, and cognitive signs together<br />
with affective numbing and distressed re-experiencing and avoidance of previous traumatic events in a person who has encountered,<br />
lived, or heard an excessively traumatic event.<br />
EMDR is a psychological method, which has proven to be effective bringing together elements of well-established approaches such as<br />
psychodynamic, cognitive, behavioral, and client-centered approaches.<br />
In recent years, there has been an interest in using the EMDR (Eye Movement Desensitization and Reprocessing) therapy. One of the<br />
reasons for this interest may be its effectiveness shown by numerous studies, especially, conducted with individuals who suffer from Post<br />
-Traumatic Stress Disorder (PTSD). EMDR is known to be an innovative approach that accelerates information processing and facilitates<br />
the integration of fragmented traumatic memories. This process is stated to allow better integration of the information that a person<br />
has to handle in the future. Recent practice guidelines and meta-analyses have designated EMDR as a first-line treatment for trauma.<br />
Although the prevalence of trauma and trauma related disorders is high in Turkey, there have been a limited number of published studies<br />
highlighting treatment options (6-8). Given the effectiveness of EMDR regarding trauma and related disorders, the utilization of the<br />
technique by a broad number of mental health professionals may not only increase the professionals’ competency in treatment of these<br />
disorders, but also may provide patients suffering from the mentioned disorders a chance to recover in a relatively short period of time.<br />
In this paper, the treatment process with Eye Movement Desensitization and Reprocessing (EMDR) of a case, who showed signs of posttraumatic<br />
stress disorder after a car accident and the need to use this effective method by clinicians more frequently and broadly in posttraumatic<br />
stress disorder patients will be discussed.<br />
Key words: Eye movement desensitization and reprocessing, therapy, trauma, post-traumatic stress disorder (PTSD)<br />
References:<br />
1. Sadock BJ, Sadock VA. Kaplan & Sadocks’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry. Ninth ed., Philadelphia, Lippincott Williams & Wilkins,2003<br />
p.623-31.<br />
2. Amerikan Psikiyatri Birliği. Psikiyatride Hastalıkların Tanımlanması ve Sınıflandırılması El Kitabı. Yeniden gözden geçirilmiş dördüncü baskı (DSM-IV-TR),Washington<br />
DC, Amerikan Psikiyatri Birliği, 2000’den çeviren E Köroğlu, Ankara, Hekimler Yayın Birliği, 2001.<br />
3. Shapiro, F., Eye Movement Desensitization and Reprocessing: Basic Principles, Protocols and Procedures, 2nd Edition, Guilford Press,Newyork, 2001.<br />
4. Bisson J, Andrew M. Psychological treatment of post-traumatic stres disorder(PTSD). Cochrane Database Syst Rev 2007;18(3):CD003388.<br />
5. Seidler GH, Wagner FE. Comparing the efficacy of EMDR and trauma-focused cognitive-behavioral therapy in the treatment of PTSD: a meya-analytic study. Psychol<br />
Med 2006;36(11):1515-22.<br />
6. Kavakcı Ö, Doğan O, Kuğu N. EMDR (eye movement desensitization and reprocessing): a different option in psychotherapy. Düşünen Adam The Journal of<br />
Psiychiatry and Neurological Sciences 2010;23(3):195-205.<br />
7. Hocaoğlu Ç, Sağlam D. Post-traumatic Stress Disorder in the Elderly: A Case Report. Klinik Psikiyatri 2007;10:223-27.<br />
8. Kavakçı Ö, Yıldırım O, Kuğu N. EMDR for Post Travmatic Stress Disorder and Test Anxiety: A Case Report Klinik Psikiyatri 2010;13:42-47.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S123<br />
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[PP-005] Ref. No: 208<br />
Cabergoline induced manic episode: A case report<br />
Rabia Nazik Yuksel, Zeynep Elyas Kaya, Nesrin Dilbaz<br />
Department of Psychiatry, Ankara Numune Training and Research Hospital, Ankara, Turkey<br />
E-mail: rabia.nky@gmail.com<br />
Cabergoline is an orally administered synthetic dopamine agonist, which is used for the treatment of hyperprolactinemia, Parkinson<br />
Disease, and antipsychotic-induced prolactin elevation.<br />
One major characteristic of cabergoline is its long duration of effect. It is highly effective in suppressing prolactin levels up to 21 days after<br />
a single 1 mg oral dose. The prolonged elimination half-life offers an advantage of once daily dosing but it might be a handicap in terms<br />
of wash-out of adverse effects like psychosis.<br />
Cabergoline has been associated with adverse reactions consistent with other dopaminergic agonists including cardiovascular,<br />
gastrointestinal, and neuropsychiatric effects. It is known that dopaminergic treatment is a remarkable risk factor for psychosis. A number<br />
of reports implicate dopamine agonists in the development of psychosis. But there is no report in the literature on dopamine agonistinduced<br />
mania. In this case, we report the first manic episode occurring after cabergoline use for hyperprolactinemia treatment. In<br />
susceptible individuals, cabergoline can cause manic episodes and cabergoline should be used more carefully considering the risk-benefit<br />
ratio.<br />
Key words: Cabergoline, manic episode, bipolar disorder, dopamine agonists, hyperprolactinemia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S124<br />
[PP-006] Ref. No: 218<br />
Substance use and eating patterns of female adolescent students<br />
Joung Sook Ahn, Jongho Shin, Ki Chang Park, Seongho Min, Min Hyuk Kim<br />
Department of Psychiatry, Wonju Medical Center, Yonsei University, Wonju, South Korea<br />
E-mail: jsahn@yonsei.ac.kr<br />
Introduction: The problems of smoking and/or drinking among female adolescents come to the front as a serious social problem, as<br />
the rate of occurrence of these behaviors among female adolescents is on the increase. Substance use disorders and eating disorders<br />
frequently co-occur in the presence of other psychiatric disorders. Although this co-occurrence suggests the possibility of shared factors<br />
in the etiology of these two problems, research to date has not established such links. Regardless of the meaning of the association, the<br />
reality that substance use disorders and eating disorders frequently co-occur has important implications for assessment, treatment, and<br />
future research, especially for female adolescents.<br />
Objectives: The first objective of this research was to estimate the rates of smoking and drinking problems among female adolescent<br />
students and the second was to examine their association with psychopathologies and eating behaviors.<br />
Methods: We surveyed 861 female adolescents, 405 students in the 8th grade of one middle school and 456 students in the 10th grade<br />
from two high schools in Wonju, South Korea. Each student completed a questionnaire that consisted of demographic data, parental<br />
monitoring, her attitude toward her parents (CATP), her own attitude toward alcohol, tobacco, and foods, BMI, and the difference between<br />
perceived and ideal body images (DoBI). The TFEQ (Three Factor Eating Questionnaire) for eating patterns and the self-report version of<br />
SDQ (Strengths and Difficulties Questionnaire-self report) for psychopathology were also administered.<br />
Results: 1) For the 8th graders, the prevalence of smoking and drinking were 8.6% and 18.4%, respectively. These prevalences were<br />
14% and 48.3% correspondingly in the 10th graders (Table 1). 2) Female adolescents with smoking and/or drinking habits, except for<br />
the 10th graders with smoking, showed inattention-hyperactivity and conduct problems more frequently than the students without<br />
substance use habits. 3) The 10th graders who reported drinking had eating patterns characterized by dietary restraints, and the 8th<br />
graders with drinking problems showed disinhibition of eating patterns (Table 2). 4) The female adolescents with a high score in the<br />
difference between perceived and ideal body image showed inattention-hyperactivity and emotional problems more frequently<br />
(Table 3).<br />
Conclusions: From these results, we suggest that middle-school girls may start smoking to reduce their weight. The lower the disinhibition<br />
score is, the higher the risk of smoking and drinking. For the high-school girls, the lower the dietary restraint score is, the higher the risk<br />
of drinking. In conclusion, smoking and drinking behaviors are closely related to externalizing problems such as inattention-hyperactivity<br />
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and conduct problems and eating behavior is mainly related to drinking rather than smoking. The association of eating behavior and<br />
drinking is likely correlated through the medium of various psychopathologies.<br />
Key words: Substance use, eating pattern, psychopathology, female adolescents.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S124-5<br />
[PP-007] Ref. No: 219<br />
Neuroleptic malignant syndrome: A case report<br />
Hale Yaci 1 , Esra Kaymak Koca 1 , Yasemin Uz 1 , Aysun Demir 1 , Aygun Akbay Ozşahin 2 , Fusun Mayda Domac 2<br />
1Department of Psychiatry, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey<br />
2Department of Neurology, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey<br />
E-mail: haleyaci@yahoo.com<br />
Summary: Neuroleptic Malignant Syndrome (NMS) is a state, which commonly presents with autonomic changes like fever exceeding<br />
40 degrees Celsius, muscle rigidity, changes in mental status, tachypnea, and fluctuations in blood pressure. It occurs mostly due to<br />
classical antipsychotic drugs with high potency. However, atypical antipsychotic drugs, such as fluoxetine, reserpine and phenothiazinelike<br />
antiemetics, can also cause NMS. We present a case of a 38 year-old patient with chronic schizophrenia, who developed NMS after<br />
ingestion of the intramuscular form of zuclopenthixol acetate 50 mg/ml twice, two days apart.<br />
Case: A 38 year-old, single, male patient with a diagnosis of chronic schizophrenia for 18 years. While being followed up with clozapine<br />
300 mg/d, amisulpride 200 mg/d for the last 6 months, upon oral administration of zuclopenthixol acetate 50 mg/ml (im) twice, two days<br />
apart, by his family for an acute psychotic flare, he presented to the emergency room with sweating, progressive dysphagia, refusal of<br />
food intake, hypersalivation, slowing of speech, dysuria, and muscle cramps. On examination, his body temperature was 39.3 degrees<br />
Celsius, heart rate was 110 bpm, blood pressure was 120/70 mm-Hg, and the patient was tachypneic (32/min). There were no pathological<br />
findings apart from urinary incontinence. On laboratory work-up: WBC=12700/mm 3 , CPK=3226 U/l, urea=74 mg/dl, creatinine=1.4 mg/dl,<br />
Fe=19 U/dl. On follow up, a mild to moderate increase in leukocytosis was seen. For hydration, 2000 cc IV fluid was given as a replacement<br />
with regards to his urinary output. All antipsychotic drugs were stopped. He was put on lorazepam 1 mg/dl because of agitation. On follow<br />
up, his leukocyte count went back to normal, CPK level was down from 3226 to 102 consecutively. Urea and creatinine levels were 20 mg/<br />
dl and 1.4 mg/dl, respectively. His oral intake returned to normal in 5 days; fluid replacement was continued for 3 more days. His rigidity<br />
was still present but to a lesser extent and after 10 days the patient was discharged with clinical recovery.<br />
Conclusion: NMS is often seen within 10 days following antipsychotic use; however, regardless of dose and duration of usage, it can<br />
be seen at any stage of therapy. There are no cases reported in the literature like ours on oral ingestion of the intramuscular form of an<br />
antipsychotic drug. We believe that as the number of case reports on NMS increase, this issue will be better understood.<br />
Key words: Neuroleptic malignant syndrome, chronic schizophrenia, zuclopenthixol acetate.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S125<br />
[PP-008] Ref. No: 223<br />
Treatment of clozapine induced obsessive compulsive behavior in a schizophrenic<br />
patient with valproic acid augmentation: A case report<br />
Fatih Canan 1 , Unsal Aydınoglu 2 , Gjergji Sinani 3<br />
1 Bolu İzzet Baysal Ruh Sağlığı ve Hastalıkları Hastanesi, Bolu, Turkey<br />
2 Atatürk Üniversitesi, Psikiyatri Anabilim Dalı, Erzurum, Turkey<br />
3 Marmara Üniversitesi, Psikiyatri Anabilim Dalı, İstanbul, Turkey<br />
E-mail: fatihcanan@gmail.com<br />
Introduction: The comorbidity of obsessive-compulsive disorders (OCD) and schizophrenia has been documented by epidemiological<br />
investigations. Within the multiple pathogenetic factors leading to OCD in schizophrenic patients, treatment with atypical antipsychotics<br />
has been proposed for a significant subgroup of these patients. Herein, we report the case of a schizophrenic patient who developed<br />
clozapine-induced obsessive compulsive symptoms that responded to valproic acid augmentation.<br />
Case Report: A 51-year-old male patient first developed paranoid delusions and auditory and visual hallucinations at the age of 23,<br />
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Poster Presentations<br />
fulfilling the diagnostic criteria of the DSM-IV for schizophrenia. He had been hospitalized several times and underwent various treatment<br />
regimens (including electroconvulsive therapy) in the past for acute schizophrenic episodes. He had been in remission with clozapine 500<br />
mg/day for approximately one year before relapse occurred as a result of treatment noncompliance. He was admitted to hospital with<br />
exacerbation of positive symptoms. He was started on clozapine 50 mg/day and titrated up to 500 mg/day. A significant improvement<br />
was observed in positive symptoms. However, he developed compulsive hand washing behavior in the 3rd week of the treatment. He had<br />
been spending 5 to 8 hours a day washing his hands although he recognized that it was senseless. He did not have a history of obsessivecompulsive<br />
disorder. We assumed clozapine-induced obsessive compulsive symptoms and gradually decreased the dosage of clozapine<br />
which resulted in aggravation of positive symptoms and elevated mood. Therefore, valproic acid 1000 mg/day was added to the regimen<br />
of clozapine 500 mg/day. Two weeks after starting valproic acid, the patient`s positive symptoms and elevated mood were significantly<br />
reduced and his compulsive hand-washing disappeared. He was discharged and in a 3 month-follow-up, he was maintained well under a<br />
combined treatment with clozapine and valproic acid.<br />
Discussion: Our patient developed hand-washing compulsion during treatment with clozapine,an atypical antipsychotic, which<br />
disappeared after augmentation of valproic acid. Although a few case reports have mentioned the efficacy of valproic acid in the treatment<br />
of OCD, there is only one case report showing alleviation of clozapine-induced OCD symptoms with valproic acid augmentation in a<br />
patient with schizophrenia. In light of our case report, we suggest that valproic acid may be a choice when treating OCD symptoms which<br />
may appear as an adverse effect of atypical antipsychotics in patients with schizophrenia. Case-controlled studies are required to establish<br />
the efficacy of valproic acid in the treatment of antipsychotic-induced OCD symptoms before definitive conclusions can be reached.<br />
Key words: Clozapine, obsessive compulsive behavior, schizophrenia, valproic acid, augmentation<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S125-6<br />
[PP-009] Ref. No: 227<br />
Treatment of bipolar disorder in adolescents: A case report<br />
Çagdas Hunkar Yeloglu 1 , Hulya Guveli 1 , Kadir Sarp 3 , Bulent Bahceci 2 , Cicecek Hocaoglu 2<br />
1Psychiatry Clinic, Rize Training and Research Hospital, Rize-Turkey<br />
2Department of Psychiatry, Rize University, Faculty of Medicine, Rize-Turkey<br />
3Gynecology and Pediatrics Hospital, Trabzon-Turkey<br />
E-mail: chocaoglu@superonline.com<br />
Bipolar disorder in adolescents is a chronic and recurrent psychiatric disorder with significant short-term and long-term morbidity. Bipolar<br />
disorder can occur with different clinical manifestations in the adolescent stage compared to the adult form and usually results in a wrong<br />
diagnosis. Mixed and rapid cycling type mania can be seen more frequently in adolescents than adults. This disorder often results in poor<br />
academic and social-family performance, legal problems, and increased risk of suicide. For these reasons, it should be treated in a timely<br />
and effective manner. However, information on the treatment of bipolar disorder in children and adolescents is limited. We discussed<br />
prospective studies with more reliable methods that have been published in the last 10 years. With the recent indication of risperidone,<br />
aripiprazole, quetiapine and olanzapine for treatment of bipolar disorders in children and adolescents, the atypical antipsychotics are<br />
rapidly becoming a first-line treatment option. The effectiveness of lithium and other mood-stabilizing drug are also supported in<br />
monotherapy and combination treatment. Studies concerning the pharmacological treatment of bipolar disorders in adolescents have<br />
commonly focused on the treatment of manic episodes, and very few data are available regarding the treatment of bipolar depression,<br />
maintenance treatments, and comorbid diseases. Also, further studies examining the safety, efficacy, tolerability and neurobiological<br />
effects of psychotropic medications in children and adolescents with or at familial risk for developing bipolar disorder are needed. In this<br />
case report, we will review clinical manifestations, differential diagnosis, and current treatment approaches of bipolar mood disorder. To<br />
this end, we will present and discuss the case, and the relevant literature, of a 16 year old female inpatient, who has received treatment at<br />
our clinic, has had a bipolar mood disorder diagnosis for 2 years and has been taking an atypical antipsychotic medication with lithium.<br />
Key words: Bipolar disorder, treatment, adolescents<br />
References:<br />
1. Kılınçaslan A, Savaş HA. Çocuk ve Ergenlerde İki Uçlu Bozukluğun İlaçla Tedavisinde Yeni Gelişmeler Güncel Psikiyatri ve Psikonörofarmakoloji 2011;1(1):24-36.<br />
2. Taylor E. Managing bipolar disorders in children and adolescents. Nat Rev Neurol 2009;5(9):484-91.<br />
3. Sayar K, Öztürk M, Özer AÖ. Üç Olgu Nedeniyle Ergenlik Döneminde Bipolar Bozukluk Van Tıp Dergisi, 2000; 7(2):66-77.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S126<br />
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[PP-010] Ref. No: 273<br />
Leukopenia and neutropenia due to venlafaxine use: A case report<br />
Erdem Onder Sonmez, Nazmiye Kaya<br />
Department of Psychiatry, Selçuk University, Meram School of Medicine, Konya-Turkey<br />
E-mail: dr_eondersonmez@hotmail.com<br />
Background: Neutropenia is a serious side effect of psychopharmacological treatment. Neutropenia is defined as less than 0.5 x 109/L<br />
mature neutrophil cells. Patients with such severe acute neutropenia are likely to experience life-threatening and sometimes fatal infections.<br />
This report includes a case, who developed leukopenia and neutropenia due to venlafaxine use and a review of the relevant literature.<br />
Case: A 27 year-old, married female patient, who had a history of major depression and used venlafaxine 75mg/day for 6 months 5 years<br />
ago. The patient reported a significant decrease in psychiatric symptoms and no side effects due to the treatment in this period. The<br />
patient reported that the symptom remission had been sustained for 4 years. She reported that complaints including anxiety, palpitation,<br />
dyspnea, paresthesia, and fear of death started recently following a psychosocial stress. A psychiatrist prescribed venlafaxine 75mg/day<br />
with a diagnosis of panic disorder. After one month a complete blood count test was performed because the patient complained of<br />
fatigue. It indicated neutropenia and leukopenia (neutrophil count, 1.2K/uL; leukocyte count, 3.26K/uL). The same test was repeated after<br />
2 weeks and it indicated a progression in severity of neutropenia and leukopenia (neutrophil count, 0.37K/uL; leucocyte count,2.38K/<br />
uL). She had no other concerning pharmacological agent. Because medical evaluations found no other medical problem associated with<br />
neutropenia, venlafaxine was stopped. Two weeks later, the neutrophil count was 2.54K/uL and the leukocyte count was 4.77K/uL. The<br />
patient’s hematological table recovered within one month.<br />
Conclusion: Neutropenia and leukopenia have never been reported during treatment with venlafaxine. A case presentation of<br />
neutropenia is reported with combined treatment of mianserin and venlafaxine. When neutropenia and/or leukopenia develop during<br />
a drug treatment the drug should be stopped immediately. Blood cell counts can return to normal after stopping the drug. In our<br />
case blood cell counts were completely normal in 2 weeks after stopping venlafaxine. It is important to consider routine blood tests in<br />
psychopharmacological treatments.<br />
Key words: Leukopenia, neutropenia, side effect, venlafaxine<br />
References:<br />
1. Anghelescu I, Klawe C, Dahmen N. Venlafaxine in a patient with idiopathic leukopenia and mirtazapine-induced severe neutropenia. J Clin Psychiatry 2002; 63(9):838.<br />
2. Andrès E, Maloisel F. Idiosyncratic drug-induced agranulocytosis or acute neutropenia. Curr Opin Hematol 2008; 15(1):15-21.<br />
3. Lucht MJ, Kleinschmidt R, Maier W, Rietschel M. Agranulocytosis during treatment with mianserin and venlafaxine. J Clin Psychopharmacol 2000; 20(4):490-1.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S127<br />
[PP-011] Ref. No: 138<br />
EMDR treatment for a sexual rape victim: A case report<br />
Mehmet Ak, Ebru Sinici, Ozgur Maden, Ali Bozkurt, Aytekin Ozsahin<br />
Department of Psychiatry, Gulhane School of Medicine, Ankara, Turkey<br />
E-mail: esinici@gmail.com<br />
Almost anyone who has had a traumatic experience might show intense stress symptoms. It is possible to see post-traumatic stress symptoms<br />
especially among people who have been raped. Recently, efforts to provide counseling for rape victims have become common. The EMDR<br />
treatment focuses on the sensorial units of the memory (emotional, cognitive, and physical) to reach the disturbing events, accelerate<br />
functions, and improve the learning process. It is thought that EMDR treatment relieves post-traumatic stress symptoms for rape victims. In<br />
this case 90 minute EMDR sessions were applied. The Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), State and Trait Anxiety<br />
Inventory-I (STAI-I), and Impact of Events Scale- Revision (IES-R) were completed before and after treatment and 1 month later in a follow up<br />
session. It was observed that the stress symptoms of the patient decreased shortly after the EMDR treatment and 1 month later in the follow<br />
up session. Although the study was conducted with one individual, in patients with sexual trauma, the EMDR application might be beneficial.<br />
Key words: Trauma, rape, EMDR<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S127<br />
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[PP-012] Ref. No: 124<br />
Influence of family and education factors on the inclination to commit crimes in<br />
Soviet times and today<br />
Elena Valzdorf<br />
Irkutsk Regional Psychoneurologic Dispensary, Irkutsk, Russia.<br />
E-mail: elenavalzdorf@yandex.ru<br />
Objective: The objectives of the research were to study the influence of education level and some family factors (alcohol addiction of<br />
parents, upbringing in a one-parent family) on the inclination to commit criminal offences in the examined individuals in Soviet times in<br />
comparison to the current situation. Material and methods: 35 reports of the Commission of forensic psychiatric experts over the period<br />
of January - March 2010 (the examined individuals of group 1) and 35 archive acts of outpatient forensic psychiatric examination that<br />
covered the period of January-March 1991 (the examined individuals of group 2) were analyzed. In total 70 men aged between 15 and 75<br />
were considered. The statistic method, comparative analysis, in combination with the data on the somatoneurological state and the data<br />
of an experimental psychological study were applied.<br />
Results: The study found out that 20 patients of group 1 were held criminally responsible under article 131 of the RF Criminal Code (CC),<br />
13 under article 132 of the RF CC, and 2 individuals were held criminally responsible under article 135 of the RF CC. Out of total 20 patients,<br />
14 had received incomplete secondary education, 7 did not receive any education at all, 6 individuals received full secondary education,<br />
4 incomplete secondary vocational education, 4 higher vocational education, and 1 patient received education in the form of 8 years of<br />
special school. The family history data showed that 10 patients were brought up in the family in which either 1 or both parents abused<br />
alcohol, 9 individuals were raised and developed in a one-parent family, 8 individuals did not have parents at all, and only 8 out of the<br />
35 patients of group 1 were brought up in secure families. The 35 patients of group 2 included 9 individuals that were held criminally<br />
responsible under article 144 of the RSFSR CC, 5 under article 108 of the RSFSR CC, 4 under each of articles 103, 145 of the RSFSR CC, 2<br />
under each of articles 117, 206, 246 of the RSFSR CC, 1 under each of articles 89, 102, 120, 148, 188, 212, 224 of the RSFSR CC. In group<br />
2 there were 15 individuals with incomplete secondary education, 13 with incomplete secondary vocational education, 5 with full<br />
secondary education and 2 with full secondary vocational education. The family history data showed that 18 patients from group 2 were<br />
brought up in the family where either one or both parents abused alcohol, 28 were raised in a two-parent secure family and 7 individuals<br />
were raised in a one-parent family.<br />
Conclusion: The study demonstrated a clear relationship between the education level and some family factors affecting the inclination<br />
to commit criminal offences. Now the number of criminal offenses against the person that are committed by uneducated individuals<br />
has increased, as well as crimes committed by those who have higher vocational education, while the number of secure families has<br />
decreased, which in turn has exacerbated the criminal situation in the country.<br />
Key words: Education factors, Soviet times, forensic psychiatric examination<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S128<br />
[PP-013] Ref. No: 108<br />
Survey of referral pathways to a crisis team<br />
Mahesh Nachnani, Stuart Beatson<br />
Department of psychiatry, Pilgrim Hospital, NHS, Boston, United Kingdom<br />
E-mail: mahesh.nachnani@nhs.net<br />
Introduction: Crisis Teams are well established in many trusts in the departments of psychiatry around the UK. The crisis team based<br />
at Pilgrim Hospital, Boston receives 1300 referrals per year approximately. Not only is it important to know what the sources of referrals<br />
to a crisis team are, but it is helpful to survey where the patients are discharged to at the time when a case is closed by the crisis team.<br />
This information will have implications in terms of service provision, as well as targeting potential sources of referrals in terms of psychoeducation<br />
of not only service users, but also of referring agencies at different tiers of mental health services, from a general practitioner<br />
to a care provider in the community.<br />
Objectives and Methods: To ascertain sources of referrals to a crisis team and the destination to which service users were discharged at<br />
the time of closure of a case by the crisis team.<br />
Results and Conclusion: N = 92 records of service users were randomly selected. They all completed their journey through the crisis team<br />
S128 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
from triage to discharge.<br />
Key words: Crisis team, referral pathways, community care<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S128-9<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-014 Ref. No: 122<br />
Fluanxol and haloperidol efficacy evaluation in treatment of schizophrenic patients<br />
Elena Valzdorf<br />
Irkutsk Regional Psychoneurologic Dispensary, Irkutsk, Russia.<br />
E-mail: elenavalzdorf@yandex.ru<br />
Objective: The purpose of the research was to study the efficacy of Fluanxol in the treatment of schizophrenic patients compared with haloperidol.<br />
Method: Research subjects were 23 paroxysmal progredient schizophrenia patients, who were stationary examined. There were 18 men<br />
and 5 women among them, 6 patients of 16 to 20 years of age and 17 patients aged between 20 to 40 years.<br />
A clinical-psychopathological research method with a psychopharmacological approach was used.<br />
Results: Three groups of patients were picked out. The first group of 9 patients included patients with an acute and subacute exacerbation,<br />
Kandinski-Klerambo syndrome, acute sensitive delusions of grandeur, of influence, of persecution with imperative pseudo hallucinations,<br />
and open thought symptoms.<br />
The second group of 4 cases included patients with paraphrenia acute exacerbations, expansive delusions, and auditory pseudo<br />
hallucinations with oneric inclusions.<br />
In both groups the therapy began with traditional neuroleptics. Haloperidol depot 5 mg was prescribed intramuscularly once every 2<br />
weeks, but haloperidol intravenously from 5 to 10 mg a day. During 7-10 days of treatment, productive psychotic symptoms were reduced<br />
only through intensity in order to change preparation closed to atypical antipsychotic drug. So Fluanxol depot from 10-20 mg was<br />
prescribed intramuscularly once every 2 weeks and at the same time patients took it from 3 to 10 mg twice a day inside. During Fluanxol<br />
therapy, psychotic symptoms were reduced after 5-7 days of treatment.<br />
The third group of 10 people included less progredient schizophrenia patients with neurosis-like negative symptomatology. Haloperidol<br />
from, 1.5 to 5 mg a day inside for 3-4 weeks of treatment, didn’t have a positive effect on the negative symptoms. Fluanxol, from 1 to 3 mg<br />
twice a day inside for 7-12 days of treatment, caused a decrease in intensity or a complete reduction in negative symptomatology, so as<br />
mimics, mood, emotions were improved. This Fluanxol effect was shown by the two first groups having negative symptoms. Most patients<br />
took it without any corrector-preparation.<br />
Conclusion: Fluanxol is more effective in the treatment of schizophrenic patients.<br />
In comparison with haloperidol it decreased positive symptomatology more quickly, decreased or completely reduced negative<br />
symptoms and only in some cases caused drug side effects.<br />
Key words: Fluanxol, haloperidol, schizophrenia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S129<br />
[PP-015] Ref. No: 241<br />
Anorexia nervosa and cannabis abuse: A case report<br />
Semra Karayılan, Atila Erol<br />
Department of Psychiatry, Sakarya University School of Medicine, Sakarya, Turkey<br />
E-mail: skryln@gmail.com<br />
Rates of comorbidity are higher in patients with eating disorders and also the number of comorbid disorders is numerous. Most<br />
comorbidities associated with eating disorders are mood disorders, anxiety disorders, personality disorders, and substance use disorders.<br />
According to past research, there is a high rate of comorbidity of alcohol-substance abuse and eating disorders. Although the majority of<br />
studies in this area are focused on the use of alcohol, studies that have identified an association between illegal substance use and eating<br />
disorders are also available. In a study in the USA, the use of cannabis with anorexia nervosa (AN) and bulimia nervosa (BN) disorders is<br />
reported to be 6-7%. In Turkey, in a study that investigated the comorbidity of eating disorders and substance use, the use of alcohol and<br />
cannabis was reported in cases of BN, but the use of psychoactive substances and cannabis was not established in cases of AN. Among<br />
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Poster Presentations<br />
eating disorders, alcohol or drug abuse are most often found in individuals with bulimia nervosa and bulimic behaviors. Also, binge eating/<br />
purging anorexics appear to be more likely than restricting anorexics to indulge in substance use. Patients with bulimia nervosa have<br />
significantly higher rates of use of amphetamines, barbiturates, marijuana, tranquilizers, and cocaine than patients with anorexia nervosa.<br />
Compounds of cannabis like tetrahydrocannabinol activate endogenous cannabinoid receptors (CB1 and CB2) in brain. Stimulating the CB1<br />
receptor is known to cause increased appetite and an antiemetic effect and because of these effects cannabinoids are included in clinical<br />
use. In this case report, an anorexia nervosa case, who was a young female patient using cannabis, will be presented. The patient, a 17 yearold,<br />
high school student, lived with her family, had complaints of weight loss and had used cannabis for three years. Before beginning to<br />
use cannabis her BMI was approximately 22, when referred to our clinic it was 15.6. She indicated that at first cannabis caused increased<br />
appetite, but excessive vomiting occurred in the first few months and then she started to exercise excessively. Although she noticed losing<br />
weight in this way, she did not stop the use of cannabis. According to a review of the literature in Turkey, such a case of cannabis use and<br />
anorexia nervosa comorbidity hasn’t previously been reported. In this respect, discussion of the case in detail is important.<br />
Key words: Anorexia nervosa, cannabis, substance abuse, eating disorders<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S129-30<br />
[PP-016] Ref. No: 249<br />
Fluoxetine-induced thrombocytopenia: A case report<br />
Atakan Yucel 1 , Mustafa Gulec 1 , Adem Aydin 2<br />
1Department of Psychiatry, Atatürk University, School of Medicine, Erzurum-Turkey<br />
2Department of Psychiatry, Yuzuncu Yil University, School of Medicine, Van-Turkey<br />
E-mail: mustafagulec78@yahoo.com<br />
Case: A 44 year old, university graduate, married male with 2 children was diagnosed with a first episode major depressive disorder<br />
and no abnormalities were observed in the routine tests, including the total blood count test carried out prior to commencing drug<br />
therapy. Afterwards the patient was prescribed fluoxetine and the daily total drug dose was set at 10 mg for the first week of treatment<br />
and 20 mg for the following 3 weeks. During the first follow up visit after thirty days, it was observed that the patient had gone into a<br />
total remission and no change was made in the pharmacotherapy. However, it was learned that thrombocytopenia was detected in the<br />
total blood count test requested by the family doctor because of a suspicion of a urinary tract infection. Since no pathology that could<br />
account for the thrombocytopenia that was detected by a hematology expert following standard consultation and further tests, the<br />
patient was transferred back to us with a suspicion of fluoxetine induced thrombocytopenia. Fluoxetine was immediately discontinued<br />
and replaced with reboxetine and similarly reboxetine was prescribed as 4 mg/day for the first week and as 8 mg/day after the first week.<br />
The thrombocytopenia of the patient went into total remission within 7 days and no problem was observed during the total blood count<br />
tests for the next 6 months.<br />
Even though the most common side effects of fluoxetine are nausea, nervousness, and insomnia, side effects of the hematological<br />
system have also been noted. To this end, there are publications which suggest possible negative effects on the number and function of<br />
thrombocytes. It is thought that the mechanism behind these hemostasis related side effects of fluoxetine is the depletion of serotonin<br />
stores by preventing the reuptake of serotonin into thrombocytes. Starting from this hypothesis, the presumption is that reboxetine,<br />
which is a pure noradrenaline reuptake inhibitor, will have no effect on these processes. In fact, there have been no reports that relate<br />
reboxetine with thrombocytopenia and/or thrombocyte functional disorders. However it should be clarified with further studies whether<br />
this is purely coincidental or if reboxetine has no effect on serotonergic systems.<br />
Conclusion: Reboxetine may be a good alternative for patients with thrombocytopenia and/or with functional thrombocyte disorders in<br />
the treatment of major depressive disorders. However, more research is required in order to reach more certain conclusions.<br />
Key words: Depression, hematological, side effect, switching, reboxetine, fluoxetine, thrombocytopenia<br />
References:<br />
1. Pai VB, Kelly MW. Bruising associated with the use of fluoxetine. Ann Pharmacother 1996; 30(7-8):786-788<br />
2. Mirsal H, Kalyoncu A, Pektaş O. Ecchymosis associated with the use of fluoxetine: case report. Turk Psikiyatri Derg 2002; 13(4):320-324<br />
3. Halperin D, Reber G. Influence of antidepressants on hemostasis. Dialogues Clin Neurosci 2007; 9(1):47-59<br />
4. Lewis G, Mulligan J, Wiles N, Cowen P, Craddock N, Ikeda M, et al. Polymorphism of the 5-HT transporter and response to antidepressants: randomised controlled<br />
trial. Br J Psychiatry 2011; 198(6):464-471<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S130<br />
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Poster Presentations<br />
[PP-017] Ref. No: 312<br />
Interethnic differences in UGT1A4 genetic polymorphisms in Mexican and<br />
Spanish populations<br />
Marisol López 1 , Pedro Dorado 2 , Alberto Ortega 1 , Eva Peñas Lledó 2 , Nancy Monroy 3 , Esther Machín 2 , María Elisa Alonso 3 , Adrián Llerena 2<br />
1 Department of Biological Systems, Universidad Autónoma Metropolitana-Xochimilco, Mexico City, Mexico<br />
2 CICAB Clinical Research Centre. Extremadura University Hospital and Medical School. Servicio Extremeño de Salud, Badajoz, Spain<br />
3 Department of Neurogenetics and Molecular Biology, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico<br />
E-mail: allerena@unex.es<br />
Clinical treatment with antiepileptics exhibits large interpatient variability. The UDP-glucuronosyltransferase (UGT) 1A4 is an enzyme<br />
responsible for the conjugation of glucuronic acid in diverse functional groups included in various antiepileptic drugs, such as lamotrigine<br />
and phenytoin. Several genetic polymorphisms of UGT1A4 have been described in different populations; among them, two nonsynonymous<br />
single nucleotide polymorphisms (SNPs) 70A>C (P24T; UGT1A4*2) and 142T>G (L48V; UGT1A4*3b), as well as a synonymous<br />
variant SNP 471T>C (C157C; UGT1A4*1b). P24T and L48V polymorphisms reduce the glucuronidation activity on various substrates.<br />
Recently, it has been shown that L48V polymorphism decreases the serum concentration of lamotrigine in patients on monotherapy or<br />
polytherapy, resulting in clinical outcome variability.<br />
The main goal of this study was to determine the allelic frequencies of UGT1A4*1b, UGT1A4*2 and UGT1A4*3b in a sample of Mexican<br />
Mestizo (MM) and Spaniard (SP) healthy volunteers. UGT1A4 genotyping is clinically important in order to identify patients who may be<br />
at an increased risk for failure of therapy and/or adverse effects to anticonvulsants such as phenytoin and lamotrigine.<br />
In this study, the allelic frequencies of these three UGT1A4 variants were determined by combined methodology of RFLPs and RT-PCR in<br />
MM and SP populations. The allelic frequencies of the three UGT1A4 polymorphisms analyzed showed interethnic differences between<br />
MM and SP, that was statistically significant for UGT1A4*1b (0.17 and 0.08, respectively; p=0.002).<br />
These data could help clinicians to improve clinical response during treatment with UGT1A4 antiepileptic drug substrates in these<br />
populations.<br />
Key words: Interethnic differences, UGT1A4, genetic polymorphism.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S131<br />
[PP-018] Ref. No: 315<br />
Influence of CYP2C9 genetic polymorphism on losartan oxidation in an<br />
Ecuadorian population<br />
Pedro Dorado, Eva Peñas Lledó, Esther Machín, Adrián Llerena, Enrique Terán, Leonardo Beltrán<br />
CICAB Clinical Research Centre. Extremadura University Hospital and Medical School. Servicio Extremeño de Salud, Badajoz, Spain. Biomedical Centre, Central University<br />
of Ecuador and Health Science College, Universidad San Francisco de Quito, Quito, Ecuador<br />
E-mail: allerena@unex.es<br />
Background: Cytochrome P450 2C9 (CYP2C9) is a polymorphic enzyme catalyzing the metabolism of several important drugs. CYP2C9<br />
metabolizes a number of therapeutically important drugs, including most nonsteroidal anti-inflammatory drugs, S-warfarin, phenytoin,<br />
and losartan. CYP2C9 is also involved in the metabolism of several important psychoactive substances (tetrahydrocannabinol, fluoxetine,<br />
amitriptyline, phenytoin, etc.). It has been reported that CYP2C9 activity is modulated by endogenous substrates such as adrenaline and<br />
serotonin. The involvement of CYP2C9 in the metabolism of melatonin has also been suggested.<br />
Losartan has recently been suggested as a selective probe for CYP2C9 metabolic activity.<br />
Objective: The aim of the study was to determine the activity of CYP2C9, using losartan as a probe drug, in relation to CYP2C9 genotype<br />
in healthy Ecuadorian subjects.<br />
Methods: A single oral dose of 50 mg losartan was given to 194 Ecuadorian unrelated subjects. Concentrations of losartan and its<br />
carboxylic acid metabolite, E3174, were analyzed by means of high-performance liquid chromatography in urine collected for 8 h. The<br />
CYP2C9 genotypes were determined in 194 subjects using specific methods for CYP2C9*2 and CYP2C9*3.<br />
Results: The frequencies of the allelic variants CYP2C9*2 and CYP2C9*3 were 0.054 and 0.015, respectively. The urinary losartan/E3174<br />
ratio was significantly higher (p=0.027) in subjects with the CYP2C9*1/*3 genotype (mean±SD, 12.4±13.8; n=6) than in subjects with the<br />
CYP2C9*1/*1 (4.9±7.0; n=167).<br />
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Poster Presentations<br />
Conclusion: This is the first most extensive population where losartan has been used as a probe drug to evaluate the CYP2C9 activity in<br />
vivo. The urinary losartan to E3174 metabolic ratio after a 50mg losartan dose was found to be a safe and useful phenotyping assay for<br />
CYP2C9 activity in vivo. The CYP2C9*3 variant allele is a major determinant of the enzyme activity, and it decreases losartan metabolism<br />
significantly, while the CYP2C9*2 allele has less impact on enzyme function.<br />
Key words: Cytochrome P450 2C9, genetic polymorphism, losartan, ecuadorian population<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S131-2<br />
[PP-019] Ref. No: 194<br />
Efficacy of progressive muscle relaxation training on anxiety, depression and<br />
quality of life in cancer patients under chemotherapy<br />
Sepideh Ershadmanesh Herizchi 1 , Isa Tt Piri 2 , Iraj Tt Asvadi 3 , Zohreh Tt Sanaat 4 , Mrs Tt Golchin 5 , Reza Tt Shabanloui 5<br />
1 Assistant Professor of Psychiatry, 2 Psychologist, 3 Professor of Oncology,<br />
4 Z.Sanaat, Assistant Professor of Oncology, 5 MS of Nursing, Hematology & Oncology Research Center-2010, Tabriz, Iran<br />
E-mail: sherizchi@gmail.com<br />
Introduction: Chemotherapy is one of the common treatment methods for cancer. However, many side effects can be seen among<br />
patients and some of them are very serious and painful. Alopecia, anorexia, vomiting, pain in the limbs, headache, and backache are some<br />
unwanted effects. On the other hand many patients suffer from psychiatric disorders especially anxiety and depression probably due to<br />
the drugs or coping with the disease state. These disorders can cause some problems in the treatment process and the Quality of life.<br />
Patients with anxiety and depression can be treated with drugs or psychotherapy.<br />
Progressive Muscle Relaxation [PMR] training is a cost effective self-help method promoting mental health in healthy participants.<br />
The aim of this study was to determine anxiety, depression, and quality of life dimensions of cancer patients undergoing chemotherapy<br />
and the effect of progressive muscle relaxation training in improving their mental health and quality of life.<br />
Materials and Methods: This research was designed as a randomized clinical trial. Sixty cancer inpatients undergoing chemotherapy<br />
in the Tabriz Hematology & Oncology ward in 2009 were randomly selected and divided into two groups, intervention or control. All<br />
participants provided a written formal consent.<br />
Anxiety, depression, and quality of life dimensions were determined with HADS and EORTC QLQ-C30 questionnaires. SPSS 16 software<br />
was employed for the data analysis.<br />
After completion of the 1st questionnaires by all participants, the case group was trained in progressive muscle relaxation in 3-6 person<br />
groups, with the aim of doing it by themselves in the hospital and after discharge 2-3 times a day. At 2 weeks and one and three months<br />
after the intervention, questionnaires were completed again by both groups, and the results were compared.<br />
Results: After initial data analysis almost all of the participants were satisfied with the learning and the experience of this technique.<br />
There was no significant difference between the scores of the case and control groups after PMR after 2 weeks and 1 month (p >0.05).<br />
However, after 3 months, anxiety, depression and quality of life dimensions were significantly improved (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-020] Ref. No: 127<br />
Anxiety reducing effects of oxytocin on the basolateral amygdala by using<br />
an electrophysiological method<br />
Oytun Erbas, Saylav Bora, Serdar Demirgoren, Gonul Peker<br />
Physiology Department, Ege University, School of Medicine, Izmir, Turkey<br />
E-mail: oytun.erbas@ege.edu.tr<br />
Objective: It has been shown by behavioral studies that oxytocin has anxiolytic effects and that oxytocin in nasal spray form suppresses<br />
amygdala activity, which is powered by anxiety as demonstrated in functional MRI studies in humans. The amygdala is a part of the<br />
limbic system and is activated in case of fear and anxiety. This study evaluated the effects of oxytocin on the basolateral amygdala using<br />
a spontaneous EEG.<br />
Material and Methods: The experiments performed in this study have been carried out according to the rules in the Guide for the Care<br />
and Use of Laboratory Animals adopted by National Institutes of Health (U.S.A) and have received consent from Ege University Animal<br />
Ethics Committee.<br />
The rats were maintained under controlled environmental conditions throughout the study: 22-24 °C ambient temperature, 12:12 lightdark<br />
cycle (light from 7:00-19:00), and standard laboratory food and tap water available ad libitum.<br />
In this study 7 Sprague-Dawley adult male rats were used, which were 8-12 weeks old. Under anesthesia a small hole was drilled. Then by<br />
taking the bregma as a reference using the stereotaxic method (coordinates Anteroposterior: - 2.8 mm, Lateral: + 4.8 mm, Ventral: - 8.5<br />
mm) (Paxinos Rat Brain), an exterior insulated bipolar EEG electrode was placed in the basolateral amygdala.<br />
Electrodes were fixed by using a dental acrylic (numerous alloys are used in the making of dental restorations). The rats were anesthetized<br />
using ketamine (40 mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP).<br />
Electrodes were placed and 3 days later, while the animals were awake in their cages, spontaneous EEG recordings were taken from<br />
the amygdala. Then, 0.9% isotonic NaCl solution was injected intraperitoneally into the rats (n = 7), and the EEG was recorded from the<br />
amygdala while they were in their cages.<br />
One day later to the same rats (n=7) oxytocin 10 IU/Kg (Synpitan 5 IU) was given IP, and 5 minutes later the oxytocin EEG records were<br />
taken in their own cage.<br />
The system recordings were taken for 20 minutes by a Biopac MP30 amplifier system in the range of the 1-60 Hz band, with 10,000<br />
amplification. During this process Delta 1-4 Hz Theta 4-8 Hz, alpha 8-12 Hz and beta 12-20 Hz waves in the EEG were accepted as the ratio<br />
of percentage in PSA (Power Spectral Analyses) methods. We affirmed electrode location histologically following euthanisation.<br />
Results: There was significant (p
Poster Presentations<br />
had no treatment up to then, and stayed in prison for three years due to injuring his chief with a knife because of delusions of persecution.<br />
Autism, flattening of affect, incoherent speech and bizarre, somatic, nihilistic delusions were found in the psychiatric examination.<br />
Flupentixol decanoate 20 mg every 15 days IM, haloperidol 20 mg/day and biperiden 10mg/day were administered first IM then orally.<br />
There was no remission even after adding ECT for ten sessions. Then clozapine was begun at 25mg/day and titrated to 500mg/day. He<br />
was discharged with symptoms which were much improved by using clozapine 500 mg/day, haloperidol 10 mg/day, biperiden 4mg/day,<br />
quetiapine 300 mg/day.<br />
In this paper a schizophrenic patient with testicular mutilation was presented and genital amputation was discussed along with reports<br />
in the literature.<br />
Key words: Schizophrenia, testicular mutilation<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S133-4<br />
[PP-022] Ref. No: 135<br />
Hoarding and mood disorder: A case report<br />
Özlem Çetinkaya Girit 1 , Fulya Maner 1 , Emine Kılınç 2 , Derya İpekçioğlu 1 , Mehmet Emin Ceylan 1<br />
1 Psychiatry Unit, Bakırköy Nueropsychiatry Research & Training Hospital, Istanbul-Turkey<br />
2NPİ Nueropsychiatric Hospital , İstanbul<br />
E-mail: fmaner@ttmail.com<br />
Hoarding is the excessive acquisition of possessions and failure to use or discard them even if the items are worthless or hazardous. The<br />
hoarder may believe that the hoarded items are very valuable, know that the accumulated items are useless, or attach a strong personal<br />
value to items. It is not clear whether hoarding is an isolated disorder or rather a symptom of another condition such as obsessive<br />
compulsive disorder. Hoarding seems to involve some neurological mechanisms which are detected by brain imaging studies. In this case<br />
report a patient with mood disorder whose predominant symptom was hoarding is presented and the status of literature about hoarding<br />
is reviewed.<br />
Key words: Hoarding, obsessive compulsive disorder, mood disorder, dementia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S134<br />
[PP-023] Ref. No: 140<br />
Effect of fish oil on treatment of premenstrual syndrome<br />
Mandana Zafari, Azar Aghamohammadi<br />
Department of Midwifery Group, Islamic Azad University, Sari Branch, Sari, Iran<br />
E-mail: mandanazafari@iausari.ac.ir<br />
Objective: Women go through many hormonal changes throughout their lives from birth to death and this causes many physical and<br />
mental challenges that are directly related to their unique reproduction delicacy. Premenstrual syndrome refers to a cyclic appearance of<br />
somatic and psychiatric symptoms in some women. Different theories and hypotheses have been proposed and discussed on this issue.<br />
Finding an effective and safe solution for the treatment of PMS has always been under consideration. The purpose of our study was to<br />
determine the effect of fish oil on treatment of premenstrual syndrome.<br />
Methods: This study was a double blind randomized placebo controlled trial. All of the medical students at the Medicine School of<br />
Mazandaran filled in the Rosignol Bonlender Questionnaire for 3 months. This questionnaire included demographic information, inclusion<br />
and exclusion criteria, check paper and the symptom list of Rosignol Bolender. A total of 200 girls suffering from the moderate and severe<br />
forms of this syndrome were selected randomly and assigned in two groups. The first group (100 girls) took a 1000 mg /day capsule of fish<br />
oil for all days of their cycle and the second group (100 girls) took placebo for all days of their cycle. The duration of this treatment was 3<br />
months. After treatment, the severity of physical, mental, and combined physical-mental symptoms were compared before and after the<br />
intervention. Also the comparison after intervention was done in two groups.<br />
Results: Based on this and based on the independent sample test, these two groups were homogeneous from the point of view of age<br />
(p = 0.287, based on independent sample test ), education level (p = 0.954, based on x2 tests), length of menstrual cycle (p = 0.305),<br />
based on independent sample test ), severity of physical symptoms before intervention ( p = 0.039 ), severity of mental symptoms before<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
intervention (p = 0.144), severity of combined physical-mental symptoms before intervention (p = 0.242) in the first group. There was a<br />
significant difference among the severity of physical (p= 0.000), mental (p= 0.000), combined physical-mental symptoms (p= 0.000) before<br />
and after intervention. The reduction in severity of physical, mental, and combined physical-mental symptoms after intervention was<br />
significant between the two groups (p= 0.000).<br />
Conclusion: Based on our results 1000mg/day fish oil may reduce the severity of physical, mental, and combined physical-mental<br />
symptoms of PMS.<br />
Key words: Premenstrual syndrome, fish oil, placebo, physical symptom, mental symptom<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S134-5<br />
[PP-024] Ref. No: 145<br />
Improvement of risperidone-induced hyperprolactinemia with the addition<br />
of aripiprazole: Case report<br />
Medine Gıynaş Ayhan, Faruk Uguz, Nazmiye Kaya<br />
Department of Psychiatry, Selcuk University,Meram School of Medicine, Konya, Turkey.<br />
E-mail: drmedineayhan@gmail.com<br />
Objective: Hyperprolactinemia is an important side effect of antipsychotic treatment. All typical antipsychotics and some atypical<br />
antipsychotics such as risperidone and amisulpiride have been shown to cause marked elevation in serum prolactin levels, whereas most<br />
other atypical antipsychotics such as quetiapine, olanzapine, clozapine, ziprasidone, and aripiprazole appear to have little or no effect on<br />
serum prolactin levels. Hyperprolactinemia can lead to gynecomastia, galactorrhea, sexual dysfunction, infertility, oligomenorrhea, and<br />
amenorrhea. It also reduces the bone mineral density and contributes to osteoporosis in the long term. These important side effects cause<br />
patients in remission not to continue treatment.<br />
Case: We report two clinical cases of risperidone-induced hyperprolactinemia and amenorrhea, who with treatment by the partial<br />
dopamine agonist aripiprazole, showed prolactin normalization.<br />
Conclusion: Addition of aripiprazole to treatment may be considered as a first option in hyperprolactinemia cases with significant<br />
improvement in psychotic symptoms.<br />
Key words: Hyperprolactinemia, amenorrhea, antipsychotic, risperidone, aripiprazole<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S135<br />
[PP-025] Ref. No: 146<br />
Atomoxetine for the treatment of ADHD in young adults with an assessment<br />
of associated functional outcomes<br />
Murat Altın 1 , Levent Alev 1 , Todd M. Durell 2 , Leonard A. Adler 3 , Dave W. Williams 2 , Ahmed Deldar 2 , James J. Mcgough 4 ,<br />
Paul E. Glaser 5 , Richard L. Rubin 6 , Elias S. Sarkis 7 , Teresa A. Pigott 8 , Bethany K. Boardman 2<br />
1 Eli Lilly and Company, Istanbul,Turkey<br />
2 Eli Lilly and Company and/or one of its subsidiaries, Indianapolis, IN, USA<br />
3 Department of Psychiatry, NYU School of Medicine; and Psychiatry Service, New York VA Harbor Healthcare System, New York, NY, USA<br />
4 UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA<br />
5 University of Kentucky, Department of Psychiatry, Lexington, KY, USA,<br />
6 Vermont Clinical Study Center, Burlington, VT, USA<br />
7 Division of Child and Adolescent Psychiatry, University of Florida, Gainesville, FL, USA<br />
8 Department of Psychiatry, University of Florida, Gainesville, FL, USA<br />
E-mail: altin_murat@lilly.com<br />
Objectives: ADHD in young adults is associated with significant impairment in multiple functional domains. This trial examined the<br />
efficacy of atomoxetine (ATX) in young adults and evaluated improvements in core ADHD symptoms and associated functional outcomes.<br />
Method: Patients aged 18-30 years were randomized to 12 weeks of double-blind treatment with ATX (n=220) or placebo (PBO, n=225).<br />
Patients in the atomoxetine treatment arm began treatment with 40 mg/day (dosed 20 mg BID) for a minimum of 7 days followed by<br />
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Poster Presentations<br />
80 mg/day (dosed 40 mg BID) for a minimum of 7 days. At Visit 5, or any visit thereafter, the dose could be increased to the maximum of<br />
100 mg/day (dosed 50 mg BID) depending upon continued ADHD symptoms. One unscheduled dose change was allowed if needed for<br />
tolerability or safety. The Conners’ Adult ADHD Rating Scale- Investigator Rated, Screening Version Total ADHD Symptoms score (CAARS<br />
– Inv:SV) with adult ADHD prompts, assessed core ADHD symptoms and was the primary efficacy measure. The adult ADHD Quality of<br />
Life-29 (AAQOL-29) scale evaluated functional outcomes in various life domains. Other assessments included Clinical Global Impression-<br />
ADHD-Severity (CGI-ADHD-S), CAARS Self Report (CAARS-S:SV), Patient Global Impression-Improvement (PGI-I), Behavior Rating Inventory<br />
of Executive Function-Adult Version Self Report (BRIEF-A), and measures for depression, anxiety, sleepiness, driving behaviors, social<br />
adaptation, and substance use. Reported means are least-squares means from last-observation-carried-forward ANCOVA models. A<br />
mixed-model repeated measures visit-wise analysis was also conducted.<br />
Results: Significant improvement (mean±SE) after ATX treatment was demonstrated on CAARS-Inv:SV (ATX [-13.6±0.8] vs. PBO [-9.3±0.8],<br />
p
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Poster Presentations<br />
domains, considered to be important in OCD patients, are also valid for Panic Disorder.<br />
Method: Our sample group included 101 Panic Disorder group, and 155 healthy volunteers with similar sociodemographic characteristics.<br />
The instruments used included the Beck Depression Inventory (BDI), State-Trait Anxiety Inventory (STAI), Panic Agoraphobia Scale (PAS), and<br />
Obsessive Beliefs Questionnaire (OBQ-44). Total and sub-scale scores of obsessive beliefs as assessed by the Obsessive Beliefs Questionnaire-44<br />
(OBQ-44) were compared between the groups. Total and sub-scale scores in the panic disorder group were re-evaluated against the state,<br />
trait, and depression factors of the State-Trait Anxiety Inventory (STAI). SPSS 18.0 for Windows was used for statistical analysis.<br />
Results: The mean age was 36.73±9.42 years in the patient group, and 34.74±12.46 years in the control group. The State Anxiety Scale<br />
total score, Trait Anxiety Scale total score, Beck Depression Inventory total score, OBQ-44 total, and subscale scores in patients with a PAS<br />
score of 12 or more were statistically significantly higher compared to the control group (p
Poster Presentations<br />
[PP-029] Ref. No: 154<br />
Cerebellar contusion presenting with pure psychiatric symptoms and cerebellar<br />
cognitive affective syndrome: A case report<br />
Baise Tıkır, Erol Göka, Makbule Çiğdem Aydemir, Sinem Duran<br />
Ankara Numune Education and Research Hospital, Department of Psychiatry, Ankara, Turkey<br />
E-mail: baisetikir@yahoo.com<br />
The cerebellum is known to be responsible for posture and motor coordination of the body. Recent studies indicate that the cerebellum<br />
has a role in conduction of higher brain functions, such as perception, affect, capacity to analyze, and memory, via neuronal connections<br />
between the cerebellum and the other regions of the brain. Schmahmann and Shermann described a new syndrome called “the Cerebellar<br />
Cognitive Affective Syndrome” (SCAS) and drew attention on cognitive functions of cerebellum. The syndrome was described in a group<br />
of patients who had impairment of executive functions, difficulties with spatial cognition, personality changes, blunt affect and language<br />
deficits in addition to primary neurological symptoms. In this case report we present a rare case of cerebellar cognitive affective syndrome<br />
presenting with pure psychiatric symptoms,who had a posterior cerebellar lobe lesion due to a contusion at the back of the skull.<br />
Key words: Cerebellar cognitive affective syndrome, cerebellum, cognitive functions<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S138<br />
[PP-030] Ref. No: 226<br />
Self-perception and anger with chest pain without cardiac etiology<br />
Esra Aydın Sünbül 1 , Murat Sünbül 2 , Fatma Feriha Cengiz 1<br />
1Erenkoy Ruh ve Sinir Hastalıkları Eğitim ve Araştırma Hastanesi, Istanbul, Turkey<br />
2Department of Cardiology, Marmara Universitesi, Istanbul, Turkey<br />
E-mail: mrm_esra@yahoo.com<br />
Objective: Physical symptoms are the most common expressions of social problems and emotional inconvenience. This problem is<br />
usually medically unexplained in patients with chest pain. ‘Chest Pain without Cardiac Etiology’ is diagnosed in more than fifty percent<br />
of patients with chest pain. Anger and suppressed hostility are important factors the development of somatic symptoms. It is important<br />
to point out that somatization in depressive disorders is due to expression of anger while somatization in anxiety is due to anger<br />
suppression. It is known that, while patients with chronic pain experience anger, they do not care enough to express it because they are<br />
in denial of this situation. The form of anger expression in patients with chronic pain may be effective in the disease process and is one of<br />
the subjects to be emphasized. Suppression of intense anger leads to the development of chronic pain and suppressed anger scores are<br />
higher than healthy controls. In this study, we compared patients with chest pain without detected cardiac etiology and healthy controls<br />
in terms of anger and self perception.<br />
Methods: Twenty five patients were included in the study. They all presented to the cardiology clinic with complaints of chest pain, but<br />
did not have any detected cardiac etiology. The healthy control group of 80 persons was organized by matching them with the patients<br />
according to their age, gender, and education. The Socio-demographical data collection form, Multidimensional Anger Scale, and Social<br />
Comparison Scale were given to both of the groups.<br />
Results: There was no significant difference between the socio-demographic features of the two groups. The non-cardiac chest pain<br />
group scored higher on the Social Comparison Scale. The healthy control group scored higher on calm behaviour and nonchalant<br />
response. Revenge for the reaction and inward looking responses were significantly higher in the non-cardiac chest pain group.<br />
Conclusions: The non-cardiac chest pain group had more negative perception of self as compared to healthy individuals, further they<br />
were found to be more negative in their forms of expressing anger. Repressed anger and hostility are important factors in the development<br />
of chronic pain. Work on the relationship between mind and body has been a topic of interest in recent years. Not just how an individual<br />
perceives himself, but also how other people perceive and relate to him, probably effects the physiological system of that individual.<br />
Key words: Chest pain without cardiac etiology, self-perception, anger<br />
References:<br />
1. Kirmayer lj, Young A. Culture and somatization: clinical, epidemiological and ethnographic perspectives. Psychosom Med 1998; 60: 420-430.<br />
2. Mayou R. Invited review: atypical chest pain. J Psychosom Res 1989; 33: 393-406.<br />
S138 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
3. Koh KB. Anger and somatization. J Psychosom Res 2003; 55:113.<br />
4. Sayar K, Bilen A, Arıkan M. Kronik ağrı hastalrında öfke, benlik saygısı ve aleksitimi. Türkiye Klinikleri Psikiyatri 2001; 2: 36-42.<br />
5. Güleç MY, Hocaoğlu Ç, Gökçe M, Sayar K. Anadolu Psikiyatri Derg 2007; 8:14-21.<br />
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Poster Presentations<br />
[PP-031] Ref. No: 155<br />
Mirtazapine treatment for weight loss and insomnia associated with methylphenidate:<br />
A chart review<br />
Sabri Hergüner, Arzu Hergüner<br />
Meram Faculty of Medicine, Department of Child and Adolescent Psychiatry<br />
E-mail: cocukergen@yahoo.com<br />
Introduction: Stimulants are used as first-line treatment for children with attention deficit hyperactivity disorder (ADHD), and their safety<br />
and efficacy are well established. Their most frequent adverse effects are sleep disturbance and decreased appetite which may limit<br />
optimal dosing and compliance. The aim of this study was to investigate the efficacy of mirtazapine on OROS methylphenidate (MPH) -<br />
induced weight loss and insomnia in children and adolescents with ADHD.<br />
Methods: We reviewed the charts of children and adolescents diagnosed with ADHD and identified 18 individuals prescribed mirtazapine for weight<br />
loss and/or insomnia while on OROS – MPH treatment. Of these, 2 discontinued mirtazapine within the first week due to excessive daytime sedation.<br />
Results: Mirtazapine was well tolerated by the remaining 16 subjects and no other side effects were reported. All subjects gained weight<br />
during concomitant mirtazapine treatment, with a mean gain of 2.1 kg. Fourteen of 16 children who had reported insomnia on MPH alone<br />
noted significant improvements in sleep after initiation of mirtazapine.<br />
Conclusion: In this chart review, mirtazapine was found to be beneficial for weight loss and insomnia associated with MPH treatment in<br />
children and adolescents with ADHD.<br />
Key words: Attention-deficit/hyperactivity disorder, children, methylphenidate, mirtazapine, insomnia, weight loss<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S139<br />
[PP-032] Ref. No: 157<br />
Rapid-onset hyponatremia induced by duloxetine in a middle-aged male with<br />
depression and somatic symptoms<br />
Jung Seok Choi, Hae Woo Lee, Jun Young Lee, Hee Yeon Jung<br />
Department of psychiatry, Smg-Snu Boramae Medical Center, Seoul, Korea<br />
E-mail: choijs@neuroimage.snu.ac.kr<br />
Duloxetine is a relatively balanced selective serotonin and noradrenaline reuptake inhibitor. We report a case of hyponatremia induced by<br />
duloxetine that developed rapidly after starting the medication in a middle-aged male with multiple somatic symptoms and depression.<br />
Two days after discontinuation of duloxetine and management with hypertonic saline as well as fluid restriction, the serum sodium level<br />
normalized. The patient had two risk factors for developing hyponatremia, namely severe weight loss and pneumonia. Therefore, when<br />
treating patients with depression and somatic symptoms, especially with risk factors for developing hyponatremia, close monitoring for<br />
clinical and laboratory evidence of hyponatremia may be essential.<br />
Key words: Duloxetine, hyponatremia, middle-aged male, somatic symptoms, depression<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S139<br />
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Poster Presentations<br />
[PP-033] Ref. No: 192<br />
Gender specific metabolic adverse effects in bipolar patients: A comparison<br />
between lithium, quetiapine and olanzapine<br />
Sermin Kesebir, Burak Baykaran, Burak Toprak, Ahmet Ertan Tezcan<br />
Erenkoy TEHMND, Istanbul, Turkey<br />
E-mail: serminkesebir@hotmail.com<br />
Objective: There is some evidence showing gender based differences in the side effects of atypical antipsychotic drugs. The aim of this<br />
study was to determine the differences between lithium, quetiapine and olanzapine with regard to their effects on metabolic variables in<br />
bipolar disorder and to assess the findings in terms of gender differences.<br />
Method: Twenty-eight female and 29 male cases diagnosed with bipolar disorder type I according to the DSM-IV, taking lithium or<br />
quetiapine or quetiapine+lithium or olanzapine or olanzapine+lithium, were evaluated consecutively. For evaluation, being in a remission<br />
period was set as a criterion for these cases. Patient interviews were carried out with SCID-I and SKIP-TURK. Blood samples were taken from<br />
the patients in order to determine PRL, blood lipids and HbA1c levels.<br />
Results: Mean age, mean age of onset, number of manic, depressive, and total episodes, functionality, and PRL levels were similar between<br />
female and male patients. BMI, HbA1c, cholesterol, triglycerides, LDL and HDL levels are found to be similar between the two groups. Both<br />
in female and male patients, no difference was found between the lithium, quetiapine and quetiapine+lithium and the olanzapine and<br />
olanzapine+lithium groups in terms of BMI, HbA1c, cholesterol, triglyceride, LDL and HDL levels. The only difference (although not significant)<br />
among the three groups was the level of cholesterol in women treated with lithium, which was found to be lower than in the other two groups.<br />
Conclusions: This insignificant difference was found while the clinical properties and PRL levels were similar among the lithium,<br />
quetiapine and quetiapine+lithium and the olanzapine and olanzapine+lithium groups. Future studies with a specific focus on this topic<br />
are needed in order to have a better understanding of the basic mechanisms of gender differences.<br />
Key words: Gender, metabolic side effect, psychotropics, bipolar disorder<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S140<br />
[PP-034] Ref. No: 161<br />
New model of psychogenic stress-induced depression and antioxidant system of rat brain<br />
Konstantin Chichinadze 1 , Tamar Domianidze 1 , Tamar Matitaishvili 1 , Ia Labadze 1 , Ann Lazarashvili 2 , Mikhail Khananashvili 1<br />
1Laboratory of Behavior and Cognitive Functions, Life Sciences Research Center, Tbilisi, Georgia<br />
2Department of Pathology, Tbilisi State University, Tbilisi, Georgia<br />
E-mail: k.chichinadze@lifescience.org.ge<br />
The present article describes results of investigation of lipid peroxidation and antioxidant enzyme activity in the brain cells of laboratory<br />
rats, that were subjected to a depression-like state. The above-mentioned state was achieved by means of a new model of depression<br />
elaborated by us. The model is based on the application of stressors of psychogenic nature.<br />
Our investigations demonstrated that in the depression-like state activity of lipid peroxidation processes increase, which was confirmed<br />
by increase of concentration of its end product – malondialdehyde, both in mitochondrial and cytosolic fractions of brain cells. In<br />
response to oxidative stress in mitochondria, activity of antioxidant system –namely the leading intracellular antioxidant superoxide<br />
dismutase (SOD) – increased. On the other hand, concentration of another important antioxidant –catalase– decreased. Most probably,<br />
the depletion of antioxidative potential of the cell, related to depression, proceeds at various speeds in various enzymatic systems.<br />
Administration of the antidepressant drug –fluoxetine– led to the normalization of intensity of lipid peroxidation and overall activity of<br />
antioxidative systems. Thus, if activity of these processes increases, antidepressants cause their down-regulation and in they decrease<br />
–antidepressants lead to their up-regulation. As a final result, this leads to normalization of cell functioning.<br />
Key words: Animal model of depression, lipid peroxidation, antidepressants<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S140<br />
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Poster Presentations<br />
[PP-035] Ref. No: 216<br />
Effects of strawberry leaf and celery seed extracts in terlipressin-induced chronic<br />
hyponatremia in rats<br />
Rehab R. Hegazy 1 , Hala F. Zaki 2 , Ola A. Sharaf 1 , Ismail E. Ismail 1 , Sanaa A. Kenawy 2<br />
1 Departement of Pharmacology, Medical Division, National Research Center, Giza, Egypt<br />
2 Departement of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt<br />
E-mail: rehab_hegazy@hotmail.com<br />
Hyponatremia (HN) is associated with mortality and morbidity risks due to development of encephalopathy and neurogenic pulmonary<br />
edema. Moreover, its rapid correction carries a high risk of development of the serious cerebral disorder known as osmotic demyelination<br />
syndrome (ODS).<br />
In the present study, chronic HN was induced in rats using a single daily administration of terlipressin (TP), a synthetic, long-acting analogue<br />
of vasopressin, for 3 days. TP-induced HN was then used to study the possible therapeutic effects of strawberry leaf extract (StrwLE) and<br />
celery seed extract (CelrSE), and to compare their effects with that resulting from rapid correction using hypertonic saline (HtNaCl). Serum<br />
sodium level, as a marker of HN, was measured following induction and treatment, respectively. The study was extended to investigate<br />
changes in locomotor activity, pain reflex and lung function using an activity cage, hot-plate test, and spirometer, respectively. Furthermore,<br />
assessment of brain nitric oxide (NO) content, that has been shown to play a role in the pathogenesis of ODS, was carried out.<br />
It was found that TP induced a profound (48 h) HN that was coupled by decreased locomotor activity, delayed pain<br />
reflex and impaired lung function. Administration of StrwLE resulted in a correction of HN with its subsequent neurological dysfunction<br />
without elevation of the brain content of NO; however, it resulted in deterioration of the lung function parameters of hyponatremic rats. These<br />
findings suggested that StrwLE is useful for treatment of chronic HN, yet, further investigations are required to study its effect on the lungs.<br />
Key words: Hyponatremia, terlipressin, rats, locomotor activity, pain reflex, lung functions<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S141<br />
[PP-036] Ref. No: 165<br />
Post traumatic stress disorder in patients with spinal cord injury and relevant factors<br />
Murat İlhan Atagün 1 , Ünal Altınok 1 , Özlem Devrim Balaban 1 , Zeliha Atagün 2 , Latif Ruhşat Alpkan 1 , Kadriye Öneş 2<br />
1Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
2İstanbul Physical Therapy and Rehabilitation Research and Training Hospital, İstanbul, Turkey<br />
E-mail: muratilhanatagun@gmail.com<br />
Objective: Although spinal cord injury (SCI) was thought to be a fatal case, development of rehabilitation approaches in the early 20th<br />
century prolonged survival rates and longevity. Physical and psychological trauma and permanent results of the injury are difficult to cope<br />
with. Post traumatic stress disorder rates following SCI range from 10 to 44%. In this study we aimed to assess PTSD frequencies in patients<br />
with SPI in Turkey and the association of PTSD to factors like depression, anxiety and caregiver burden.<br />
Methods: Eighty four patients with SCI (mean age= 40.5±15.97; 40 female, 44 male) and caregivers (n=83; mean age=43.72±14.37; 67<br />
female, 16 male) were enrolled. Patients with mental retardation, premorbid psychiatric disorder, comorbid central nerve system disease<br />
and patients with professional caregivers were excluded. Clinican administered post traumatic stress disorder rating scale (CAPS), the Beck<br />
depression and anxiety, and Zarit caregiver burden scales were assessment tools.<br />
Results: Although they had experienced traumatic events, 32.1% (n=27) of the patients did not have PTSD, while 40.5% (n=34) had<br />
PTSD. About 28.6% of these had acute PTSD symptoms and 11.9% (n=10) had had PTSD symptoms in the past. Patients with PTSD had<br />
statistically significant higher scores of depression, anxiety and caregiver burden.<br />
Discussion: Perception of stress may be influenced by several factors including personality and economical factors. Expression of feelings<br />
may increase stress tolerance. The differing results may be due to the factors above as well as methodologies, different stages of assessed<br />
samples, social and cultural differences, and tolerance to stress. On the other hand, some negative effects of PTSD are screened in this<br />
study. These negative factors may influence adjustment of the disabled person and thus may cause a vicious circle.<br />
Key words: Spinal Cord Injury, post traumatic stress disorder, depression, anxiety, caregiver burden<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S141<br />
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Poster Presentations<br />
[PP-037] Ref. No: 230<br />
A comparison before and after using lamotrigine in long term continued treatment:<br />
the effect of blood levels<br />
Sermin Kesebir 1 , Fisun Akdeniz 2 , Aysun Demir 1 , Mustafa Bilici 1<br />
1 Erenkoy TEHMND, Istanbul, Turkey<br />
2 Ege University, Psychiatry, Izmir, Turkey<br />
E-mail: serminkesebir@hotmail.com<br />
Objective: The purpose of this study is that determine whether or not the efficacy of lamotrigine, which is an anticonvulsant with a<br />
stabilizer quality in neuronal membranes and has inhibitor activity in sodium and calcium channels and presynaptic neurons, is related<br />
to blood levels in bipolar disorder. We compared the period before and after lamotrigine use in bipolar cases and studied if there was any<br />
relationship between lamotrigine blood levels and clinical progress.<br />
Method: Forty cases, diagnosed with bipolar disorder type I according to the DSM-IV, and taking lamotrigine for at least two years<br />
together with any mood stabilizer (lithium, anticonvulsants or atypical antipsychotics), were evaluated consecutively. For evaluation,<br />
being in remission period was set as a criterion for these cases. Patient interviews were carried out with the SCID-I in bipolar cases. Before<br />
or after protective treatment, the SCIP-TURK Mood Disorders Diagnosis and Patient Registration Form were filled in by the patients and<br />
their relatives. Later blood samples were taken from the bipolar cases in order to analyze lamotrigine blood levels.<br />
Results: In the bipolar cases, when comparing before and after long term maintenance of lamotrigine, it was determined that after using<br />
lamotrigine, total episode and depressive episode frequency decreased, episode severity was less (p< 0.001, 0.039, and 0.04, respectively)<br />
and the fast onset and termination ratio decreased (p= 0.027). When evaluated according to these variables, in long term maintenance,<br />
the ratio of good treatment response to lamotrigine among bipolar cases was 77.5%. In cases with good treatment response to<br />
lamotrigine, while lamotrigine doses were found to be similar to the others (135.5±52.7/155.6±69.7 mg/day), lamotrigine blood levels<br />
were found to be higher (3.8±1.9/2.0±1.1 µg /ml) (p= 0.005). No correlation was shown between lamotrigine dose and lamotrigine blood<br />
levels (r= 0.185, p= 0.254).<br />
Conclusion: As a result, lamotrigine is an efficient choice in long term maintenance treatment of bipolar disorder. The relationship of this<br />
efficacy to lamotrigine blood levels must be explored in future studies.<br />
Key words: Lamotrigine, bipolar disorder, blood level<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S142<br />
[PP-038] Ref. No: 172<br />
ICAM, VCAM and E-selectin levels in first episode schizophrenic patients<br />
Semine Özdoğan Kavzoğlu, Aytül Gürsu Hariri<br />
Erenköy Research and Training Hospital for Neuropsychiatry, Istanbul, Turkey<br />
E-mail: sokavzoglu@hotmail.com<br />
Objective: It is known that mortality rates in schizophrenic patients with cardiovascular diseases are twice as high as other diseases.<br />
Some of the research has revealed that the risks of cardiovascular disease were dependent on adhesion molecules. The main adhesion<br />
molecules are intracellular adhesive molecule (ICAM-1), vascular cell adhesive molecule (VCAM-1) and E-selectin. The aim of this study<br />
was to determine whether or not ICAM-1, V-CAM-1 and E-selectin levels, which are considered as possible biological determinants in the<br />
prognosis and progression of atherosclerosis, change with treatment in schizophrenic patients with respect to controls.<br />
Method: In the Erenköy Research and Training Hospital for Neuropsychiatry, 50 patients who were diagnosed with first episode<br />
schizophrenia according to the DSM-IV-TR diagnostic criteria and had never received antipsychotic treatment and a control group<br />
consisting of 50 healthy volunteers were enrolled the study. At the beginning of the study (n=50) and after the third month (n=39), ICAM,<br />
VCAM, E-selectin, Fasting Blood Glucose, Total Cholesterol, LDL Cholesterol, HDL Cholesterol and Triglyceride levels were checked in the<br />
plasma of each patient and compared with each other. For the control group, the same biochemical parameters were investigated only at<br />
the beginning of the study. In order to assess the termination of the acute episode, the patient group was given the Positive Symptoms<br />
Assessment Scale (SAPS) and Negative Symptoms Assessment Scale (SANS) in the beginning and at the end of the third month.<br />
Results: In the first episode schizophrenic patients, the average age was 30.14±7.50 years. In the patients, the beginning ICAM-1 levels<br />
were lower than the control group (t= 3.41, p=0.001) and increased during treatment (t=-6.73 p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
levels were similar to the control group (t=-1.23, p=0.223; t=-0.32 p=0.750, respectively). In addition, after treatment the VCAM-1 level was<br />
determined to be lower than the pretreatment level (t=7.17, p
Poster Presentations<br />
[PP-040] Ref. No: 176<br />
Tardive akathisia with aripiprazole: A case report<br />
Ömer Şenormancı, Oya Gönüllü Güçlü, Ramazan Konkan, Yavuz Altunkaynak, Güliz Şenormancı<br />
Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
E-mail: senorman_7@hotmail.com<br />
Tardive akathisia is characterized by feelings of restlessness, discomfort, and tension causing the patient to be unable to settle down and<br />
sit still. The patient should also be taking a long term antipsychotic medication without any recent changes in dosage or type, and no<br />
withdrawal of antiakathisic drugs. Aripiprazole is a potent partial agonist that shows high affinity binding to dopamine (D2) and serotonin<br />
(5HT1a) receptors and is an antagonist at 5HT2a, 5HT2b receptors. Although there are a number of case reports about arippiprazole<br />
causing acute akathisia, only one tardive akathisia case, who was a nonpsychotic female patient, has been reported so far. In this case<br />
tardive akathisia with aripiprazole developed in a patient who had diagnoses of mental retardation and psychotic disorder not otherwise<br />
specified and who was treated by supplementary drugs without stopping aripiprazole.<br />
Key words: Antipsychiotics, aripiprazole, extrapyramidal side effects, atypical antipsychotics, tardive akathisia, tardive syndromes<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S144<br />
[PP-041] Ref. No: 178<br />
Comparing mental disorders between divorced couples and normal<br />
couples in a city of Iran<br />
Majid Kazemi 1 , Sima Karimi 2 , Hadi Hasankhani 3 , Somayeh Kazemi 4<br />
1 Rafsanjan University of Medical Science, Iran<br />
2 Islamic Azad University- Sirjan Branch, Iran<br />
3 Tabriz University of Medical sciences, Iran<br />
4 Islamic Azad University- Mashhad Branch, Iran<br />
E-mail: maj_kaz@yahoo.com<br />
Background: The family is the first and the most important source for fulfilling needs of human beings including love, satisfaction and<br />
peace. One serious difficulty in couple’s lives is the phenomenon of divorce, which recently has been increasing in Iran. Divorce has a lot<br />
of negative effects, both physical and psychological, on couples.<br />
Objective: The aim of this study was to compare mental disorders between the couples who were divorced and normal couples in a town<br />
in Iran.<br />
Method: This research was causal –comparative on couples in Sirjan in 2010. Seventy couples were chosen voluntarily and randomly<br />
based on the duration of their marriage from couples applying for divorce and refereeing to the administration of justice and normal<br />
couples. The questionnaire symptom checklist-90-revised (SCL-90-R) was used. The data were collected and analyzed.<br />
Results: The averages of mental disorder scores between two groups in nine dimensions were compared and showed different<br />
significances. People who had gotten divorced had more high scores comparing the total coefficient of global severity index (GSI).<br />
The findings revealed that the divorced couples had higher GSIs and a significant correlation was observed (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-042] Ref. No: 238<br />
Suicide rate in Oman in the period between January 2000 and December 2010<br />
Saif Salam Al Hashmi, Ahmed Ali Al Sabri, Nasser Mubarak Al Felati<br />
Armed forces hospital, Muscat, Oman<br />
E-mail: nouralmanar@gmail.com<br />
Background: Suicide rates have been explored in different parts of the world, including many Arab /Islamic countries. To our knowledge,<br />
no study has been conducted in Oman so far.<br />
Objective: To examine the rate of suicide in the Sultanate of Oman in a ten year period (2000-2010).<br />
Method: The data kept at the Royal Oman Police Forensic Department were queried for the presence of suicide as a cause of death for a<br />
10 year period (2000-2010)<br />
Results: The total number of suicide cases in Oman in that period was 599, with 59.9 cases every year. Omanis account for 8.7 cases every<br />
year.<br />
Conclusion: Based on our data the suicide rate in Oman was found to be 2 /100,000 /year. This puts Oman in the group of low suicide<br />
rate countries in the world.<br />
Key words: Suicide rate, Oman, ten year period<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S145<br />
[PP-043] Ref. No: 179<br />
The effect of the recitation of the Quran on depressed patients in the psychiatry<br />
department of Moradi hospital in Rafsanjan (IRAN)<br />
Ali Ansari, Tayebeh Negahban, Ahmad Reza Sayyadi<br />
Rafsanjan University of Medical Sciences<br />
E-mail: shibonraf@yahoo.com<br />
Background and Objective:: Depression is a common psychiatric disorder and has a huge impact on human life. Data published in<br />
scientific sources suggest that about one hundred million cases are diagnosed annually. Depression comprises about 35 to 45% of<br />
all mental disorders in Iran. Unfortunately, this figure is rising day by day and it is necessary to look for new and modern methods for<br />
treatment and prevention of this psychiatric disorder. One of the non- medicinal methods of treatment is music therapy, which seems to<br />
be a safe and effective therapeutic method. Reading the Koran with a pleasant voice can be regarded as a kind of agreeable Gnostic music.<br />
The main purpose of this research was to determine the effect of the recitation of the Koran on depression.<br />
Methods: This study was a semi-experimental one and included all the depressed patients who had been hospitalized in the psychiatry<br />
department of the Rafsanjan Moradi Center. The sampling time period was one year. The patients were divided into two groups randomly,<br />
(30 people in the experimental and 30 in the control group). The selection of the subjects was based on the psychiatrist’s diagnosis, Beck’s<br />
depression scale and the condition of the patients. The questionnaires were filled out for the case group. Recitation of Yousof Verse of<br />
the Koran by Abdolbaset, was transmitted for the case group, for 15 minutes every other day for 7 sessions. At the end of the first two<br />
weeks of hospitalization, both of the groups were retested by another questionnaire and the results were analyzed by paired t- test and<br />
Student’s t test by EPI6.<br />
Results: The result of this research showed that the Koran reciting had a beneficial effect on the depressed patients (p
Poster Presentations<br />
[PP-044] Ref. No: 239<br />
Dissociative symptoms associated with piracetam use: a case report<br />
Adem Aydın 1 , Pınar Güzel Özdemir 1 , Yavuz Selvi 1 , Faruk Uğuz 2<br />
1 Department of Psychiatry, Yuzuncu Yıl University, Van, Turkey<br />
2 Department of Psychiatry, Selcuk University, Konya, Turkey<br />
E-mail: adem.dr@gmail.com<br />
Piracetam is a cyclic derivative of a gamma-aminobutyric acid drug that is often used in neurology practice (1). It has antithrombotic and<br />
neuroprotective properties and improves cognitive performance (2).<br />
In this article, a case report, piracetam is used for combined therapy, but after piracetam use, dissociative symptoms like depersonalization<br />
and derealization were detected.<br />
Case: A 29-year-old female patient applied to the psychiatric clinic with the following complaints: Intense discomfort, alienation from herself,<br />
perceiving herself odd , that perception that her hands and feet were bigger, feeling like not living in the society, the feeling that colors and<br />
sizes of objects seemed abnormal, and feelings of alienation from objects and people in her surroundings. These complaints continued for<br />
10 days and she had never had any psychological complaints before. She also expressed that these complaints bothered her greatly. Except<br />
for these complaints, she did not describe any other abnormality in perception and thought content. She did not have prominent depressive<br />
symptoms and psychosocial stress in her history. One month ago, she had seen a neurologist for vertigo. She was diagnosed with peripheral<br />
vertigo and prescribed betahistine 16mg/day. After this medication, she described a marked reduction in the vertigo, however since she did<br />
not get rid of her complaints completely, after 12 days she was prescribed piracetam 2400mg/day as combination treatment.<br />
On psychiatric examination, she was conscious, oriented normally, anxious,appeared ready to cry, thought contents were normal, positive<br />
depersonalization and derealization in the perception, psychomotor activation was normal. Nothing abnormal was detected in her<br />
hemogram, biochemistry, serum B12, thyroid function tests, EEG, and brain MRI.<br />
In clinical follow-up, since there was a connection between the patient’s administration of piracetam and the dissociative indications,<br />
piracetam was stopped. Betahistine was continued in the same dosage. It was observed in daily observation that after a day, a decrease<br />
in her dissociative symptoms began and in 5 days they had totally disappeared. In further follow up visits dissociative symptoms were<br />
not observed in a month.<br />
The dissociative symptoms like derealization and depersonalization were started with addition of piracetam to the treatment, and<br />
diminished quickly after piracetam was stopped. This directed us to think that those dissociative symptoms were related to the piracetam<br />
administration. This relation is not established in literature (3).<br />
Trauma is usually reported as the origin of dissociative symptoms. There generally is childhood period trauma and dissociative symptoms<br />
come up in later life. There is still no etiopathogenesis described related to development of dissociative symptoms. Traumatic stress and<br />
neurobiological theories are basic models suggested in etiology (3). In the medication studies, depersonalization is the basic dissociative<br />
symptom in dissociation’s neurobiological theories. In those studies, it is also shown that serotonergic and glutamate receptors have a<br />
role in depersonalization (3).<br />
We think that this case report which shows the administration of piracetam and development of dissociative indications may contribute<br />
to the neurobiological theories on dissociative disorder’s etiology.<br />
Key words: Dissociative symptoms, piracetam<br />
References:<br />
1. Değirmenci E, Şahiner T, Erdoğan Ç. Long Term Effects of Piracetam on Spectral Analysis of EEG in Alzheimer’s Disease and Minimal Cognitive Impairment. Klinik<br />
Psikofarmakoloji 2006;16:93-7<br />
2. Winbland B. Piracetam: a review of pharmacological properties and clinical uses. CNS Drug Rev 2005;11:169-82<br />
3. Wınnica K, Tomasiak M, Bielawska A. Piracetam-an old drug with novel properties? Acta Poloniae Pharmaceutica- Drug Research 2005;62:405-409<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S146<br />
S146 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-045] Ref. No: 181<br />
Reversible normoprolactinemic galactorrhea induced by fluoxetine<br />
Fatih Canan 1 , Ünsal Aydınoğlu 2 , Gjiergji Sinani 3<br />
1 Bolu Izzet Baysal Mental Health Hospital, Bolu, Turkey<br />
2 Department of Psychiatry, Ataturk University, Erzurum, Turkey<br />
3 Department of Psychiatry, Marmara University, Istanbul, Turkey<br />
E-mail: fatihcanan@gmail.com<br />
Introduction: Several drugs can cause galactorrhea and it’s etiology needs to be differentiated from other local or neuroendocrinological<br />
causes. All conventional antipsychotic drugs block D2 receptors on lactotroph cells and thus remove the main inhibitory influence on<br />
prolactin secretion. Tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors are less frequent<br />
causes. There is evidence that serotonin may stimulate prolactin release directly via postsynaptic 5-HT receptors in the hypothalamus or<br />
indirectly via 5-HT mediated inhibition of tubuloinfundibular dopaminergic neurons. However, galactorrhea due to antidepressants is<br />
not consistently associated with elevated prolactin levels, which may suggest still unexplained mechanisms of antidepressant-induced<br />
galactorrhea.<br />
We report a case of euprolactinemic galactorrhea in a woman with generalized anxiety disorder while on treatment with fluoxetine.<br />
Case Report: A 29-year-old woman visited a psychiatric outpatient clinic with complaints of excessive and uncontrollable worry about<br />
minor life events, feeling restlessness, irritability, muscle tension, tiring easily, and poor sleep that started 8 months prior to admission. She<br />
had no history of endocrine or reproductive pathology or psychiatric problems. She was diagnosed as having generalized anxiety disorder<br />
according to the DSM-IV criteria and was started on fluoxetine 20 mg per day. After 4 weeks of medication, her symptoms diminished.<br />
However, she developed unilateral galactorrhea (the nonpuerperal discharge of milk-containing fluid from the breast). She had no history<br />
of galactorrhea. She first noticed the discharge on treatment day 21 and described it as white-creamy and from the right nipple. She did<br />
not notice any bloody, greenish, or foul-smelling discharge, nor did she report any sexual dysfunction. She consulted her gynecologist,<br />
who recommended a mammogram and breast ultrasonography. The pregnancy test was negative. The results of these tests and breast<br />
examination were normal. Serum prolactin level on treatment day 28 was 18.18 ng/mL (reference range: 2.5-29 ng/mL). Because her<br />
galactorrhea developed after the initiation of fluoxetine, her medication was discontinued. Buspirone 5 mg/day was started and gradually<br />
raised to 20 mg/day. Eight days after stopping fluoxetine, the patient reported reduction and cessation of galactorrhea. At the 3 month<br />
follow-up visit, the patient was well maintained on buspirone and there was no re-emergence of galactorrhea.<br />
Discussion: Although galactorrhea caused by the use of fluoxetine has been reported earlier, the commonly perceived cause is<br />
hyperprolactinemia. Fluoxetine has been shown to potentiate elevation of prolactin levels from other stimuli, including insulin,<br />
fenfluramine, and 5-HT. However, hyperprolactinemia is not the only mechanism responsible for the development of SSRI-induced<br />
galactorrhea. The exact mechanism of galactorrhea remains unknown in many cases.<br />
Our patient developed galactorrhea without hyperprolactinemia after beginning fluoxetine therapy. The strict temporal relationship<br />
between the use of the drug and the onset of galactorrhea, as well as the resolution once treatment was discontinued, suggests a causal<br />
link between the two phenomena.<br />
To the best of our knowledge, we are the first to report an association with fluoxetine use and galactorrhea without elevated prolactin<br />
levels. Clinicians should consider fluoxetine as a possible cause of galactorrhea even with normal prolactin levels. Future research should<br />
investigate the precise mechanisms of antidepressant-induced normoprolactinemic galactorrhea.<br />
Key words: Fluoxetine, galactorrhea<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S147<br />
S147
Poster Presentations<br />
[PP-046] Ref. No: 240<br />
Influence of polymorphism of the norepinephrine transporter gene (SLC6A2) and<br />
alpha-2 adrenergic receptor gene (ADRA2A) on regional cerebral blood flow<br />
in a Korean ADHD sample: a preliminary study<br />
Younghui Yang 1 , Jaewon Kim 2 , Boongnyun Kim 2 , Minsup Shin 2 , Soochurl Cho 2<br />
1 Department of Psychiatry, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea<br />
2 Division of Child and Adolescent Psychiatry, Seoul National University Hospital, Seoul, Republic of Korea<br />
E-mail: nauyoung@gmail.com<br />
Some genes related to the noradrenergic system have been investigated as candidate genes in Attention Deficit Hyperactivity Disorder<br />
(ADHD). Through functional brain imaging studies, it has been reported that brain areas such as the prefrontal cortex (PFC), dorsal<br />
anterior cingulate cortex, and striatum show abnormal findings in ADHD patients. We have investigated whether there was an association<br />
between polymorphism of the noradrenergic system related genes (SLC6A2 and ADRA2A) and regional cerebral blood flow (rCBF) in a<br />
Korean ADHD sample.<br />
Methods: A total of thirty-six children (31 boys and 5 girls, mean age: 8.9 (± 1.84) years) participated in this study. Subjects were recruited<br />
from the outpatient’s clinic of child and adolescent psychiatry in the Seoul National University Hospital. The diagnosis of ADHD was made<br />
based on the DSM-IV-TR. All patients were drug naïve at the time of image acquisition. Genotyping of SLC6A2 (G1287A, -3081(A/T)) and<br />
ADRA2A (Dral, Mspl) was done. SPM8 (Statistical parametric mapping 8) was used to compare images between the two groups divided<br />
by each genotype.<br />
Results: Children with the G/A and A/A genotypes at the SLC6A2 G1287A polymorphism showed decreased rCBF in the right inferior<br />
temporal gyrus and the left middle temporal gyrus compared to children with G/G genotype (uncorrected p-value< 0.001). In ADRA2A<br />
Mspl polymorphism, children with the C/G and C/C genotypes showed increased rCBF in the left striatum and the left cingulate gyrus and<br />
decreased rCBF in the left cerebellar vermis compared to children with G/G genotype.<br />
There were no significant rCBF alterations across genotypes in the SLC6A2 -3081(A/T) and ADRA2A Mspl genes.<br />
Conclusion: This study showed that the noradrenergic system related genes might be associated with functional brain abnormalities in<br />
children with ADHD.<br />
Key words: ADHD, neuroimaging, SLC6A2, ADRA2A<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S148<br />
[PP-047] Ref. No: 129<br />
Do we need specialist clinics to monitor metabolic side effects on chronic<br />
bipolar patients in Treatment? – Audit of management of bipolar disorder against<br />
NICE guidelines in South Staffordshire NHS Trust, UK<br />
Fiesal Jan, Vanathi Kennedy<br />
Foundation House, St. Georges’ Hospital, Corporation Street, ST16 3AG, Stafford<br />
E-mail: khalidnoma@hotmail.com<br />
Objective: To highlight the pharmacological management of patients with Bipolar Affective Disorder and to evaluate whether the<br />
management meets the current standards as set up by recognised guidelines, especially those underlined by NICE guidelines.<br />
Method: The audit data were collected from a patient population from the West patch of South Staffordshire and focussed on inpatients<br />
from the 2 adult units based at Stafford and a psychiatric ICU. It also included a minimum of 5 patients of both genders from all the<br />
community teams. The selection was random and not based on severity or duration of the disorder, co-morbidity or other accompanying<br />
diagnoses, for e.g, Personality disorder.<br />
The audit tool was devised by the clinical audit coordinator in conjunction with clinicians.<br />
Results: Twenty of twenty-eight 28 patients (72%) were on mood stabilizers, either lithium or sodium valproate, with sodium valproate<br />
the more preferred drug.<br />
Twelve of twenty-eight (43%) were on antipsychotics. Three of seven (43%) patients, who did not respond to combination treatment,<br />
were started on lamotrigine.<br />
In 21/22 (95%) of the patients, antidepressants were stopped.<br />
S148 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
Nine of the twenty-eight (32%) patients continued to be on antidepressants even after resolution of the depressive episode.<br />
The compliance of monitoring for physical side effects during the initial period of starting medications was not satisfactory with only:<br />
19/24 (79%) monitored for renal disease,<br />
18/24 (75%) monitored for diabetes,<br />
15/24 (63%) monitored and advised about obesity and<br />
15/24 (63%) drug levels checked regularly.<br />
In 4/28 (15%), there was no documentation about any physical health monitoring.<br />
Only in 50-60% of patients had the monitoring been done annually, but it was regardless of any recognised guidelines.<br />
In 19/26 (73%) the patient’s preference of drug choices was recorded.<br />
In 21/28 (75%) patients, there was documentation about discussion of potential benefits and side effects of the medications.<br />
Five of twenty-eight (18%) patients who were prescribed valproate were of child bearing age; 4 were advised to use contraception and<br />
one had been sterilized.<br />
Clinical implications: Monitoring cognitive function tests is often dependent on patient mental health, illness, age, and lack of side<br />
effects.<br />
Patient preference for drugs should be taken into consideration.<br />
Evidence should be documented regarding clinical need or history of risk on antidepressant medication.<br />
Evidence of long term treatment with antidepressants after resolution of a depressive episode should be documented in the patient<br />
notes.<br />
Annual check-ups of parameters should be documented by either the GP or Mental Health Team. However, weight and BP machines may<br />
not be available at clinic appointments. There is a need for closer understanding among clinicians about the responsibility for initiation<br />
and maintenance of close physical monitoring.<br />
Discussions should be held with women of child bearing age regarding contraception.<br />
Teams to monitor the need for referral to specialist Bipolar Units should be available, regardless of any cost implications.<br />
Key words: Bipolar, mood disorder, mood stabiliser, antipsychotics, physical health monitoring, serum drug levels, cognitive side effects, relapse,<br />
pregnant women<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S148-9<br />
[PP-048] Ref. No: 186<br />
Assessment of risk of absenteeism in elemantary school students<br />
Kültegin Ögel 1 , Gülşah Karadayı 2 , Zeynep Karaman 3 , Hediye Atıcı Arıcan 3 , Niyazi Kaya 3 , Uğur Karaman 3 , Ahmet Murat Altuğ 3<br />
1Acibadem University Medical Faculty<br />
2Yeniden Society<br />
3Ministry of National Education Primary School Department<br />
E-mail: ogelk@ogelk.net<br />
Finding a resolution to the absenteeism problem is important in terms of children’s development. It is necessary that the risk of<br />
absenteeism is determined in an early stage and an early warning system is established to prevent absenteeism. For this reason,<br />
development of an assessment tool was targeted.<br />
Methods: A qualitative research design was carried out at the first stage of the study. During this research procedure, 97 teachers, 53<br />
administrators, 73 elementary school students who hadleft school, and 76 of their parents who were selected to represent the overall<br />
structure of the population in Turkey were included in the study. With the information retrieved from this research, a scale named the Risk<br />
Assessment Form (RIDEF) was developed. RIDEF consists of 111 questions within 9 risk categories.<br />
The second stage of the study was carried out with 3871 students studying in 21 schools from 5 different cities, which were selected at<br />
the first stage. While 49.5% (n=1924) of the students were between the ages of 7 and 12, 48% (n=1859) of the students were between 13<br />
to 16 years of age. The mean age was 12.27±1.87 years. The mean of days of unexcused absences of those students within the 2009-2010<br />
academic year, during which time this research was implemented, was 6.62±8.93 days and the mean of days of their unexcused absences<br />
the year before was 6.08±7.21 days.<br />
At the second stage, the RIDEF was applied to the same students 15 days after the first application and also a different interviewer filled<br />
the form for half of the students. The School Atmosphere Scale was applied during the study, as well.<br />
Results: When the total score derived from the scale was compared with the Pearson correlation analysis the interrater reliability was<br />
found as r= 0.96 (p
Poster Presentations<br />
Based on the risk indicators obtained from RIDEF, the Cronbach alpha validity of the scale was calculated as 0.79. When any item is<br />
removed from the scale, the value of the internal consistency coefficient varies between 0.77 and 0.79.<br />
It has been observed that there is a statistically significant level of correlation between the School Atmosphere Scale and RIDEF sub-scales<br />
(r=0.51, p=0.001).<br />
As a result of the analysis, categorized risk indicators were grouped under two factors, which accounted for 44.73% of the total variance<br />
with eigen values over one. The first factor, consisting of 4 items grouped under the title of individual problems related to childhood,<br />
explains 30.98% of the variance and the second factor, consisting of 5 items with the title social and economic problems related to the<br />
family, accounts for 13.75% of the variance.<br />
The mean scores of the risk points derived from all of the categories showed a statistically significant difference between students with<br />
high and low levels of absenteeism.<br />
Discussion: This research study showed that the RIDEF is a reliable and valid scale in determining the risk of absenteeism.<br />
Key words: Absenteeism, assessment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S149-50<br />
[PP-049] Ref. No: 185<br />
Effectiveness of an addiction treatment program called SAMBA: A pilot study<br />
Kültegin Ögel 1 , Ceren Koç 2 , Bircan Karalar 2 , Aslı Başabak 2 , Alper Aksoy 2 , Mebrure İşmen 3 , Romina Yeroham 2<br />
1Acibadem University Medical Faculty<br />
2Yeniden Society<br />
3Umraniye Prison<br />
E-mail: ogelk@ogelk.net<br />
Description of SAMBA program: SAMBA (Sigara, Alkol ve Madde Bağımlılığı Tedavi Programı / Tobacco, Alcohol, and Drug Addiction<br />
Treatment Program) is a treatment program which is designed to treat tobacco, alcohol, and drug addiction problems.<br />
Development of SAMBA: Before developing this program, a comprehensive literature review was done. Addiction treatment programs<br />
that are still applied in addiction centers in Turkey were reviewed. Necessary meetings with the specialists working in the addiction field<br />
were conducted. The weaknesses and strengths of the programs were discussed with the specialists and expectations from an addiction<br />
program were reviewed. SAMBA was developed according to the findings of the literature review and suggestions made in the meetings<br />
with professionals.<br />
The Content of SAMBA: SAMBA is a program that is based on Cognitive Behavioral Theory. In some sessions, some interventions that are<br />
based on Mindfulness and Acceptance Therapy are used. In addition, in some sessions, some techniques of Dialectical Behavior Therapy<br />
and Emotion Regulation are applied.<br />
The Structure of SAMBA: SAMBA is composed of 7 modules and 13 sessions. The modules of SAMBA are:<br />
1. The Effects of Drugs, Alcohol, and Tobacco<br />
2. Motivation<br />
3. Mindfulness<br />
4. Anger and Stress Management<br />
5. Relapse Prevention<br />
6. Communication Skills<br />
7. Thinking Errors<br />
Each session lasts around one and half to two hours. All sessions are designed in an interactive mode. It contains activities and didactic<br />
lectures.<br />
SAMBA should be applied in group format and by professionals such as psychologists, social workers and psychiatrists.<br />
Pilot Study: The pilot Study of SAMBA was carried out at Ümraniye T-Type Prison. The first pilot scheme was applied with a group that<br />
consisted of members who are alcohol and drug addicts. After all the modules were applied, feedback from the group members was<br />
collected. According to the feedback, necessary changes were made. Afterwards, the second pilot scheme was done with other members<br />
who were again alcohol and drug addicts from the same prison. Based on the feedbacks, SAMBA was reviewed and reached its final form.<br />
The results showed that there was a significant difference between the pre-test and post-test of the dimensions of Anger and Stress<br />
Management (Z= -1.919, p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
There was not a significant difference between the results pre-test and post-test of the dimension of Motivation. The results showed that<br />
the participants were not well-informed about relapse prevention. Therefore, it is suggested that the focus of the program should be on<br />
relapse prevention.<br />
According to the results of the feedback form, 66.6% of the participants claimed that they have learned moderate or very much information<br />
from the SAMBA program. 91.6% of the participants claimed that the trainers were moderately or very much successful. Lastly, 75% of the<br />
participants reported that they had the opportunity to participate and share ideas during the sessions again moderately or very much.<br />
Key words: Addiction, psychotherapy, treatment, effectiveness<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S150-1<br />
[PP-050] Ref. No: 187<br />
Psychometric properties of different forms of the Addiction Profile Index (BAPI)<br />
Kültegin Ögel 1 , Aslı Başabak 2 , Ceren Koç 2 , Alper Aksoy 2 , Gülşah Karadayı 2<br />
1Acibadem University Medical Faculty<br />
2Yeniden Society<br />
E-mail: ogelk@ogelk.net<br />
The Addiction Profile Index (BAPI) is composed of 37 items and 5 subscales assessing the characteristics of substance use, dependency<br />
diagnosis, the effect of substance use on the person’s life, craving, and the motivation to quit using substances. The reliability and validity<br />
of the scale were reported in a very recent study.<br />
In these current studies, we aimed to develop a clinician-administered form (BAPI-U), clinical form (BAPI-II) and a short form of BAPI (BAPI-K).<br />
Study 1: Psychometric properties of clinician-administered form of BAPI<br />
Items of the BAPI were changed to a clinician asked type. In the original BAPI 5-point likert ratings were used. In this questionnaire we<br />
used 3-point likert ratings.<br />
A total of 150 male inmates were recruited from the Umraniye, Istanbul T-type prison. Cinical Psychologists and guardians of the prison<br />
conducted face-to-face interviews with inmates to complete the BAPI.<br />
The BAPI-U items were found to be significantly correlated with the self-reported form (0.89). High correlations between interviewer<br />
ratings in all subscales were found. Factor analyses yielded four factors for the BAPI-U, which were similar to the BAPI.<br />
It was concluded that the BAPI-U has similarities with the BAPI and therefore it may be applied by non-clinical professionals (such as<br />
nurses, guardians etc) after a short training period.<br />
Study 2: Development and psychometric properties of the clinical form of the BAPI<br />
It is important to know the factors causing alcohol or substance dependence disorders in order to choose the treatment modality and to<br />
prevent relapses.<br />
In order to assess depression, anxiety, anger, and assertiveness, new items were added to the original BAPI items. This new instrument<br />
was named the BAPI-II.<br />
The research sample was similar to study 1. The Beck Depression Inventory, Rathus Assertiveness Inventory, Multi-dimensional Anger<br />
Scale and STAI-1 were used in this study.<br />
The Cronbach Alpha value of the whole scale was found to be 0.79. The self and clinican administered rating correlations were statistically significant.<br />
The correlation of the BAPI-II with the other scales was high. One factor was obtained and 54.34% of the variance was explained by this factor.<br />
High correlations were found between the ratings of psychologists and prison guardians in all subscales. This shows that the BAPI may be<br />
administered by non clinical professionals efficiently.<br />
Study 3: Development and psychometric properties of the short form of the BAPI<br />
This study was conducted to develop a shorter version of the BAPI to be used as a screening tool. The study was carried out with 1200<br />
people in 7 different prisons. Based on the results of the statistical analyses, some questions were removed. The short version of the BAPI<br />
is composed of 23 questions and is named as BAPI-K.<br />
The correlation between the original form and the short version of the form was found to be very high (0.96). Both subscales of the two<br />
scales were found to be correlated. The scores of the correlations of the BAPI with CAGE and AUDIT were also found to be statistically<br />
significant. The internal consistency of the new scale was found to be satisfactory (0.89).<br />
The results have shown that the BAPI-K is a valid and reliable instrument, and can be used as a screening tool.<br />
Key words: Addiction, assesment, questionnaire<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S151<br />
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[PP-051] Ref. No: 199<br />
Aripiprazole treatment for the choreoathetoid movements and psychotic<br />
symptoms of Huntington’s disease: A case report<br />
Sevinç Ulusoy, İzgi Alnıak, Kasım Fatih Yavuz, Tuğba Kara<br />
Bakirkoy Research and Training Hospital for Psychiatry and Neurology, Istanbul, Turkey<br />
E-mail: tugbakara111@yahoo.com<br />
Introduction: Huntington’s Disease, that is caused by CAG trinucleotide repeat expansion in the IT15 gene located on the short<br />
arm of chromosome 4, is an autosomal dominant, progressive neurodegenerative disorder characterized by motor, cognitive, and<br />
psychopathological symptoms (1). The disease is accompanied by a variety of psychiatric disorders and its incidence rates range from 33<br />
to 76%. Although depression is the most common accompanying psychiatric disorder, anxiety, obsessive-compulsive disorder, irritability<br />
and manic and psychotic symptoms may be associated with Huntington’s Disease (2).<br />
In this case report, we discuss the effectiveness of aripiprazole on the motor and psychiatric symptoms of a patient with Huntington’s<br />
disease, who had psychotic symptoms.<br />
Case: Two years ago, psychotic symptoms developed in addition to existing neurological symptoms in a fifty-year-old patient who was<br />
known to have had Huntington’s disease for twenty years.<br />
After one month of 30 mg/day aripiprazole treatment for a diagnosis of ‘Psychotic Disorder Due to a General Medical Condition’, a<br />
significant decline was observed in the motor and psychotic symptoms that had been present at the beginning of the disease.<br />
Discussion: Although the pathogenesis of the Huntington’s disease has not been exactly solved, the glutamatergic and dopaminergic<br />
systems with striatal neurodegeneration are thought to be responsible for the clinical signs of the disease (3).<br />
By the consideration of this process it is conceivable that aripiprazole, which is used in the treatment of psychosis and chorea, may be a<br />
well-tolerated agent for its effects on the negative and positive symptoms with low metabolic and extrapyramidal side effects.<br />
Key words: Aripiprazole, choreoathetoid movement, Huntington’s disease<br />
References:<br />
1. Walker FO: Huntington’s disease. Lancet 2007; 369:218–228<br />
2. van Duijn E, Kingma EM, van der Mast RC: Psychopathology in verified Huntington’s disease gene carriers. J Neuropsychiatry Clin Neurosci 2007, 19:441-8.<br />
3. Paoletti P, Vila I, Rife´ M, et al: Dopaminergic and glutamatergic signaling crosstalk in Huntington’s disease neurodegeneration: the role of p25/ cyclin-dependent<br />
kinase 5. J Neurosci 2008; 28:1090–1101<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S152<br />
[PP-052] Ref. No: 189<br />
Acute effects of Bacopa monnieri on mood in healthy young adults<br />
Chris Neale, Sarah Benson, Con Stough, Andrew Scholey<br />
Centre for Human Psychopharmacology, Swinburne University, Melbourne, Australia<br />
E-mail: chrisneale02@gmail.com<br />
Objectives: Previous research has identified that Bacopa monnieri (BM) improves aspects of cognitive functioning such as attention,<br />
speed of information processing and verbal learning with chronic dosing (300mg daily). To date there have been no reports of acute<br />
neurocognitive benefits of BM where acute testing has been evaluated; only one known study has reported on acute Bacopa measures[1].<br />
It is possible that in this previous study the cognitive instruments were not demanding enough to detect acute effects. This study is the<br />
first acute dose ranging study of BM using multi-tasking cognitive assessment and measurement of mood.<br />
Methods: Seventeen healthy young adults took part in this double-blind, placebo-controlled three-period crossover study. They were<br />
administered 300 mg BM, 600 mg BM, or a matching placebo on different days with a seven-day washout period between visits. The<br />
treatment order was determined using a Latin Squares design. Following baseline assessment, participants were administered the day’s<br />
treatment and further assessment took place 1 h and 4 h later. The assessments included the Purple multi-tasking framework (MTF) and<br />
the Bond-Lader mood visual analogue scales (administered before and after each 20 min MTF session). The MTF is a 20 minute framework<br />
where participants are required to complete four tasks simultaneously. Tasks include Stroop, maths, tracking and working memory.<br />
Results: There was a significant, dose-dependent effect of treatment on ratings of alertness favouring the 600 mg treatment at both<br />
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Poster Presentations<br />
post-dose assessment times. There was a trend for dose-related effects on performance of the MTF, in particular for the Stroop task, where<br />
there was an advantage for the 300 mg dose.<br />
Conclusions: This is the first demonstration of acute neurocognitive effects of BM. The combination of increased alertness for 600 mg and<br />
better selective attentional performance for 300 mg suggests that mood and cognitive processes can be dissociated and that different<br />
doses of Bacopa may benefit different neural mechanisms.<br />
Further participants are needed for this cohort to increase the statistical power of these findings.<br />
Key words: Bacopa monnieri, nutraceuticals, mood, cognition<br />
References:<br />
1. Nathan, P.J., et al., The acute effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy normal subjects, in Human Psychopharmacology:<br />
Clinical & Experimental. 2001, John Wiley & Sons Ltd. 1996. p. 345-351.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S152-3<br />
[PP-053] Ref. No: 201<br />
Anxiety and depressive symptom levels among adolescents with risk taking behaviour<br />
Nuray Sarp 1 , Aylin Aksoy Çoban 2 , Kültegin Ögel 3<br />
1Acıbadem Fulya Hospital, Psychiatry service, Psychology Department, İstanbul, Turkey<br />
2Acıbadem Fulya Hospital, Psychiatry service, Istanbul, Turkey<br />
3Acıbadem University School of medicine, Department of Mental Heath Disease, Istanbul, Turkey<br />
E-mail: ogelk@ogelk.net<br />
Background: In our country, risk taking behavior has increased among adolescents in recent years. Risky behaviours are defined as<br />
behaviors that affect an adolescent’s health and wellness and daily life directly or indirectly. These behaviours can cause potential<br />
negative results. Bullying, smoking, using alcohol or drugs, early or unprotected sexual activity, skipping school, elopement, damaging<br />
friends and self destruction are the most frequent risky behaviors among adolescents. Through previous research, it has been shown that<br />
the moods of adolescents with risky behaviors differ from other adolescents. Thus it is thought that there may be an association between<br />
risky behavior and depression and anxiety.<br />
Objective: This study investigated the differences between adolescents with risky behaviour and the ones with non-risky behaviour in<br />
terms of depressive and anxiety symptom levels.<br />
Methods: The participants were from different regions and different socio-economic statuses. A total of 3483 students from forty-three<br />
schools (12 vocational high schools, 23 state schools and 6 private high schools ) and104 classes were included in this study. The multistage<br />
cluster sampling method was used for the selection of the sample. In the study, YSR 11-18 (Youth Self Report) and a questionnaire,<br />
which was developed by the researchers, were used. The research survey consisted of 238 items; The questions covered demographical<br />
information, parent and region features, problems about school life, risky behaviours, neglect and abuse, disease, trauma, and health.<br />
Results: In this study, 45.5% of participants were female, 54.5% were male. According to the analysis of each risky behaviour, significant<br />
differences were found for depressive and anxiety symptom levels between groups.<br />
Adolescents who exhibit bullying, elopement, self destruction, commit crimes, and have damaging friends are more likely to show<br />
anxiety and depressive symptoms compared to non-risky behavior adolescents.(p=0.000). In addition, the level of depressive and anxiety<br />
symptoms of drug users were higher than the level of depressive and anxiety symptoms of non-users (depressive; p=0.000, anxiety;<br />
p=0.019).<br />
Adolescents who are carrying a weapon, using alcohol, working in a job and skipping school had a higher level of only depressive<br />
symptoms (p=0.0000). On the other hand, only the high level anxiety group had unprotected sexual activity (p=0.092).<br />
Conclusions: A comparison of non-risky behavior adolescents to risky behavior adolescents showed significant differences in terms of<br />
anxiety and depressive symptom levels and these symptom levels changed according to the risky behaviour type.<br />
Key words: Adolescents, anxiety symptom levels, depressive symmptom levels, risky behavior<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S153<br />
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Poster Presentations<br />
[PP-054] Ref. No: 153<br />
The relationship between mental health and academic achievement among<br />
Kordestan high school students<br />
Fayegh Yousefi, Srwa Mohamadzadeh<br />
Department of Psychiatry at Kordestan University of Medical Sciences, Sanandaj, Kordestan, Iran<br />
E-mail: fyousefi_kms@yahoo.com<br />
Objective: Academic achievement is one of the important factors to which parents, teachers and society pay attention and also, it is<br />
related to students’ mental health. The main objective in the present study was to determine the relationship between students’ mental<br />
health and their academic achievement.<br />
Method: The sample of this study was 1662 high school students (765 males and 908 females) in the age range of 14-19 years. The<br />
sampling method of this study satisfied random sampling. Also, data were gathered by using the GHQ-28. The GHQ-28 is an instrument<br />
to determine mental health and it includes four scales measuring depression, anxiety, somatization and social function. The reliability of<br />
this scale is 0.91 by Cronbach’s alpha.<br />
Results: The results of the present study showed that 45.4% of the respondents had a lack of mental health. Based on the results of the<br />
current study, the low rate of lack of mental health (42.2%) was in the first grade of high school while, the high rate of loss of mental health<br />
were among Pre-University students.<br />
In addition, the results from the present study indicated that there is significant relationship between the education of the respondents’<br />
father and students’ mental health (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
abusers. In the ROC analyses, the area under the curve was found to be 0.90. The ROC analysis has shown that the area under the curve<br />
for alcohol abusers was 0.81 and for substance abusers was 0.93 (Graph 1 and 2).<br />
The BAPI craving subscale was found to be consistent with the PACS and the motivation subscale was found to be consistent with the<br />
SOCRATES. The BAPI total score showed a significant correlation with the MATT average score and the composite score of the Medical<br />
Condition, Substance Use, and Legal Status and Family Social Relations subscales of the ASI questionnaire.<br />
Discussion: The results have shown that psychometric properties of the BAPI are satisfactory for alcohol and substance abusers. The<br />
psychometric properties of the total scale and the data of alcohol and substance abuse are similar. Finally, we can say that the BAPI can<br />
assess both alcohol and substance abuse rather than just alcohol use.<br />
Key words: Addiction, alcohol, assessment<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S154-5<br />
[PP-056] Ref. No: 160<br />
Death anxiety among terminally ill inpatients<br />
Marjan Anvar Abnavi, Ali Javadpour, Sahand Mohamadzadeh<br />
Department of Psychiatry, Shiraz University of Medical Sciences, Shiraz, Iran<br />
E-mail: anvarm@sums.ac.ir<br />
Objective: In spite of the certainty of death, people seem unable to escape anxiety at the prospect of it. Death anxiety contributes<br />
to important emotional and behavioral consequences. The aim of this study was to investigate the relationship of death anxiety with<br />
variables such as severity of illness, depression, and religious beliefs.<br />
Methods: The study is a cross-sectional descriptive study. The data were collected by using a demographic questionnaire, the Templar<br />
Death Anxiety Scale, the Beck Depression Questionnaire, the Cumulative Illness Rating Scale and the Religious Attitude Questionnaire.<br />
Stepwise multiple regression analysis was conducted to identify the factors that influenced the degree of death anxiety.<br />
Results: A group of one hundred and fifty persons, (50 severely ill patients, 50 relatives, and 50 normal controls) completed the<br />
questionnaires. Death anxiety score was 7.2 in attendants, 5.3 in patients, and 4.4 in the control group. Depression and severity of illness<br />
had a positive correlation with death anxiety (p
Poster Presentations<br />
study, the Cronbach alpha coefficient of the questionnaire was calculated to be 0.88 for patients and 0.80 for experts, which was very<br />
satisfactory. The data were analyzed by the SPSS software and Lisrel through the factor analysis method.<br />
Results: Based on the responses of 401 patients and 406 experts, the current situation of access to medical care in the public hospitals<br />
of Iran has lower than average quality and most of the patients and experts gave a low rating to each of the 5 factors of accessibility<br />
in the current situation. In addition, the findings showed that the structure of access to medical care in Iranian public hospitals has a<br />
5-dimensional structure containing individual characteristics, service providing system, social-geographic features, health policy making<br />
and management strategies. The relationship among the 5 dimensions was meaningful from 0.13 for the correlation of health policy<br />
making with the individual characteristics to 0.40 for the correlation of health policy making with the management strategies.<br />
Conclusions: The findings show that the service providing system had the highest quality and was the most effective factor on having<br />
access to medical care structure. It seems that it can be helpful to pay attention to the above factors especially in programming and policy<br />
making to improve access to medical care by distributing the standardized number of beds and specialists based on the population of<br />
each region, training, organizing, and managing the human resources, and improving the service providing system process.<br />
Key words: Feature, access, access to health care, medical care<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S155-6<br />
[PP-058] Ref. No: 174<br />
Smoking behaviour during the course of paroxetine treatment: A case report<br />
Neslihan Akkişi Kumsar, Atila Erol<br />
Sakarya Training and Research Hospital, Sakarya, Turkey<br />
E-mail: drneslihanakkisi@yahoo.com<br />
Selective serotonin reuptake inhibitors are used for the treatment of a wide range of psychiatric disorders, although nicotine craving<br />
attributed to the use of serotonin reuptake inhibitors especially paroxetine has not yet been reported in the literature. Here we present<br />
a case, who developed nicotine craving and started to smoke cigarettes after initiation of 20mg/day paroxetine, and discuss possible<br />
mechanisms of this side effect while reviewing current status of the literature. A 25 year-old female patient was evaluated at our outpatient<br />
clinic and diagnosed with generalized anxiety disorder. She was given paroxetine 20mg/day for four weeks. While her symptomatology<br />
improved by the second week of the treatment, she complained of nicotine craving at the fourth week. During psychiatric assessment<br />
there was not any history of smoking, alcohol or any other substance use disorder. She mentioned that she started smoking one package/<br />
day after starting the paroxetine treatment. The craving for nicotine decreased after the drug was discontinued and she quit smoking<br />
within two weeks. We did not find any report of smoking behaviour attributed to SSRIs in the literature, although there is a study about<br />
decreased smoking behaviour during paroxetine treatment. To the best of our knowledge this case is the first one in the literature. More<br />
research is needed to exlore nicotine craving and SSRIs.<br />
Key words: Craving, cigarette, paroxetine<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S156<br />
[PP-059] Ref. No: 190<br />
Development of a SNP genotyping panel and a medical decision support algorithm<br />
to predict drug response in schizophrenia<br />
Hüseyin Alper Döm 1 , Mehmet Ali Döke 2 , Yemliha Yener Tuncel 1 , Gürkan Üstünkar 3 , Yeşim Aydın Son 4<br />
1 Middle East Technical University, Bioinformatics Graduate Program Ankara, Turkey<br />
2 Middle East Technical University, Department of Biological Sciences, Ankara, Turkey<br />
3 Middle East Technical University, Informatics Institute, Department of Information Science, Ankara, Turkey<br />
4 Middle East Technical University, Informatics Institute, Department of Health Informatics, Ankara, Turkey<br />
E-mail: h.alper.dom@gmail.com<br />
Genome Wide Association Studies (GWAS) of Single Nucleotide Polymorphisms (SNPs) is leading the development of personalized<br />
medicine approaches to predict and diagnose diseases or to determine drug response in individual patients. As the basic research<br />
provides all the genomic information and interpretation of these data, translational research has to be conducted in order to develop<br />
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genomic diagnostics to apply this information into practice in medical clinics. In this perspective, our goal is to design a diagnostic assay<br />
for the Prediction of Drug Response for Schizophrenia to especially guide the initial selection of antipsychotics based on the individual<br />
genomic information of the patients.<br />
Initially a literature search has been done to identify previously described SNPs associated with schizophrenia that are known to effect<br />
the response to antipsychotics or predict the side effects of antipsychotic drugs. Twenty-two SNPs are identified, that map to 8 genes.<br />
Next, we have applied the novel AHP based SNP prioritization approach implemented in the METU-SNP software for GWAS to the SNP<br />
Genotyping data for the European American population (from dbGAP database), with 1351 patients and 1378 controls genotyped for<br />
over 729454 SNPs. The 22 SNPs selected based on the literature were cross-checked with the results of GWAS and prioritized in order to<br />
finalize the pharmacogenomics of the SNP (p-SNP) panel for schizophrenia and to determine the order of SNPs to be targeted in the assay<br />
development process. The pyro-sequencing approach was used during the development of the assay to determine the genotypes of the<br />
patients for the SNPs selected for the panel. After the next phase of our project, which is the development and optimization of primer<br />
sets, is completed a validation study will be designed in collaboration with psychiatric clinics for the described p-SNP kit panel and the<br />
supporting software that is in-line, for development of easy translation of the genotyping results to support the clinical decision of the<br />
choice of therapy.<br />
Application of personalized medicine approaches and utilizing genomic diagnostic assays as presented here will eliminate or decrease<br />
the number of trials-and-errors in selecting sthe right treatment and dosage for particuler patient, and will also minimize emergency<br />
visits due to side effects of the drugs. In addition, the prescription of the right medicine and treatment plan at the initial diagnosis<br />
of schizophrenia will increase trust between healthcare professionals and patients, which in return is expected to provide higher<br />
cooperation and adherance rates of patients to their treatment. Overall the personalized medicine approach is expected to decrease the<br />
cost of healthcare in psychiatry and other disciplines, while offering higher quality healthcare.<br />
Key words: Pharmacogenomics, personalized medicine, translational medicine, genomic diagnostics, medical decision support systems, GWAS,<br />
SNP genotyping, METU-SNP, schizophrenia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S156-7<br />
[PP-060] Ref. No: 200<br />
Basal ganglial hemorrhage induced mania<br />
Barış Yılbaş 1 , Murat Gönen 2<br />
1Department of Psychiatry, Elbistan State Hospital, Elbistan-K.Maraş, Turkey<br />
2Department of Neurology, Elbistan State Hospital, Elbistan-K.Maraş, Turkey<br />
E-mail: barisyilbas@mynet.com<br />
Neuroimaging studies on mood disorders concentrate on the limbic system, especially on the hippocampus and amygdala. Accumulating<br />
evidence suggests an association between abnormalities of the basal ganglia and mood disorders. We present a case of mania following<br />
basal ganglial hemorrhage.<br />
A 30-year old male, with no history of bipolar disorder, was admitted to the emergency room with complaints of euphoria and decreased<br />
need for sleep. During psychiatric assessment, he exhibited grandiosity, psychomotor activation, irritability, and flight of ideas. The<br />
patient,whose cranial MRI showed hemorrhage in the basal ganglia, was hospitalized with a diagnosis of mood disorder due to a general<br />
medical condition. Lorazepam 5mg/day and olanzapine 10mg/day was started. On the tenth day of treatment his episode ended.<br />
The basal ganglia are interconnected with the limbic system and prefrontal cortex and therefore are implicated in bipolar disorder.<br />
Key words: Basal ganglia hemorrhage, mania<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S157<br />
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Poster Presentations<br />
[PP-061] Ref. No: 233<br />
Evaluation of cognitive functions in euthymic bipolar patients using<br />
mono- and multi- drug treatments<br />
Birgül Elbozan Cumurcu 1 , Rıfat Karlıdağ 1 , Şükrü Kartalcı 1 , Işıl Göğcegöz Gül 1 , Süleyman Demir 2 , Bahar Yeşil 1<br />
1 Inonu University Medical Faculty, Turgut Ozal Medical Center, Department of Psychiatry, Malatya, Turkey<br />
2 Gaziosmanpasa University School of Medicine, Department of Psychiartry, Tokat, Turkey<br />
E-mail: baharyesilege@hotmail.com<br />
Objective: Some studies on patients suffering from bipolar disorder show that in active and remission periods of the disorder there are<br />
cognitive insufficiencies (1,2,3). The causes of cognitive insuffuciencies in bipolar disorder is not understood yet. We anticipate that multidrug<br />
usage has more adverse effects on cognitive functions than mono- drug usage and our aim in this study was to investigate effects of<br />
drugs used in treatment of bipolar disorder on cognitive functions. In this study we evaluated the cognitive functions of bipolar patients<br />
who were in their euthymic period taking mono- and multi-drug regimens and compared them with a healthy control group.<br />
Methods: Eighty bipolar I and II patients diagnosed based on the DSM-IV criteria and 80 healthy controls were included in the study and<br />
two groups matched according to age, sex, and education aspects. The patients and controls gave written informed consent to participate<br />
in the study. The necessary approval and ethic committee reviews and permits were obtained prior to the study. The patients were<br />
evaluated using a psychiatric interview, the Young Mania Scale and the Hamilton Depression Rating Scale. A large neurocognitive battery<br />
(Wechsler Memory Scale-Revised, Stroop,Verbal Memory Processes Scale) was used for neurocognitive assessment.<br />
Results: In most cognitive tests the results of the patient group were worse than the control group. The Verbal Memory Processes<br />
Scale-learning scores and long term memory scores were higher in the patients on a mono-drug regimen. All other tests did not show<br />
significant differences.<br />
Conclusions: Our study showed that the cognitive function of bipolar patients had deficiencies not only in active periods of bipolar<br />
disorder but also in remission periods, like previous studies (4,5,6).<br />
The Verbal Memory Processes Scale learning scores and long term memory scores showed better results in patients using a mono-drug<br />
compared to the ones on a multi-drug regimen. Other tests did not show significant differences. Future studies with larger number of<br />
patients may show different results. Also other studies to investigate the effects of each drug group on cognitive functions in bipolar<br />
patients are needed.<br />
Key words: Bipolar disorder, cognitive functions, euthymia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S158<br />
[PP-062] Ref. No: 247<br />
Adult ADHD symptoms in cannabis dependence and the importance of<br />
comorbidity in Adult ADHD<br />
Umut Mert Aksoy, Şennur Günay Aksoy, Fulya Maner<br />
Bakirkoy Research And Teaching Hospital For Neuropsychiatry, İstanbul, Turkey<br />
E-mail: drumutmertaksoy@gmail.com<br />
Background: Adult Attention Deficit Hyperactivity Disoeder (A-ADHD) is one of the most important neuropsychiatric disorders originating<br />
in childhood. According to the last epidemiological studies, ADHD can be persistent into adulthood. Sixty percent of childhood ADHD<br />
cases present with at one or more symptoms in adulthood (Biedermann 2000, Wilens 2006). A prevalance rate of 4.4% of adults has been<br />
reported for ADHD (Fayyad 2007, Kessler 2006).<br />
Comorbidity with alcohol and substance use disorders in A-ADHD is also common and reported as 50%, which is 2-3 times more common<br />
than in the normal population (15%) (Katusic 2005). A-ADHD is reported to be an independent risk factor for substance abuse. Comorbid<br />
substance use disorders have been observed at rates of 9-30& (Wilens 2006).<br />
Individuals with substance use dişorders comorbid with A-ADHD do not differ in substance preference from individuals without A-ADHD<br />
comorbidity. Cannabis is the most abused substance.<br />
Objective: We aimed to demonstrate the existence and intensity of Adult ADHD symptoms in cannabis dependent individiuals and<br />
discuss the importance of comorbid A-ADHD.<br />
Methods: Seventy patients participated and gave informed consent. The participants were selected from patients who underwent<br />
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inpatient treatment in the Department for Addiction at Samsun Neuropsychiatry Hospital. Diagnostic interviews were conducted for<br />
cannabis dependence syndrome (ICD 10; DSM-IV); the earliest interview was after 21 days of detoxification therapy. For assesment, the<br />
Adult ADD/ADHD DSM IV based Diagnostic Screening and Rating Scale was used. The reliability, validity, and transliteral equivalance study<br />
had been performed by Günay et.al in 2005 (Günay 2006). The scale was developed by Prof. Dr.Turgay, former Director of the Toronto<br />
ADHD Clinic, Ontario,Canada. It is a self assessment scale.<br />
General total and subscale mean scores and standard deviation of the ADHD scale according to group factors were calculated. Mean<br />
ADHD total and subscale scores were compared by using the group variable independent t test. The analyses were conducted using SPSS<br />
for Windows 16.00.<br />
Results: The ADHD general total mean scores and subscale mean scores were compared between the groups. Considerably higher scores<br />
were observed in cannabis dependent individuals.<br />
Twenty-two patients met the criterion of inattention whereas 24 patients met both the criteria of hyperactivity and inattention. Twentyfour<br />
patients were re-evaluated and interviewed and Adult ADHD was diagnosed.<br />
Five individuals in the control group met the criterion of inattention, and there were no individuals who met the criteria for both<br />
hyperactivity and inattention.<br />
All three subdimensions of the Turgay Adult ADHD Scale were found to be statistically higher in the cannabis dependent patients.<br />
Conclusions: As this study shows, Adult ADHD is highly represented in cannabis dependent patients.(in our sample 35% of patients were<br />
diagnosed with Adult ADHD).<br />
The awareness of the ADHD diagnosis in Turkey has rapidly increased over time. However it is not commonly researched, diagnosed, or<br />
treated in adult psychiatric units. A major difficulty may be that ADHD has been misdiagnosed because comorbidity is common and 90%<br />
of A-ADHD patients present with another psychiatric disorder in clinical practice. Recent studies clearly show a strong relation between<br />
ADHD and addiction, which supports the idea that a high percentage of drug dependent individuals are also suffering from undiagnosed<br />
A-ADHD. Individuals who are diagnosed and treated are less vulnerable to addiction (Biedermann 1999)<br />
Key words: Adult ADHD, cannabis dependency, substance use<br />
References:<br />
1. Biederman J, Mick E, Faraone SV (2000) Age-de¬pendent decline of symptoms of attention deficit hyperactivity disorder: impact of remission definition and<br />
symptom type. Am J Psychiatry 157:816–818<br />
2. Wilens TE (2006) Attention-deficit/hyperactivity disorder and the substance use disorders: the nature of the relationship, subtypes at risk, and treatment issues.<br />
Psychiatr Clin North Am 27:283–30.<br />
3. Fayyad J, De GR, Kessler R et al (2007) Cross-national prevalence and correlates of adult attentionDeficit hyperactivity disorder. Br J Psychiatry 190:402–409<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S158-9<br />
[PP-063] Ref. No: 270<br />
Ganser syndrome as a dissociative disorder: A case report<br />
Beliz Soyer, Jülide Kenar, Kader Semra Karataş<br />
Erenkoy Mental and Nervous Diseases Training and Research Hospital, Istanbul, Turkey<br />
E-mail: blz_syr@hotmail.com<br />
Ganser syndrome was first described in 1898 by Sigbert Ganser in 4 prisoners. Initially, it was believed to be rare, occurring mainly in<br />
forensic settings. Hence, it was referred to as prison psychosis. Later, such cases were reported more frequently in non-forensic settings.<br />
The syndrome has found a place in both the ICD-10 and DSM-IV, despite controversy about its existence and distinctiveness. This disorder<br />
was previously classified as a fictitious disorder; currently, it is classified under ‘dissociative disorder not otherwise specified.’ We report a<br />
case of a 38 year old woman with Ganser syndrome. The symptoms started 9 months after the death of her brother’s children.<br />
Key words: Ganser Syndrome, vorbeireden, dissociative disorder<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S159<br />
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Poster Presentations<br />
[PP-064] Ref. No: 272<br />
Escitalopram induced galacthorrea: Phenomenon presentation<br />
Aslı Aktümen Bilgin 1 , Birmay Çam 2<br />
1 Zonguldak Atatürk Devlet Hastanesi Psikiyatri Kliniği, Zonguldak, Turkey<br />
2 Gönen Devlet Hastanesi Psikiyatri Kliniği Balıkesir, Turkey<br />
E-mail: draslibilgin@gmail.com<br />
Hyperprolactinemia can present with many physical symptoms such as galactorrhea, amenorrhea, infertility and osteoporosis and<br />
can also cause psychological problems like depression and anxiety. Hyperprolactinemia is mostly seen as a side effect of antipsychotic<br />
medications and rarely can also occur as a side effect of an SSRI. Hyperprolactinemia and galactorrhea as adverse effects of escitalopram<br />
are rarely encountered. In this text we present a case, who developed hyperprolactinemia and galactorrhea on the sixth day of treatment.<br />
The prolactin level decreased to normal after stopping the medication.<br />
Key words: Escitalopram, galactorrhea, hyperprolactinemia<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S160<br />
[PP-065] Ref. No: 276<br />
Amisulpride use in treatment of Tourette’s disorder<br />
Yasemen Taner, Hande Ayraler Taner<br />
Departmant of Child and Adolescent Psychiatry, Gazi University, Ankara, Turkey<br />
E-mail: taneryasemen@yahoo.com<br />
Tourette’s disorder is a neuropsychiatric disease characterised by chronic vocal and motor tics that leads to severe psychosocial disability.<br />
Many old and new generation antipsyshotics had been used in the treatment of Tourette’s Disorder, especially antipsychotics which have<br />
strong effects on D2 receptors. Amisulpride is an antipsychotic which has strong effects on D2 and D3 receptors. Parkinsonism, endocrine<br />
system side effects, and weight gain are less frequent than with the other antipsychotics. Amisulpride is safely used in the treatment of<br />
schizophrenia and the other psychoses in adults. In this case report we discuss amisulpride use in 3 cases with Tourette’s disorder. These<br />
cases previously used other antipsychotics for Tourette’s disorder treatment. Amisulpride was used at a dose of 75-200 mg/day. After<br />
treatment in all three of these cases, the Yale Global Tic Severity Scale score decreased.<br />
Key words: Tourette’s disorder, amisulpride<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S160<br />
[PP-066] Ref. No: 299<br />
Lithium associated glossodynia syndrome: A case report<br />
Hasan Toğul<br />
Gata Haydarpasa Training Hospital, İstanbul, Turkey<br />
E-mail: hasan_togul@hotmail.com<br />
Lithium revolutionized the treatment of bipolar disorder and continues to be the most widely used treatment for this disorder. There<br />
are several side effects that result from lithium carbonate therapy and among the most commonly reported are polydipsia, polyuria,<br />
tremor and weight gain. There have also been reports of various skin lesions with lithium treatment. The following case report suggests<br />
that mucosal lesions may possibly result from lithium therapy. Glossodynia is commonly seen in old female patients. In our case, a 45<br />
year old male had glossodynia after lithium carbonate therapy. The patient’s symptoms were under control with a lithium regimen for a<br />
year. He stopped using lithium in January 2011 and one and a half months later he was hospitilazed because of dysphoric mania. After<br />
his hospitalization, lithium therapy was started again. Three weeks later he reported mucosal ulcerations in the mouth, with associated<br />
soreness of the tongue. The tongue appeared inflamed, with cracks or irregular reddish areas. He was evaluated by a dermatologist, who<br />
diagnosed him with glossodynia. No other medical causes for the lesions were found; the lesions were presumed to be secondary to<br />
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Poster Presentations<br />
lithium treatment. His lithium treatment was stopped and glossodynia treatment begun. Shortly thereafter, his glossodynia symptoms<br />
disappeared. Psychotropic medications can cause mucosal ulcerations and it is important to consider these side effects in the differential<br />
diagnosis and and begin treatment as soon as possible.<br />
Key words: Lithium carbonate, glossodynia, side effects<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S160-1<br />
[PP-067] Ref. No: 300<br />
Two cases of affective disorder due to immunosuppresive treatment<br />
that followed renal transplantation<br />
Hüseyin Ünübol, Başak Ünübol, Jülide Güler, Alper Ünal<br />
Erenkoy Mental Health Education and Research Hospital, İstanbul, Turkey<br />
E-mail: hunubol@hotmail.com<br />
The advent of effective immunosuppressive medicines in the mid-1980s, most notably cyclosporine, revolutionized solid-organ transplant<br />
surgery. For the first time, survival rates reached acceptable levels and rendered organ transplantation a reasonable, non-experimental<br />
standard of medical practice. From the beginning, the immunosuppressive medications were noted to have significant neurological and<br />
psychiatric side effects. From that time to this, the neuropsychiatric side effects such as subjective anxiety or jitteriness, along with tremor,<br />
have served as endpoints in the clinical titration of the the most frequently used immunosuppressive medications, cyclosporine and<br />
tacrolimus. Experience over the past 15 years, however, has established the fact that there are other neuropsychiatric side effects, varying<br />
from seizures, stroke, and profound cognitive impairment to very subtle forms of neuropsychiatric difficulty. Here we present two cases<br />
that underwent uncomplicated renal transplantation and after the immunosuppressive therapy, developed psychiatric symptoms. The<br />
first case was a 29 year old woman with psychotic mania, and the second was a 25 year old male with severe depression that followed a<br />
hypomanic episode (1-3).<br />
Case No 1: A 29 year-old female patient, with a history of kidney transplantation 9 months ago, developed<br />
insomnia, nervousness, mobility, speaking too much, aggressive behavior towards her mother at home, destruction of items, thinking<br />
people were trying to poison her, self-talk in the office, increased skepticism, left her workplace without permission, angry and rowdy<br />
behavior.<br />
History: No previous psychiatric treatment. No family history of substance abuse and psychiatric illness. Surgery for kidney transplantation<br />
9 months ago. Twenty mg/day oral olanzapine treatment was started.<br />
Mycophenolate Mofetil 1000 mg tb 2*1 07:30 and 19:30, prednisolone 5 mg tb 1*2 07:30, cyclosporine 100 mg tb 1*1 19.30 cyclosporine<br />
100 mg tb 1*1 21:30 therapy was continued.<br />
Blood samples for monitoring of cyclosporine levels were sent outside the center. MPPI, Rorschach, and psychometric examinations were<br />
performed and she was evaluated in the direction of psychotic process. PMA is returning to normal; irritability and the patient’s insight<br />
improved on olanzapine 20 mg/day treatment and she was discharged.<br />
Case No 2: A 25 year-old, male patient, with a history of kidney transplantation 4 years ago. The symptoms included unhappiness,<br />
reluctance, discomfort, passive thoughts of death, and insomnia.<br />
Hisstory Kidney transplant in 2007. Approximately 1.5 years ago he had increased speech and movement and affective elation observed<br />
indicated a hypomanic episode in the hospital outpatient clinic as the patient was evaluated. Risperidone 2 mg/day treatment was<br />
started. Two months ago the patient presented with depressive symptoms and started sertraline 50 mg/day, quetiapine 25 mg/day, 500<br />
mg 2 * 2, Mycophenolate mofetil, prednisolone 5 mg, 1 * 1, tacrolimus 1 mg tb 2 * 2, a month after inpatient treatment, the patient became<br />
euthymic, anxiety resolved, and after the disappearance of suicidal ideation the patient was discharged.<br />
Key words: Renal transplantation, immunosuppresive treatment, depression, affective disorder<br />
References:<br />
1. Trzepacz PT, Brenner R, Van Thiel DH. A psychiatric study of 247 liver transplantation candidates. Psychosomatics 1989;30: 147-153.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S161<br />
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Poster Presentations<br />
[PP-068] Ref. No: 303<br />
Varenicline induced psychotic disorders: A case report<br />
İkbal İnanlı, İbrahim Eren, Tahsin Etli<br />
Konya Eğitim ve Araştırma Hastanesi Beyhekim Psikiyatri Kliniği, Konya, Turkey<br />
E-mail: ikbalcivi@yahoo.com<br />
Varenicline is a new agent, commonly used to assist individuals with smoking cessation. There is an increase in case reports of psychiatric<br />
disorders induced or activated by using the agent. Due to the agent’s mechanism of actions, it is possible to make this correlation. Patients<br />
who have a mental illness or high-risk persons should be careful about using this drug. In this report, the case of a psychotic disorder<br />
induced by varenicline is presented.<br />
Key words: Psychotic disorder, smoking cessation, varenicline<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S162<br />
[PP-069] Ref. No: 309<br />
Affective disorders and catatonia: Report of two cases<br />
Feride Büyükşahin, Jülide Güler, Başak Ünübol, Hüseyin Ünübol, Alper Ünal<br />
Erenkoy Mental Health Education and Research Hospital, İstanbul, Turkey<br />
E-mail: basakctf@hotmail.com<br />
Catatonia refers to a broad group of movement abnormalities usually associated with schizophrenia, but also found in other disorders<br />
such as mania, depression, many neurological disorders (especially those involving the basal ganglia, limbic system, diencephalon, and<br />
frontal lobes), systemic metabolic disorders, and toxic drug states. Catatonia is often neglected when screening and examining psychiatric<br />
patients. Undiagnosed catatonia can increase morbidity and mortality, illustrating the need to effectively screen patients for presence<br />
of catatonia, as well as their response to treatment. We describe the clinical presentation of catatonia in a 32 year-old woman with<br />
schizoaffective disorder and in a 25 year-old woman with severe psychotic depression.<br />
Key words: Catatonia, mood disorders, depression<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S162<br />
[PP-070] Ref. No: 224<br />
The relationship of incarceration, past suicide attempts, depression, anxiety and<br />
attention deficit hyperactivity disorder in cases of anti-social personality disorder<br />
Hakan Balıbey 1 , Türker Türker2, Zülküf Perdeci 1 , Nalan Bayar 1 , Mehmet Boran Evren 1<br />
1 Department of Psychiatry Ankara Military Hospital, Ankara, Turkey<br />
2 Department of Public Health Division of Epidemiology Gulhane Military Medical Faculty, Ankara, Turkey<br />
E-mail: hbalibey@gmail.com<br />
Bacgrounds and Objective: Even though attention deficit/hyperactivity disorder (ADHD) has been considered as a childhood disorder<br />
for a long time, currently it is widely accepted that this is a disorder that continues well into adulthood. Attention deficit hyperactivity<br />
disorder (ADHD) is a chronic developmental psychiatric disorder, which starts in early childhood, although its primary symptoms can<br />
still be observed in adulthood. The main symptoms are attention loss, impulsiveness, and hyperactivity which result in mental, social,<br />
and educational/occupational problems in adulthood (1). The current study aimed to study the relationship of incarceration, suicide<br />
attempts, depression, anxiety, and attention deficit hyperactivity disorder in men, who had been diagnosed with antisocial personality<br />
disorder (APD). There are previous studies in the literature for equivalent diagnoses (2,3). METHODS: A total of 80 subjects, 44 of whom<br />
were diagnosed with antisocial personality disorder according to the DSM-IV-TR diagnostic criteria in Ankara Military Hospital psychiatry<br />
clinic and 36 controls, who did not have a psychiatric diagnosis were included in the study. The subjects had been administered a semistructured<br />
interview form for identifying their demographic properties, criminal history, and past suicide attempts. The subjects had also<br />
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Poster Presentations<br />
been given the Wender-Utah rating scale, Hamilton anxiety scale, and Hamilton depression scales. The diagnosis of anti-social personality<br />
disorder has been corroborated by a second mental health professional for all such cases.<br />
Results: There was a statistically significant difference between the Wender-Utah test scores of the APD group and the control group<br />
(p
Poster Presentations<br />
motivations for the use of antipsychotic prescription by psychiatrists.<br />
Five hundred and sixty patients, who applied to the psychiatry clinic of the SSK Ankara Education and Research Hospital in 2004 and<br />
were diagnosed with schizophrenia and 423 patients who presented to the same clinic (name changed to the Psychiatry Clinic of Dışkapı<br />
Yıldırım Beyazıd Education and Research Hospital) in 2009 and were diagnosed with schizophrenia were included in the study. The data<br />
were recorded on the data gathering form that we prepared and included socio-demographic information and details of medication use.<br />
We determined that 77.5 percent of the schizophrenic patients were prescribed atypical antipsychotics in single or combined (typicalatypical<br />
or atypical-atypical) form in 2004. Forty-five percent of patients were using typical antipschotics as monotheraphy or in<br />
combination. In 2009, 91.7 percent of patients were using atypical antipschotics in single or combined form. Only 19.9 percent of patients<br />
were taking typical antipschotics in single or combined form. Using atypical antipsychotics reduced the use of typical antipsychotics<br />
by a significant amount ( χ2=246.26 and p
References:<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
1. Segura-Bruna N, Rodriguez-Campello A, Puente V, Roquer J. Valproate-induced hyperammonemic encephalopathy. Acta Neurol Scand 2006; 114(1):1-7.<br />
2. Chen WT, Yen DJ, Yu HY, Liao KK. Valproate-induced encephalopathy. Zhonghua Yi Xue Za Zhi (Taipei) 2001; 64(8):474-8.<br />
3. Wadzinski J, Franks R, Roane D, Bayard M. Valproate-associated hyperammonemic encephalopathy. J Am Board Fam Med 2007; 20(5):499-502.<br />
4. Gurjar M, Singhal S, Baronia AK, Azim A, Poddar B. Valproate-induced hyperammonemic encephalopathy: A reminder of rare complication of valproate. J Emerg<br />
Trauma Shock 2011; 4(2):321-2.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S164-5<br />
[PP-074] Ref. No: 274<br />
Two cases of tardive dyskinesia associated with the use of paliperidone ER and<br />
their management<br />
Ömer Yanartaş, Yücel Yılmaz, İshak Saygılı, Selma Bozkurt Zincir, Ümit Başar Semiz<br />
Erenkoy Mental Health and Disorders Training and Research Hospital, Istanbul, Turkey<br />
E-mail: yanartas2005@yahoo.com<br />
Paliperidone is an extended-release (ER) medication used in the treatment of schizophrenia and the recommended dose range is 3-12<br />
mg/day (1). Tardive dyskinesia (TD) associated with the use of antipsychotics is characterized by involuntary choreic-athetoid movements<br />
occurring in the late stages of the treatment. Choreathetoid movements mostly occur around the mouth and face and athetoid<br />
movements alone mostly occur on the head-neck and pelvis (2, 3). We hereby present two cases of perioral dyskinesia who were using<br />
paliperidone, and discuss their response to the treatment.<br />
Both patients were females in their 20s and had been diagnosed with paranoid schizophrenia according to the DSM-IV-TR diagnostic<br />
criteria. Both patients had been using olanzapine before being switched to paliperidone ER. Olanzapine treatment had been discontinued<br />
due to side effects and treatment failure. The durations of paliperidone ER use were 9 months and 1 year, respectively; the doses of<br />
paliperidone ER were 9 and 12 mg/day that is consistent with the literature in terms of side effect risk (4). In one of the cases, the<br />
occurrence of side effects in combination with a psychotic exacerbation led to a change in antipsychotic drug therapy. In the other case,<br />
the drug was not discontinued due to the remission of initial psychotic symptoms and satisfaction of the patient with the treatment;<br />
however, the drug dose was reduced. In the treatment of TD associated with the use of paliperidone ER, one case responded to vitamin<br />
E 400 MU/day and omega 3 fatty acids while the other was administered propranolol 40 mg/day and clonazepam 1 mg/day. After one<br />
month, the scores of both patients on the extrapyramidal symptoms assessment scale were markedly reduced. The patient who had the<br />
psychotic exacerbation also had a history of childhood trauma, which we feel had negatively influenced the course of the treatment.<br />
Young age and female sex, and drug use for more than 6 months may increase the risk of TD in patients taking paliperidone; the use of<br />
vitamin E, omega 3 fatty acids, propranolol, and clonazepam may lead to a significant improvement in symptoms.<br />
Key words: Extrapyramidal side effects, paliperidone, tardive dyskinesia<br />
References:<br />
1. Janicak PG, Winans EA. Paliperidone ER: a review of the clinical trial data Neuropsychiatric Disease and Treatment 2007:3(6) 869–883.<br />
2. Kaplan HI, Sadock BJ Synopsis of Psychiatry: Eighth ed. Baltimore: Williams & Wilkins, 1998<br />
3. Bernstein JG. Drug Therapy in Psychiatry. Third ed. St.Louis: Mosby-Year Book, 1995<br />
4. Meltzer HY, Bobo WV, Nuamah IF, Lane R, Hough D, Kramer M, Eerdekens M. Efficacy and tolerability of oral paliperidone extended-release tablets in the treatment<br />
of acute schizophrenia: pooled data from three 6-week, placebo-controlled studies. J Clin Psychiatry 2008 May;69(5):817-29.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S165<br />
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Poster Presentations<br />
[PP-075] Ref. No: 301<br />
Effects of agmatine in rats with chronic unpredictable mild stress<br />
Feyza Arıcıoğlu 1 , Tijen Utkan 2<br />
1 Department of Pharmacology and Psychopharmacology Research Unit, Marmara University, Faculty of Pharmacy, Istanbul, Turkey<br />
2 Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey<br />
E-mail: feyza.aricioglu@gmail.com<br />
Depression is one of the most common psychiatric disorders which is a leading cause of total disability and economic burden.<br />
Although there are medications that alleviate depressive symptoms, they have serious limitations. Therefore better understanding of<br />
the neurobiology of the disease is required. Agmatine (l-amino-4-guanidinobutane) is an endogenous amine synthesized from the<br />
decarboxylation of arginine. Agmatine has been quantified in nearly all of the organs of the rat including brain and plasma. Agmatine<br />
exerts a wide range of biological activities on several organ systems, including the central nervous system, where it has been proposed<br />
to act as a neurotransmitter. Agmatine interacts with the imidazoline receptors, alpha-2-adrenoceptors, nicotinic cholinergic receptors,<br />
and serotonergic 5-HT3 receptors. It selectively modulates the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors in rat<br />
hippocampal neurons via an interaction between the guanidino group of agmatine and the NMDA channel pore and is an endogenous<br />
inhibitor of all isoforms of nitric oxide synthase. Agmatine is released from neurons and has neuroprotective properties. The present study<br />
was designed to evaluate the effect of agmatine in a chronic unpredictable mild stress (CUMS)-induced depression model.<br />
Animals were allocated to the following study groups: animals not exposed to CUMS (Control group, n=12), animals exposed to CUMS for<br />
5 weeks (CUMS group, n=12), and animals exposed to CUMS and treated with agmatine (CUMS+Agmatine group, n=12). The control and<br />
CUMS groups were injected with saline and the CUMS+Agmatine group was injected with agmatine 40 mg/kg, i.p. daily throughout the<br />
experiment. CUMS was applied as previously described with a minor modification. Briefly, the CUMS and CUMS+Agmatine groups were<br />
subjected to different types of stressors: restraint for 4 h, cage tilting for 24 h, wet bedding for 24 h, swimming in 40C cold water for 5<br />
min, swimming in 45 C hot water for 5 min, pairing with another stressed animal for 48 h, level shaking for 10 min, nip tail for 1 min, and<br />
inversion of the light/dark cycle for 24 h. These nine stressors were randomly applied for 5 weeks, during which each stressor was applied<br />
for 4-5 times. The rats received one of these stressors per day and the same stressor was not applied continuously for 2 days so that<br />
animals could not predict the occurence of stimulation. The control group not receiving stress treatment had free access to food and water<br />
but all groups were food and water deprived 24 h before the sucrose consumption test only. After 5 weeks, the sucrose consumption,<br />
sucrose preference and forced swimming tests were performed.<br />
The results of this study showed that agmatine administration during CUMS suppressed CUMS-induced depression-like behavioral<br />
changes, including a reduction in sucrose preference, body weight, locomotor activity, and a decrease in immobility time in the forced<br />
swimming test. Our findings suggest that agmatine may have a protective effect either by inhibiting oxidative damage and/or by<br />
modulating neuronal activity in CUMS. Based on these findings, agmatine, as an endogenous molecule, has a promising effect and further<br />
studies are required to understand the underlying mechanism.<br />
Key words: Agmatine, sucrose preference, forced swimming test, chronic unpredictable mild stress<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S166<br />
[PP-076] Ref. No: 302<br />
A case of obsessive compulsive disorder with psychotic features that suffered<br />
from sexual trauma<br />
Fatma Fariha Cengiz, Esra Aydın Sünbül<br />
Erenköy Psychiatric Training and Research Hospital, İstanbul, Turkey<br />
E-mail: dr_ffatmacengiz@yahoo.com.tr<br />
Introduction: Although the relationship between obsessive compulsive disorder (OCD) and psychosis is a noteworthy phenomenon, the<br />
limits of the two disorders have not been defined. Eisen and Rasmussen (1993) evaluated a total of 475 patients with OCD and 14% were<br />
identified as having psychotic symptoms in addition to OCD. They classified the patients into 4 groups: 6% OCD without insight, OCD<br />
and schizophrenia (4%), OCD and delusional disorder (2%), OCD and schizotypal personality disorder (3%) (1). In clinical observation it is<br />
seen that, the shift from an obsession to a delusion is described when insight into obsessive signs is lost and resistance abandoned. These<br />
delusions do not signify a schizophrenic diagnosis but represent reactive affective or paranoid psychoses (3).<br />
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Poster Presentations<br />
Case: A 32 year old single man, who has not been a soldier, presented with aggressive, contamination, sexual, need for symmetry, somatic<br />
obsessions; checking, washing, counting, need for confession compulsions; thinking he was followed by the secret service, sense of anal<br />
burning, and inability to sleep. His mood and affect were anxious, speech increased, and associations were dispersed. He had a history<br />
of sexual abuse by his brother. Obsessive symptoms started at the age of 12, feeling some problems about his gender, anxiety about<br />
his future, sleeplessness and not talking to people at 16. After 15 days he had talked about the sexual abuse with her mother, who died<br />
because of a myocardial infarction and he started to blame himself. He lost 15 kg in 6 months and started to experience auditory and<br />
visual hallucinations. He was treated with many antipsychotics, SRIs, TCAs, and benzodiazapines. He had a hypomanic attack under the<br />
treatment of aripiprazole. In the Rorschach test he showed schizoid reactions and dissociation in 2003. He was hospitalized 2 times. At his<br />
last visit his treatment was sertraline 200 mg/day and olanzapine 5 mg/day. The appearance of the psychotic symptoms occurred, when<br />
the depressive symptoms started. Olanzapine was increased to 10 mg/day after sleeplessness and psychotic symptoms flared up. The last<br />
Rorschach test assessed the patient as being in pregenital organization and requiring close control of affective and psychotic symptoms.<br />
Discussion: The clinical observations emphasize the interest in OCD patients with psychosis, who are neglected often. The shift from<br />
an obsession to delusion is triggered by stress and is generally transient (2). The strong association between psychotic features and<br />
depressive features in OCD may also have important implications in the treatment strategies (3). OCD represents a psychopathological<br />
spectrum varying along a continuum of insight and requires careful clinical observation and treatment.<br />
Key words: Obsesive compulsive disorder, psychosis, sexual trauma<br />
References:<br />
1. Eisen JL, Rasmussen SA. Obsessive-compulsive disorder with psychotic features. J Clin Psychiatry1993; 54(10):373-379.<br />
2. Özerdem A. Obsesif-Kompulsif Bozukluk ve Psikoz Üzerine Bir Gözden Geçirme. Klinik Psikiyatri 1998;2:98-102<br />
3. Khess CDJ, Das J, Parial A et. al. Obsesive Compulsive Disorder with psychotic features.Hong Kong J Psychiatry1999;9(1): 21-25<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S166-7<br />
[PP-077] Ref. No: 304<br />
Priapism associated with zuclopenthixol treatment: A case report<br />
Alparslan Asil Budaklı, Mehmet Alpay Ateş, Ayhan Algül<br />
GATA Haydarpasa Education Hospital, İstanbul, Turkey<br />
E-mail: asil.budakli@gmail.com<br />
Background: Priapism is pathologically prolonged and painful penis erection, usually without sexual desire or stimulation. Priapism is<br />
classified as veno occlusive low flow (ischemic) and arterial high flow (non ischemic). The low flow–ischemic type is the most common<br />
type of priapism and if it is untreated, leads to irreversible ischemic cavernosal tissue changes. The causes include generally certain<br />
medications, although the mechanism for drug-induced priapism is unknown (1-4).<br />
Here we discuss, in light of the literature, a 62-year-old- male paranoid schizophrenic patient, who had been treated with oral<br />
zuclopenthixol since 1995 and developed an acute and painful erection.<br />
Case: It was revealed that the patient, who presented with priapism, that hadcontinued for a week, took zuclopenthixol 20 mg a day for<br />
2 days prior to the veno occlusive priapism.<br />
After emergency urological treatment, the psychiatric examination revealed paranoid psychosis. Zuclopenthixol was stopped and<br />
risperidone 6 mg/day and biperiden 4 mg/day were prescribed. A week later he was discharged from hospital.<br />
Discussion: In many cases it has been reported that psychotropic drugs may cause priapism. Some of them are trazadone, chlorpromazine,<br />
haloperidol, zuclopenthixol, olanzapine, ziprasidone, and clozapine (3). Although the mechanism of priapism associated with antipsychotics is not<br />
clear, it is thought to be related to blockage that is mediated by the alpha receptors in the corpora cavernosa of the penis (3). Similarly, the capacity<br />
of zuclopenthixol to induce priapism is thought to be due to its antagonist activity on alpha-1 adrenergic receptors (1,3).<br />
Therefore it is important that clinicians must take notice of side effects of antipsychotics, including rarely seen ones.<br />
Key words: Zuclopenthixol, priapism, side effect, drug induced, antipsychotics<br />
References:<br />
1. J Salado, A Blazquez, R Diaz-Simon, F Lopez-Munoz, C Alamo and GG Rubio Priapism associated with zuclopenthixol: Ann Pharmacother June 1, 2002 vol. 36 no. 6 1016-1018<br />
2. Brichart N, DElavierre D, Peneau M, İbrauhim H, Mallek A. Priapism induced with antipsychotic medications: a series of four patients. Prog.Urol. 2008 Nov; 18 (10):<br />
699-73.Epub 2008 Jun 10.<br />
3. Sood S, James W and Bailon MJ. Priapism associated with atypical antipsychotic medications. a review. Int Clin Psychopharmacol 2008; 23: 9-17<br />
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Poster Presentations<br />
4. Şükrü Kartalcı, Işıl Göğceğöz Gül, Rıfat Karlıdağ, Birgül Elbozan Cumurcu Recurrent priapism during quetiapine treatment case report; Bulletin of Clinical<br />
Psychopharmacology, Vol: 20, N.: 4, 2010 327-328<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S167-8<br />
[PP-078] Ref. No: 113<br />
Prescribing patterns and inappropriate use of medications in patients referred to<br />
doctors in Ardabil City of Iran<br />
Firouz Amani, Amin Shaker<br />
Iran- Ardabil University of Medical Sciences, Iran<br />
E-mail: biostat.f@gmail.com<br />
Objective: To determine the drug use patterns and descriptive analysis of prescriptions among patients who visited doctors in Ardabil City.<br />
Methods: A retrospective study was carried out on 2000 randomly selected prescriptions from all registered prescriptions in Ardabil City<br />
using data from two insurance organizations. Data were obtained on demographics, prescribing indicators and potentially inappropriate<br />
medications. The collected data were analyzed by descriptive statistical methods using SPSS software.<br />
Results: From all prescriptions, 822 (41 %) were for men and 1178 (59%) were for women. The mean age of the subjects was 31.6 ± 21.3<br />
years ranging from 1 to 91. On thousand three hundred and six (65.3%) of all prescriptions were from general practitioners and others from<br />
specialists. The mean number of drugs per prescription was 3.58±1.3 ranging from 1 to 9. Dexamethasone, with 219 (24.7 %) prescriptions,<br />
was the most commonly prescribed medication. The total number of medications prescribed in all the prescriptions was 7158 while the<br />
mean number of medications per encounter was 3.6. Antibiotics, with 52.8% of the prescriptions, were the most prescribed drug group.<br />
Conclusion: The results showed that the mean of prescription drugs per encounter and the rate of prescription injection drugs were more<br />
than the global standards. Also, the pattern of prescription drugs was inappropriate. It is necessary to reduce irrational prescription of<br />
drugs to patients by monitoring and control indicators of medical doctors who prescribe higher numbers of prescriptions.<br />
Key words: Pattern, drug utilization, inappropriate medications<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S168<br />
[PP-079] Ref. No: 305<br />
Bipolar affective disorder and normal pressure hydrocephaly: A case report<br />
Kader Semra Karataş 1 , Jülide Güler 1 , Özgür Bilgin Topçuoğlu 2 , Ebru Damla Bostancı 1 , Beliz Soyer 1<br />
1Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Psychiatry, İstanbul, Turkey<br />
2Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Neurology, İstanbul, Turkey<br />
E-mail: drsemraocak@yahoo.com<br />
Background: The subject of this study was how affective disorders are related to structural changes in the brain. The use of lithium in<br />
affective disorders can cause pseudotumor cerebri, which has been reported in the literature, although there is no information about the<br />
occurrence of normal pressure hydrocephalus. We detected normal pressure hydrocephalus in a patient diagnosed with bipolar affective<br />
disorder 10 years ago and treated with lithium.<br />
Case: A 55 year-old woman, housewife, not working, lives in Istanbul with her husband and children. She was diagnosed with bipolar<br />
affective disorder 10 years ago and treated with lithium. She had hand tremors, weakness and dizziness and was admitted to hospital.<br />
The patient was dehydrated, walking with small steps, showed balance difficulty and urinary incontinence. The patient was admitted<br />
to the psychiatric unit. A neurology consultation and cranial MRI were requested. The patient was thought to have normal pressure<br />
hydrocephalus. Lumbar puncture was performed twice. The patient was diagnosed with arrested hydrocephalus; CSF flow could not be<br />
identified. A CSF dynamic MRI was requested and the patient was transferred to neurosurgery.<br />
Discussion: There are publications about the relationship between structural brain abnormalities and affective disorders. Hydrocephalus,<br />
by definition, is the accumulation of CSF in the ventricular system due to an imbalance between production and absorption of CSF.<br />
Presenting symptoms include memory impairment, urinary incontinence symptoms, and ventriculomegaly (2,3). The etiology of<br />
normal pressure hydrocephalus can include head trauma, metabolic problems, endocrinopathies, infectious and immunological<br />
conditions; danazol, tamoxifen, oxytocin, tetracycline, indomethacin, lithium, drugs such as retinol are mentioned (2.4). Normal pressure<br />
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Poster Presentations<br />
hydrocephalus is not known to be associated with lithium in the literature. Lithium is known for its relationship with pseudotumor cerebri.<br />
Taking into account the patient saw benefits from lithium, it was decided to postpone to a change to the mood stabilizer.<br />
Key words: Bipolar affective disorder, lithium, normal pressure hydrocephalus, structural brain abnormalities<br />
References:<br />
1. Arnone D, Cavanagh J, Gerber D, Lawrie SM, Ebmeier KP, Mclntosch AM. Magnetic resonance imaging studies in bipolar disorder and schizophrenia: meta-analysis.<br />
BJPsych 2009; 195:194-201.<br />
2. Görgülü O, Yurt A, Özer FD, Turan Y. Normal basınçlı hidrosefali ön tanılı 26 hastanın analizi. Demans Dergisi 2003; 3:117-120.<br />
3. Kempton MJ, Geddes JR, Ettinger U, Williams SCR, Grasby PM. Meta-analysis, Database, and Meta-regression of 98 Structural Imaging Studies in Bipolar Disorder.<br />
Arch Gen Psychiatry. 2008;65:1017-32.<br />
4. Levine SH, Puchalski C. Pseudotumor cerebri associated with lithium therapy in two patients. J Clin Psychiatry. 1990; 51:251-3.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S168-9<br />
[PP-080] Ref. No: 307<br />
Agmatine attenuats cognitive impairment and oxidative damage following chronic<br />
unpredictable mild stress: A behavioral, biochemical, and histological study<br />
Salih Gümrü 1 , Emre Yarcı 1 , Özer Şehirli 1 , Yusufhan Yazır 2 , Tijen Utkan 3 , Feyza Arıcıoğlu 1<br />
1 Department of Pharmacology and Psychopharmacology Research Unit, Marmara University, Faculty of Pharmacy, Istanbul, Turkey<br />
2 Department of Histology and Embryology, Kocaeli University, Medical Faculty, Kocaeli, Turkey<br />
3 Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey<br />
E-mail: salihgumru@gmail.com<br />
Agmatine (l-amino-4-guanidinobutane) is an endogenous polycationic amine synthesized by the decarboxylation of arginine by the<br />
enzyme arginine decarboxylase and hydrolysed by agmatinase. Agmatine has been quantified in nearly all organs including brain. It<br />
has been proposed to act as a novel neuromodulator in the mammalian brain. Previous studies have shown that endogenous agmatine<br />
interacts with a number of receptor subtypes such as, imidazoline, 2-adrenergic and N-methyl-D-aspartate. It also blocks other ligandgated<br />
cationic channels, including nicotinic receptors, and inhibits all three isoforms of nitric oxide synthase. Although there are papers<br />
showing that agmatine may have a modulator role in learning and memory, the question of whether it is able to reverse impaired learning<br />
and memory still remains. This study was planned to investigate the effect of agmatine on cognitive functions and oxidative damage<br />
following chronic unpredictable mild stress (CUMS).<br />
Rats were allocated to the following study groups: animals not exposed to CUMS (control group, n=12), animals exposed to CUMS for<br />
5 weeks (CUMS group, n=12), animals exposed to CUMS and treated with agmatine (CUMS+Agmatine Group, n=12). The control and<br />
CUMS groups were injected with saline and the CUMS+Agmatine group was injected with agmatine 40 mg/kg, i.p. daily throughout the<br />
experiment. CUMS was applied according a previous study with a minor modification. Briefly, the CUMS and CUMS+Agmatine groups<br />
were subjected to different types of stressors: restraints for 4 h, cage tilting for 24 h, wet bedding for 24 h, swimming in 40C cold water for<br />
5 min, swimming in 45 C hot water for 5 min, pairing with another stressed animal for 48 h, level shaking for 10 min, nip tail for 1 min, and<br />
inversion of the light/dark cycle for 24 h. These nine stressors were randomly applied for 5 weeks. The rats received one of these stressors<br />
per day and the same stressor was not applied continuously for 2 days so that animals could not predict the occurence of stimulation.<br />
After 5 weeks, animals were tested in the passive avoidance (PA) and Morris’s water maze (MWM) tasks to evaluate learning and memory<br />
functions. At the end of the experiment, the brains of the rats were either removed freshly for malondialdehyde (MDA), glutathione (GSH)<br />
levels and myeloperoxidase (MPO) activity or removed with 4% paraformaldehyde perfusion for c-fos, glial fibrillary acidic protein (GFAP)<br />
and brain-derived neurotrophic factor (BDNF) determination immunohistochemically in cortex and hippocampus.<br />
There was a significant defect in cognitive functions of the CUMS group whereas agmatine treatment significantly reversed this effect<br />
both in the PA and MWM tests. A decrease in GSH and an increase in MDA and MPO levels in the CUMS group were significantly inhibited<br />
with agmatine treatment, which were considered markers of oxidative damage. In the immunohistochemical experiments, it was found<br />
that c-fos and GFAP were overexpressed and BDNF was decreased in the CUMS group whereas data for the agmatine treatment group<br />
were similar to those of the control group. The findings of the current study clearly showed beneficial effects of agmatine on cognitive<br />
impairment and oxidative damage in CUMS.<br />
Key words: Agmatine, BDNF, c-fos, chronic unpredictable mild stress, GFAP, malondialdehyde, glutathione, myeloperoxidase<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S169<br />
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Poster Presentations<br />
[PP-081] Ref. No: 308<br />
Ceruloplasmin levels before and after treatment in patients with depression:<br />
A case-control study<br />
Mehmet Cemal Kaya 1 , Yasin Bez 1 , Salih Selek 2 , Haluk Asuman Savaş 3 , Hakim Çelik 2 , Hasan Herken 4<br />
1 Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey<br />
2 Harran University School of Medicine, Department of Psychiatry, Sanliurfa, Turkey<br />
3 Gaziantep University School of Medicine, Department of Psychiatry, Gaziantep, Turkey<br />
4 Pamukkale University School of Medicine, Department of Psychiatry, Denizli, Turkey<br />
E-mail: mcemalkaya@yahoo.com<br />
Objective: Ceruloplasmin is a serum protein synthesized by hepatocytes and involved in both copper and iron metabolism. It is an<br />
acute phase reactant and has antioxidant capacity (1). Deficiency of ceruloplasmin is thought to cause neural cell damage secondary to<br />
decreased mitochondrial energy production and increased lipid peroxidation, and iron associated free radicals (2,3). Ceruloplasmin, an<br />
antioxidant agent, has previously been investigated in some psychiatric disorders like schizophrenia and obsessive compulsive disorder<br />
(4). Studies about ceruloplasmin in depression are relatively scarce (5). In this prospective study, we aimed to determine the serum<br />
ceruloplasmin levels of depressive patients before and after treatment, to compare them those of healthy control subjects and to assess<br />
any possible association of ceruloplasmin levels to treatment response.<br />
Methods: Among the admissions to the Psychiatry Outpatients Clinic of Gaziantep University Medical Faculty Hospital 19 (8 males, 11<br />
females) patients who were diagnosed with major depressive disorder according to the DSM-IV criteria and 40 (17 males, 23 females)<br />
healthy control subjects have been included in the study. The patients received naturalistic antidepressant treatment during the 8 weeks<br />
period after the diagnosis. The serum ceruloplasmin levels and the Hamilton Depression Rating Scale (HAM-D) scores of the patients<br />
were measured before and after the 8 week period of antidepressant treatment. Blood collection for ceruloplasmin measurement was<br />
done only once for the healthy control subjects. The measurement of ceruloplasmin levels was conducted according to the standard<br />
procedures.<br />
Results: The ceruloplasmin levels of patients both before and after antidepressant treatment were significantly higher than those of<br />
control subjects (t=7.569, p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-082] Ref. No: 159<br />
Foetality in schizophrenia<br />
Elif Mutlu, Mehmet Emin Ceylan, Agah Aydın<br />
Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
E-mail: elifmutlu@yahoo.com<br />
Objective: The aim of this study was to evaluate common morphological and neurological features of schizophrenia from an ontogenetic<br />
perspective and to propose a new conceptual approach to schizophrenia, in which early foetal marks persist without diminishing in<br />
comparison to other people.<br />
Material and Methods: Fifty patients diagnosed with schizophrenia from the Bakırköy Research and Training Hospital for Psychiatry,<br />
Neurology and Neurosurgery were chosen for the study group. The control group consists of fifty healthy male subjects. The ages of<br />
all subjects varied between 18 and 65. All of the subjects were informed about the study and their written consents were obtained.<br />
Sociodemographic data of all subjects were recorded and the Waldrop Minor Physical Anomalies Scale, the NES ( neurological evaluation<br />
scale), and the Edinburgh Handedness Inventory were applied.<br />
Results: We found significantly higher scores among schizophrenic patients in comparison to healthy subjects both in the NES total and<br />
all four sub-categories of the scale. The minor physical anomalies scores, head circumference, and hypertelorism were significantly higher<br />
in the schizophrenic group. In addition, for hand-eye dominancy, we observed more tendency to be crosswise.<br />
Conclusion: Some characteristics of schizophrenia such as hypertelorism, large head circumference, high palate, thin muscle and<br />
bone structure, primitive reflexes, mental and behavioral characteristics could be evaluated as a separate ontogenetic entity.Evaluating<br />
schizophrenia within the context of a neurodevelopmental hypothesis, as an evolutionary process, in which foetal traits persist, would<br />
contribute to our understanding of the disorder’s ambigous nature and phenomenology.<br />
Key words: Schizophrenia, foetality, ontogenesis<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S171<br />
[PP-083] Ref. No: 182<br />
Metabolic changes in the acute phase with olanzapine treatment<br />
Mehmet Ak 1 , Abdullah Bolu 1 , Süleyman Akarsu 1 , Deniz Sezlev 2 , Tülin Yanık 2 , Özcan Uzun 1 , Fuat Özgen 1 , Aytekin Özşahin 1<br />
1Department of Psychiatry, Gulhane Military Medical Faculty, Ankara, Turkey<br />
2METU, Faculty of Science, Biology department, Ankara, Turkey<br />
E-mail: drmehmetak@gmail.com<br />
Introduction: Atypical antipsychotics are used in treatment of psychotic disorders and severe behavior disorders. Despite the lack of extra<br />
pyramidal side effects, they cause metabolic disorders (such as hyperlipidemia, weight gain, glucose intolerance), which are important<br />
causes of mortality (1). The exact mechanisms of these side-effects of atypical antipsychotics have not been identified so far and therefore<br />
and protective measures could not be established (2). In this study we aimed to examine the acute phase changes in blood lipid profile<br />
and body mass index while using olanzapine.<br />
Materials and Methods: Twenty four patients, who were diagnosed with first-episode psychotic disorder and received olanzapine<br />
treatment in the Department of Psychiatry, Gulhane Military Medical Faculty, were enrolled in the study. The serum lipid levels and fasting<br />
blood sugars were measured before the treatment and four weeks after the treatment; body mass index was calculated and the data<br />
obtained were compared.<br />
Results: The comparison of pre- and post-treatment data showed significant increases in the weight gain, measurement of waist<br />
circumference, body mass index, total cholesterol, and VLDL levels (p
Poster Presentations<br />
References:<br />
1. Jin H., Meyer J.M., Mudaliar S., Jeste D.V., 2008. Impact of atypical antipsychotic therapy on leptin, ghrelin, and adiponectin. Schizophrenia Research 100 (2008)<br />
70–85.<br />
2. Yazıcı K. Yazıcı A., 2008. Weight Increase Induced by Antipsychotic drugs:What is the role of genes? Bulletin of Clinical Psychopharmacology 2008;18:59-70.<br />
3. Chagnon YC. Susceptibility genes for the side effect of antipsychotics on body weight and obesity.Curr Drug Targets 2006; 12: 1681-1695<br />
4. Evans WE, Johnson JA. Pharmacogenomics: the inherited basis for interindividual differences in drug response. Annu Rev Genomics Hum Genet 2001; 2: 9-39<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S171-2<br />
[PP-084] Ref. No: 183<br />
Do cultural factors effect clinical manifestations of OCD? Clinical features of<br />
a Turkish sample<br />
Ramazan Konkan 1 , Ömer Şenormancı 1 , Oya Güçlü 1 , Erkan Aydın 1 , Mehmet Z. Sungur 2<br />
1 Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
2 Marmara University School of Medicine, İstanbul, Turkey<br />
E-mail: ramazankonkan@gmail.com<br />
Objective: In the present study we evaluated the clinical characteristics of OCD patients monitored in an outpatient program and<br />
compared them with other cultures.<br />
Method: The study included 116 OCD patients who presented to the clinics at the Bakirköy Research and Training Hospital for Psychiatry,<br />
Neurology and Neurosurgery, met the inclusion criteria, volunteered to participate in the study after being diagnosed and were referred<br />
by two psychiatrists. The diagnosis was confirmed using the Structured Clinical Interview Form for the DSM-IV Axis I Disorders (SCID-I). An<br />
inquiry form was developed for obsessive compulsive symptoms based on the obsessions and compulsions included in the Yale-Brown<br />
Obsession Compulsion Scale (Y-BOCS) according to their incidence and a sociodemographic form from the SCID-I clinical interview guide.<br />
Results: Our sample consisted of 30 male (25.9%) and 86 female (74.1%) patients. The mean age was 34.96±10.23 years. The most<br />
common obsessions were impurity-contamination (49.1%), followed by doubt (20.7%) and religious (11.2%) obsessions. Secondary<br />
obsessions included doubt (53.4%), impurity-contamination (14.7%) and sexual obsessions (9.5%), respectively. In tertiary obsessions,<br />
21 patients reported presence of symmetry-exactness (18.1%), 13 patients reported doubt (11.2%), 10 patients reported sexual (8.6%)<br />
obsessions, and 43 patients (37.1%) had no tertiary obsessions (Table 1). Ninety-six percent of patients had accompanying compulsions.<br />
The most common compulsions were cleaning and washing (53.4%), checking (26.7%) and repetitive ritual behavior (7.8%).DISCUSSION:<br />
The most common obsession in the present study was impurity/contamination with a rate of 49.1% in line with the literature, followed by<br />
doubt obsessions of 20.7%. The most common compulsion reported in literature is washing accompanied by obsession of contamination,<br />
and it is followed by checking. Similarly, in our study, the primary compulsion was cleaning and washing with a rate of 53.4%, followed by<br />
checking (26.7%) and repetitive ritual behaviors (7.8%). Although the first two obsessions and compulsions are in line with the literature,<br />
the tertiary obsessions reported as aggressive or sexual obsessions in the literature were replaced by religious obsessions (11.2%) in our<br />
sample. An intercultural study showed that religious obsessions were the most common obsessions with 60% in the Egyptian sample,<br />
and 50% in the Saudi sample. However, the rate of religious obsessions was 6% in the U.S., 5% in the United Kingdom, and 11% in India.<br />
Studies on Jewish populations showed similar results with the Muslim populations, with a religious obsession rate of 50%. We believe that<br />
the rate of religious obsession is associated with our country’s position, being at the junction of Western and Eastern cultures. Relatively<br />
lower rate of sexual obsessions compared to the literature may result from the fact that obsessions related with sexuality may be more<br />
difficult to report than other obsessions in our population.<br />
Key words: Clinical manifestation, cultural differences, OCD<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S172<br />
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Poster Presentations<br />
[PP-085] Ref. No: 196<br />
Reliability and validity of Turkish version the Brief Fear of Negative Evaluation<br />
Scale II (BFNE-II) among male patients with alcohol dependency<br />
Cüneyt Evren, Selime Çelik, Reşide Aksoy, Turan Çetin, Müge Ülkü, Sera Yiğiter, Elif Mutlu<br />
Bakırköy Training and Research Hospital for Psychiatry, Neurology and Neurosurgery, Alcohol and Drug Research, Treatment and Training Center (AMATEM), İstanbul, Turkey<br />
E-mail: cuneytevren@yahoo.com<br />
Background and Objective: The construct of fear of negative evaluation consists of feelings of apprehension about others’ evaluations,<br />
distress over these negative evaluations, and the expectation that others will evaluate one negatively (1). The Brief Fear of Negative<br />
Evaluation Scale (BFNE) is a measure of a person’s tolerance for the possibility they might be judged disparagingly or hostilely by others<br />
(2). The aim of this study was to determine the reliability, validity and factorial structure of the Turkish translation of the BFNE-II in male<br />
alcohol dependent inpatients.<br />
Methods: Participants were 155 consecutively admitted male alcohol dependents. Patients were investigated with the BFNE-II, the Social<br />
Phobia Scale (SPS), the Social Interaction Anxiety Scale (SIAS) and the Liebowitz Social Anxiety Scale (LSAS). The BFNE-II was repeated in<br />
136 of these 155 patients after 2 weeks.<br />
The BFNE is composed of 12 items describing fearful or worrying cognition. Eight of the twelve items describe the presence of fear or<br />
worrying, while the remaining four items describe the absence of fear or worrying (3). In the BFNE-II (4) reversed items are corrected.<br />
Results: The Turkish version of the BFNE-II was found to be compatible with the original scale. In alcohol dependents the internal<br />
consistency coefficient (Cronbach’s alpha) was 0.91 for the BFNE-II. For each of the items, the corrected item-total correlation values were<br />
between 0.57 and 0.84 (p
Poster Presentations<br />
when meeting and talking with other people”’ (1). Thus the two companion measures were designed to distinguish between scrutiny fears<br />
and concerns about interaction. The scales correspond to the DSM-III-R descriptions of Social Phobia--Circumscribed and Generalised<br />
types, respectively. In this study, the reliability and validity of the Turkish translation of the Social Phobia Scale (SPS) and Social Interaction<br />
Anxiety Scale (SIAS) in male alcohol dependent inpatients were determined.<br />
Method: The study was conducted with hospitalized patients between August 2008 and March 2009 in the Bakirkoy State Hospital<br />
for Mental Health and Neurological Disorders, AMATEM (Alcohol and Drug Research, Treatment and Education Center) in Istanbul.<br />
Participants were 155 consecutively admitted male alcohol dependents. Diagnoses of alcohol dependence and social anxiety disorder<br />
were made with the SCID-I modules of these disorders. Patients were investigated with the SPS, the SIAS (2), the Brief Fear of Negative<br />
Evaluation II (BFNE-II) and the Liebowitz Social Anxiety Scale (LSAS).<br />
Results: The Turkish versions of both the SPS and the SIAS were found to be compatible with the original scales. In alcohol dependents,<br />
the internal consistency coefficient (Cronbach’s alpha) was 0.92 for the SPS and 0.93 for the SIAS. For each of the items, the corrected<br />
item-total correlation values were between 0.21 and 0.68 (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-088] Ref. No: 217<br />
Venlafaxine-mirtazapine combination in the treatment of post traumatic stress disorder<br />
Abdullah Bolu, Süleyman Akarsu, Cemil Çelik, Barbaros Özdemir, Kamil Nahit Özmenler<br />
Department of Psychiatry, Gulhane Military Medical Faculty, Ankara, Turkey<br />
E-mail: abdullah_bolu@yahoo.com<br />
Introduction: Posttraumatic stress disorder (PTSD) is an incapacitating clinical syndrome characterized by intrusive recollections,<br />
emotional numbing and withdrawal, cue-related responses, and psychological and physiological hyperarousal. In the treatment of PTSD<br />
pharmacotherapy must be supported with psychotherapy to increase the success of treatment. In this study we aimed to evaluate the<br />
effect of venlafaxine-mirtazapine combination in the PTSD patients, who did not respond to antidepressant treatment at<br />
adequate dose for an adequate duration.<br />
Material and Methods: The hospital records of the patients who were diagnosed with PTSD according to DSM-IV diagnostic criteria and<br />
did not respond to adequate doses of an antidepressant treatment for adequate duration were examined retrospectively. Data of the<br />
patients (n=28), whose treatment were venlafaxine- mirtazapine combination, were obtained. These data were IES-R, Hamilton Anxiety<br />
scale and Hamilton Depression Scale scores.<br />
Results: IES-R score, Hamilton Anxiety, Hamilton depression scores of 28 patients who were diagnosed with PTSD were evaluated. A<br />
significant decrease in IES-R total, IES-R avoidance, Hamilton Anxiety and Hamilton depression scores (p> 0.05) with adequate dose and<br />
duration of venlafaxine-mirtazapine treatment were detected. The same change was not accompanied in IES-R hyperarousal and IES-R<br />
intrusive test scores.<br />
Conclusion: Post-traumatic stress disorder treatment takes longer and sometimes becomes chronic. According to the results of this study,<br />
venlafaxine- mirtazapine combination can be used in the treatment of PTSD patients who did not respond to antidepressant treatment<br />
at adequate doses for an adequate duration.<br />
Key words: Mirtazapine, posttraumatic stress disorder, PTSD, venlafaxine<br />
References:<br />
1. McDougall SJ, Widdop RE, Lawrence AJ (2004) Medial prefrontal cortical integration of psychological stress in rats. Eur J Neurosci; 20: 2430-2440.<br />
2. Radley JJ, Rocher AB, Janssen WG, Hof PR, McEwen BS, Morrison JH (2005) Reversibility of apical dendritic retraction in the rat medial prefrontal cortex following<br />
repeated stress. Exp Neurol; [Epub ahead of print].<br />
3. Kılıçoğlu A. Stress and effects of brain: A review. New Symposium Journal; July 2007, Volume 45, İssue 3<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S175<br />
[PP-089] Ref. No: 221<br />
Efficacy and 3-month follow-up of repetitive transcranial magnetic stimulation<br />
(rTMS) in treatment resistant depression: Three cases<br />
Onur Durmaz, Mehmet Alpay Ateş, Mesut Çetin, Servet Ebrinç, Cengiz Başoğlu, Ayhan Algül<br />
Department of Psychiatry, GATA Haydarpasa Training Hospital, Istanbul, Turkey<br />
E-mail: drodurmaz@gmail.com<br />
Introduction: rTMS(Repetitive Transcranial Magnetic Stimulation) is an effective non-invasive cortical stimulation method that is being used<br />
in the treatment of drug resistant major depressive disorder. The underlying mechanism of effect of rTMS has not been fully understood<br />
yet. Neuromodulation, neuroplasticity, and cortical excitability are the most accepted theories (1). Even though the post-treatment effect of<br />
rTMS in depression is well known, little is known about its lasting effect (2).Therefore in this report we investigated the effect of add-on rTMS<br />
treatment with 3 month follow-up after treatment in 3 outpatient cases diagnosed with drug resistant unipolar major depression.<br />
Case 1: A 33 year-old female patient was diagnosed with major depressive disorder and received venlafaxine 300 mg/day for two years.<br />
An add-on 15 sessions of DLPFC rTMS (20 Hz, 110% MT, 1000p/d) was applied due to insufficient medication response. The MADRS and<br />
HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after treatment. The MADRS scores were<br />
found to be 37, 11, 2 and 4, while the HAM-A scores were found to be 35, 9, 5 and 6, respectively.<br />
Case 2: A 35 year-old male patient was diagnosed with major depressive disorder since age 12 and received escitalopram 20 mg/day for<br />
three months. An add-on 15 sessions of DLPFC rTMS (20 Hz,110% MT,1000p/d) was applied due to insufficient medication response. The<br />
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Poster Presentations<br />
MADRS and HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after treatment. The MADRS<br />
scores were found to be 28, 10, 5 and 5, while the HAM-A scores were found to be 33, 18, 7 and 6, respectively.<br />
Case 3: A 44 year-old male patient was diagnosed with major depressive disorder since age 15 and received venlafaxine 375 mg/day and<br />
ziprasidone 40 mg/day for five months. An add-on 15 sessions of DLPFC rTMS (20 Hz,110% MT,1000p/d) was applied due to insufficient<br />
medication response. The MADRS and HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after<br />
treatment. The MADRS scores were found to be 29, 9, 6 and 7, while the HAM-A scores were found to be 28, 13, 10 and 8, respectively.<br />
Conclusion: Maintenance of improvement in major depression treatment has been another concern apart from efficacy of current<br />
interventions. rTMS is an effective method as monotherapy and also as add-on treatment of depression. In this study each of three<br />
patients responded favorably to rTMS. In the post-treatment course, significiant improvement was maintained at the 3-month follow-up.<br />
Given its relatively benign side effect profile, long lasting therapeutic effect, and more practical non-invasive application than ECT, we<br />
conclude that rTMS can be considered as an optional treatment before ECT in treatment-resistant depression patients.<br />
Key words: rTMS, resistant depression, treatment, follow-up, maintenance<br />
References:<br />
1. Pell GS, Roth Y, Zangen A.Modulation of cortical excitability induced by repetitive transcranial magnetic stimulation: Influence of timing and geometrical<br />
parameters and underlying mechanisms. Prog Neurobiol. 2010 Nov 5.<br />
2. Bortolomasi M, Minelli A, Fuggetta G, Perini M, Comencini S, Fiaschi A, Manganotti P.Long-lasting effects of high frequency repetitive transcranial magnetic<br />
stimulation in major depressed patients. Psychiatry Res. 2007 Mar 30;150(2):181-6.<br />
3. Hadley D, Anderson BS, Borckardt JJ, Arana A, Li X, Nahas Z et all. Safety, tolerability, and effectiveness of high doses of adjunctive daily left prefrontal repetitive<br />
transcranial magnetic stimulation for treatment-resistant depression in a clinical setting. J ECT. 2011 Mar;27(1):18-25.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S175-6<br />
[PP-090] Ref. No: 225<br />
The effects of brain-derived neurotrophic factor Val66Met polymorphism on<br />
executive functioning in patients with obsessive-compulsive disorder<br />
Raşit Tükel 1 , Hakan Gürvit 2 , Berna Özata 1 , Banu Aslantaş Ertekin 1 , Erhan Ertekin 1 , Bengi Baran 2 , Şükriye Akça Kalem 2 ,<br />
Nalan Öztürk 1 , Güher Saruhan Direskeneli 3<br />
1 Istanbul University, Istanbul Faculty of Medicine, Department of Psychiatry, İstanbul, Turkey<br />
2 Istanbul University, Istanbul Faculty of Medicine, Department of Neurology, İstanbul, Turkey<br />
3 Istanbul Faculty of Medicine, Department of Physiology, Istanbul University, İstanbul, Turkey<br />
E-mail: rtukel@gmail.com<br />
Objective: In the present study, we investigated the association between the brain-derived neurotrophic factor (BDNF) Val66Met<br />
polymorphism and performance on tests measuring executive functions in a sample of patients with obsessive-compulsive disorder<br />
(OCD).<br />
Method: A total of 71 patients diagnosed with OCD by the DSM-IV criteria were included in the study. All patients were assessed using the<br />
Yale-Brown Obsessive-Compulsive Scale and the Hamilton Depression Rating Scale. Patients also performed the Wisconsin Card Sorting<br />
Test (WCST), the Trail Making Test part A (TMT A) and part B (TMT B), the Tower of London Test (ToL), the Verbal Fluency Test (semantic and<br />
lexical fluency) and the Stroop Test. Genomic DNA was extracted from whole blood. The single nucleotide polymorphism (G/A) leading<br />
to amino acid substitution at the 66 codon in the BDNF gene (dbSNP number rs6265) was screened by a polymerase chain reaction<br />
and restriction digestion analysis in the DNA samples. The performance of the patients on the neuropsychological tests of executive<br />
functioning was compared between the patients with Val/Val genotype and Met carriers.<br />
Results: Subjects with Val/Val genotype and Met carriers (Met/Met or Val/Met genotypes) did not differ on socio-demographic and clinical<br />
factors, except for the age of onset of the illness, which was earlier in subjects with Val/Val genotype than Met carriers. The performances on the<br />
TMT B and TMT B-A, the Stroop Test, and the two measures of the ToL were found to be significantly lower in the Met-allele carriers, compared<br />
to the Val/Val group. There were no significant differences in the WCST and the Verbal Fluency Test performances between the two groups.<br />
Conclusions: These findings suggest that the BDNF Met allele may be associated with poorer performance on neuropsychological tests<br />
of executive functions in OCD patiens.<br />
Key words: Brain-derived neurotrophic factor, executive functions, obsessive-compulsive disorder, polymorphism<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S176<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-091] Ref. No: 228<br />
Diagnostic confusion about OCD and schizophrenia: A case report<br />
Sevgi Gül Kabak, Mustafa Burak Baykaran, Selma Bozkurt Zincir<br />
Erenköy Mental Health Training and Research Hospital, İstanbul, Turkey<br />
E-mail: sbozkurtzincir@yahoo.com<br />
Introduction: Both obsessions and delusions are based on wrong, absurd and extreme ideas and it is thought that they could be<br />
separated on the basis of the presence of insight. Between obsessions and delusions there is the protection of insight and the ability to<br />
resist compulsive thoughts and/or behaviors. The insight of obsessive patients against obsessions may be protected or completely lost<br />
(1). In this paper, the diagnostic process in a patient with OCD, who also had delusions, is discussed.<br />
Case: A 30 year-old, married, female patient applied to the hospital with complaints of unhappiness, suspiciousness, self-reproach, thoughts<br />
of death, hearing noises and insomnia. The patient had a four year medical history. She considered her 6 year-old son as her “love.” Four<br />
years ago she had sexual feelings towards her female collegues and she thought that her feelings were mutual and her thoughts could be<br />
read by them. During psychiatric examination, her thought content had Schneiderian symptoms such as paranoia, thought withdrawal,<br />
thought insertion, and reference delusion. Just after the hospitalization and evaluation, the patient was medicated with 6 mg/day risperidone<br />
and 2 mg/day biperiden for a preliminary diagnosis of schizophrenia. Later the preliminary diagnosis was changed to atypical obsessivecompulsive<br />
disorder and her treatment was changed to sertraline 200 mg/day, quetiapine 300 mg/day and clonazepam 2 mg/day. Due to the<br />
fact that after a 10-day period of improvement, her reference delusion and fear of death had restarted, and inappropriate affect was detected,<br />
a treatment regimen of pimozide 2mg/day, sertraline 200mg/day, clomipramine 75mg/day, clonazepam 2mg/day had been prescribed.<br />
The difference between the facts and the idea had been discussed through a cognitive approach. After 12 days, her affect recovered and<br />
obsessive thoughts decreased, therefore the patient was discharged from hospital on the previously mentioned treatment. After 2 months,<br />
there had been no psychotic symptoms, she had been able to cope with distress better and her psycho-social functioning had been fine.<br />
Discussion: The frequency of psychotic symptoms in OCD was detected at the ratio of 0.7-12.3% in a former study and 14% psychotic<br />
symptoms and 4% schizophrenia was reported in another study. Thomsen and Jensen demonstrated that 5% of 135 OCD patients, who<br />
applied to the hospital for the first time, were later diagnosed as schizophrenic (3). Despite the psychotic nature of OCD that has been<br />
noticed for a long time, modern classification systems still refer to OCD as an anxiety disorder. Although the DSM-IV mentions poor<br />
insight in OCD, there has been no objective description for what degree of insight should be accepted as poor. The diagnostic criteria and<br />
treatment of schizo-obsessions and whether the patients who have schizophrenia and OCD comorbidity should be considered as schizoobsessive<br />
disorder are still under discussion(2).<br />
Key words: Comorbidity, differential diagnosis, obsessive compulsive disorder, schizophrenia<br />
References:<br />
1. Aydın A. Ceylan ME. Türkcan A. Şizofrenide Obsesif Kompulsif Fenomenler: Bir Gözden Geçirme. Klinik Psikofarmakoloji Bülteni 2008;18:222-234<br />
2. Demir EY. Aslan S. Şizo-Obsesif Bozukluk: Tanı, Sınıflandırma ve Tedavi. Türkiye’ de Psikiyatri 2005;7(1):38-43<br />
3. Güleç G. Güneş E. Yenilmez Ç. Obsesif Kompulsif Belirtileri Olan Şizofreni Hastalarının Şizofreni ve Obsesif Kompulsif Bozukluk Hastaları İle Karşılaştırılması. Türk<br />
Psikiyatri Dergisi 2008;19(3):247-256<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S177<br />
[PP-092] Ref. No: 232<br />
Is vaginismus a specific phobia?<br />
Ramazan Konkan 1 , Meltem Bayrak 1 , Oya Güçlü 1 , Ömer Şenormancı 1 , Mehmet Z. Sungur 2<br />
1 Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey<br />
2Marmara University School of Medicine, İstanbul, Turkey<br />
E-mail: ramazankonkan@gmail.com<br />
Objective: Although vaginismus is classified under the title of “sexual pain disorders”, its etiological roots are still controversial. It has been<br />
suggested that vaginismus should be considered as a phobic reaction resulting in an avoidance behavior due to a dominant fear of pain. It<br />
has also been argued that, in patients with vaginismus, other fears usually accompany the fear of pain during coitus. Excessive sensitivity<br />
particularly in the genital area is said to prevail in vaginismus. In our study, patients with vaginismus were compared to a healthy group<br />
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Poster Presentations<br />
in terms of commonly seen phobias, amplified perception of somatic sensations and sensitivity to pain<br />
Method: As a part of a different aspect of a vaginismus trial 40 subjects with vaginismus, who was referred to the Sexual Functioning<br />
Disorders outpatient clinic and agreed to take part in the study and 50 women of the control group who described penile penetration<br />
difficulty and pain during coitus, were evaluated. The participiants were evaluated using a sociodemographic form developed by the<br />
researchers, the SCL-90-R (Symptom Checklist-90-Revised), and the Somatosensory Amplification Scale Halam and Hafner (1977) fear<br />
checklist. The data were analysed using the SPSS for Windows 10.0 statistical packet program and P
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-094] Ref. No: 291<br />
Switching to fluoxetine due to sertraline-induced urinary incontinence: A case report<br />
Pınar Güzel Özdemir 1 , Adem Aydın 1 , Mustafa Güleç 2 , Emine Füsün Akyüz Çim 1<br />
1 Yuzuncu Yil University, Medical Faculty, Department of Pyschiatry, Van, Turkey<br />
2 Ataturk University, Medical Faculty, Department of Pyschiatry, Erzurum, Turkey<br />
E-mail: pguzelozdemir@yahoo.com<br />
Urinary incontinence is involuntary leakage of urine. It is not life-threatening but adversely affects the quality of life (1). The patient usually<br />
complains about frequent or periodic urinary incontinence in small amount or just leakage.<br />
Here we report a case of urinary incontinence induced with sertraline and resolved after sertraline was discontinued.<br />
Case: A 38 year-old married female patient presented to our clinic with complaints such as boredom, avolution, and depression. In<br />
her history, there was no psychiatric treatment or treatment with any other medications. On her psychological examination, she was<br />
cooperative, oriented, replying to questions briefly and properly. Her affect was depressive. The patient was diagnosed with depressive<br />
disorder and prescribed sertraline 50mg/day. She was suggested to come to the clinic for follow up after 3 weeks, however she came back<br />
a week later complaining of urinary incontinence. Without any pressure feeling, she developed urinary incontinence which negatively<br />
affected her daily activities. Her medication was changed to fluoxetine 20mg/day from sertraline 50mg/day. Her urinary incontinence<br />
complaint disappeared 2 days after. On the follow-up the patient did not have any urinary incontinence.<br />
We presented a case report of urinary incontinence, which developed after starting sertraline. In the literature, there are case reports<br />
about sertraline induced urinary incontinence and switching to fluoxetine (1,2).<br />
Despite extensive research, the mechanism of enuresis has not been clarified in detail. Continence is maintained by alpha-adrenergically<br />
mediated constriction of the bladder sphincter (3). Sertraline has alpha-adrenergic blockage, which may partially explain urinary incontinence<br />
in our case.<br />
Enuresis is usually underdiagnosed because of clinicians do not ascertain about it or the masking of this side effect by multiple drugs such<br />
as antimuscarinic or noradrenergic agents (3).<br />
Fluoxetine may be a choice in sertraline induced urinary incontinence cases in the treatment of depression and anxiety disorders. Larger<br />
case series are needed on this issue.<br />
Key words: Urinary incontinence, sertraline, fluoxetine<br />
References:<br />
1. Votolato NA, Stern S, Caputo RM: Serotonergic antidepressants and urinary incontinence Int Urogynecol J Pelvic Floor Dysfunct 2000;11:p 386–8.<br />
2. Maalouf Fadi T, Gilbert Andrew R. Sertraline-Induced Enuresis in a Prepubertal Child Resolves after Switching to Fluoxetine. J Child Adolesc Psychopharmacol<br />
2010;20:161<br />
3. Andersson KE: Advances in the pharmacological control of the bladder. Exp Physiol 1999;84:195–213<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S179<br />
[PP-095] Ref. No: 292<br />
The relationship between the serum bilirubin levels and metabolic syndrome<br />
in schizophrenia patients<br />
Filiz Karadağ 1 , Hasan Herken 1 , Bünyamin Kaptanoğlu 2 , Yaşar Enli 2 , Özgür Kalkancı 1 , Ceyhan Balcı Şengül 3 , Hüseyin Alaçam 1<br />
1 Pamukkale University Medical Faculty Psychiatry Department, Denizli, Turkey<br />
2 Pamukkale University Medical Faculty Biochemisry Department, Denizli, Turkey<br />
*Denizli State Hospital, Denizli, Turkey<br />
E-mail: filizlal@yahoo.com<br />
Objective: Especially with the use of atypical antipsychotics, the increase of the metabolic side effects constitutes a major problem<br />
in schizophrenia patients. Serum bilirubin levels have been reported to be associated with insulin resistance, abdominal obesity, and<br />
metabolic syndrome (MS) (1,2). However, the relationship between MS parameters and bilirubin levels has not been investigated in<br />
schizophrenia patients. It has been reported that antipsychotic drugs do not cause significant changes in serum bilirubin levels (3).<br />
The objective of this study was to investigate the association between bilirubin levels and the parameters associated with MS in<br />
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Poster Presentations<br />
schizophrenia patients.<br />
Methods: Ninety one schizophrenic patients (38 female, 53 male) receiving antipsychotics for at least one year were included in the study.<br />
The parameters associated with MS were as follows: Body mass index, body weight, waist circumference, systolic and diastolic blood<br />
pressure, fasting blood glucose, insulin, serum triglycerides, HDL cholesterol levels, and the insulin resistance as calculated by using the<br />
value HOMA (homeostasis model assessment). The criteria were based on ATP-III criteria for metabolic syndrome (Adult Treatment Panel<br />
III). Statistical analysis was performed by using SPSS 17.0 (for Windows).<br />
Results: Serum triglyceride levels were inversely correlated with serum direct bilirubin (p=.006) and positively correlated with indirect/<br />
direct bilirubin ratio (p =. 002). Serum HDL levels (p=.018) showed a significant positive correlation with indirect/direct bilirubin ratio.<br />
Waist circumference (p=.048) showed a significant negative correlation with serum total bilirubin. The levels of insulin (p =.038) and value<br />
of HOMA (p =.015) were inversely correlated with serum direct bilirubin.<br />
The rate of metabolic syndrome was significantly lower in the patients with highest quartile (75-100) of the serum direct bilirubin levels<br />
than the other quartiles (p=.022).<br />
In these patients, the ratio of the patients that meet criteria for metabolic syndrome according to levels of the fasting triglyceride (p=.013)<br />
and HDL (p=.040) was significantly lower than others. Additionally, the means of body weight (p=.026), waist circumference (p=.022), and<br />
serum triglyceride levels (p=.039) of these patients were found significantly lower.<br />
Conclusions: In this study we found that bilirubin levels are associated with metabolic syndrome and its parameters and high levels of<br />
serum direct bilirubin may be associated with the lower risk for MS in schizophrenia patients; similar to the healthy individuals (1,2,4).<br />
Our study is the first study investigating this issue. Our results may be important for the following aspects: High serum direct bilirubin<br />
levels may serve as an easily applicable, inexpensive marker indicating lower MS risk for schizophrenic patients. Additionally, it may be<br />
possible to prevent antipsychotics induced metabolic side effects by avoiding the drugs with higher risk for MS, in the patients with low<br />
levels of direct bilirubin. Due to the relatively limited number of patients and cross-sectional nature, our results required to be confirmed<br />
by longitidunal studies with larger samples.<br />
Key words: Schizophrenia, metabolic syndrome, bilirubin, antipsycotic drug<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S179-80<br />
[PP-096] Ref. No: 293<br />
Olanzapine abuse: A case report<br />
Neslihan Akkişi Kumsar, Atila Erol<br />
Sakarya Training and Research Hospital, Sakarya, Turkey<br />
E-mail: drneslihanakkisi@yahoo.com<br />
Introduction: Olanzapine is a thienobenzodiazepine which specifically blocks 5-HT2A and D2 receptors and additionally blocks<br />
muscarinic (M1), H1, 5-HT2C, 5-HT3.5-HT6, a l, and D4 receptors. It has greater affinity for 5-HT2 receptors than for D2 receptors (Kelly,<br />
Conley & Carpenter 2005). Olanzapine has consistently been found to be significantly superior to placebo and comparable with, or<br />
superior to, haloperidol for the treatment of overall, positive, and negative symptoms of schizophrenia. In this case, we want to report a<br />
case of olanzapine abuse.<br />
Case Report: A 48-year old, primary school graduate, married, female patient was admitted to our psychiatry clinic with tachycardia,<br />
insomnia, and anxiety. In psychiatric assessment, she mentioned that her symptoms have been similar for 15 years and in the last 3 years<br />
she has used citalopram 40 mg/d and olanzapine 10 mg/d and after this treatment her symptoms decreased. During psychiatric treatment<br />
when her consequent doctor wanted to stop the olanzapine treatment, she did not succeed and the patient had anxiety, insomnia, and<br />
anger and reported decreased symptoms after using the drug again<br />
Discussion: Besides medications with obvious abuse potential such as benzodiazepines and methyphenidate and other stimulants, abuse<br />
of a number of commonly prescribed psychiatric medications has been reported. The abuse of anticholinergic drugs was first reported<br />
in 1960 with the description of a patient, who increased her trihexyphenidyl to achieve antidepressant and euphoriant effects. Recently,<br />
abuse of quetiapine for its sedative and anxiolytic effects has been reported. The abuse risk of quetiapine has been also reported in our<br />
country and Kaya et al. studied the abuse risk of quetiapine with prisoners. In the literature there are only two cases of olanzapine abuse.<br />
Key words: Abuse, olanzapine<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S180<br />
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Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-097] Ref. No: 123<br />
Various reasons for self-destructive acts and objects used to commit them in 1991<br />
Elena Valzdorf<br />
Irkutsk Regional Psychoneurologic Dispensary<br />
E-mail: elenavalzdorf@yandex.ru<br />
Objective: The objective of the research was to study and assess the reasons for self-destructive acts committed by the individuals that<br />
underwent outpatient forensic psychiatric examination in 1991 and to give a brief characteristic of the objects used to commit the selfdestructive<br />
acts.<br />
Methods: The statistical method and comparative analysis were employed to study the historical data of 30 archive acts of outpatient<br />
forensic psychiatric examinations covering the period of January-March, 1991.<br />
Results: The analysis of the archive of acts revealed 30 males aged between 15 and 51 (the age range of 20 and 41 dominated). The<br />
reasons for committing self-destructive acts by the examined individuals who underwent outpatient forensic psychiatric examination in<br />
1991 included the following: Conflicts with people around them (in 12 patients), conflict situations with parents and other close relatives<br />
(sister, brother, wife) (in 5), conflicts with inmates in place of imprisonment (in 4), conflict situations during military service (for example,<br />
a self-destructive act was committed by a serviceman to be closer to his parents house) 9in 3), an effect of command hallucinations in 2,<br />
ongoing investigation (in 1), conflict with loved ones (woman) (in 1), protest (investigator refused to allow relatives to visit the patient) (in<br />
1), and severe headache in combination with high blood pressure (the suicide was attempted to ease the pain) (in 1). Also according to<br />
the archive documents of forensic psychiatric examination 18 out of 30 individuals used sharp, cutting, or piercing objects (razor, kitchen<br />
knife, or pen knife, glass, fragment of a broken mirror, wire, sharpened coin, cigar case, etc.), 3 individuals used washing line or belt, 3<br />
patients used a medicine in tablet form, 1 individual used a medicine in liquid form, and 1 patient used the effect of low temperatures<br />
(long deliberate stay in cold weather in winter).<br />
Conclusion: The research findings demonstrated that the most common reasons for self-destructive acts committed by the examined<br />
patients in 1991 were conflict situations with individuals, out of prison, and in the society rather than conflicts in place of imprisonment<br />
or in place of military services. The objects used to commit self-destructive acts included: Sharp, cutting, or piercing objects (most often<br />
razor and kitchen knife), washing line, and a medicine in tablet form (antibiotics, phenazepam, cyclodolum, etc.).<br />
Key words: Self-destructive acts, outpatient forensic psychiatric examination, archive documents<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S181<br />
[PP-098] Ref. No: 296<br />
Topiramate induced acute psychotic disorder<br />
Serkan Barlak, Alpay Ateş, Cengiz Başoğlu, Servet Ebrinç<br />
Department of Psychiatry, GATA Haydarpasa Training Hospital, Istanbul, Turkey<br />
E-mail: drserkanbarlak@yahoo.com.tr<br />
Introduction: The use of topiramate has increased in recent years. It is now used in several specialties to treat a wide range of medical<br />
conditions. A small number of case reports describes psychosis as an adverse event of topiramate. While using topiramate as an option<br />
for treatment-resistant epilepsy, clinicians need to be aware of the possibility of topiramate-induced psychosis in patients who have<br />
not previously had a psychotic episode. Although there is a small literature in neurology journals regarding psychiatric adverse events<br />
in epileptic patients, the psychiatric literature is silent about the topic. We report a patient without a previous history of psychosis, who<br />
developed psychosis after use of topiramate.<br />
Case: The patient on multiple antiepileptic drugs with refractory tonic-clonic epilepsy was prescribed topiramate. The patient developed<br />
definite psychotic symptoms including auditory halucinations and paranoid-persecutory delusions and other behavioral symptoms<br />
fifteen days after beginning topiramate. The psychotic and other psychiatric symptoms resolved quickly with discontinuation of<br />
topiramate and by using a second-generation antpsychotic drug.<br />
Discussion: Topiramate was originally discovered as an oral hypoglycaemic, afterwards was approved as an anticonvulsant agent and is<br />
now used as an adjunct to various treatments. The several mechanisms of action include inhibition of sodium conductance, decreased<br />
frequency of generated action potentials, activated gamma-aminobutyric acid activity, inhibition of AMPA receptor, and weak inhibition<br />
of carbonic anhydrase (1). The mechanism underlying psychotic symptoms induced by topiramate is not clear, but overactivity of<br />
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Poster Presentations<br />
ascending dopaminergic pathways due to GABAergic inhibition of the substantia nigra has been proposed (3). The true prevalence of<br />
topiramate-induced psychosis is not known. Although there have only been a few case reports of topiramate-induced psychosis, an<br />
antiepileptic drug survey group found the incidence to be 1.5% in 596 patients (2). The risk of this side effect may be greater in the general<br />
population as studies of topiramate exclude patients with past psychiatric history and past psychiatric history is the most important<br />
predictor for psychiatric adverse events. As epilepsy could overlap with psychiatric conditions at a rate of 50-60% including mood, anxiety,<br />
and psychotic disorders, clinicians should be cautious in diagnosing drug–induced psychosis.<br />
Key words: Topiramate, antiepileptic, drug-induced psychosis<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S181-2<br />
[PP-099] Ref. No: 170<br />
Glass-aating behaviour with radiological findings: A pica case<br />
Neslihan Akkişi Kumsar, Atila Erol<br />
Sakarya Training and Research Hospital, Sakarya, Turkey<br />
E-mail: drneslihanakkisi@yahoo.com<br />
Pica is the persistent, compulsive ingestion of non-nutritive substances, which includes eating disorders with unusual cravings. Etiologies<br />
of consumption of common and bizarre substances range from mineral deficiencies and helminthic infestations to cultural preferences.<br />
Recently, pica has been linked to obsessive-compulsive (OCD) spectrum disorders.<br />
Although there are few epidemiological studies and likely underreporting by embarrassed patients, pica exists in all ages, races, genders,<br />
and geographical regions. Lower socioeconomic groups, young children, pregnant women, or nursing mothers with increased nutritional<br />
demands are at higher risk, as well as those with brain damage, epilepsy, mental retardation, psychosis, or dementia.<br />
Case Report: A 32-year-old, primary school graduate, unemployed, male patient referred to psychiatry clinic with glass eating behavior<br />
for 10 years. There was not any history of psychiatry referral before the development of glass eating craving. He was referred to psychiatry<br />
clinic with this craving and had difficulty to quit eating glass. In psychiatric examination we found cleaning and control obssessions.<br />
The cranial MRI showed decrease in size of in corpus callosum, enlargement in Sylvian fissure and sulcus, asymmetry in III. and lateral<br />
ventricules.<br />
Discussion: In literature we did not a pica case like this one regarding glass eating. Even most pica cases are associated with element<br />
deficiency in our case there was not any deficiency. Because of obsessive symptoms, it might be associated with obsessive spectrum<br />
disorders with radiological findings. In OCD spectrum disorders, pica should also be considered and radiological investigation must<br />
always be done.<br />
Key words: Obsessive compulsive spectrum, pica, corpus callosum<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S182<br />
[PP-100] Ref. No: 209<br />
The use of bupropion in treatment Kleptomania’s: Two cases<br />
Özyıl Öztürk Sarıkaya 1 , Demet Güleç Öyekçin 2<br />
1Bursa Devlet Hastanesi, AMATEM Birimi, Bursa, Turkey<br />
2On Sekiz Mart ÜTF Psikiyatri AD, Çanakkale, Turkey<br />
E-mail: ozyilsarikaya@yahoo.com<br />
Objective: Kleptomania is an impulse control disorder, which is characterized by one’s uninterrupted impulse of stealing objects<br />
that needed neither for use nor for value, in a repetitive uncontrollable manner (1). Studies stated that those with kleptomania are<br />
accompanied by other psychiatric conditions such as mood disorders, other impulse control disorders, or substance abuse and addiction<br />
(2).<br />
For the treatment, selective serotonin reuptake inhibitors, mood stabilizers, and opioid receptor antogonists have been shown to be<br />
effective. In recent years, treatment for pathological gambling and trichotillomania as other impulse control disorders in which naltrexone<br />
and bupropion were studied for effective treatment of pathological gambling and trichotillomania, bupropion has been found to be as<br />
effective as naltrexone (3-4).<br />
S182 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
The effectiveness of bupropion for treatment of kleptomania, which is classified as an impulse control disorder, is discussed on two cases<br />
in this report.<br />
Case 1: A 34 year-old married, women, graduated from high school presented with fatique, stress, lack of motivation, and complaints of<br />
staying in house, which lasted for the last two months in March, 2011. She had been stealing objects which were not important for her<br />
or she didn’t need for a year. She stated that she felt joy during kleptomanic behaviour and later felt guilty and depressed and she could<br />
not leave the house.<br />
She had substance abuse history and had been treated for major depression.<br />
SCID-I revealed she had major depressive disorder recurring type and kleptomania.<br />
For treatment, bupropion was given 150 mg/day initially, then increased to 300 mg/day. The depressive symptoms were apperently<br />
reduced in 8th week of the treatment. In 12th week, psychiatric examination revealed that functionalty, stealing impulse, and behaviour<br />
healed clearly.<br />
Case 2: A 25 year-old single,women, graduated from high school presented with hypersomnia, eating too much, lying, suicide thoughts,<br />
and stealing things that she didn’t need. Kleptomanic behaviour had begun one year ago.<br />
She was told to be overweight when she was 8 year-old and tried to commit suicide when she was attending to secondary school. She<br />
had been shopping compulsively for 3-4 years.<br />
SCID-I revealed that she had major depressive disorder recurring type and kleptomania.<br />
Bupropion 150 mg/day was started initially, then 300 mg/day was given for treatment. The depressive symptoms were reduced markedly<br />
in the 10th week of the treatment. Desire and impulses to steal, hyperphagia, and suicide thoughts were found to be treated.<br />
Discussion: There are studies (3-4) showed bupropion to be effective for treatment of pathological gambling and trichotillomania, both<br />
of which are impulse control disorders. We investigated the effectiveness of bupropion treatment in two cases, who had kleptomania<br />
and co-existing mood disorder. To our knowledge this is the first case report bupropion is used for kleptomania treatment. Larger and<br />
controlled studies on kleptomania would make it possible to understand the pharmacotherapy and etiology of this disorder better.<br />
References:<br />
1. Hocaoğlu Ç, Kandemir G. The use of SSRI (Selective Serotonin Reuptake Inhibitors) in kleptomania’s treatment: case reports. Bulletin of Clinical Psychopharmacology<br />
2004;14:204-8.<br />
2. Bayle FJ, Caci H, Millet B, Richa S, Olie JP. Psychopathology and comorbidity of psychiatric disorders in patients with kleptomania. Am J Psychiatry 2003;160(8):1509-13.<br />
3. Bhanji NH, Margolese HC. Alternative pharmacotherapy for trichotillomania: a report of successful bupropion use. J Clin Psychiatry 2004;65(9):1283.<br />
4. Dannon PN, Lowengrub K, Musin E, Gonopolski Y, Kotler M. Sustained-release bupropion versus naltrexone in the treatment of pathological gambling: a<br />
preliminary blind-rater study. J Clin Psychopharmacol 2005; 25(6):593-6.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S182-3<br />
[PP-101] Ref. No: 251<br />
A randomized, double-blind, placebo-controlled trial of celecoxib augmentation of<br />
sertraline in the treatment of a drug-naïve women with major depression<br />
Farshad Hashemian 1 , Marzieh Majd 1 , Seyed Mohammad Hosseini 2 , Ali Sharifi 1 , Maryam Vahdat Shariat Panahi 3 , Ofogh Bigdeli 1<br />
1 Department of Clinical Pharmacy, Islamic Azad University, Pharmaceutical Sciences Branch, Tehran, Iran<br />
2 Department of Psychiatry, Hamedan University of Medical Sciences, Hamedan, Iran<br />
3 Islamic Azad University, Tehran Medical Branch, Iran<br />
E-mail: majd.marzie@gmail.com<br />
Objectives: A growing body of evidence strongly suggests that inflammatory process and immune responses are involved in the<br />
pathophysiology of depression. While depression itself is considered a heterogeneous disorder, the involvement of immune system<br />
further complicates the matter.<br />
Meanwhile, several antidepressant medications (e.g. fluoxetine) have been reported to exert immunomodulatory properties, which may<br />
affect human immune system and may partly contribute to their efficacy. Moreover, it must be noted that immune response/system<br />
profoundly varies between the genders due to differences in sex hormones. However, there have been no controlled studies investigating<br />
the benefits of celecoxib augmentation therapy in treatment-naïve women with depression.<br />
To increase the homogeneity of the study population, the present study was designed to examine the antidepressant effects of celecoxib<br />
augmentation of sertraline in the treatment of female drug-naïve patients with depression for 8 weeks.<br />
Methods: Forty female patients diagnosed with first episode of major depression according to DSM-IV-TR criteria were recruited for this<br />
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study. The inclusion criteria were: 1. First episode of major depression, 2. Female gender, 3. Antidepressant-naïve, 4. Age between 18 and<br />
50 years, and 5. Hamilton depression rating scale (17 items) score ranging from 18 to 36. The patients with history of other psychiatric<br />
disorders, significant suicidal ideation, liver and kidney dysfunction, and cardiovascular disorders were excluded. The patients were<br />
randomly assigned into two equal groups receiving either sertraline 50-100 mg/day plus celecoxib 100 mg twice daily or sertraline 50-100<br />
mg/day plus placebo twice daily. The participants were assessed by Hamilton depression and anxiety rating scale at baseline, and 4th and<br />
8th weeks of the treatment. The data were analyzed by Mann-Whitney U test and Fisher’s exact test. The trial was registered in Iranian<br />
Registry of Clinical Trials (IRCT registration number: IRCT201009043106N3). This study was approved by Azad University Pharmaceutical<br />
Sciences Ethics Committee (No: 4114).<br />
Results: No significant differences were observed between two groups regarding demographicals characteristics and the Hamilton<br />
depression score at baseline. The mean Hamilton depression score decreased from 26.14 (SD=5.51) at baseline to 12.42 (SD=5) at 4th<br />
week and from 26.22 (SD=5.38) at baseline to 17.33 (SD=5.24) at 4th week in the celecoxib and placebo groups, respectively. Celecoxib<br />
group showed significantly greater decrease in Hamilton scores compared to placebo (P< 0.05) at the end of week 4. The mean decrease<br />
in Hamilton score was greater in the treatment group compared to placebo over 8 weeks, although it was not statistically significant. In<br />
addition, remission rate (HamD scores
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
[PP-103] Ref. No: 298<br />
Adult primary enuresis nocturna: A case report<br />
Yücel Yılmaz, Ömer Yanartaş, İshak Saygılı, Aytül Gürsü Hariri<br />
Erenkoy Mental Health Training And Research Hospital, Istanbul, Turkey<br />
E-mail: yilmazyucel@live.com<br />
Introduction: Nocturnal enuresis (bed-wetting) is a hereditary, medical condition, which effects both children and adults (1). Beside this<br />
there is few studies on pevalance of enuresis nocturna (EN) among adults. EN cases are seldomly reported. Although most of the patients<br />
recover spontaneusly from EN, in the resistant cases illness persist through adulthood (2). The patients who have frequent bed-wetting in<br />
their childhood have greater risk for persistence of symptoms (3).<br />
Case: A 29-year-old single, male patient does not work. The patient has been suffering from bed-wetting at nights, 2-3 times per week<br />
since his early childhood. He reports that he never had a long period free from bed-wetting at nights. He was suffering from bedwetting<br />
only at nights and never had daytime wetting. The patient reported that bedwetting becomes more frequent when he was under stress or<br />
felt unhappy about something and decreased in frequency when he felt less stressed out. While his military service, for a short period his<br />
symptoms had stopped when his millitary service was over his symptom has started again. In last six months, after he has suffered from<br />
thoughts of worthlessness, relationship issues with his father, and some economic problems his bed-wetting frequency increased. After<br />
his first application to the Erenkoy Mental Health Training And Research Hospital outpatient clinic, a consultation with a neurologist and a<br />
urologist was planned. He had been examined separately by a urologist, a neurologist and a psychiatrist. Several investigations had been<br />
performed in which they could not detect any organic disease. These investigations included urine analysis, abdominal USG, cranial MRI,<br />
and EEG. According to the results of these investigations, organic etiology was ruled out and 25 mg/day imipramine had been commenced.<br />
Later we increased imipramine dosage to 50 mg/day and added behavioral homework to the treatment. In his familiy history, there were<br />
similar symptoms in his brother wich had persisted until age 15th, and in his cousin which had persisted until he turned to 19 years old. The<br />
treatment response of the patient was good; his compliance with pharmacological treatment and behavioral therapy techniques was good.<br />
Discussion: Our case, according to DSM-IV-TR diagnostic criteria, was fulfilling the criteria for enuresis nocturna and major depressive<br />
disorder on axis I. His problems about his functionality and his relationship with his father have caused an increase in his depressive<br />
symptoms and his bed-wetting. We think that patient’s good response to treatment is related to his high motivation in his first psychiatric<br />
application and his compliance with behavioral threapy. It is compatible with literature data that the relatives of the patient have similar<br />
symptoms.<br />
Key words: Enuresis nocturna, imipramine, behavioral therapy<br />
References:<br />
1. Yaluğ İ, Ünsalan N, Özten E, Öztep Kuruoğlu S, Tufan AE. Erişkinde ikincil enürezis nokturna: Bir olgu sunumu. Anadolu Psikiyatri Dergisi 2006; 7:185-190<br />
2. Burgu B, Gokce MI, Gucuk A, Soygur T. Prospective evaluation of factors affecting the response and relapse rates to desmopressin therapy in male monosymptomatic<br />
enuretic adults. Urology 2009; 74: 915–919<br />
3. Yeung CK, Sihoe JD, Sit FK, Bower W, Sreedhar B, Lau J. Characteristics of primary nocturnal enuresis in adults: an epidemiological study. BJU Int 2004; 341-345<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S185<br />
[PP-104] Ref. No: 311<br />
Major depressive disorder and the 5-HTTLPR in Spanish and Mexican populations<br />
Pedro Dorado 1 , Hugo Trejo 2 , Elisa Alonso 2 , Eva Peñas Lledó 1 , Adrián Llerena 1 , Marisol López 3<br />
1Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain<br />
2National Institute of Neurology and Neurosurgery Manuel Velasco Suárez. Mexico City, Mexico<br />
3Metropolitan Autonomous University-Campus Xochimilco, Mexico City, Mexico<br />
4Co-Principal Investigators<br />
E-mail: allerena@unex.es<br />
Preliminary evidence of an increased risk of suffering from MDD for individuals carrying the 5HTTLPR S allele was described in 70 Spanish<br />
patients [1].<br />
The present study aimed to analyze the potential relevance of the 5-HTTLPR genotypes and the risk of suffering from MDD in Mexicans<br />
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and Spaniards.<br />
One hundred and twenty-two (70 previously analyzed) white Spanish and 101 Mexican Mestizo patients with a diagnosis of MDD (DSM-<br />
IV) were studied. Additionally, 327 Spaniards and 153 Mexican Mestizo healthy volunteers were also studied by a previously reported PCR<br />
method [1]. Genotypes and allele frequencies were compared between MDD patients and HVs by two-tailed Fisher’s test.<br />
The frequencies of 5HTTLPR LL, LS and SS genotypes in the Spanish population (MDD vs. HV) were 19.7 vs. 28.8%, 54.9 vs. 50.5% and 25.4<br />
vs. 19.9 %. In the Mexican Mestizo population the frequencies in the MDD vs. HV groups were 14.9 vs. 18.3%, 49.5 vs. 55.6%, and 35.6 vs.<br />
26.1% for 5HTTLPR LL, LS, and SS genotypes, respectively. The frequencies of 5-HTTLPR genotypes of the four groups (MDD and HV from<br />
Spain and Mexico) corresponded to those predicted by the Hardy–Weinberg law.<br />
The odds ratio associated with the 5-HTTLPR-S allele were 1.72 (95% CI: 1.04-2.85) and 1.28 (95% CI: 0.64-2.55) for the MDD in comparison<br />
with the HV group in Spaniards and Mexicans, respectively.<br />
The frequency of S was higher than the frequency of L allele in both MDD groups. In the Spanish population, the S allele was significantly<br />
higher (p
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
Present data support CYP2C9 and CYP2C19 genotyping prior to phenytoin treatment in order to prevent adverse events. Consistently, for<br />
patients carrying CYP2C9 and CYP2C19 defective alleles, valproate instead of phenytoin should be recommended to treat SE.<br />
Grant: The study has been partly supported by the Institute of Health Carlos III-FIS and the European Union (FEDER) Grants, PI10/02010<br />
and CP06/00030 (P Dorado) and from PRIS Extremadura, Consejería de Sanidad y Dependencia, FundeSalud PRIS10043. This study was<br />
coordinated in the networks CIBERSAM and CAIBER, which are initiatives of ISCIII (Spain).<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S186-7<br />
[PP-106] Ref. No: 314<br />
Influence of CYP2D6 genetic polymorphism on fluoxetine and amitriptyline<br />
clinical response<br />
M. López 1 , E. Peñas Lledó 2 , H. Trejo 1 , P. Dorado 2 , J. Guerrero 2 , M. E. Alonso 3 , A. Llerena 2<br />
1Metropolitan Autonomous University-Campus Xochimilco, Mexico City, Mexico.<br />
2Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain<br />
3National Institute of Neurology and Neurosurgery Manuel Velasco Suárez. Mexico City, Mexico<br />
E-mail: allerena@unex.es<br />
Cytochrome P450 2D6 (CYP2D6) is involved in the metabolism of many antidepressants. It is characterized by a high individual variability<br />
in catalytic activity mainly due to >75 CYP2D6 alleles that determine metabolizer status. The role of CYP2D6 genetic polymorphism in<br />
the metabolism of amitriptyline and fluoxetine was previously demonstrated [LLerena et al, 2004]. Herein, we analyzed the relevance<br />
of CYP2D6 genetic polymorphism for the clinical response to the antidepressant drugs fluoxetine and amitriptyline. Sixty-five patients<br />
(DSM-IV) diagnosed with major depression and a score equal or greater than 17 on the Hamilton-Depression (HAM-D) were prospectively<br />
studied. They were treated either with fluoxetine or amitriptyline under antidepressant monotherapy. The informed written consent was<br />
obtained from all patients. Clinical Response was evaluated with HAM-D. The patients were evaluated every month. A two months period<br />
evaluation is reported here. The patients with a 50% decrease on HAM-D were considered as “responders.” CYP2D6 genotyping was<br />
assayed by PCR-RFLP and RT-PCR. The first month evaluation showed that 49 out of the initial 65 remained (16 dropped-out) in the study<br />
and second month evaluation showed that 41 patients remained (8 more dropped-out). Among responders there were 56.6% and 60% to<br />
fluoxetine, and 50% and 70% to amitriptyline, at first and second follow up evaluations, respectively. The responders were characterized<br />
by presenting one or two CYP2D6 active genes. Furthermore, the number of active genes was related to better clinical response in both<br />
drugs. The percentage of responders was higher for those with two active genes than for patients carrying just one: (a) fluoxetine, 81 %<br />
vs.18 % at first month; 87% vs. 13% at second month; (b) amitriptyline, 60 % vs.40 % at first month; 83% vs. 17% at second month. All<br />
ultrarapid metabolizers (n=3 UMs; those with more than two CYP2D6 active genes) were found to drop out during the first month. The<br />
only poor metabolizer patient in the study (PM; with none CYP2D6 active genes) was found among “non-responders” in both follow-up<br />
evaluations. The number of CYP2D6 active genes seems to be related to clinical response to the antidepressant drugs amitriptyline or<br />
fluoxetine. Among responders, the frequency of patients carrying two CYP2D6 active genes is higher than those with one copy. Moreover,<br />
UMs and PMs were not found in this group.<br />
Grants: Supported by grants from the Spanish Ministry of Health Instituto de Salud Carlos III and EU-FEDER PI10/02758, CP06/00030 (PD);<br />
AEXCID (9IA006) Junta de Extremadura and EU-FEDER (BS10023) and Consejo Nacional de Ciencia y Tecnología de México (Nº 59366). This<br />
work was coordinated by Network Red Iberoamericana de Farmacogenética y Farmacogenómica (CYTED206RT0290).<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S187<br />
[PP-107] Ref. No: 137<br />
Evaluation of insight and functional recovery in patients with schizophrenia<br />
Aykut Karahan, Ahmet Tiryaki, Baykal İskender, Evrim Özkorumak<br />
Karadeniz Teknik Üniversitesi, Tıp Fakültesi, Psikiyatri Ana Bilim Dalı, Trabzon, Turkey<br />
E-mail: baykal.iskender@gmail.com<br />
Objective: Despite the fact that functional remission is the most important goal for the treatment of schizophrenia, standard definitions<br />
have not yet been made due to differences in measurement methods, the variability in the course of the disease, cognitive levels of the<br />
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Poster Presentations<br />
patients, and psycho-social factors. Nevertheless, there exists an accumulation of knowledge regarding factors, which influence functional<br />
remission. Insight levels of patients influence their level of functionality, while causing problems in treatment adherence and social<br />
adaptation. The purpose of this study was to examine the factors which influence schizophrenia patients’ levels of insight and functional<br />
remission.<br />
Methods: In this cross-sectional descriptive study, 70 outpatients between the ages of 18-65, who applied to the Karadeniz Technical<br />
University, Psychiatry Clinic and were diagnosed with schizophrenia according to DSM-IV, were evaluated. The patients who reported they<br />
agree to take part in the study by signing the consent form were included in the study. The patients who had a history of traumatic brain<br />
injury and/or any disease which affects the central nervous system, whose Clinical Global Impression (CGI) disease severity low score was<br />
above four, who were taken as inpatients to the hospital in the last two months or whose treatment was changed were excluded from<br />
the study. The patients were evaluated by using respectively socio-demographic data collection form, clinical interview structured for<br />
DSM (SCID-I), the Positive and Negative Syndrome Scale (PANSS), Calgary Depression Scale (CDS), the Functional Remission of General<br />
Schizophrenia Scale (FROGS), Schedule for Assessing the Three Components of Insight (SAI-E), and cognitive test battery.<br />
Results: Insight levels of the patients determined through the SAI-E, were found to be highly correlated with the PANSS positive, negative,<br />
and general psychopathology, Stroop Test, Controlled Word Association Test (FAS), and Trail Making Test A-B scores. In the regression<br />
analysis, PANSS total score, Stroop Test, and FAS scores were the predictors of insight.The FROGS functional levels of patients were found<br />
to be related with occupational status, sex, age of onset of illness, comorbid psychiatric illness, PANSS positive, negative, and general<br />
psychopathology, CDS, SAI-E, FAS, Trail Making Test, Stroop Test, and Wisconsin Card Sorting Test. In the regression analysis, occupational<br />
status, comorbid obsessive compulsive disorder, PANNS negative and general psychopathology, and FAS scores were the predictors of<br />
patients functional status.<br />
Conclusion: Although insight levels of patients are basically related to cognitive functions, it has been reported in previous studies that<br />
clinical symptoms can cause changes in the levels of insight depending on the course of the disease. The relationship between insight<br />
and depression can vary depending on the severity of the depression, patients’ defense mechanisms, and internalized stigma levels. The<br />
effects of clinical symptoms of schizophrenia, levels of cognitive function, and levels of insight and employment status on the patients’<br />
functionality levels are prominent.<br />
Key words: Schizophrenia, functional remission, insight, cognitive functions<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S187-8<br />
[PP-108] Ref. No: 205<br />
Comparison of superoxide dismutase, glutathione peroxidase, and adenosine<br />
deaminase activities between respiratory and nocturnal subtypes of patients with panic disorder<br />
Osman Özdemir 1 , Yavuz Selvi 1 , Halil Özkol 2 , Yasin Tülüce 2 , Lutfullah Beşiroğlu 1<br />
1 Department of Psychiatry,Yuzuncu Yil University, Van, Turkey<br />
2 Department of Medical Biology, Yuzuncu Yil University, Van, Turkey<br />
E-mail: drosmanozdemir@yahoo.com<br />
Background: Panic Disorder (PD) is a heterogeneous disease and panic attacks are divided according to the different symptom clusters as<br />
respiratory, nocturnal, nonfearful, cognitive, and vestibular subtypes. Oxidative stress (OS) is produced by free radicals which are named as<br />
reactive oxygen species (ROS). They can be evaluated indirectly by measurement of some antioxidant enzyme levels such as superoxide<br />
dismutase (SOD), catalase (CAT), or glutathione peroxidase (GSH-Px). PD is known to be associated with a high frequency of comorbid<br />
immunological and increased expression of T lymphocytes compared to controls. Adenosine deaminase (ADA) has been accepted as an<br />
important enzyme in the maturation and function of T lymphocytes. The aetiology of panic disorder is yet to be fully understood. There<br />
is mounting evidence indicating that ROS may have an important role in the pathogenesis of PD.<br />
Objective: In the present study we aimed to compare SOD, GSH-Px, and ADA activities in panic disorder patients with/without nocturnal,<br />
respiratory subytypes, and healthy subjects. Thus to evaluate the effects of OS and inflammatory process on pathogenesis of PD and to<br />
determine biological parameters in the subtypes of PD.<br />
Methods: The study comprised of 60 patients with PD and 30 healthy control subjects. Panic Attack Symptom Checklist (PASC), Panic and<br />
Agoraphobia Scale (PAS), Hamilton Depression Rating Scale (HAM-D), and Hamilton Anxiety Rating Scale (HAM-A) were administered to the<br />
patients. A nocturnal panic attack is defined as an abrupt waking from sleep in a state of panic attack. The respiratory subtype is four of the<br />
following five symptom criteria during an individual’s most recent severe panic attack: Feeling of choking or smothering sensations; shortness<br />
of breath; chest pain or discomfort; numbness or tingling sensations; and fear of dying. The nonrespiratory subtype is operationalized as that<br />
which does not meet the mentioned symptom criteria. The biochemical analyses were made after all the blood samples were collected. The<br />
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Poster Presentations<br />
laboratory analyses of investigation were conducted in Department of Medical Biology, Faculty of Medicine, at the University of Yuzuncu Yil.<br />
Results: We found that SOD and GSH-Px blood activities of patients were significantly lower, and ADA activities of patients were higher<br />
than the healthy controls. All of the activities were not significantly different between respiratory and nocturnal subtypes. There were<br />
no significant relationships between the duration of illness and Panic-Agoraphobia (PAS) scores of patients with nocturnal subtypes.<br />
Hamilton Depression Rating Scale (HAM-D) and Hamilton Anxiety Rating Scale (HAM-A) scores of the patients with nocturnal subtype<br />
were significantly higher than the patients without nocturnal subtype. When examining the correlations between these variables and<br />
enzyme levels, there was only a positive correlation between duration of disease and serum activities of GSH-Px.<br />
Conclusion: In conclusion, SOD and GSH-Px ADA activities of the patients with PD are different from healthy subjects. Our results suggest<br />
that oxidative and inflammatory processes may play role in pathophysiology of PD. These findings may support the idea that both<br />
nocturnal and respiratory subtypes of PD have different symptom clusters of the same disease.<br />
Key words: Panic disorder, subtypes, oxidative stress<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):188-9<br />
[PP-109] Ref. No: 106<br />
The neural and cognitive effects of Bacopa Monniera: An fMRI study<br />
Chris Neale 1 , Andrew Scholey 1 , Matthew Hughes 1 , Patrick Johnston 2<br />
1 Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University of Technology, Melbourne, Australia<br />
2 Department of Psychology, University of York, York, England<br />
E-mail: chrisneale@swin.edu.au<br />
Objectives: Bacopa Monniera is an ayurvedic herbal medicine used in Indian medicine as a memory tonic. Animal models have shown<br />
that it is an antioxidant (1), a memory enhancer (2), and an antidepressant (3). Human trials have had variable results, but spatial memory,<br />
attention, and information processing tasks seem to be affected by Bacopa.<br />
Given the improvements shown the RVIP task as a result of a 12 week Bacopa intervention, an fMRI methodology was employed to see<br />
how Bacopa affects the brain during this task. The improved performance in these tasks suggests Bacopa may modulate task specific brain<br />
regions. This investigation looks at the effects of Bacopa on the BOLD signal in the RVIP task over a 90 day intervention.<br />
Method: The study utilized a double blind, placebo controlled, crossover design where all participants completed a 90 day course of<br />
both Bacopa (300mg daily) and placebo during the study. The participants were aged between 40 and 65 years and in good health.<br />
Interventions were separated by a 120 day washout period. Scans were undertaken on a 3T Siemens TRIO magnet before and after each<br />
90 day intervention where participants would complete two runs of the task per scan visit.<br />
The RVIP task is a block design which requires participants to respond when they see three odd or even numbers in a stream of numbers<br />
presented at 100/minute. The control block requires a response when a zero is seen in the stream of numbers. Blocks last for 1 minute and<br />
are repeated 3 times per condition in each of two experimental runs per scan.<br />
Results: Data collection is ongoing at present. Baseline data show a bilateral increase in BOLD activation in the precentral gyrus and<br />
precuneus with activation extending to the left inferior frontal gyrus (n=7, p=.005) when compared with control using a task greater than<br />
baseline mask. Behavioural data suggest fewer ‘hits’ in the active task compared to control task.<br />
Conclusions: The methodology of the study sets a gold standard for clinical trials using nutraceuticals and fMRI. Given the ongoing nature<br />
of the study, conclusions are merely speculative at this point. However, the task looks to be a sensitive reflection of sustained attention.<br />
We anticipate that the 90 day intervention of Bacopa will affect the BOLD signal in these particular regions of interest.<br />
Key words: Bacopa monniera, fMRI, nutraceuticals, human cognition<br />
References:<br />
1. Bhattacharya et al (2000) Antioxidant Activity of Bacopa Monniera in Rat Frontal Cortex, Striatum and Hippocampus. Phytotherapy Research, 14, 174 – 179<br />
2. Hota et al (2009) Bacopa monniera leaf extract ameliorates hypobaric hypoxia induced spatial memory impairment. Neurobiology of Disease, 34 (1) 23-39<br />
3. Sairam et al (2001) Prophylactic and curative effects of Bacopa monniera in gastric ulcer models. Phytomedicine, 8 (6) 423-430<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S189<br />
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[PP-110] Ref. No: 98<br />
Methlyphenidate induced thrombocytopenia in a pediatric patient with<br />
ADHD and stuttering<br />
Serdal Özdemir, Fatma Ayık Özdemir<br />
İnönü Üniversitesi Tıp Fakültesi Turgut Özal Tıp Merkezi Psikiyatri AD, Malatya, Turkey<br />
E-mail: serdoktor@yahoo.com<br />
Stuttering and attention deficit hyperactivity disorder (ADHD) can be seen together. Anemia or thrombocytopenia, rarely even pancytopenia<br />
may occur as a side effect of medications used to treat both disorders. Thrombocytopenia, although it may be seen in some cases using<br />
methylphenidate, occurs rarely. An 8 year-old boy was brought to our outpatient clinic by his family with the complaints of stuttering, attention<br />
deficit, and hyperactivity. After the psychiatric evaluation and history were conducted and psychometric tests were applied. One month later<br />
methylphenidate 18mg/day was started for the treatment of ADHD. Soon after initiation of medication, petechia developed on both lower<br />
extremities of the patient. CBC showed isolated thrombocytopenia and te patient was followed by hematology clinic. On the 6th day upon<br />
stopping mehtlyphenidate, the thrombocyte count returned to normal. We also discussed possible mechanisms of thrombocytopenia.<br />
Key words: Isolated thrombocytopenia, petechia, methylphenidate<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S190<br />
[PP-111] Ref. No: 245<br />
Use of mirtazapine and olanzapine in treatment of major depressive disorder with<br />
psychotic features developed during pregnancy: A case report<br />
Mustafa Güleç 1 , Yavuz Selvi 2 , Ünsal Aydınoğlu 1<br />
1 Atatürk Üniversitesi Tıp Fakültesi, Psikiyatri Anabilim Dalı, Erzurum, Turkey<br />
2 Yüzüncü Yıl Üniversitesi Tıp Fakültesi, Psikiyatri Anabilim Dalı, Van, Turkey<br />
E-mail: mustafagulec78@yahoo.com<br />
Objctive: To contribute to the of treatment of major depressive disorder with psychotic features developing during pregnancy<br />
Case: A 25 year-old, married, female patient was 13 weeks pregnant and diagnosed with major depressive disorder (MDD) with psychotic<br />
features. She was a housewife with primary school degree and was admitted to inpatient unit. The obstetrician did not find any fetal<br />
anomalies. The patient was put on mirtazapine and olanzapine, doses of which ranged between 15-30mg/day and 5-10 mg/day,<br />
respectively during her two months hospitalization. In her follow up, 15 days after discharge, olanzapine dose was decreased to 5 mg/day,<br />
but mirtazapine was continued at 30mg/day until delivery. To decrease neural tube defect risk folic acid 5mg/day was prescribed during<br />
the treatment, as well. She gave birth to a live and healthy baby on the expected due date during her outpatient treatment.<br />
The information regarding the safety of use of mirtazapine and olanzapine during pregnancy primarily rely on case reports. While<br />
there were no fetal abnormalities in majority of cases regarding olanzapine use (1,2), there are some reports including hip dysplesia (3),<br />
meningocele ve ankyloblepharon (4), atrioventricular channel defect and unilateral pes equinovarus (5). However, more cases and studies<br />
are needed to explore, whether these cases were coincidental or due to teratogenic effects of olanzapine. Currently available publications<br />
(6,7,8,9) report that major malformation risk in general population does not increase with the use of mirtazapine during pregnancy. The<br />
reports from our country are parallel to the reports in the literature (10,11).<br />
Results: Even in majority of cases no fetal abnormalities were reported regarding olanzapine use during pregnancy, large case series are<br />
needed to have more evidence for stronger judgments. Also even mirtazapine does not look like a teratogenic agent, is should be used<br />
with caution during pregnancy and babies that are exposed to mirtazapine should be followed closely.<br />
Key words: Depression, pregnancy, safety, mirtazapine, olanzapine, teratogenicity<br />
References:<br />
1. Littrell KH, Johnson CG, Peabody CD, Hilligoss N. Antipsychotics during pregnancy. Am J Psychiatry 2000; 157(8):1342<br />
2. Mendhekar DN, War L, Sharma JB, Jiloha RC. Olanzapine and pregnancy. Pharmacopsychiatry 2002; 35(3):122-123<br />
3. Spyropoulou AC, Zervas IM, Soldatos CR. Hip dysplasia following a case of olanzapine exposed pregnancy: a questionable association. Arch Womens Ment Health<br />
2006; 9(4):219-222<br />
4. Arora M, Praharaj SK. Meningocele and ankyloblepharon following in utero exposure to olanzapine. Eur Psychiatr 2006; 21(5):345-356<br />
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Poster Presentations<br />
5. Yeshayahu Y. The use of olanzapine in pregnancy and congenital cardiac and musculoskeletal abnormalities. Am J Psychiatry 2007; 164(11):1759-1760<br />
6. Lennestål R, Källén B. Delivery outcome in relation to maternal use of some recently introduced antidepressants. J Clin Psychopharmacol 2007; 27(6):607-613<br />
7. Way CM. Safety of newer antidepressants in pregnancy. Pharmacotherapy 2007; 27(4):546-552<br />
8. Djulus J, Koren G, Einarson TR, Wilton L, Shakir S, Diav-Citrin O, et al. Exposure to mirtazapine during pregnancy: a prospective, comparative study of birth<br />
outcomes. J Clin Psychiatry 2006; 67(8):1280-1284<br />
9. Einarson TR, Einarson A. Newer antidepressants in pregnancy and rates of major malformations: a meta-analysis of prospective comparative studies.<br />
Pharmacoepidemiol Drug Saf 2005; 14(12):823-827<br />
10. Yaris F, Kadioglu M, Kesim M, Ulku C, Yaris E, Kalyoncu NI, et al. Newer antidepressants in pregnancy: prospective outcome of a case series. Reprod Toxicol 2004;<br />
19(2):235-328<br />
11. Guclu S, Gol M, Dogan E, Saygili U. Mirtazapine use in resistant hyperemesis gravidarum: report of three cases and review of the literature. Arch Gynecol Obstet<br />
2005; 272(4):298-300<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S190-1<br />
[PP-112] Ref. No: 253<br />
Effects of group musical therapy on inpatients with schizophrenia: A preliminary study<br />
Selma Bozkurt Zincir 1 , Ümit Başar Semiz 1 , Aynil Yenel 1 , Emel Başoğlu 1 , Mustafa Bilici 1 , Cumhur Tulay 2<br />
1 Erenköy Mental Health Training and Research Hospital, İstanbul, Turkey<br />
2 Science, Culture, and Art Society (BIKSAD)<br />
E-mail: sbozkurtzincir@yahoo.com<br />
Background: Since ancient times, music has been used as a therapy method and has been considered to have some good effects on<br />
the human body and mental health (1, 2, 5). Music might have beneficial effects on human life such as physiological functions, quality of<br />
life, and psychosocial functioning. There is a wide acceptance about musical therapy practices for various disorders. This generalization<br />
may mean that schizophrenia patients could have some benefits from musical therapy, too (1- 3). There is not enough scientific evidence<br />
emphasizing the efficacy of musical therapy which is applied to severe mental disorders and has recovery potential for some deficits (2, 4).<br />
Objectives: The first aim of this study was to examine the feasibility of music therapy for inpatients with schizophrenia, who need acute<br />
care and also to explore its effects on mental health, general psychosocial functioning, and satisfaction with patient care.<br />
Method: Forty-five patients with schizophrenia were randomly assigned to a study group (n=15) and a control (n=30) group in a ward for female<br />
schizophrenia inpatients. Both groups received medication and standard care for their disorder. Additionally, the study group underwent group<br />
music therapy with classical Turkish music tones for twelve sessions over four weeks. The assessment included measures of psychotic symptoms<br />
using the Positive and Negative Syndrome Scale (PANSS), the Brief Psychiatric Rating Scale (BPRS), and quality of life and subjective satisfaction<br />
with musical experiences. All of the measurement tools were applied before the randomization and weekly until the study was completed.<br />
Results: This study demonstrated that music therapy for schizophrenia inpatients, who need acute care because of psychotic excitation,<br />
is feasible. The comparison of the groups also showed that music therapy has significant advantages on improvement of interpersonal<br />
relationships and general psychosocial functioning.<br />
Conclusions: This study is the first musical group therapy trial with classical Turkish music tones in schizophrenic patients. Musical activity<br />
diminishes negative symptoms, reduces social isolation, and improves patients’ abilities to adapt to the social environment in the community after<br />
discharge from the hospital. Therefore, music therapy may increase the therapeutic alliance of schizophrenic patients in the long term.<br />
Key words: Music therapy, schizophrenia, inpatient, quality of life<br />
References:<br />
1. Altınölçek H. Türklerde psikiyatrik hastaların rehabilitasyonunda müziğin terapötik etkileri. Popüler Psikiyatri Dergisi 2006; 34: 16- 19.<br />
2. Talwar N, Crawford MJ, Maratos A, Nur U, McDermott O, Procter S. Music therapy for inpatients with schizophrenia: Exploratory randomised controlled trial. British<br />
Journal of Psychiatry 2006; 189: 405- 409.<br />
3. Ulrich G, Houtmans T, Gold C. The additional therapeutic effect of group music therapy for schizophrenia patients: A randomised study. Acta Psychiatrica<br />
Scandinavica 2007; 116: 362- 370.<br />
4. Hayashi N, Tanabe Y, Nakagawa S,et al. Effects of group musical therapy on inpatients with chronic psychosis: A controlled study. Psychiatry and Clinical<br />
Neurosciences 2002; 56: 187- 193.<br />
5. Gold C, Heldal TO, Dahle T, Wigram T. Music therapy for schizophrenia or schizophrenia-like illnesses (Review). Cochrane Database of System Reviews. 2005, 2: 1- 20.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S191<br />
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Poster Presentations<br />
[PP-113] Ref. No: 255<br />
Clinical correlations of childhood trauma and dissociation in a sample of female<br />
inpatients diagnosed with schizophrenia spectrum disorders and severe<br />
nonpsychotic disorders: the preliminary data<br />
Selma Bozkurt Zincir, Ümit Başar Semiz, Aysun Demir, Yücel Yılmaz, Sevgi Gül Kabak<br />
Erenköy Mental Health Training and Research Hospital, Istanbul, Turkey<br />
E-mail: sbozkurtzincir@yahoo.com<br />
Background: There is recent increasing interest in the relationship between early childhood trauma and the risk of developing psychotic<br />
experiences later in life (2,3). Although a large number of studies of psychiatric patients, a majority of whom have a psychotic disorder,<br />
indicate that the prevalence of childhood trauma in this group is high, whether childhood trauma is of etiological importance in psychosis<br />
remains controversial (1, 2, 4).<br />
Objectives: In the present study, we aimed to investigate the possibility of a link between psychotic disorders and childhood traumatic<br />
experiences by comparing trauma exposure in a group of female patients with a diagnosis of psychotic disorders to a group diagnosed<br />
with severe non-psychotic disorders. The secondary purpose of this study was to examine the clinical correlations between trauma<br />
exposure, dissociative phenomena, and psychiatric symptomatology and psychosocial functioning for these two groups.<br />
Methods: Patients with psychotic disorders, mostly schizophrenic (n=54), and with a non-psychotic diagnosis (n=24), were recruited<br />
at the Women’s Clinic of the Istanbul Erenköy Mental Health Hospital. The data were collected through a semi-structured interview for<br />
demographic, psychiatric, and trauma histories. Psychotic symptoms were measured by using the Positive and Negative Symptom Scale<br />
(PANSS). At the main interview, the Childhood Traumatic Questionnaire (CTQ), Dissociative Experiences Scale (DES), Traumatic Experiences<br />
Checklist (TEC), and SCL-90-R were administered to all participants by psychiatrists, who were blind to trauma history.<br />
Results: In this preliminary study, high prevalence rates of childhood traumatic experiences and dissociative phenomenon were found in<br />
a sample of consecutively admitted moderately ill psychotic inpatients. Another finding of the present study was that emotional abuse<br />
during childhood was most strongly correlated with the experience of dissociative symptoms in adult schizophrenia patients. Additionally,<br />
in this group a history of trauma was significantly related to somatization, poor communication skills, and depressive symptoms.<br />
Conclusions: The results of this study are consistent with previous studies raising the possibility that such trauma is of etiological<br />
importance in schizophrenia and other related disorders (4-6).<br />
Key words: Childhood trauma, dissociation, psychosis, schizophrenia<br />
References:<br />
1. Schafer I, Harfst T, Aderhold V, Briken P, Lehmann M, Moritz S, Read J, Naber D. Childhood trauma and dissociation in female patients with schizophrenia spectrum<br />
disorders an exploratory study. J Nerv Ment Dis 2006; 194: 135- 138.<br />
2. Spence W, Mulholland C, Lynch G, Mchugh S, Dempster M, Shannon C. Rates of childhood trauma in a sample of patients with schizophrenia as compared with a<br />
sample of patients with non-psychotic diagnosis. Journal of Trauma & Dissociation 2006; 7(3): 7- 22.<br />
3. Lysaker PH, LaRocco VA. The prevalence and correlates of trauma-related symptoms in schizophrenia spectrum disorder. Comprehensive Psychiatry 2008; 49: 330- 334.<br />
4. Larkin W, Read J. Childhood trauma and psychosis: Evidence, pathways, and implications. J Postgrad Med 2008; 54(4): 287- 293.<br />
5. Bendall S, Jackson HJ, Hulbert CA, McGorry PD. Childhood trauma and psychotic disorders: a systematic, critical review of the evidence. Schizophrenia Bulletin 2008; 34(3): 568- 579.<br />
6. Morgan C, Fisher H. Environmental factors in schizophrenia: childhood trauma- a critical review. Schizophrenia Bulletin 2007; 33(1): 3- 10.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S192<br />
[PP-114] Ref. No: 256<br />
Comparison of neurocognitive skills between generalized anxiety disorder<br />
and premenstrual dysphoric disorder patients: A controlled study<br />
Selma Bozkurt Zincir, Aynil Yenel, Selvinaz Çınar Parlak, Gülnihal Şimşek, Arzu Bayrak, Dicle Bilge, Ümit Başar Semiz, Mustafa Bilici<br />
Erenköy Mental Health Training and Research Hospital, Istanbul, Turkey<br />
E-mail: sbozkurtzincir@yahoo.com<br />
Background: Recently, there has been increased interest in the ability of female reproductive hormones to impact psychoneurological<br />
processes involving the interplay of several body systems. This lends reliability to the view of premenstrual dysphoric disorder (PMDD)<br />
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Poster Presentations<br />
as a disorder founded in real biochemical disturbances (1,2). Although the effects of the menstrual cycle on emotional state and<br />
cognitive function have been only recently systematically studied, they have long been recognized. Previously published studies yielded<br />
inconsistent data in terms of cognitive tests throughout the cycle phases (1, 3, 4).<br />
Objective: This study aimed to compare the effects of cyclic reproductive hormonal changes on cognitive, emotional, and behavioral function<br />
in childbearing age female patients with generalized anxiety disorder (GAD) and those with premenstrual dysphoric disorder (PMDD).<br />
Method: One of psychiatric samples was a group of PMDD (n = 42), and the other was a group of GAD patients (n = 36), who had 20 and<br />
higher on the Hamilton Anxiety Scale (HAM-A) score. An age matched healthy control group (n = 40) was also included in the study. The<br />
psychiatric rating scales were applied twice according to the menstrual phases. The frontal assessment battery, Stroop test, and Weschler<br />
verbal memory tests were applied for the evaluation of neurocognitive changes with respect to follicular and late luteal phases.<br />
Results: There was a significant increase in dysphoric mood during the luteal phase in women with PMDD compared to their follicular phase<br />
and compared to the GAD women and the control group. Taken together with the repeated measures and the data analysis, the GAD group<br />
had significantly worse performance regarding overall neurocognitive functions in their luteal phase (particularly memory skills, attention,<br />
and psychomotor function) as compared to the PMDD group, whereas the control group had significantly better performance overall.<br />
Conclusions: Even though neurocognitive impairments seen in the women with PMDD were partly due to the dysphoric mood during<br />
the late luteal phase, it seems to be related to the physiological and psychoneurological processes in which female reproductive<br />
hormones may have a central role.<br />
Key words: Neurocognitive functions, premenstrual dysphoric disorder, generalized anxiety disorder, female reproductive hormones<br />
References:<br />
1. Farage MA, Osborn Thomas W, MacLean AB. Cognitive, sensory, and emotional changes associated with menstrual cycle: a review. Arch Gynecol Obstet. 2008; 278: 299- 307.<br />
2. Reed SC, Levin FR, Evans SM. Changes in mood, cognitive performance and appetite in the late luteal and follicular phases of the menstrual cycle in women with<br />
and without PMDD (Premenstrual Dysphoric Disorder). Horm Behav. 2008; 54: 185- 193.<br />
3. Morgan M, Rapkin A. Cognitive flexibility, reaction time, and attention in women with premenstrual dysphoric disorder. J Gend Specif Med. 2002; 5: 28- 36.<br />
4. Morgan M, Rapkin AJ, D’Elia L, Reading A, Goldman L. Cognitive functioning in premenstrual syndrome. Obstet Gynecol. 1996; 88: 961- 966.<br />
5. Resnick A, Perry W, Parry B, Mostofi N, Udell C. Neuropsychological performance across the menstrual cycle in women with and without premenstrual dysphoric<br />
disorder. Psychiatry Research 1998; 77:147- 158.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S192-3<br />
[PP-115] Ref. No: 259<br />
Evaluation of olfactory function and olfactory bulb volume in major depressive disorder<br />
Meral Akbıyık, Oğuz Karamustafalıoğlu<br />
Şişli Etfal Research and Teaching Hospital, Department of Psychiatry, İstanbul, Turkey<br />
akbiyikmeral@gmail.com<br />
Objective: The purpose of this study was to assess olfactory function and olfactory bulb volume in patients with major depressive<br />
disorder (MDD) in comparison to normal subjects.<br />
Method: Twenty treatment-free premenopausal, 25-45 year-old women diagnosed with long-term, severe MDD at the Şişli Etfal Research<br />
and Teaching Hospital psychiatric outpatient clinics and 20 healthy women matched by age, education, smoking behavior, and frequency<br />
of upper respiratory tract infection participated in this study.<br />
Odor threshold, discrimination, and identification functions were assessed by Sniffin’ sticks. Olfactory bulb volumes were calculated by<br />
manual segmentation of acquired T2-weighted coronal slices according to a standardized protocol.<br />
Results: When OB volumes of patients and controls were analyzed with a two-way Analysis of Covariance, with age and education as the<br />
covariate and group as a factor, the patients had significantly larger OBs than the controls (right p=0.011; left p
Poster Presentations<br />
[PP-116] Ref. No: 261<br />
Fluoxetine induced hypomanic shift in a bulimic patient: A case report<br />
Mustafa Özten, Atila Erol<br />
Department of Psychiatry, Sakarya University, Faculty of Medicine, Sakarya, Turkey<br />
E-mail: drozten@yahoo.com<br />
In the psychopharmacological treatment of bulimia nervosa (BN), antidepressants have a positive effect on mood and reduce the related<br />
preoccupation with body weight and the number of binge eating episodes. Research with antidepressants such as imipramine, desipramine,<br />
trazodone, phenelzine, amitriptyline and mianserin has been conducted to investigate their efficacy in the treatment of bulimia. A higher dose<br />
of the fluoxetine (60 mg/day) was shown to be effective in BN and has received FDA approval. Comorbidity of eating disorders with mood,<br />
anxiety, and substance use disorders is common. The presence of additional psychiatric disorders impairs compliance with treatment and makes<br />
treatment difficult by increasing severity and chronicity. The treatment of bulimia nervosa with fluoxetine is adversely affected by the presence<br />
of a mood disorder. High dose fluoxetine should be used for BN to be effective, but these high doses may increase the risk of a manic shift.<br />
When using fluoxetine in patients with a history of bipolar mood disorder (BiPMD) or a positive family history of BiPMD, clinicians need to be<br />
careful because of the possibility of a manic shift. There is not any developed algorithm for psychopharmacological treatment with comorbidity<br />
of BiPMD and BN; generally the use of agents that have a positive effect on both disorders is recommended, although such a medication is not<br />
available. Negative effects on weight gain or other negative interactions of mood stabilizers in BN, makes it difficult to use them. Like other<br />
antidepressants SSRIs may also cause a manic shift. The use of antidepressant doses of fluoxetine for mood and anxiety disorders are known to<br />
carry a risk for a manic or hypomanic shift. Hence, detailed examination of cases, where there is history of mood disorder or family history of mood<br />
disorder, is recommended. Using high dose fluoxetine in BN also increases the possibility of manic or hypomanic shifts. The use of fluoxetine 60<br />
mg in a patient with BN caused a hypomanic shift, even though there was no history of bipolar disorder or a positive family history. A review of<br />
the treatment demonstrated that 60 mg of fluoxetine did not result in a significant decrease in symptoms and adequate treatment response.<br />
Retrospectively inadequate response to the treatment was associated with the presence of comorbid BiPMD.<br />
Key words: Bulimia nervosa, fluoxetine, hypomania, mania<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S194<br />
[PP-117] Ref. No: 262<br />
Schizophrenia and Mega Cisterna Magna: A case report<br />
Semra Karayılan, Atila Erol<br />
Department of Psychiatry, Sakarya University Faculty of Medicine, Sakarya, Turkey<br />
E-mail: skryln@gmail.com<br />
The cerebellum, which is known in general as an organ to control coordination, balance, and fine motor movements, has been demonstrated<br />
to have an important role in cognitive functions by using anatomical and functional imaging methods. The anomaly of mega cisterna magna<br />
is one of the various lesions of the posterior fossa which can influence cerebellar functions like cerebellar hypoplasia/agenesis, vermis<br />
hypoplasia/agenesis, Dandy-Walker malformation or variant, persistent Blake’s pouch, arachnoid cyst, Joubert syndrome, and tumors of the<br />
posterior fossa. Mega cisterna magna (MCM) is a developmental malformation of the posterior fossa, where morphologically the vermis and<br />
cerebellar hemispheres are intact. Associated structural brain anomalies are common with mega cisterna magna and especially, MCM may<br />
be a component of the Dandy-Walker variant (with cerebellum hypoplasia) or Dandy-Walker syndrome (with cerebellum agenesia). Our<br />
knowledge about the relationship between this anomaly and psychiatric disorders is limited to very few case reports available. In this article,<br />
we report a case of schizophrenia associated with mega cisterna magna. A 35-year-old married patient (house wife, graduated from primary<br />
school) was brought to our clinic by her relatives with complaints of disorganized and inappropriate speech, strange behavior, and fear of<br />
people. She had auditory and visual hallucinations and delusions of reference and persecution. Up to five months ago she had no psychiatric<br />
or neurological symptoms or history. Her symptoms began with social isolation, decrease of self-care, and positive psychotic symptoms.<br />
Neurological examination and EEG examination were normal, but mega cisterna magna was discovered in her cranial magnetic resonance<br />
imaging scan. The patient was treated with risperidone 6mg/day for four weeks and was discharged after remission of psychotic symptoms.<br />
The prevalence and prognostic significance of MCM has not been defined completely yet. Memory and verbal fluency were found to be lower<br />
in cases of mega cisterna magna than in controls. Schizophrenic patients are known to have problems of memory and verbal fluency, too.<br />
The role of the cerebellum in schizophrenia has been highlighted by Andreasen’s hypothesis of ‘cognitive dysmetria’. This hypothesis suggests<br />
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Poster Presentations<br />
that the cerebellum has a role in the general dyscoordination of sensorimotor and mental processes which are seen in schizophrenic patients.<br />
The following observations demonstrating the involvement of the cerebellum are determined in studies of schizophrenic patients: high<br />
prevalence of neurological soft signs, dyscoordination, abnormal posture, balance problems, impaired eye blink conditioning and impaired<br />
adaptation of the vestibular-ocular reflex. Abnormal cerebellar activations have been showed in functional imaging studies. In the context of<br />
this case, the relationship of schizophrenia with cerebellar anomalies was reviewed.<br />
Key words: Schizophrenia, mega cisterna magna, cerebellum, brain imaging methods<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S194-5<br />
[PP-118] Ref. No: 263<br />
Congenital hypogonadism and comorbid anorexia nervosa in a male patient:<br />
A case report<br />
Mustafa Özten, Atila Erol<br />
Department of Psychiatry, Sakarya University, Sakarya, Turkey<br />
E-mail: drozten@yahoo.com<br />
Male hypogonadism results from a failure of the testes to produce adequate androgen. Patients have low circulating testesterone in<br />
combination with clinical symptoms such as osteopenia, increased adiposity, decreased muscle mass, decline in energy and stamina,<br />
decreased cognitive function, decreased libido and erectile dysfunction. The cause may be primary (genetic anomaly) or secondary (defect in<br />
hypothalamus or pituitary), but often presents with the same symptomatology. Hypogonadal patients who are both symptomatic and who<br />
have clinically significant alterations in laboratory values are candidates for treatment. Testosterone replacement therapy is widely applied.<br />
The prevalence of eating disorders in men as compared to women is less than ten times and also shows differences in the course of the<br />
disease and the causes of its appearance. Social, genetic, psychological factors, personality traits and a history of trauma are considered to<br />
play a role in the development of anorexia nervosa (AN). In addition, steroid hormones affect the development of eating disorders and eating<br />
behavior. Homosexuality, asexuality and sexual role disorders are known to be more common in male patients with AN. AN is associated<br />
with notable medical complications and affects many systems like a general medical disease. One of the systems that is affected by AN is<br />
the genitourinary system; hypogonadism is one of the known complications of AN. Endocrine abnormalities such as hypogonadotropic<br />
hypogonadism mediate some of the clinical manifestations. Most of the endocrine changes that occur in AN are physiological adaptations<br />
to starvation and are usually reversible with weight gain. Prolonged AN or cachexia can cause hypogonadism. In this article we report a<br />
man, who had suffered from hypogonadism since infancy with no treatment and developed AN at age 18. Congenital hypogonadism with<br />
comorbid AN is a rare illness. As a result of the interaction of hypogonadism with anorexia nervosa the patient developed a sexual identity<br />
crisis, which is important in its clinical and theoretical aspects, since he suffered from delayed puberty, no secondary sexual characteristics,<br />
and no ejaculation or erection although he was 22 years old. Up to now only one case from Japan is reported in the literature with congenital<br />
hypogonadism and anorexia nervosa. Hypogonadism with comorbid anorexia nervosa has not been listed as a case in the Turkish indices yet.<br />
Key words: Anorexia nervosa, congenital hypogonadism, male patient<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S195<br />
[PP-119] Ref. No: 275<br />
Review of diagnosis and treatment of pregnant psychiatric patients in a state hospital<br />
Kader Semra Karataş, Jülide Güler, Aytül Hariri<br />
Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Psychiatry, İstanbul, Turkey<br />
E-mail: drsemraocak@yahoo.com<br />
Background: Because of the physiological changes during pregnancy there are changes of pharmacokinetic and pharmacodynamic<br />
characteristics, and there are differences in the treatment of psychiatric disorders in this period.<br />
Objective: The aim of this study was to evaluate the sociodemographical features, diagnoses, and treatments of 20 pregnant psychiatric<br />
inpatients that were hospitalized between August 2010 and August 2011.<br />
Method: The sociodemographical features, diagnoses, and treatments of the patients were evaluated retrospectively.<br />
Results: The percentages of diagnoses of the patients were as follows: schizophrenia 27.3%, bipolar affective disorder manic episode<br />
S195
Poster Presentations<br />
22.7%, bipolar affective disorder depressive episode 9.1%, unipolar depression 27.4%, and obsessive compulsive disorder, dissociative<br />
disorder, and schizoaffective disorder, each 4.5%. When the treatments of the patients were evaluated according to their diagnosis<br />
we found that 13.6% of schizophrenia patients were treated with ECT, 9.09% with haloperidol and 4.5% with atypical antipsychotics;<br />
the patients with bipolar depression were treated with mood stabilizers and ECT plus mood stabilizers at the same rate of 4.5%; 18.1%<br />
of the patients with mania were treated with ECT plus haloperidol; and of the unipolar depressed patients 13.6% were treated with<br />
psychotherapy and 9.09% with ECT and haloperidol.<br />
Conclusion: ECT was used commonly as a treatment option in our patient group. ECT treatment was added onto haloperidol treatment<br />
in severe cases. This treatment is consistent with the recommendations of the APA and with those in the literature.<br />
Key words: Pregnancy, mental illness, treatment, ECT, antipsychotic drugs<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S195-6<br />
[PP-120] Ref. No: 278<br />
Peripheral edema associated with mirtazapine: Presentation of a case<br />
Birmay Çam 1 , Hüseyin Kurt 2<br />
1Gönen Devlet Hastanesi Psikiyatri Kliniği, Gönen, Balıkesir, Turkey<br />
2Gönen Devlet Hastanesi İç Hastalıkları Kliniği, Gönen, Balıkesir, Turkey<br />
E-mail: birmaycam@mynet.com<br />
In the medical literature, occurrence of edema during treatment with mirtazapine is stated as the least frequently reported side effect. A<br />
case of edema occurring during mirtazapine treatment is reported below.<br />
Case: A 34 year-old female patient was admitted to the psychiatric ward with a diagnosis of recurrent depressive disorder. There were no specific<br />
findings in the patient’s medical history other than high blood pressure and irregularly administered antihypertensive drugs. There was no use<br />
of alcohol or illicit drugs. The treatment regimen of the patient included escitalopram 5 mg daily, alprazolam 0.5 mg daily, and hydroxyzine 12.5<br />
mg daily. Mirtazapine 15 mg daily was added to the medical treatment, as the depression and insomnia continued. The day after beginning<br />
the treatment with mirtazapine pretibial edema developed. The CBC, ALT, AST, GGT, ALP, bilirubin, albumin, urea, creatinine, Na, K, Cl, Ca, urine<br />
analysis, thyroid function tests and chest X-ray were repeated and all were within normal limits, as before. Cardiac insufficiency, cirrhosis, nephrotic<br />
syndrome, and venous insufficiency, all of which can cause edema, were ruled out by the internal medicine consult. The patient was not in the<br />
premenstrual period and not pregnant. It was also reported that such a side effect was observed during the administration of escitalopram to the<br />
patient. The edema was assessed as being due to mirtazapine. The edema decreased three days after the cessation of the mirtazapine treatment<br />
and the administration of furosemide 40 mg/day at the recommendation of internal medicine. It disappeared ten days later. Escitalopram 10<br />
mg daily and hydroxyzine 25 mg daily were continued. The patient, whose depressive symptoms decreased and anxiety disappeared, has<br />
continued to be followed up as an outpatient after discharge. The patient’s depressive symptoms did not recur and her blood pressure remained<br />
within normal limits although she did not receive any antihypertensive treatment. She had no edema at her two month follow up visit. Her CBC,<br />
electrolytes, biochemical and thyroid function tests, and urine analysis all remained within normal limits.<br />
Discussion: In our case, the occurrence of edema simultaneously with the administration of mirtazapine, the exclusion of systemic<br />
diseases that can cause edema, the lack of continuation or recurrence of the edema even as the patient remained on escitalopram<br />
between the previous and the current depressive episodes, and finally the disappearance of the edema right after the cessation of<br />
mirtazapine treatment made us to think that the edema was caused by mirtazapine. In the medical literature, it is reported that MAOIs,<br />
escitalopram, and sertraline can cause edema. Kutscher et al. reported that peripheral edema occurred in a male patient of 60 years of age<br />
after the use of mirtazapine and disappeared right after the cessation of mirtazapine treatment (1,2,3,4). More detailed studies should be<br />
conducted to explore and understand this issue better.<br />
Key words: Edema, mirtazapine<br />
References:<br />
1. Remick RA,Froeze C,Keller FD(1989)Common side effects associated with monoamine oxidase inhibitors.Prog Neuropsychopharmacol Biol Psychiatry 13:497-504.<br />
2. Masdrakis VG,Oulis P,Kouzoupis AV,Masdrakis GV,Soldatos CR(2009)Bilateral ankle oedema in a patient taking escitalopram.World J Biol Psychiatry 10:939-41.<br />
3. Dadic-Hero E,Ružic K,Grahovac T,Graovac M,Palijan TZ,Sepic-Grahovac D(2011) Allergic reactions--outcome of sertraline and escitalopram treatments.Psychiatr<br />
Danub. Mar;23(1):120-2.<br />
4. Kutscher EC,Lund BC,Hartman BA(2001)Peripheral edema associated with mirtazapine. Ann Pharmacother.35(11):1494-5.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S196<br />
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Poster Presentations<br />
[PP-121] Ref. No: 280<br />
Abuse of tianeptine: A case report<br />
Hüsameddin Özer, Atilla Erol<br />
Sakarya Teaching and Research Hospital, Psychiatry Clinic, Sakarya, Turkey<br />
E-mail: husamozer@mynet.com<br />
Tianeptine is an atypical antidepressant, which modestly enhances the mezolimbic release of dopamine. Tianeptine is an antidepressant<br />
that is accepted as not being abused by patients. However, there have been some case reports regarding abuse and/or addiction to it.<br />
The abuse of tianeptine is rare and so far has only been reported in patients with pre-existing multi substance abuse disorders. A total of<br />
141 cases of abuse were reported between 1989 and 2004. The patients usually sought and experienced a psychostimulant effect. The<br />
stimulant effect of tianeptine has been specifically emphasized in some case reports of tianeptine abuse in the literature.<br />
In this poster, a twenty year-old female patient, who received tianeptine treatment for depression and developed tianeptine dependence<br />
is presented. In our case, the patient was taking sixty pills daily. Although she took sixty pills, her biological tolerance was excellent and<br />
hepatic and hematological parameters were not affected, similar to the findings of other reports in the literature.<br />
This case emphasizes that while prescribing tianeptine treatment clinicians should be careful using it in patients with substance abuse<br />
problems, as reported by other case reports in the literature.<br />
Key words: Tianeptine abuse, tianeptine dependence<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S197<br />
[PP-122] Ref. No: 282<br />
GWAS with AHP based SNP prioritization approach to identify SNP biomarkers<br />
for Alzheimer’s disease<br />
Onat Kadıoğlu 1 , Gürkan Üstünkar 2 , Yeşim Aydın Son 3<br />
1 Middle East Technical University, Bioinformatics Graduate Program Ankara, Turkey<br />
2 Middle East Technical University, Informatics Institute Department of Information Science, Ankara, Turkey<br />
3 Middle East Technical University, Informatics Institute Department of Health Informatics, Ankara, Turkey<br />
E-mail: onat.kadd@gmail.com<br />
Genome wide association studies (GWAS) is defined as search for biological variance associated with certain phenotypes and diseases<br />
among individuals in a population depending on statistical analysis. Combined p-value approach has been introduced recently and<br />
is defined as the second-wave GWAS. It helps mapping of significant SNPs to genes and pathways to evaluate SNP-gene-disease<br />
associations. Identification of enriched genes and pathways significantly associated with diseases can be performed via this approach.<br />
The major bottleneck of current standard GWAS approaches is the prioritization of statistically significant results. Our group has recently<br />
developed a novel Analytical Hierarchical Process (AHP) based on a structured SNP prioritization algorithm. SNPs are scored according<br />
to their biological relevance in terms of their genomic location and functional consequence, evolutionary conservation, and genedisease<br />
association. The recently developed METU-SNP application integrates GWAS, combined p-value while utilizing AHP based SNP<br />
prioritization algorithms. Combined p-value and AHP prioritization approach for GWAS of Alzheimer’s Disease (AD) has been utilized for<br />
the SNP-disease association of AD for the first the time in this study with METU-SNP software.<br />
The results from the analysis of two different sets of AD genotyping data with the newly proposed AHP based prioritization yield promising<br />
results for both datasets. For the ADNI data, all the top 100 SNPs according to AHP scoring map to OMIM associated genes and 18 of<br />
them map to AD linked genes. For the GenADA data, all the top 100 SNPs according to AHP scoring map to OMIM associated genes and<br />
37 of them map to AD linked genes. Glycolysis and gluconeogenesis, leukocyte migration, axon guidance, actin filament polymerization,<br />
cell adhesion, DNA fragmentation during apoptosis, fatty acid metabolism, and negative regulation of cell proliferation are common<br />
pathways residing at top 100 pathways according to combined p-value for pathways that are observed in GWAS results of both data sets.<br />
GWAS of both data with METU-SNP confirms the literature for AD associated genes; A2M, ABCA1, ACE, APOA1, APP, CHRNA7, IL1A,<br />
LDLR, LPL, MPO, PTGS2, SORL1. rs3781835 at SORL1, rs4343, and rs4351 at ACE1 are SNPs with high AHP scores are also listed to be AD<br />
associated at PharmGKB database. Moreover, CT and TT genotype of rs6313 at HTR2A gene indicates resistance to the treatment with<br />
antipsychotic drugs for AD patients presenting delusional symptoms. As presented here METU-SNP is a powerful tool with a novel AHP<br />
based prioritization algorithm implemented, which can lead to discovery of new associations at SNP, gene, and pathway level. In near<br />
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future, we expect that these new associations described through GWAS here and in other studies will lead to development of personalized<br />
medicine approaches with application in pharmacogenomics and psychopharmacology.<br />
Key words: AHP, Alzheimer’s disease, biomarker, GWAS, personalized medicine, pharmacogenomics, SNP prioritization<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S197-8<br />
[PP-123] Ref. No: 287<br />
A case report of a relapse in a major depression patient with valsartan/hydrochlorothiazide<br />
Alev Büyükkınacı, Devrim Öztürk Can, Gökçe Silsüpür<br />
Boylam Psychiatry Hospital, Ankara, Turkey<br />
E-mail: alevkilicoglu@gmail.com<br />
It is known that some drugs can cause depression. In particular, there is evidence that barbiturates, vigabatrine, topiramate, flunarizine,<br />
corticosteroids, mefloquine, efavirenz, and interferon alpha have been shown to cause depression (1). Angiotensin II is a strong<br />
vasopressor with various physiological effects especially regulating blood pressure. It regulates water retention and aldosterone secretion.<br />
Angiotensin II has two known receptors, AT1 and AT2. Valsartan is a non-selective angiotensin AT selective blocker, which prevents<br />
angiotensin binding to AT2 receptors and controls hypertension in this way (2). It has been shown that angiotensin converting enzyme<br />
polymorphism is related to relapse in major depression patients after partial sleep deprivation and this was related to its effect on the<br />
dopaminergic system (3). This finding shows that drugs targeting the angiotensin system may effect depression. Here we present a case<br />
with recurrent depression who was in remission and relapsed after she was given an antihypertensive medication containing valsartan<br />
and hydrochlorothiazide. She was a 56 year old single woman, living alone. She had a depressive episode in 1983 for the first time and had<br />
other episodes in 1997, 2001, and the last one in 2003. After having used venlafaxine and paroxetine, she was given citalopram in 2003 at<br />
40 mg/day, which she has been using until now. She did not have any depressive attacks after 2003. She was given an antihypertensive<br />
containing valsartan and hydrochlorothiazide 3 months before she presented to our clinic. After taking the medication she had reluctance,<br />
despondency, intense feelings of guilt with statements like “she will not be even accepted to hell.” There were no stressors that the patient<br />
or her relatives defined. The patient was admitted to our clinic after her symptoms increased the month prior to her admission. Since there<br />
were published articles on depression triggered by valsartan and similar antihypertensives and since the patient’s symptoms started after<br />
taking the medication, we continued on her drug regimen with citalopram 40 mg/day and changed her antihypertensive medication to<br />
a calcium channel blocker, amlodipine. After 2 weeks her symptoms started to decrease. We concluded that her depression was triggered<br />
by valsartan. This case is important for showing that medications affecting the angiotensin system can trigger depression and there is a<br />
need to study the role of the angiotensin system in the etiology of depression.<br />
Key words: Valsartan, antihypertensives, depression, relapse<br />
References:<br />
1. Celano CM, Freudenreich O, Fernandez-Robles C, Stern TA, Caro MA, Huffman JC. Depressogenic effects of medications: a review.Dialogues Clin Neurosci.<br />
2011;13(1):109-25.<br />
2. Black HR, Bailey J, Zappe D, Samuel R.Valsartan: more than a decade of experience. Drugs. 2009;69(17):2393-414.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S198<br />
[PP-124] Ref. No: 158<br />
Monosymptomatic hypochondriacal psychosis: A case report<br />
Yasemin Şimşek, Gökçe Elif Sarıdoğan, Ebru Şahan, Melike Nebioğlu, Cem Cerit, Mecit Çalışkan<br />
Haydarpaşa Numune Hastanesi Psikiyatri Kliniği, İstanbul, Turkey<br />
E-mail: cemcerit@yahoo.com<br />
Introduction: The somatic type of delusional disorder is also recognized as monosymptomatic hypochondriacal psychosis. According<br />
to the DSM-IV, the disorder is characterized by the presence of a somatic delusion in which the person has a false belief of having some<br />
physical defect or a general medical condition (1). The most substantial characteristic of the aforementioned disorder is the demand of<br />
the patient attributing the symptoms to a serious physical illness, and seeking medical advice continuously in an effort to find transient<br />
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Poster Presentations<br />
relief by being informed of the absence of a disease (2).<br />
Case Presentation: A 26- year old, female patient was admitted to an outpatient psychiatric clinic with complaints of having a possible ocular<br />
disease, which may cause blindness. Her symptoms included her irises deviating involuntarily, her eyes moving incoherently, and having a<br />
feeling in her eyes as if they are being drawn away. A previous psychiatric admission of the patient was reported to be 3 years ago with the<br />
complaints of dysmorphism and tremor in her hands and having a serious disorder relevant to her hands for which she was seen by several<br />
specialists although she wasn’t convinced by their answers. Although, thereafter she was hospitalized and was treated with several mood<br />
stabilizers and antipsychotic medications for the following three years in outpatient clinics, a full remission could not be achieved.<br />
She was hospitalized again. Her physical and neurological examination didn’t reveal any biological anomalies. It was noticed that she was<br />
touching her eyes constantly and her speech was focused on her bodily sensations so that she couldn’t maintain her attention on any<br />
other topic. In the contents of her thoughts, she had somatic delusions as defined above. She was treated with pimozide, started with 2mg<br />
and increased up to a dose of 6 mg/day gradually. Her condition was observed to improve with a decrease in intensity of her symptoms,<br />
increased interest, improved self-care, decrease in the amount of her speech and becoming more functional.<br />
Discussion: Because there was no increase in psychomotor activity and the content of speech was solely about the sensations in her eyes,<br />
we did not diagnose her with an affective disorder. We arrived at the diagnosis of monosymptomatic hypochondriacal psychosis after<br />
evaluating the cues such as the worry about having an eye disease, not being persuaded with the medical examinations and diagnosis,<br />
lack of any other psychotic symptoms, delusions being only about bodily sensations, several admissions to non-psychiatric physicians,<br />
and her resistance to treatment with multiple drugs. In the literature there are cases reporting surgery, which was not required, such as an<br />
operation to treat a patient stating that he had a lumbar nerve root compression (3). In the present case the patient presented to internal<br />
medicine and ophthalmology clinics at the beginning insisting that she needed an eye operation. In a study on 23 patients it has been<br />
reported that these cases have responded well to pimozide (4).<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S198-9<br />
[PP-125] Ref. No: 288<br />
Amisulpride in the treatment of treatment resistant tic disorder: A case report<br />
Onat Yılmaz, Mehmet Alpay Ateş, Gülşah Meral, Cengiz Başoğlu, Ayhan Algül, Servet Ebrinç, Mesut Çetin<br />
GATA Haydarpasa Training Hospital, Department of Psychiatry, Uskudar, Istanbul, Turkey<br />
E-mail: onatyilmaz@yahoo.com<br />
Introduction: Tics are sudden, recurrent, involuntary motor movements or vocalizations caused by involuntary contractions of motor<br />
or vocal muscles. Typically these disorders are characterized by early childhood onset and are more common in the male population.<br />
Genetic, neurobiological, neurochemical and environmental factors play a role in the pathogenesis, and malfunctioning of the basal<br />
ganglia is thought to be responsible for the disease. The presence of abnormalities in the EEG of some patients, worsening of the tics with<br />
administration of dopamine agonists, and improvement of tics with antidopaminergic agents are some of the known biological evidence.<br />
Amisulpride, with a pure antidopaminergic activity, and thus being used effectively in the treatment of Tourette’s syndrome, makes it a<br />
candidate to treat other tic disorders, as well. In this report, an adult patient diagnosed with “Tic Disorder Not Otherwise Specified,” who<br />
was previously treated with several antidepressant and antipsychotic drugs, is cured with amisulpride.<br />
Case presentation: A 21-year-old single male patient was admitted to the hospital complaining of impairment in interpersonal relations,<br />
difficulties in social adaptation due to the involuntary repetition of certain movements. His complaints had started at the age of nine after<br />
his uncles were killed. Though the patient was tried on different treatment regimens, but he had no benefits. Because of his tics, he hardly<br />
finished his primary school education and was not able to work for a long time.<br />
In history there were no perinatal or neonatal complications and he was born by spontaneous vaginal birth. As the sixth of eleven children,<br />
his developmental history was normal. There was no family history of any mental illness, epilepsy, alcoholism, or movement disorder.<br />
On his admission to the unit, he was given amisulpride 200mg/day and the dosage was increased to 400mg/day in three days. He had a<br />
score of 15 in motor tics on admission and he had a score of 3 for motor score (80% decrease) at the third week of the treatment. No side<br />
effects were observed and he was discharged at the end of the third week. All of the signs were in remission on the follow up after two<br />
months.<br />
Discussion: Contrary to the antipsychotics effecting both D1 and D2 receptors in the nigrostriatal pathway, antipsychotics of the<br />
benzamide group, which work as selective D2 receptor antagonists, are effective in the treatment of tic disorders. As the most preferred<br />
drug in this group, amisulpride causes less extrapyramidal side effects by selectively acting on the limbic regions rather than striatal<br />
regions. In the literature, there are case reports of amisulpride’s effective use in tic disorders.<br />
Clinicians should keep in mind that, with less side effect risk compared to conventional antipsychotics and the benefits of its mechanism<br />
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Poster Presentations<br />
of action, amisulpride might be the drug of choice in tic disorders. On the other hand, larger controlled clinical trials should be planned<br />
on this issue.<br />
Key words: Tic disorders, echopraxia, amisulpride, side effect<br />
References:<br />
1. Turan M, Çilli AS. Tik bozuklukları. Genel Tıp Derg. 1999;9(3):117-21<br />
2. Fountoulakis KN, Lacovides A, Kaprinis GS. Successful treatment of Tourette’s disorder with amisulpride, Ann Pharmacother. 2004; 3: 901.<br />
3. Leysen JE, Janssen PMF, Heylen L, Gommeren W, Van Gompel P, Lesage As.Receptor interactions of new antipsychotics: relation to pharmacodynamic and clinical<br />
effects. Int J Psychiatry Clin Pract; 1998; 2(Suppl.1): 3-17.<br />
4. Ates MA, Algül A, Semiz UB, Güneş C, Çetin M. Tedaviye dirençli Gilles de la Tourette sendromunda amisülpirid kullanımı: Bir olgu sunumu. Yeni Sempozyum Dergisi.<br />
2009; 47:1: 16-18.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S199-200<br />
[PP-126] Ref. No: 290<br />
Evaluation of patients with obstructive sleep apnea syndrome referred to the sleep<br />
disorders unit of a university hospital<br />
Evrim Özkorumak 1 , Haluk Hıdıroğlu 2 , Ahmet Tiryaki 1 , İsmail Ak 1<br />
1 Karadeniz Technical University, Psychiatry Department, Trabzon, Turkey<br />
2 Ataköy State Mental Health Hospital, Trabzon, Turkey<br />
E-mail: evrimozkorumak@yahoo.com<br />
Introduction: Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive episodes of apnea and hypopnea, and decrease in<br />
oxygen saturation (1). The relationship of OSAS and other medical conditions has been explored in the research literature while the relationship<br />
between OSAS and mental health has not been sufficiently investigated yet. The aim of this study was to determine the distribution of mental<br />
disorders and the type of distribution of mental disorders within clinical features of OSAS from the point of view of psychiatry.<br />
Method: The patients, who were referred to the sleep disorders unit of Karadeniz Technical University, Faculty of Medicine Hospital for<br />
1 year were considered the population for this study. A total of 102 patients, with a diagnosis of OSAS according to polysomnography<br />
and patients with no exclusion criteria composed the sample of the study. The patients were classified according to the ICSD-2 (The<br />
International Classification of Sleep Disorders) with polysomnography. Sociodemographical and clinical features of the patients were<br />
recorded. The Montgomery Asberg Depression Rating Scale, the Beck Depression Inventory and the Epworth Sleepiness Scale were<br />
administered. Psychiatric diagnoses were made by interviews based on the DSM-IV Axis I Disorders (SCID-I).<br />
Results: According to the ICDSD-2, 19.6% (n=20) of the patients had a mild, 29.4% (n=30) had a moderate and 51,0% (n=52) had a severe<br />
form of OSAS. The distribution of sex, marital status, and occupation are shown in Table I. The means of weight and height of the whole<br />
sample were 91.15±16.78kg and 168.23±8.76cm, respectively. Fifty-seven point nine percent of the patients (n=59) had had a psychiatric<br />
referral previously, 42.2% of them (n=43) did not. According to the body mass index (BMI), 5.9% of patients (n=6) were within normal<br />
limits, 30.4% were (n=31) overweight, 54.9% were obese (n=59) and 8.8% were morbidly obese (n=9). The Epworth Sleepiness Scale total<br />
score was significantly higher in severe OSAS patients (p=0.002). The relationship of mild and moderate OSAS with BMI was significant<br />
(p=0.010). The median age of severe OSAS patients was significantly higher than mild OSAS patients (p=0.0529).<br />
Thirty-one point four percent (n=32) of patients had 1 diagnosis according to the SCID-I, 22.5% (n=23) had more than one diagnosis, and<br />
46.1% (n=47) did not have any diagnosis. The total scores of the BDI and the MADRS were 5.49±9.05 and 5.82±9.40, respectively.<br />
Discussion: There are many risk factors for OSAS. Male predominance is present for adult OSAS patients. The number of male patients was<br />
higher than female patients in this study. One of the most important risk factor is obesity (2). Most of the patients were obese or morbidly<br />
obese in our group. The detected depression rate was correlated with many studies which reported higher depression rates in OSAS (2-5).<br />
In this study the rate of anxiety disorders was higher than in the healthy population while being similar or lower than the rate estimated<br />
in previous studies with OSAS patients.<br />
Conclusion: Mental disorders associated with medical diseases are important clinical syndromes effecting morbidity and mortality.<br />
Recognizing the symptoms and signs of OSAS is important. Regarding this issue, further studies with larger samples comparing different<br />
subgroups are needed.<br />
Key words: Obstructive sleep apnea, mental diseases<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S200<br />
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Poster Presentations<br />
[PP-127] Ref. No: 286<br />
Clozapine use in idiopathic tardive dystonia and paranoid schizophrenia comorbidity:<br />
A case report<br />
Mustafa Güleç, Elif Oral, Esat Fahri Aydın<br />
Department of Psychiatry, Medical Faculty, University of Atatürk, Erzurum, Turkey<br />
E-mail: mustafagulec78@yahoo.com<br />
Objective: To present brief idea about a suitable and safe antipsychotic usage in patient with schizophrenia and tardive dystonia.<br />
Method: Results will be discussed.<br />
Results:<br />
Case: A 42-year-old woman with diagnose of first episode and drug naïve schizophrenia presented with involuntary movements in her<br />
orobuccal region, including tongue and lips. At first administration, routine biochemical and hematological assessments were normal, and<br />
patient had positive and negative features of schizophrenia. According to the information received her relatives, although she has not taken<br />
any antipsychotic medication, her involuntary movements has been risen 18 month earlier her antipsychotic treatment. These movements<br />
were consulted with neurology clinic. Her brain MRI, EEG, and further assessments including detailed neurological examination, jaw MRI was<br />
normal, and specialist of neurology suggested that the clozapine usage may be helpful because of the possible idiopathic tardive dystonia.<br />
Clozapine medication was started with gradually, although there was not enough proof about prior antipsychotic usage and anatomical<br />
or functional deficit. During her hospitalization, all of the involuntary movements were recovered with 200 mg/day clozapine, and more<br />
than 35% percent decrease was observed at her positive (SAPS) and negative (SANS) scale assessments with 600 mg /day clozapine. In this<br />
period, there was no side effect except moderate sialorrhea. Etiology of the idiopathic tardive dystonia is still remaining unclear, and data<br />
for treatments is receiving from the case reports. There is some evidence about efficacy of clozapine treatment (1,2). In addition, there is a<br />
consensus about that clozapine can cause extrapyramidal side effects rarely and effective treatment option for schizophrenia as well (3). On<br />
the other hand, tendency of the general psychiatry practice would prefer to this molecule in the resistant schizophrenia which is describe as<br />
show no remission despite of two different kinds of antipsychotic usage for minimum six weeks (4). In this case, clozapine usage in the first<br />
line seems to be necessary because of the idiopathic tardive dystonia. It may be clarified with further studies whether this case was remitted<br />
incidentally or this remission was related with antagonistic effects of clozapine on the receptors of D1.<br />
Conclusion: Clozapine may be a first line treatment option for the drug naïve patients with first episode schizophrenia and tardive<br />
dystonia. However, we need further studies performed with wide case series to achieve this kind of opinion.<br />
Key words: Tardive dystonia, neurological, schizophrenia, clozapine, safety, efficacy<br />
References:<br />
1. Kwan Y, Sim K. Resolution of tardive dystonia in a patient with bipolar disorder treated with clozapine: a case report. Prog Neuropsychopharmacol Biol Psychiatry<br />
2010; 34(1):238-239.<br />
2. Aukst-Margetic B, Margetic B. Treatment of generalized tardive dystonia with clozapine. Psychiatr Danub 2008; 20(3):329-331.<br />
3. Asenjo Lobos C, Komossa K, Rummel-Kluge C, Hunger H, Schmid F, Schwarz S, et al. Clozapine versus other atypical antipsychotics for schizophrenia. Cochrane<br />
Database Syst Rev 2010; (11):CD006633.<br />
4. Kane J, Honigfeld G, Singer J, Meltzer H. Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine. Arch Gen Psychiatry<br />
1988; 45(9):789-796.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S201<br />
[PP-128] Ref. No: 306<br />
The clinical use of Buprenorphine-Naloxone in the opioid-dependent patient<br />
with Hepatitis C<br />
Tuğba Kara, Arzu Çiftçi<br />
Bakirkoy Research and Training Hospital for Psychiatry and Neurology, Istanbul<br />
E-mail: tugbakara111@yahoo.com<br />
Introduction: Guidelines for the treatment of opioid dependence which developed by organizations such as American Society<br />
of Interventional Pain Physicians (ASIPP) and the American Psychiatric Association (APA) recommend extensive treatment with<br />
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Poster Presentations<br />
pharmacological treatments such as methadone, buprenorphine, buprenorfine-naloxone as well as psychosocial therapy. Buprenorphine-<br />
Naloxone therapy is being used effectively as an alternative treatment to entering patients into a methadone outpatient clinics (1). The<br />
clinical relevant effect of buprenorphine depends on m-opioid receptor agonism (2).<br />
Case: 16-years-old male patient with opioid dependence diagnosed according to DSM-IV criteria entered CEMATEM ( Child and<br />
Adolescent Alchol and Substance Treatment Centre ) clinic for out-patients in Bakirkoy Research and Training Hospital for Psychiatry and<br />
Neurology and a week later the patient has been hospitalized. Liver enzyme levels were normal and opiat value was found as positive in<br />
sub-threshold in routine controls and after 6- 8 hours Buprenorfin-Naloksan combination (Suboxone) treatment was received the patient<br />
experienced withdrawal symptoms.In patient’s routine blood tests, hepatitis C virus (HCV) was determined and the patient developed<br />
significiantly elevated liver enzyme levels during buprenorphine-naloxone treatment.<br />
Conclusions: Although Buprenorphine has been used clinically in the early 1970s, it’s metobolism has not been fully unterstood already<br />
(3). Buprenorphine was mainly metobolized by N-dealkylation and glucuronidation of buprenorphine and norbuprenorphine by CYTP450<br />
isoforms in liver ( 4). For non-hepatitis subjects, buprenorphine treatment showed no evidence of altered liver enzyme levels.<br />
In contrast, AST and ALT levels increased significantly with buprenorphine treatment among patients with a history of hepatitis (5).<br />
Liver enzym values significiantly elevated in this case with hepatitis C received Buprenorphine-Naloxone combination treatment.<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S201-2<br />
[PP-129] Ref. No: 105<br />
The use of z hypnotics in the management of insomnia in forensic psychiatric<br />
units in Oxford, England<br />
Hasanen Ali Altaiar<br />
Oxford Health NHS Trust, Littlemore Hospital, Oxford, ox4 4xn, UK<br />
E-mail: hasanen.al-taiar@oxfordhealth.nhs.uk<br />
Objectives: Insomnia has an estimated prevalence of 30% in general population and its prevalence is higher among psychiatric patients. In 1987 a<br />
survey showed around half of psychiatric patients received a hypnotic medication. Also people with mental health problems have an increased risk of<br />
developing dependence on hypnotics. “Z-drugs” are benzodiazepine like medications and are used as primary pharmacological treatment for insomnia.<br />
They include zolpidem, zaleplon, and zopiclone. Zopiclone is not available in the US, although its active stereoisomer, eszopiclone is available. NICE<br />
guidelines recommend trying non-pharmacological interventions such as sleep hygiene prior to considering “z drugs.” The symptoms, findings of<br />
evaluation, and the reasoning behind prescribing “z drugs” should be documented in medical and nursing notes. The maximum duration should not be<br />
longer than 2 weeks when “z drugs” were used.<br />
The aims of this study included: To review if ‘z-drugs’ were prescribed according to the NICE guidelines, whether “insomnia” was documented in patient<br />
charts or not, if other measures were tried before prescribing a “z drug,” and if the reason for switch was documented, in case of switching from one “z<br />
drug” to another.<br />
Methods: We reviewed all the progress notes and medication charts for a 6-month duration between January 1-June 30, 2010 for all of the inpatients (n=<br />
74) in the 6 forensic wards at the Littlemore Hospital. We identified the patients, who were prescribed “z drugs” for insomnia, and reviewed their records.<br />
Results: We found out that only 3 patients were prescribed “z drugs,” which was zopiclone 7.5mg/day for all of three cases. All orders were for as needed<br />
basis use. Insomnia was recorded in medication charts, but not in the notes section. Non-pharmacological measures were tried in only one of the patients<br />
and documentation was found in one case, too. The maximum duration was not documented and there was no revision in original orders.<br />
Conclusions: Based on our data the “z drugs” are rarely used in forensic units of Littlemore Hospital. The only prescribed one was zopiclone and it was<br />
used only for a couple of days. The documentation regarding use of those medications was rare and no case of switch to another “z drug” was found.<br />
Checking for the response to the treatment and conducting the study in general wards beside forensic units would have improved this study and<br />
provided more patients, who were prescribed those medications.<br />
The majority of forensic patients are on high doses of antipsychotics or rapid tranquilizers, which might help to cope with insomnia. We found that<br />
other than documentation the standards were followed by the Trust. As forensic patients were supervised at all times on-call doctors should be able to<br />
prescribe Z hypnotics, when needed. The use of sleep hygiene in treatment of insomnia should be encouraged for all patients.<br />
Key words: Z hypnotics, forensic, psychiatric, z drugs, Oxford<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S202<br />
S202 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
[PP-130]<br />
Pathological gambling: A case report<br />
Mehmet Fatih Tastan, Haluk A. Savas<br />
Gaziantep University, Medical School, Department of Psychiatry, Gaziantep, Turkey<br />
E-Mail: mfatihtastan@yahoo.com, drhaluksavas@hotmail.com<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Poster Presentations<br />
Pathological gambling(PG), is a disorder which is growing everyday with the increasing prevalence of opportunities for play, usually properly diagnosed,<br />
treatment can be difficult and increasingly restricting the individual’s living area. PG, for the first time in 1980, by The Union of American psychiatry has<br />
been recognized as a disorder and the DSM-3 was unable to resist the urge to gamble as a continuous and progressive definition of a “Impulse Control<br />
Disorders Not Elsewhere Classified” has been included under the heading. Physiological symptoms of DSM-3-R were included in the PG, “the excitement is<br />
to be obtained to provide the desired amount of bets or the need to increase the frequency of hearing,” such as tolerance and “gambling oynayamayınca<br />
hearing restlessness or irritability, such as” withdrawal symptoms participated in the diagnostic criteria. We present a case of PG, 28 year old male patient<br />
who is treated with quetiapin and cognitive behavioral treatment (CBT). With CBT, we did daily psychotherapeutic interview and patient had discovered<br />
his cognitive distortion. Also we saw that SSRIs, Naltrexone, Lithium and Carbamazepine could be used in PG treatment. Patient was externed after 11<br />
days hospitalizing. At the controls we obtained that patient had not gamble again. As a result this was the effect of Cognitive Behavioral Treatment.<br />
Key words: Pathological gambling, cognitive behavioral treatment, cognitive distortion<br />
Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S203<br />
S203
(±)-3-4-methylenedioxymethamphetamine S36<br />
1-benzylpiperazine S36<br />
5-HT1B A-161T S108<br />
Absence convulsion S118<br />
Absenteeism S150<br />
Abuse S180<br />
Academic achievement S154<br />
Academic performance S58<br />
Acceptance S105<br />
Access S156<br />
Access to health care S156<br />
Addiction S54, S42, S83, S109, S151, S155<br />
ADHD S57, S66, S73, S96, S97, S136, S148<br />
Adolescence S96<br />
Adolescents S126, S153<br />
ADRA2A S148<br />
Adult ADHD S159<br />
Adult attention deficit hyperactivity disorder S163<br />
Affective disorder S161<br />
Agmatine S166, S169<br />
Agranulocytosis S46<br />
AHP S198<br />
Alcohol S155<br />
Alcohol abuse S173, S174<br />
Alcohol dependence S108<br />
Alexithymia S56<br />
Alkaline phosphatase S116<br />
Alloxan S116<br />
Alzheimer’s disease S52, S198<br />
Amenorrhea S135<br />
Amisulprid S160, S200<br />
Amplified perception of somatic sensations S178<br />
Amygdala S110, S133<br />
Anger S138<br />
Animal model of depression S140<br />
Anorexia S92<br />
Anorexia nervosa S130, S195<br />
Antidepressant S38, S39, S43, S51, S81, S121, S136, S140<br />
Antiepileptic S182<br />
Antihypertensives S198<br />
Antioxidant S170<br />
Antioxidant vitamins S74<br />
Antipsychotic S63, S135, S144, S149, S167<br />
Antipsychotic development S50<br />
Antipsychotic drug S180, S196<br />
Antisocial personality disorder S163<br />
Anxiety S69, S163, S132, S133, S141, S155<br />
Anxiety disorders S40, S67, S68<br />
Anxiety models S69<br />
Anxiety symptom levels S153<br />
Archive documents S181<br />
Aripiprazole S135, S144, S152<br />
Assessment S150, S151, S155<br />
Atherosclerosis S143<br />
Atomoxetine S136<br />
Attachment S56<br />
Attention deficit hyperactivity S58<br />
Attention deficit hyperactivity disorder S95, S139<br />
Atypical antipsychotics S63, S144, S164, S171<br />
Augmentation S126<br />
Autism S72<br />
Avoiding behavior S122<br />
Bacopa monniera S108, S153, S189<br />
Basal ganglia hemorrhage S157<br />
BDNF S91, S169<br />
Behavioral therapy S185<br />
Bilirubin S180<br />
Binge eating S54<br />
Biogenic amines S51<br />
Biological rhythm S88, S89<br />
Biomarker S102, S198<br />
Bipolar S36, S57, S149<br />
Bipolar affective disorder S169<br />
Bipolar disorder S39, S59, S98, S100, S124, S126, S140, S142, S158<br />
Blood level S142<br />
Blood sugar S111<br />
Body dysmorphic disorder S143<br />
Brain imaging methods S195<br />
Brain injury S136<br />
Brain microdialysis S36<br />
Brain-derived neurotrophic factor S176<br />
Bright light S89<br />
Bulimia S92<br />
Bulimia nervosa S95, S194<br />
Buprenorphine S35<br />
Bupropion S113, S121, S143<br />
C-fos S169<br />
Cabergoline S124<br />
Calcium S72, S123<br />
Cannabis S37, S83, S130<br />
Cannabis dependency S159<br />
Caregiver burden S141<br />
Catatonia S162<br />
CBT S105, S106, S111<br />
Cerebellar cognitive affective syndrome S138<br />
Cerebellum S138, S195<br />
Cerebral ischemia S112<br />
Ceruloplasmin S170<br />
Subject Index<br />
Character S34, S54<br />
Chemotherapy S132<br />
Chest pain without cardiac etiology S138<br />
Child S36, S57<br />
Childhood trauma S79, S86, S192<br />
Children S74, S75, S97, S139<br />
Cholinesterase inhibitors S136<br />
Choreoathetoid movement S152<br />
Chronic schizophrenia S125<br />
Chronic unpredictable mild stress S166, S169<br />
Chronotherapeutics S89<br />
Cigarette S156<br />
Clinical characteristics S82<br />
Clinical manifestation S172<br />
Clozapine S46, S126, S201<br />
CNR1 1359 G/A S108<br />
Co-morbidity S96, S97<br />
Cognition S34, S91, S153<br />
Cognitive behavior therapy S40, S41<br />
Cognitive functions S83, S136, S138, S158, S188<br />
Cognitive processing of emotions S56<br />
Cognitive side effects S149<br />
Combination drug therapy S40<br />
Community care S129<br />
Comorbidity S92, S95, S177<br />
Complementary and alternative medicine S65<br />
Confidence interval S104<br />
Congenital hypogonadism S195<br />
Corpus callosum S182<br />
COX-2 inhibitor S184<br />
Craving S156<br />
CRH S51<br />
Crisis team S129<br />
Cultural differences S172<br />
Cytochrome P450 2C9 S132<br />
Cytokines S70<br />
D-serine S50<br />
Death S155<br />
Deep brain stimulation S61<br />
Dementia S62, S134<br />
Depression S36, S38, S39, S43, S57,S60, S60, S64, S65, S70,<br />
S77, S78, S81, S82, S85, S87,S89, S130, S132, S139, S141, S145,<br />
S155, S161, S162, S163, S170, S178, S184, S190, S193, S198<br />
Depression treatment S58<br />
Depressive symmptom levels S153<br />
Descriptive statistics S104<br />
Development S74<br />
Diabetic rats S116<br />
Differential diagnosis S177<br />
Diltiazem S119<br />
Dissociation S192<br />
Dissociative disorder S159<br />
Dissociative symptoms S146<br />
Divorce S144, S184<br />
Don Juanism S52<br />
Dopamine S49, S63<br />
Dopamine agonists S124<br />
DRD2 TaqIA S108<br />
Drug S100, S103<br />
Drug discovery S62<br />
Drug induced S167<br />
Drug-induced psychosis S182<br />
Drug interactions S97<br />
Drug safety S48<br />
Drug utilization S168<br />
Dual diagnosis S109<br />
Duloxetine S115, S139<br />
E-selectin S143<br />
Eating disorders S54, S92, S93, S94, S130<br />
Eating pattern S125<br />
Echopraxia S200<br />
Ecstasy S36<br />
ECT 196<br />
Ecuadorian population S132<br />
Edema S196<br />
Education S65<br />
Education factors S128<br />
EEG S110, S133<br />
Effectiveness S151<br />
Efficacy S38, S136, S201<br />
Electroconvulsive therapy S174<br />
Electromagnetic induction S117<br />
EMDR S106, S127<br />
Emotion regulation S40<br />
Emotionality S34<br />
Enuresis nocturna S185<br />
Environmental risk S52<br />
Erectile dysfunction S137<br />
Escitalopram S160<br />
Essential fatty acids S66<br />
Estrogen S77<br />
Euthymia S158<br />
Evidence based treatment S41<br />
Executive functions S176<br />
Exercise S91<br />
Extrapyramidal side effects S144, S165<br />
Eye movement desensitization and reprocessing S123<br />
Fear of negative evaluation scale S173
Female adolescents S125<br />
Female reproductive hormones S193<br />
Fish oil S135<br />
Flight safety S103<br />
Fluanxol S129<br />
Fluoxetine S113, S130, S147, S179, S194<br />
FMRI S62, S108, S189<br />
Foetality S171<br />
Follow-up S176<br />
Forced swimming test S166<br />
Forensic S202<br />
Forensic psychiatric examination S128<br />
Functional outcomes S136<br />
Functional remission S188<br />
Functioning S86<br />
GABA S51<br />
Galactorrhea S147, S160<br />
Ganser Syndrome S159<br />
Gating S49<br />
Gender S140<br />
Generalized anxiety disorder S193<br />
Generalized convulsion S118<br />
Genes S52<br />
Genetic S68S 100<br />
Genetic association S46<br />
Genetic polymorphism S131, S132<br />
Genomic diagnostics S157<br />
GFAP S169<br />
Ginseng augmentation therapy S114<br />
Glia S50, S51<br />
Glossodynia S161<br />
Glutamate S40, S49, S50, S51, S69, S70<br />
Glutathione S169<br />
Glycine S50<br />
GOT S116<br />
GPT S116<br />
Guidelines S98, S100<br />
GWAS S157, S198<br />
Hallucination S121<br />
Haloperidol S129<br />
Happiness S34<br />
Harm minimization S42<br />
Health S34<br />
Hematological S130<br />
Heroin S109<br />
Hippocampal neurogenesis S91<br />
HIV/AIDS S42<br />
HLA-system S46<br />
Hoarding S134<br />
Homework assignments S41<br />
HPA axis S51<br />
Human characteristics S34<br />
Human cognition S108, S189<br />
Huntington’s disease S152<br />
Hyperammonemic encephalopathy S164<br />
Hyperprolactinemia S124, S135, S160<br />
Hypersexual disorders S52<br />
Hypersomnia S44<br />
Hypochondriasis S105<br />
Hypoglycemia S78<br />
Hypomania S194<br />
Hyponatremia S139, S141<br />
Hypothalamic-pituitary-thyroid axis S77<br />
ICAM-1 S143<br />
Imipramine S185<br />
Immunosuppresive treatment S161<br />
Impulse control disorder S53<br />
Impulsivity S94<br />
In vitro analysis S115<br />
Inappropriate medications S168<br />
Individualized medicine S101<br />
Inflammation S184<br />
Information processing disorder S49<br />
Inpatient S191<br />
Insight 188<br />
Insomnia S139<br />
Insulin S78<br />
Insulin resistance S78<br />
Interethnic differences S131<br />
Iron deficiency S74<br />
Isolated thrombocytopenia S190<br />
Ketamine S49, S69<br />
Lack of self confidence S111<br />
Lactation S48, S71, S71<br />
Lamotrigine S142<br />
Lateral ventricle S61<br />
Learning S112<br />
Leukopenia S127<br />
Lipid peroxidation S140<br />
Lithium S169<br />
Lithium carbonate S161<br />
Locomotor activity S141<br />
Long QTc S119<br />
Losartan S132<br />
Lung functions 141<br />
Magnetic resonance imaging S61<br />
Maintenance S176<br />
Maintenance phase S100<br />
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org<br />
Subject Index<br />
Major depressive disorder S115<br />
Male patient S195<br />
Malondialdehyde S169<br />
Management S95<br />
Mania S157, S194<br />
Manic episode S124<br />
Marital conflict S144, S184<br />
Mechanism of action S63<br />
Medical care S156<br />
Medical decision support systems S157<br />
Medical diseases S67<br />
Medical marijuana S37<br />
Medication S40, S43<br />
Mega cisterna magna S195<br />
Melatonin S75<br />
Mental diseases S200<br />
Mental disorder S144, S184<br />
Mental health S154<br />
Mental illness S196<br />
Mental symptom S123, S135<br />
Mentalizing S56<br />
Metabolic syndrome S180<br />
Metabolic S171<br />
Metabolic side effect S140<br />
Methadone S35, S114<br />
Methadone substitution therapy S137<br />
Methylphenidate S139, S190<br />
Metoprolol S119<br />
METU-SNP S102, S157<br />
MGLU receptors S70<br />
Middle-aged male S139<br />
Mindfulness S40, S105<br />
Mirtazapine S139, S175, S190, S196<br />
Mixed mania S98<br />
Modafinil S44<br />
Models S49<br />
Molecular diagnostics S102<br />
Mood S89, S91, S153<br />
Mood disorder S77, S79, S134, S149, S162<br />
Mood stabiliser S149<br />
MRI S62<br />
Music therapy S191<br />
Myeloperoxidase S46, S169<br />
NADPH-oxidase S46<br />
Neuroactive steroids S50, S51<br />
Neurocognitive functions S193<br />
Neurodegeneration S90, S91<br />
Neurodevelopment S49<br />
Neurodevelopmental disorders S75<br />
Neurogenesis S193<br />
Neuroimaging S36, S62, S148<br />
Neuroleptic malignant syndrome S125<br />
Neurological S201<br />
Neurological co-morbidity, treatment S97<br />
Neurological deficits S164<br />
Neuromodulation S117<br />
Neuropathic pain S59<br />
Neuroplasticity S90<br />
Neuroprotection S112<br />
Neuroprotective effect S90<br />
Neuroregeneration S91<br />
Neurotrophic factors S70<br />
Neutropenia S127<br />
Nicotine S112<br />
Nitric oxide S50<br />
NMDA S40, S70<br />
NMDA receptor S49, S69<br />
Non-seasonal affective disorder S89<br />
Normal pressure hydrocephalus S169<br />
Nutraceuticals S108, S153, S189<br />
Nymphomania S52<br />
Obesity S94<br />
Obsessive beliefs S137<br />
Obsessive compulsive behavior S126<br />
Obsessive compulsive disorder S71, S134, S176, S177<br />
Obsessive compulsive spectrum S182<br />
Obstructive sleep apnea S200<br />
Occupation S58<br />
OCD S59, S137, S172<br />
Olanzapine S171, S180, S190<br />
Olfaction S193<br />
Oman S145<br />
Omega fatty acids S75<br />
Omega-3 fatty acids S64<br />
Ontogenesis S171<br />
Opioid dependence S35<br />
Opioid withdrawal syndrome S114<br />
Orally disintegrating olanzapine S115<br />
Outpatient forensic psychiatric examination S181<br />
Oxford S202<br />
Oxidative stress S170, S189<br />
Oxytocin S76, S133, S118<br />
P value S104<br />
Pain S54, S55, S81, S82<br />
Pain reflex 141<br />
Pain threshold S178<br />
Paliperidone S165<br />
Panic disorder S78, S106, S122, S137, S189, S71
Panic symptoms S122<br />
Paroxetine S156<br />
Pathological gambling S53, S174<br />
Pattern S168<br />
Pentylenetetrazol (PTZ) S118<br />
Perinatal depression S64<br />
Persistent symptoms S86<br />
Personality S34<br />
Personality disorder S178<br />
Personalized medicine S102, S157, S198<br />
PET S62<br />
Petechia S190<br />
Pharmacogenetics S63, S101<br />
Pharmacogenomics S102, S157, S198<br />
Pharmacological treatment S93<br />
Pharmacology S93<br />
Pharmacotherapy S53, S93<br />
Phobias S178<br />
Physical activity S91<br />
Physical health monitoring S149<br />
Physical symptom S123, S135<br />
Pica S182<br />
Pilots S103<br />
Piracetam S146<br />
Placebo S38, S123, S135<br />
Polymorphism S63, S100, S108, S176<br />
Polypharmacy S164<br />
Post traumatic stress disorder S141<br />
Post-partum blues S163<br />
Post-traumatic stress disorder (PTSD) S123, S175<br />
Pregnancy S35, S48, S71, S190, S196<br />
Pregnant women S149<br />
Premenstrual dysphoric disorder S193<br />
Premenstrual syndrome S123, S135<br />
Priapism S167<br />
Progesterone S77<br />
Progressive muscle relaxation S132<br />
Psychiatric S202<br />
Psychiatric disorders S37, S48, S62, S74, S77<br />
Psychiatry S65, S74, S101, S109<br />
Psychopathology S125<br />
Psychopharmacotherapy S71<br />
Psychosis S83, S167, S178, S192<br />
Psychospiritual interventions S42<br />
Psychostimulants S44<br />
Psychosurgery S61<br />
Psychotherapy S53, S95, S105, S106, S151<br />
Psychotic disorder S80, S162<br />
Psychotropic drugs S48, S88, S90, S103<br />
Psychotropics S140<br />
PTSD S59, S106, S175<br />
Quality of life S132, S191<br />
Quantitative EEG S58<br />
Questionnaire S151<br />
Racine scale S118<br />
Radial-arm maze S112<br />
Rape S127<br />
Rapid antidepressant efficacy S69<br />
Rat S68<br />
Rat behaviour S36<br />
Rational drug use S102<br />
Rats S141<br />
Reaction time S113<br />
Reboxetine S130<br />
Reference memory S112<br />
Referral pathways S129<br />
Rehabilitation S86<br />
Relapse S149, S198<br />
Religious beliefs S155<br />
Renal transplantation S161<br />
Repetitive transcranial magnetic stimulation (rTMS) therapy S58<br />
Resistant depression S176<br />
Risk factors S137<br />
Risky behavior S153<br />
Risperidone S135<br />
RTMS S176<br />
Safety S190, S201<br />
Schizophrenia S49, S50, S59, S61, S63, S77, S80, S86, S126,<br />
S129, S134, S143, S157, S164, S171, S177, S180, S188,<br />
S191, S192, S195, S201<br />
Scientific basis S63<br />
SCL-90 S144<br />
Seasonal affective disorder S89<br />
Self-destructive acts S181<br />
Self-perception S138<br />
Serotonin S49, S63<br />
Serotonin syndrome S36<br />
Sertraline S179<br />
Serum drug levels S149<br />
Sexual dysfunction S80, S103<br />
Sexual trauma S167<br />
Side effect S63, S103, S127, S130, S161, S167, S200<br />
Sigma receptor S112<br />
Single Nucleotide Polymorphisms (SNPs) S102<br />
SLC6A2 S148<br />
Subject Index<br />
Sleep S43, S89<br />
Sleep deprivation S87, S89<br />
Smoking cessation S162<br />
SNP genotyping S157<br />
SNP prioritization S198<br />
SNRI S55<br />
Social anxiety S173, S174<br />
Social behaviour S76<br />
Social Phobia Scale S174<br />
Social Interaction Anxiety Scale S174<br />
Sodium valproate S164<br />
Somatic symptoms S139<br />
Somatization S56, S105<br />
Somatoform S105<br />
Soviet times S128<br />
SPECT S62<br />
Spinal Cord Injury 141<br />
SSRI S55, S103<br />
St. John’s Wort S65<br />
Stress S111<br />
Structural brain abnormalities S169<br />
Substance abuse S83, S130<br />
Substance P S51<br />
Substance use S125, S159<br />
Subtypes S189<br />
Sucrose preference S166<br />
Sudden cardiac death S119<br />
Suicide rate S145<br />
Switching S130<br />
Synaptic plasticity S91<br />
Tardive akathisia S144<br />
Tardive dyskinesia S165<br />
Tardive dystonia S201<br />
Tardive syndromes S144<br />
Temperament S54<br />
Ten year period S145<br />
Teratogenicity S190<br />
Terlipressin S141<br />
Testicular mutilation S134<br />
Testosterone S77<br />
Thalamic EEG S118<br />
The quran reciting S145<br />
Therapeutic relationship S41<br />
Therapy S109, S123<br />
Thinking S34<br />
Thrombocytopenia S130<br />
Thyroid hormones S77<br />
Tianeptine abuse S197<br />
Tianeptine dependence S197<br />
Tic disorders S200<br />
TMS S59<br />
Topiramate S182<br />
Tourette’s disorder S160<br />
Transcranial magnetic stimulation (TMS) S60, S117<br />
Transcultural psychiatry S37<br />
Transcultural psychiatry in USA S37<br />
Transgenic S68<br />
Translational medicine S157<br />
Trauma S56, S80, S123, S127<br />
Treatment S87, S89, S93, S96, S101, S105, S126, S151, S174, S176, S196<br />
Treatment outcome S41<br />
Treatment principles and pitfalls S41<br />
Treatment resistance S86<br />
Treatment resistant depression S85<br />
Turkish American cases S37<br />
Typical and atypical antipsychotics S110<br />
Typical antipsychotics S164<br />
UGT1A4 S131<br />
Unintended pregnancy S163<br />
Units S202<br />
Urinary incontinence<br />
Vaginismus S178<br />
Vagus nerve stimulation S60<br />
Valproic acid S126<br />
Valsartan S198<br />
Varenicline S162<br />
VCAM-1 S143<br />
Venlafaxine S127, S175<br />
Ventricular arrhythmias S119<br />
Vigilance-promoting agents S44<br />
Visual and auditory tasks S113<br />
Vitamin D S72, S116<br />
Volumetry S193<br />
Vorbeireden S159<br />
Weight loss S139<br />
Well-being S34<br />
Wellness S34<br />
Wender-Utah rating scale S163<br />
Z hypnotics S202<br />
Zinc deficiency S116<br />
Zinc supplementation S73<br />
Ziprasidone S119<br />
Zuclopenthixol S167<br />
Zuclopenthixol acetate S125<br />
γ –hydroxybutyrate S44
Abalı O. S97<br />
Abnavi M. A. S155<br />
Abolghasemi S. S111<br />
Abtahi M. M. S111<br />
Adler L. A. S135<br />
Adzlin U. B. S42<br />
Aghamohammadi A. S122, S134, S163<br />
Ahl J. S115<br />
Ak İ. S200<br />
Ak M. S54, S127, S171, S174<br />
Akarsu S. S171, S175<br />
Akbıyık M. S193<br />
Akça Ö. F. S72<br />
Akdeniz F. S142<br />
Akkaya C. S81<br />
Aksoy A. S150, S151<br />
Aksoy R. S173<br />
Aksoy Ş. G. S158<br />
Aksoy U. M. S158<br />
Alaçam H. S179<br />
Alev L. S114, S115, S135<br />
Algül A. S59, S167, S175, S199<br />
Allahtavakoli M. S112<br />
Alnıak İ. S152<br />
Alonso M. E. S131, S185, S187<br />
Alowesie R. M. S136<br />
Alpkan L. R. S141<br />
Altaiar H. A. S202<br />
Altın M. S114, S115, S135<br />
Altındağ A. S55<br />
Altınok Ü. S141<br />
Altuğ A. S149<br />
Altunkaynak Y. S144<br />
Amani F. S168<br />
Anderson I. S38<br />
Annagür B. B. S94<br />
Ansari A. S145<br />
Antón J. M. S186<br />
Arıcan H. A. S149<br />
Arıcıoğlu F. S70, S166, S169<br />
Arun K. S47<br />
Ashna S. M. S117<br />
Askari K. S111<br />
Aslan S. S85<br />
Asvadi I. T. S132<br />
Atagün M. İ. S141<br />
Atagün Z. S141<br />
Ateş M. A. S167, S175, S181, S199<br />
Atila Erol S194<br />
Atmaca M. S121<br />
Ay M. E. S108<br />
Ay Ö. İ. S108<br />
Aydemir M. Ç. S101, S138<br />
Aydemir Ö. S90<br />
Aydın A. S87, S130, S146, S171, S178, S179<br />
Aydın E. S121, S136, S172<br />
Aydın E. F. S201<br />
Aydın M. D. S60<br />
Aydın S. S58<br />
Aydınoglu U. S125, S143, S147, S190<br />
Ayhan Bilgiç S73<br />
Ayhan M. G. S135<br />
Aziz S. A. S137<br />
Baharudin A. S137<br />
Bahçeci B. S65, S126<br />
Bakar A. K. B. A. S42<br />
Baker G. B. S35, S50, S68<br />
Bakım B. S59<br />
Balaban Ö. D. S141<br />
Balıbey H. S91, S123, S162<br />
Balikci A. S123<br />
Baran B. S176<br />
Barlak S. S181<br />
Başabak A. S150, S151<br />
Başoğlu C. S175, S181, S199<br />
Başoğlu E. S191<br />
Bayar N. S162<br />
Baykaran M. B. S140, S177<br />
Bayrak A. S192<br />
Bayrak M. S177<br />
Author Index<br />
Beatson S. S128<br />
Beltrán L. S131<br />
Benson S. S152<br />
Beşiroğlu L. S188<br />
Bez Y. S98, S170<br />
Bigdeli O. S113, S183<br />
Bilge D. S192<br />
Bilgin A. A. S160<br />
Bilici M. S142, S191, S192<br />
Boardman B. K. S135<br />
Bolu A. S171, S175<br />
Bora S. S109, S117, S133<br />
Bostancı E. D. S168<br />
Bozkurt A. S127, S174<br />
Brueckl T. S44<br />
Budaklı A. A. S167<br />
Buturak Ş. V. S60<br />
Büyükkınacı A. S198<br />
Büyükşahin F. S162<br />
Can D. Ö. S198<br />
Canan F. S125, S143, S147<br />
Cascorbi I. S45<br />
Cengiz F. F. S138, S166<br />
Cerit C. S198<br />
Cetin M. S78, S175, S199<br />
Ceylan M. E. S133, S134, S171, S178<br />
Chichinadze K. S140<br />
Cho S. S148<br />
Choi J. S. S139<br />
Cloninger C. R. S34<br />
Cumhur Tulay S191<br />
Cumurcu B. E. S158<br />
Çalışkan M. S198<br />
Çam B. S160, S196<br />
Çelenk S. S163<br />
Çelik C. S175<br />
Çelik H. S170<br />
Çelik S. S173<br />
Çetin T. S173<br />
Çetingüç M. S102<br />
Çiftçi A. S201<br />
Çim E. F. A. S179<br />
Çoban A. A. S153<br />
Dalkilic A. S37, S93<br />
Deldar A. S135<br />
Demir A. S125, S142, S192<br />
Demir S. S158<br />
Demirel B. S163<br />
Demirgoren S. S133<br />
Deveci E. S77<br />
Dilbaz N. S124<br />
Diler R. S. S36, S57<br />
Direskeneli G. S. S176<br />
Doğan S. S52<br />
Doksat K. M. S56<br />
Domac F. M. S125<br />
Domianidze T. S140<br />
Dorado P. S131, S185, S186, S187<br />
Döke M. A. S156<br />
Döm H. A. S156<br />
Duran S. S138<br />
Durell T. M. S135<br />
Durmaz O. S175<br />
Dursun S. S50, S68<br />
Durukan İ. S66<br />
Ebrinç S. S71, S175, S181, S199<br />
Efe M. S108<br />
Eker E. S51<br />
Elbi H. S67<br />
Elboğa G. S55<br />
Enli Y. S179<br />
Erbas O. S109, S117, S118, S133<br />
Erdal M. E. S108<br />
Erdem M. S80, S174<br />
Eren İ. S99, S162<br />
Ermis A. S133<br />
Erol A. S92, S129, S156, S180, S182, S194, S195, S197<br />
Ersoy M. A. S85<br />
Ertekin B. A. S176<br />
Ertekin E. S176
Etli T. S162<br />
Evren C. S80, S154, S173<br />
Evren M. B. S162<br />
Evren V. S117<br />
Farjad S. S112<br />
Felati N. M. A. S145<br />
Girit O. C. S133, S134<br />
Glaser P. E. S135<br />
Golchin M. T. S132<br />
Göka Erol S138<br />
Gönen M. S157<br />
Guerrero J. S187<br />
Gulec M. S130<br />
Guveli H. S126<br />
Güçlü O. S121, S136, S172, S177<br />
Güçlü O. G. S144<br />
Gül I. G. S158<br />
Güleç H. S55<br />
Güleç M. S78, S89, S179, S190, S201<br />
Güler J. S161, S162, S168, S195<br />
Gümrü S. S169<br />
Günay H. S68<br />
Güner S. S106<br />
Gürol D. T. S154<br />
Gürvit H. S176<br />
Güven M. S83<br />
Habil M. H. S42<br />
Hamdikene M. S115<br />
Hariri A. G. S142, S185, S195<br />
Hasankhani H. S144, S184<br />
Hashemian F. S113, S183<br />
Hashmi S. S. A. S145<br />
Hegazy R. R. S141<br />
Hergüner A. S139<br />
Hergüner S. S139<br />
Herizchi S. E. S132<br />
Herken H. S108, S170, S179<br />
Hıdıroğlu H. S200<br />
Hızlı G. S58<br />
Hisim O. S133<br />
Hnidek . S48<br />
Hobbs D. S114<br />
Hocaoglu C. S64, S126<br />
Hofmann S. S40<br />
Horacek Jiri S49<br />
Hosseini S. M. S183<br />
Höschl C. S48, S49<br />
Hudson A. L. S35<br />
Hughes M. S108, S189<br />
Ibrahim N. S137<br />
Ismail I. E. S141<br />
İnanlı İ. S162<br />
İpekçioğlu D. S134<br />
İskender B. S187<br />
İşmen M. S150<br />
Jaafar N. R. N. S137<br />
Jan F. S148<br />
Jarrott B. S112<br />
Javadpour A. S155<br />
Johnston P. S108, S189<br />
Jung H. Y. S139<br />
Kabak S. G. S177, S193<br />
Kadıoğlu O. S197<br />
Kalem Ş. A. S176<br />
Kalkancı Ö. S179<br />
Kaptanoğlu B. S179<br />
Kara T. S152, S201<br />
Karadağ F. S62, S154, S179<br />
Karadayı G. S149, S151<br />
Karadere M. E. S163<br />
Karagianis J. S114<br />
Karahan A. S187<br />
Karalar B. S150<br />
Karaman U. S149<br />
Karaman Z. S149<br />
Karamustafalıoğlu O. S193<br />
Karataş K. S. S159, S168, S195<br />
Karayılan S. S129, S194<br />
Karimi S. S144, S184<br />
Karlıdağ R. S158<br />
Author Index<br />
Kartalcı Ş. S158<br />
Kavzoğlu S. Ö. S142<br />
Kaya M. C. S66, S170<br />
Kaya N. S127, S135, S149<br />
Kaya Z. E. S124<br />
Kazantzis N. S41<br />
Kazemi M. S144, S184<br />
Kazemi S. S144, S184<br />
Kechrid Z. S115<br />
Kenar J. S159<br />
Kenawy S. A. S141<br />
Kennedy V. S148<br />
Kesebir S. S140, S142<br />
Khananashvili M. S140<br />
Kheirabadi G. R. S116<br />
Kılıç S. S104<br />
Kılınç E. S134<br />
Kırlı S. S39, S81<br />
Kim B. S148<br />
Kim J. S148<br />
Kim M. H. S124<br />
Kirsch I. S38<br />
Koca E. K. S125<br />
Koç C. S150, S151<br />
Konkan R. S121, S136, S144, S172, S177<br />
Korkmaz S. S121<br />
Kuloglu M. S121<br />
Kumsar N. A. S156, S180, S182<br />
Kurt H. S196<br />
Kuru T. S163<br />
Kültür S. E. Ç. S73<br />
Labadze I. S140<br />
Lalies M. S35<br />
Lazarashvili A. S140<br />
Lee H. W. S139<br />
Lee J. Y. S139<br />
Lledó E. P. S131, S185, S186, S187<br />
Llerena A. S45, S131, S185, S186, S187<br />
López M. S131, S187, S185<br />
Machín E. S131<br />
Mackay M. S50<br />
Maden O. S127<br />
Mahmodi G. S111, S155<br />
Majd M. S113, S183<br />
Maner F. S53, S133, S134, S158, S178<br />
Maracy M. R. S116<br />
Martin P. R. S35<br />
Matitaishvili T. S140<br />
Mazlum B. S74<br />
Mcgough J. J. S135<br />
Melledo J. M. S50<br />
Meral G. S199<br />
Meyers A. S115<br />
Min S. S124<br />
Mislan N. S137<br />
Mitchell N. D. S50, S69<br />
Mohamadzadeh S. S154, S155<br />
Mohr P. S48<br />
Mokri A. S113<br />
Molavi H. S111<br />
Monroy N. S131<br />
Moshtaghian J. S111<br />
Mutlu E. S171, S173, S178<br />
Nachnani M. S128<br />
Nasiripour A. A. S155<br />
Neale C. S108, S152, S189<br />
Nebioğlu M. S198<br />
Negahban T. S145<br />
Nuray Atasoy S76<br />
Oakes T. M. M. S115<br />
Oral E. S88, S201<br />
Ortega A. S131<br />
Ozşahin A. A. S125, S127<br />
Ögel K. S105, S149, S150, S151, S153, S154<br />
Öneş K. S141<br />
Öyekçin D. G. S182<br />
Özata B. S176<br />
Özbek K. S114, S115<br />
Özçelik N. B. V. S61<br />
Özçetin A. S103<br />
S208 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Özdemir B. S175<br />
Özdemir F. A. S190<br />
Özdemir O. S188<br />
Özdemir P. G. S146, S179<br />
Özdemir S. S190<br />
Özen N. E. S68<br />
Özer H. S197<br />
Özgen F. S171<br />
Özkol H. S188<br />
Özkorumak E. S64, S187, S200<br />
Özmen M. S90<br />
Özmenler K. N. S175<br />
Özşahin A. S171, S174<br />
Özten M. S194, S195<br />
Öztürk M. S57<br />
Öztürk N. S176<br />
Palenicek T. S49<br />
Panahi M. V. S. S183<br />
Paparrigopoulos T. S42, S43<br />
Papavasiliou A. S44<br />
Park K. C. S124<br />
Parlak S. Ç. S192<br />
Peker G. O. S117, S133<br />
Perdeci Z. S162<br />
Perreault A. S35<br />
Pieri M. C. S109<br />
Pigott T. A. S135<br />
Piri I. T. S132<br />
Prakash A. S115<br />
Ranjkesh M. S116<br />
Rashid R. A. S42<br />
Raskin J. S114<br />
Rubin R. L. S135<br />
Sabri A. A. A. S145<br />
Sabri Hergüner S74<br />
Saglam S. S121<br />
Sahmelikoglu O. S133<br />
Salehi M. S116<br />
Sanaat Z. T. S132<br />
Sarıdoğan G. E. S198<br />
Sarıkaya Ö. Ö. S182<br />
Sarkis E. S. S135<br />
Sarp K. S126<br />
Sarp N. S153<br />
Savaş H. A. S170<br />
Saygılı İ. S164, S165, S185<br />
Sayyadi A. R. S145<br />
Scholey A. S108, S152, S189<br />
Seifertova D. S48<br />
Selek S. S170<br />
Selvi Y. S88, S146, S188, S190<br />
Semerci B. S96<br />
Semiz Ü. B. S164, S165, S191, S192<br />
Sezlev D. S171<br />
Shabanloui R. T. S132<br />
Shafaie J. S112<br />
Shaker A. S168<br />
Sharaf O. A. S141<br />
Sharifi A. S113, S183<br />
Sheehan D. S115<br />
Shin J. S124<br />
Shin M. S148<br />
Shohrati M. S113<br />
Sidi H. S137<br />
Silsüpür G. S198<br />
Sinani G. S125, S143, S147<br />
Sinici E. S127<br />
Soldatos C. R. S43<br />
Son Y. A. S101, S156, S197<br />
Sonmez E. O. S127<br />
Sook A. J. S124<br />
Soyer B. S159, S168<br />
Spaniel F. S49<br />
Stough C. S152<br />
Sundar A. S. S46<br />
Sungur M. Z. S41, S121, S136, S172, S177<br />
Sünbül E. A. S138, S166<br />
Author Index<br />
Sünbül M. S138<br />
Şahan E. S198<br />
Şehirli Ö. S169<br />
Şengül C. B. S100, S108, S179<br />
Şenormancı G. S144<br />
Şenormancı Ö. S53, S121, S136, S144, S172<br />
Şimşek G. S192<br />
Şimşek Y. S198<br />
Tabatabayi M. S. S113<br />
Taner E. S63<br />
Taner H. A. S160<br />
Taner Y. S160<br />
Tarhan N. S58<br />
Tellioglu T. S37<br />
Terán E. S131<br />
Tezcan A. E. S140<br />
Thirunavukarasu M. S46, S47<br />
Tıkır Baise S138<br />
Tiryaki A. S187, S200<br />
Toğul H. S160<br />
Topçuoğlu Ö. B. S168<br />
Toprak B. S140<br />
Torres E. L. S186<br />
Tosun M. S84<br />
Trejo H. S185, S187<br />
Treuer T. S114<br />
Tuncel Y. Y. S156<br />
Turan T. S76<br />
Tükel R. S176<br />
Tülüce Y. S188<br />
Türkbay T. S95<br />
Türker T. S162<br />
Uğur M. S75<br />
Uguz F. S70, S135, S146<br />
Uhr M. S44<br />
Ulusoy S. S152<br />
Utkan T. S166, S169<br />
Utkan T. S169<br />
Uz Y. S125<br />
Uzun Ö. S171<br />
Ülkü M. S173<br />
Ünal A. S97, S161, S162<br />
Ünay D. S62<br />
Ünübol B. S161, S162<br />
Ünübol H. S161, S162<br />
Üstünkar G. S156, S197<br />
Valesova V. B. S49<br />
Valzdorf E. S128, S129, S181<br />
Williams D. W. S135<br />
Würz A. S104<br />
Yaci H. S125<br />
Yanartaş Ö. S164, S165, S185<br />
Yang Y. S148<br />
Yanık T. S171<br />
Yarcı E. S169<br />
Yavuz K. F. S152, S163<br />
Yazır Y. S169<br />
Yeloglu Ç. H. S126<br />
Yenel A. S191, S192<br />
Yeroham R. S150<br />
Yeşil B. S158<br />
Yılbaş B. S157<br />
Yıldız M. S86<br />
Yılmaz O. S199<br />
Yılmaz Y. S164, S165, S185, S192<br />
Yiğiter S. S173<br />
Yousefi F. S154<br />
Yucel A. S130<br />
Yuksel R. N. S124<br />
Yüce M. S96<br />
Yücel B. S94<br />
Yükselir C. S174<br />
Zafari M. S111, S122, S134, S155, S163<br />
Zakaria H. B. S42<br />
Zaki H. F. S141<br />
Zepeda N. S35<br />
Zincir S. B. S79, S165, S177, S191, S192