SYMPOSIA

With Contributions of

Dear Colleagues, 

INTRODUCTION and WELCOME 

We are very proud to invite you and to have the honour to host you at the “4 th International Congress on 

Psychopharmacology” which will be held in Antalya on November 23-27, 2011 as the Turkish Association for Psychopharmacology 

(TAP) Conference. 

The theme of the congress is: “Innovations and continuity in psychiatry & psychopharmacology: better care for better 

health.” 

We haven chosen to combine two key concepts as the main theme of this conference: ‘Innovations” and “Continuity”. This 

is simply to reflect the fact that the field of psychopharmacology has been progressing rapidly with very novel psychotropic 

medications being launched faster then ever. 

Furthermore, many patients with mental illness present with a wide-range of psychiatric and medical co-morbidities which 

require the treating clinician to have an up-to-date knowledge of psychotropic medications to be able to provide effective and 

optimal treatments. Therefore, “continuity” refers to the fact that there is a gap between evidence-based practice guidelines 

and actual care in clinical practice for patients with mental illnesses, a lack of “continuity” of knowledge to be shared with the 

clinician. One of the objectives of this conference is to fill this gap by our rich scientific programme! 

This year’s conference will help participants and clinicians to be able to discuss and to gain insight into translating the latest 

evidence-based research into actual clinical practice, to assess where new psychotropic medications fit into patient-centred 

treatment strategies and to get direct guidance on the toughest clinical challenges to help patients presenting with complex 

psychiatric needs. 

This conference will be a wonderful opportunity, not only to present the results of your work, but also to meet, to 

communicate and to discuss research issues with other colleagues from the field in a beautiful and sunny part of the World. 

There is no doubt that the 4 th International Congress on Psychopharmacology will provide a warm and an elite atmosphere 

in Antalya for discussions, solutions, and practical suggestions about daily practice problems and issues. We hope that 

this will an opportunity for you, to refresh, update, and expand your knowledge in the major and challenging domains of 

psychopharmacology, biological psychiatry, neuroscience and neuroimaging, by contributions from Turkish and international 

researchers and clinicians. The Congress aims to create an interactive platform, where all participants are encouraged to ask 

questions and share their experiences about difficult and treatment resistant cases. 

As always and as expected, the Congress will bring together scientists from Turkey and other internationally renowned 

scientists to share experiences and ideas on the latest developments in psychopharmacology at the conference, symposia, 

debates, bilateral and multilateral discussion sessions, and satellite symposia. This congress will also dedicate time to ‘meet the 

specialist’ sessions and courses, which will be held by distinguished scientists in the field. 

Furthermore, the traditional “The Poster Presentation Research Incentive Awards” will also be presented at the 4 th 

International Congress on Psychopharmacology to the top three posters selected by the jury. 

The most exciting and novel aspect of this Congress is that it is the first International conference organized by TAP. 

We will be hosting fellow Associations, and fellow participants who are part of these Associations, from all over the world 

including Canada, Malaysia, India, The Czech Republic, Greece, China, Hungary, USA, The UK, Australia, Israel, Iran, Russia, 

Germany, The Netherlands, and The Ukraine. 

Furthermore, there will be joint symposia with International Fellow and Partner Associations at this meeting. It is hoped that 

this will increase International research collaborations. 

Abstracts of all the presentations submitted to the 4 th International Congress on Psychopharmacology will be published in 

the latest issue of the Bulletin of Clinical Psychopharmacology as a supplement. This will ensure that these presentations are 

available to be accessed at the SCI-E. 

We hope that the conference will be a fruitful and enjoyable experience for all participants and we are looking forward to 

meeting you in beautiful and sunny Antalya, Turkey! 

The 4 th ICP Organizing Committee

Turkish Association for Psychopharmacology 

4 th International 

Congress on Psychopharmacology 

“Innovations and continuity in psychiatry & 

psychopharmacology: better care for better health” 

November 23-27, 2011 

Antalya, Turkey 

PROGRAM 

www.psychopharmacology2011.org

Cengiz Han AÇIKEL 

Feyza ARICIOĞLU 

Murad ATMACA 

Glen BAKER (Canada) 

Cengiz BAŞOĞLU 

Alican DALKILIÇ (USA) 

Rasim Somer DİLER (USA) 

Serdar DURSUN (Canada) 

Servet EBRİNÇ 

Atila EROL 

Ayhan ALGÜL 

M. Alpay ATEŞ 

İsmail AK 

Lütfullah BEŞİROĞLU 

Mustafa BİLİCİ 

Sunar BİRSÖZ 

Ömer BÖKE 

M. Emin CEYLAN 

Mecit ÇALIŞKAN 

Murat DEMET 

Nesrin DİLBAZ 

H. Murat EMÜL 

Cüneyt EVREN 

Ömer GEÇİCİ 

Erdal IŞIK 

Fatih KARAASLAN 

Nesrin KARAMUSTAFALIOĞLU 

CO-CHAIRS 

Mesut ÇETİN 

Oğuz KARAMUSTAFALIOĞLU 

PROGRAM COMMITTEE MEMBERS 

Ömer GEÇİCİ 

Ali Saffet GÖNÜL 

Hasan HERKEN 

Numan KONUK 

Samet KÖSE (USA) 

David OSSER ( USA) 

Haluk A. SAVAŞ 

Tahir TELLİOĞLU (USA) 

Tümer TÜRKBAY 

Ömer YANARTAŞ 

SECRETARIAT TREASURERS 

EXECUTIVE COMMITTE 

Yasin BEZ 

Gökay ALPAK 

Nazmiye KAYA 

Selim KILIÇ 

Selçuk KIRLI 

Erhan KURT 

Ömer ÖZBULUT 

Bengi SEMERCİ 

Ümit Başar SEMİZ 

Aytekin SIR 

M. Zihni SUNGUR 

M. Hakan TÜRKÇAPAR 

Özcan UZUN 

İlhan YARGIÇ 

Ümit YAŞAR 

Kazım YAZICI 

Mustafa YILDIZ 

COMMITTEES

Nihat ALPAY 

Rüstem AŞKIN 

Ömer AYDEMİR 

İbrahim BALCIOĞLU 

Mustafa BAŞTÜRK 

Erhan BAYRAKTAR 

Meral BERKEM 

Can CİMİLLİ 

Ali ÇAYKÖYLÜ 

Orhan DOĞAN 

M. Kerem DOKSAT 

Ali DORUK 

Alaattin DURAN 

Engin EKER 

Ercan ABAY 

Mehmet Yücel AĞARGÜN 

Fisun AKDENİZ 

Tunç ALKIN 

Köksal ALPTEKİN 

Jules ANGST (Switzerland) 

Zehra ARIKAN 

Çiğdem AYDEMİR 

Cahide AYDIN 

Nazan AYDIN 

İsmail Hakkı AYHAN 

Glen BAKER (Canada) 

David BALDWIN (UK) 

Reha BAYAR 

Oğuz BERKSUN 

Mansur BEYAZYÜREK 

Michel BOURIN (France) 

Charles BOWDEN (USA) 

Adnan CANSEVER 

John COOKSON (UK) 

Behçet COŞAR 

Duran ÇAKMAK 

Abdülkadir ÇEVİK 

Ali Savaş ÇİLLİ 

Ayşen ÇOŞKUN 

Bülent ÇOŞKUN 

Bill DEAKIN (UK) 

Melissa DELBELLO (USA) 

Yunus Emre EVLİCE 

Max FINK (USA) 

Guy GOODWIN (UK) 

ORGANIZING COMMITTEE 

Hayriye ELBİ METE 

Hüsnü ERKMEN 

Ertuğrul EŞEL 

Erol GÖKA 

Mustafa GÜLTEPE 

Hayrettin KARA 

İsmet KIRPINAR 

Işın Baral KULAKSIZOĞLU 

Bekir Aydın LEVENT 

Özgür ÖNER 

Aytekin ÖZŞAHİN 

Mücahit ÖZTÜRK 

M. Kemal SAYAR 

Sefa SAYGILI 

INTERNATIONAL SCIENTIFIC ADVISORY BOARD 

Başak ÖZÇELİK 

Erol GÖKA 

Peykan GÖKALP 

Bahar GÖKLER 

Ayça GÜRDAL KÜEY 

Hatice GÜZ 

David GREENBERG (Israel) 

Çiçek HOCAOĞLU 

İlkin İÇELLİ 

Rene S. KAHN (The Netherlands) 

Ayhan KALYONCU 

Emine KILIÇ 

Neşe KOCABAŞOĞLU 

Stan KUTCHER (Canada) 

Levent KÜEY 

Lee Wei LIM (Netherlands) 

Karl LOOPER (Canada) 

Herbert MELTZER(USA) 

Levent METE 

Hasan MIRSAL 

Nahit MOTAVALLI MUKADDES 

Norbert MULLER (Germany) 

Donald Hugh MYRICK (USA) 

Ziad NAHAS (USA) 

Andrew NIERENBERG (USA) 

David NUTT (UK) 

Jim Van OS (The Netherlands) 

David OSSER (USA) 

Timuçin ORAL 

Süha ÖZAŞKINLI 

Haluk ÖZBAY 

Ayşegül ÖZERDEM 

COMMITTEES 

Levent SEVİNÇOK 

Vedat ŞAR 

Cem ŞENGÜL 

Lut TAMAM 

Bilgen TANELİ 

Ertan TEZCAN 

Musa TOSUN 

Tayfun TURAN 

Raşit TÜKEL 

Müfit UĞUR 

Medaim YANIK 

Yankı YAZGAN 

Ayşegül YILDIZ 

Salih ZOROĞLU 

Fuat ÖZGEN 

Mine ÖZKAN 

Sedat ÖZKAN 

Mine ÖZMEN 

Nurgül ÖZPOYRAZ 

Özden PALAOĞLU 

Özkan PEKTAŞ 

Jorge A. QUIROZ (USA) 

Gary SACHS (USA) 

Armağan SAMANCI 

Bilgin SAYDAM 

Seher SOFUOĞLU 

Haldun SOYGÜR 

Atilla SOYKAN 

Ahmet Rıfat ŞAHİN 

Rajiv TANDON (USA) 

Işık TUĞLULAR 

Zeliha TUNCA 

Ömer TUNCER 

Hamdi TUTKUN 

Ümran TÜZÜN 

Berna ULUĞ 

Aylin ULUŞAHİN 

Tayfun UZBAY 

Alp ÜÇOK 

Süheyla ÜNAL 

Simavi VAHİP 

Hans Peter VOLZ (Germany) 

Axel WÜRZ (UK) 

Olcay YAZICI 

Nevzat YÜKSEL 

Joseph ZOHAR (Israel)

JOINT SYMPOSIUMS WITH INTERNATIONAL PARTNER SOCIETIES 

Canadian College of 

Neuropsychopharmacology (CCNP) 

Czech NeuroPsychopharmacological 

Society (CNPS) 

Hellenic Society for the Advancement 

of Psychiatry and Related Sciences 

Ian ANDERSON 

Kandasamy ARUN 

Glen BAKER 

Tanja BRUECKL 

Ingolf CASCORBI 

C. Robert CLONINGER 

Alican DALKILIÇ 

Rasim Somer DİLER 

Serdar DURSUN 

Serdar GÜNER 

Mohamed Husain HABIL 

Stefan HOFMANN 

Jirí HORÁCEK 

Cyril HOSCHL 

Alan Leslie HUDSON 

Nikolaos KAZANTZIS 

INVITED INTERNATIONAL SPEAKERS 

CV’s of international guest speakers can be found at 

www.psychopharmacology2011.org 

Irving KIRSCH 

Adrián LLERENA 

Peter R. MARTIN 

Pavel MOHR 

Tomas PALENICEK 

Thomas J. PAPARRIGOPOULOS 

Antigone S. PAPAVASILIOU 

Rusdi Abd. RASHID 

Umi Adzlin SILIM 

Constantin R. SOLDATOS 

A. Shyam SUNDAR 

Tahir TELLİOĞLU 

Manickam THIRUNAVUKARASU 

Axel WÜRZ 

Hazli ZAKARIA 

Joseph ZOHAR 

SPEAKERS 

The International Union of Basic and 

Clinical Pharmacology (IUPHAR) 

Turkish Association for Cognitive 

Behaviour Psychotherapy (TACBP) 

International Association for 

Cognitive Psychotherapy (IACP) 

Indian Psychiatric Society Malaysian Psychiatric Association

NOVEMBER 23, 2011 WEDNESDAY 

TIME HALL A HALL B HALL C 

13.30 ARRIVING TO HOTEL - REGISTRATION 

15.00-16.00 

OPENING CONFERENCE 

Evolution of human brain functions: Identifying 

psychobiological targets for promoting well-being 

Claude Robert Cloninger, USA 

16.30-17.00 COFFEE BREAK 

17.30-19.30 

PS-01 

Epigenetics or genetics: Gene-environment 

interactions over the life - span 

PS-02 

Behavioral addictions and treatments: 

Review of recent data 

ABBREVIATIONS OC Opening Conference KL Lecture PS Symposium MD Debate JS Joint Symposium KC Course WS Workshop 

AT A GLANCE 

PS-03 

Painful syndromes in psychiatry and their 

managements

NOVEMBER 24, 2011 THURSDAY 

TIME HALL A HALL B HALL C HALL D HALL E 

09.00-10.30 

KL-01 

Treatment of opioid 

dependence 

during pregnancy 

Peter R. Martin, USA 

PS-04 

Adult attention - deficit 

hyperactivity disorder 

(ADHD) and comorbidity 


11.00-12.30 

MD-01: DEBATE 

Antidepressants are not 

associated with suicide risk 

Serdar Dursun, Canada 

Nesrin Dilbaz, Türkiye 

Hakan Türkçapar, Türkiye 

PS-06 

Neuroimaging in 

psychopharmacology: An 

update 

12.30-13.30 LUNCH 

13.30-14.30 

14.30-16.00 

SATELLITE SYMPOSIUM 

MD-02: DEBATE 

Antidepressants are useful 

in treatment of depression 

M. Zihni Sungur, Türkiye 

Ian Anderson, UK 

Irving Kirsch, UK / USA 


16.30-18.00 

KL-02 

Benzylpiperazine; a major 

contaminant of ecstasy, 

induces marked changes 

in rat brain neurochemistry 

and behavior 

Alan Leslie Hudson, Canada 

JS-01 

International Association for 

Cognitive Psychotherapy (IACP) 

Advances and problems in 

Cognitive Behavior Therapy 

(CBT) 


18.30-20.30 

20.30-22.30 

JS-02 

Malaysian Psychiatric 

Association 

Malaysian perspective of 

substance dependence 

PS-07 

The rationale of 

antipsychotic combinations 

in schizophrenia: 

Epidemiological and clinical 

evidences 

PS-05 

Brain mapping, TMS, NVS, 

biofeedback and deep brain 

stimulation in treatment of 

psychiatric disorders 

POSTER SESSIONS 

ORAL SESSIONS 

PS-08 

Advances in complementary 

alternative psychotropic 

drugs: Fish oil (omega-3 

fatty acids), vitamine B12, 

folate ve other add-on 

therapies in psychiatric 

disorders 

KC-04 

Mindfulness and acceptance 

based therapies 

Kültegin Ögel, Türkiye 


COURSE 

KC-01 

Biostatistics - Basic 

part 1 

Selim Kılıç, Türkiye 

KC-02 

Biostatistics - 

Intermediate part 1 

Cengiz Han Açıkel, Türkiye 

AT A GLANCE 

THERAUPATIC ALLIENCE 

EDUCATION PROGRAM 

15.00-19.00 

THERAUPATIC ALLIENCE 

EDUCATION PROGRAM 

Hakan Türkçapar 

Sponsored by

NOVEMBER 25, 2011 FRIDAY 

AT A GLANCE 


09.00-10.30 

KL-03 

Unipolar versus bipolar depression 

in children: What do we know 

about the etiology, diagnosis, and 

treatment? 

Rasim Somer Diler, USA 

PS-09 

From preclinical studies to clinical 

practice in anxiety disorders 


11.00-12.30 

MD-03: DEBATE 

Antidepressants are useful in the 

treatment of bipolar disorders 

Haluk Savaş, Türkiye 

Selçuk Kırlı, Türkiye 

Kaan Kora, Türkiye 

PS-11 

Psychotropic drug treatments 

during pregnancy and lactation 

12.30-13.30 LUNCH 

13.30-14.30 

14.30-16.00 


PS-13 

Hormones and psychiatric 

disorders 

PS-14 

Clinical course of psychiatric 

disorders associated with trauma 

and treatment issues 


16.30-18.00 

KL-04 

Transcultural psychiatry (a 

comparison of USA - Türkiye and 

sample cases) 

Alican Dalkılıç, USA 

JS-03 

Hellenic Society for the Advancement 

of Psychiatry and Related Sciences 

Disorders of sleep and wakefulness 

and their pharmacological 

management 


18.30-20.30 

20.30-22.30 

21.30 

JS-04 

The International Union of Basic 

and Clinical Pharmacology 

(IUPHAR) 

Pharmacogenomics of 

psychoactive drugs 

“DÜŞÜNEN ŞARKILAR” 

SOSYAL PROGRAM 

PS-16 

Marijuana; from mellow to 

madness 

PS-10 

Will glutamatergic modulators be 

a target for the future therapy of 

depression? 

PS-12 

Vitamin and mineral 

supplementation in treatment of 

childhood psychiatric disorders 

COURSE 

KC-03 

CBT in somatization disorders 

Axel Würz, UK 

PS-15 

Depression and pain 

PS-17 

Overcoming treatment resistance: 

An update 

WS-01 

Management of panic disorder 

Serdar Güner, The Netherlands 

COURSE and WORKSHOP 

KC-01 


part 2 


KC-02 



Cengiz Han Açıkel, Türkiye

NOVEMBER 26, 2011 SATURDAY 

NOVEMBER 27, 2011 SUNDAY 


AT A GLANCE 


09.00-10.30 

JS-05 

Indian Psychiatric Society 

Current concept of obsessive 

compulsive disorder (OCD) 

KL-05 

Medical marijuana use in 

psychiatry 

Tahir Tellioğlu, USA 


11.00-12.30 

KL-06 

Early intervention in anxiety and 

depression: What we know, what 

we don’t know and what we 

should know? 

Joseph Zohar, Israel 

PS-19 

Are the effects of 

psychopharmacological and 

other therapeutic approaches 

neuroregenerative or 

neurodegenerative? Review of 

recent data 

12.30-13.30 LUNCH 

13.30-15.30 

JS-06 

Czech NeuroPsychopharmacological 

Society (CNPS) 

From models of schizophrenia 

to clinical outcome: A 

psychopharmacological perspective 

PS-21 

Treatment approaches to 

comorbidities of ADHD 


16.00-18.00 

JS-07 

Canadian College of 

Neuropsychopharmacology 

Advances in psychotropic drug 

development: Promising novel targets 

and agents for psychiatric disorders 

PS-22 

How to fight with bipolar disorder? 

From guidelines to clinical 

practice: Myths and realities 


18.30-20.30 

WS-02 

Residency and fellowship training 

and short-term research / clinical 

possibilities in psychiatry in USA 

Tahir Tellioğlu, USA 

Alican Dalkılıç, USA 

PS-18 

Chronobiotics and 

chronotherapeutics in psychiatry 

PS-20 

Controversial topics in eating 

disorders 

PS-23 

Individualized medicine: 

Focus on pharmacogenetics 

KC-05 

EMDR course 


TIME HALL A 

09.00-10.30 

COURSE and WORKSHOP 

KC-01 


part 3 


PS-24 

Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety 


11.00-12.00 CLOSING and AWARDS CEREMONY 

KC-02 



Cengiz Han Açıkel, Türkiye

13.30 

15.00-16.00 

17.30-19.30 

17.30-19.30 

17.30-19.30 

Arriving to hotel - registration 


NOVEMBER 23, 2011 WEDNESDAY 

Chairperson: M. Kemal Sayar, Türkiye 

16.30 - 17.00 COFFEE BREAK 

PS-01: Epigenetics or genetics: Gene-environment interactions over the life - span 

PS-02: Behavioral addictions and treatments: Review of recent data 

PS-03: Painful syndromes in psychiatry and their managements 

SCIENTIFIC PROGRAM 

HALL A 

Evolution of human brain functions: Identifying Claude Robert Cloninger, USA 

psychobiological targets for promoting well-being 

Co-chairs: Neşe Kocabaşoğlu, Türkiye - Alan Leslie Hudson, Canada 

From genes to epigenetics: Etiopathogenic mechanisms of diseases Ahmet Korkmaz, Türkiye 

Psychiatric disorders: Genes or childhood traumas? Ümit Başar Semiz, Türkiye 

ADHD: Genetics and /or acquired? Özgür Öner, Türkiye 

Psychosis: Genes and /or addictive subtances? Ali Doruk, Türkiye 

Alzheimer’s dementia: Genes and /or life-style? Engin Eker, Türkiye 

Alzheimer’s disease, genes and biomarkers Işın Baral Kulaksızoğlu, Türkiye 

Co-chairs: Bekir Aydın Levent - Lütfullah Beşiroğlu, Türkiye 

Co-chairs: Abdülkadir Çevik - Erol Göka, Türkiye 

HALL B 

Internet addiction Lut Tamam, Türkiye 

Shopping addiction Levent Sevinçok, Türkiye 

Pathological gambling Ömer Şenormancı, Türkiye 

From Don Juanism and nymphomania to hypersexual disorders Sultan Doğan, Türkiye 

Trichotillomania Ramazan Konkan, Türkiye 

Is binge eating a type of addiction? Fulya Maner, Türkiye 

HALL C 

Personality characteristics of pain in psychiatric disorders Mehmet Ak, Türkiye 

At the pain junction fibromyalgia syndrome and depression M. Kemal Sayar, Türkiye 

Alexithymia and painful syndromes Hüseyin Güleç, Türkiye 

Differences of SSRI and SNRI antidepressants of painful Abdurrahman Altğndağ, Türkiye 

syndromes treatments in psychiatry 

Hypnotherapy for painful syndromes in psychiatry M. Kerem Doksat, Türkiye

09.00-10.30 

11.00-12.30 

13.30-14.30 

14.30-16.00 

16.30-18.00 

18.30-20.30 




HALL A 

KL-01: Treatment of opioid dependence during pregnancy Peter R. Martin, USA 

Chairperson: Nazan Aydın, Türkiye 


MD-01: Antidepressants are not associated with suicide risk 

Moderator : Serdar Dursun, Canada 

Proponent : Nesrin Dilbaz, Türkiye 

Opponent : Hakan Türkçapar, Türkiye 

12.30 - 13.30 LUNCH 


MD-02: Antidepressants are useful in treatment of depression 

Moderator : M. Zihni Sungur, Türkiye 

Proponent : Ian Anderson, UK 

Opponent : Irving Kirsch, UK / USA 


KL-02: Benzylpiperazine; a major contaminant of ecstasy, induces Alan Leslie Hudson, Canada 

marked changes in rat brain neurochemistry and behavior 

Chairperson: İlhan Yargıç, Türkiye 


JS-02: Malaysian Psychiatric Association 

Malaysian perspective of substance dependence 

Co-chairs: Mohamed Husain Habil, Malaysia - Haluk Savaş, Türkiye 

Drug problems and harm reduction approach in Malaysia Mohamed Husain Habil, Malaysia 

National methadone maintenance therapy program (MMTP): Hazli Zakaria, Malaysia 

An update of five pilot projects in Malaysia 

Spiritually enhanced drug addiction rehabilitation (SEDAR) program: Rusdi Abd Rashid, Malaysia 

The innovative ways to upscale MMTP in Malaysia 

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 

Co-chairs: Alan Leslie Hudson, Canada - Nesrin Dilbaz, Türkiye 

ADHD and prognosis Yasemen Işık Taner, Türkiye 

ADHD in adults: Impulsivity components and links with aggression Yankı Yazgan, Türkiye 

ADHD and substance use Cengiz Tuğlu, Türkiye 

ADHD and mood disorders in children Rasim Somer Diler, USA 

ADHD and psychotic disorders Cengiz Başoğlu, Türkiye 

Academic and occupational problems in ADHD Mücahit Öztürk, Türkiye 

11.00-12.30 PS-06: Neuroimaging in psychopharmacology: An update 

16.30-18.00 


Co-chairs: Peter Martin, USA - Ali Saffet Gönül, Türkiye 

Neuroimaging studies in dementia, psychiatric disorders, drug discovery and more... Devrim Ünay, Türkiye 

Imaging of the serotonergic system in depression and anxiety Murad Atmaca, Türkiye 

Can psychiatric disorders be predicted by neuroimaging studies? Ali Saffet Gönül, Türkiye 

What is the real meaning of ventricular enlargement in schizophrenia? Buğçe Vedin, Türkiye 

From two dimensions to the third dimension 

12.30 - 13.30 LUNCH 



JS-01: International Association for Cognitive Psychotherapy (IACP) 

Advances and problems in Cognitive Behavior Therapy (CBT) 

Co-chairs: M. Zihni Sungur, Türkiye - Stefan Hofmann, USA 

18.30-20.30 PS-07: The rationale of antipsychotic combinations in schizophrenia: Epidemiological and clinical evidences 

Co-chairs: Pavel Mohr, Czech Republic - İsmail Ak, Türkiye 


HALL B 

Recent advances in the treatment of anxiety disorders Stefan Hofmann, USA 

Recent advances in translating science into practice: Collaborative Nikolaos Kazantzis, Australia 

empiricism and engagement with homework assignments 

As an evidence based approach CBT: Alarms in the treatment and M. Zihni Sungur, Türkiye 

application mistakes 


Comorbidity vs co-occurrence in schizophrenia Özcan Uzun, Türkiye 

What are the scientific bases of the use of atypical antipsychotics? Ender Taner, Türkiye 

Pharmacogenetics and antipsychotic combinations Filiz Karadağ, Türkiye 

Is there any connection between depression and schizophrenia? Abdullah Akpınar, Türkiye 

Between extrapyramidal and metabolic side effects of antipsychotics: What can we do? Erdal Işık, Türkiye 

Other side effects of antipsychotics: What can we do? H. Murat Emül, Türkiye


HALL C 

09.00-10.30 PS-05: Brain mapping, TMS, NVS, biofeedback and deep brain stimulation in treatment of psychiatric disorders 

Co-chairs: Ercan Abay, Türkiye 

Brain mapping and computerized EEG treatment and biofeedback Mert Savrun, Türkiye 

of psychiatric disorders 

Transcranial Magnetic Stimulation (TMS) as a treatment for depression Ayhan Algül, Türkiye 

What is the best method of targeting TMS for depression? Novel rTMS Nevzat Tarhan, Türkiye 

depression treatment protocols 

What does transcranial magnetic stimulation (TMS) promise in Bahadır Bakım, Türkiye 

psychiatric disorders other than depression? Future perspectives 

Deep brain stimulation as an alternative treatment for Mehmet Aydın, Türkiye 

neuropsychiatric disorders 

Nervus Vagus Stimulation (NVS) in depression treatment Sadiye Visal Buturak, Türkiye 


11.00-12.30 POSTER SESSIONS 

14.30-16.00 ORAL SESSIONS 

Co-chairs: Haluk Savaş - Ayhan Algül, Türkiye 

12.30 - 13.30 LUNCH 

Co-chairs: Ali Saffet Gönül - Yasin Bez, Türkiye 




18.30-20.30 PS-08: Advances in complementary alternative psychotropic drugs: Fish oil (omega-3 fatty acids), 

vitamine B12, folate ve other add-on therapies in psychiatric disorders 

Co-chairs: Manickam Thirunavukarasu, India - Mesut Çetin, Türkiye 


What are the mechanisms of omega-3 fatty acids, vitamine B12, Cemal Kaya, Türkiye 

folate and other add-on therapies in psychiatric disorders? 

Omega-3 fatty acids in ADHD treatment İbrahim Durukan, Türkiye 

Are omega-3 fatty acids useful in maintenance treatments? Armağan Samancı, Türkiye 

Is fish oil promising in treating depression during pregnancy and lactation? Evrim Özkorumak, Türkiye 

Can St. John’s Wort be an alternative treatment of depression? Çiçek Hocaoğlu, Türkiye 

Complementary medicine alternatives in other psychiatric disorders Bülent Bahçeci, Türkiye 

(sleep, pain, etc.)

20.30-22.30 KC-01: Biostatistics - Basic part 1 


20.30-22.30 KC-02: Biostatistics - Intermediate part 1 


20.30-22.30 KC-04: Mindfulness and acceptance based therapies 

Kültegin Ögel, Türkiye 

15.00-19.00 THERAUPATIC ALLIENCE EDUCATION PROGRAM 

Hakan Türkçapar 

Sponsored by 


COURSES 

HALL D 

HALL E 

HALL C 

KC-01 & KC-02 Course participants should bring NOTEBOOK or NETBOOK with them. 

KC-01 & KC-02 Course registration is limited to 15 people for each and early application is recommended to register. 

There is no limit to the number of participants for courses other than KC-01 and KC-02 courses which are limited with 15 

participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro 

THERAUPATIC ALLIENCE EDUCATION PROGRAM 

Theraupatic Allience Education Program is limited to 40 people. Early application is recommended to register.

09.00-10.30 

11.00-12.30 

13.30-14.30 

16.30-18.00 




HALL A 

KL-03: Unipolar versus bipolar depression in children: What do Rasim Somer Diler, USA 

we know about the etiology, diagnosis, and treatment? 

Chairperson: Tümer Türkbay, Türkiye 


MD-03: Antidepressants are useful in the treatment of bipolar disorders 

Moderator : Haluk Savaş, Türkiye 

Proponent : Selçuk Kırlı, Türkiye 

Opponent : Kaan Kora, Türkiye 

12.30 - 13.30 LUNCH 


14.30-16.00 PS-13: Hormones and psychiatric disorders 

Co-chairs: Constantin Soldatos, Greece - İbrahim Balcıoğlu, Türkiye 

The hypothalamic - pituitary - adrenal axis Ertuğrul Eşel, Türkiye 

Thyroid axis Tayfun Turan, Türkiye 

Effects of oxytocin on the social behavior Nuray Atasoy, Türkiye 

Insulin Mesut Çetin, Türkiye 

Sex steroids Erdem Deveci, Türkiye 

Melatonin Müfit Uğur, Türkiye 


KL-04: Transcultural psychiatry (a comparison of USA - Türkiye Alican Dalkılıç, USA 

and sample cases) 

Chairperson: Erol Göka, Türkiye 


18.30-20.30 JS-04: The International Union of Basic and Clinical Pharmacology (IUPHAR) 

Pharmacogenomics of psychoactive drugs 

Co-chairs: Ingolf Cascorbi, Germany - Feyza Arıcıoğlu, Türkiye 

Role of polymorphic drug transporters in treatment resistant depression Tanja Brueckl, Germany 

Relationship between pharmacogenetic traits and personality Adrián Llerena, Spain 

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 

Co-chairs: Hayriye Elbi - Raşit Tükel, Türkiye 

Behavioral models in anxiety disorders Hüseyin Günay, Türkiye 

Pharmacological models in anxiety disorders M. Murat Demet, Türkiye 

Genetic models in anxiety disorders Nurper Erberk Özen, Türkiye 

New drug molecules in pre-clinical applications of anxiety disorders Raşit Tükel, Türkiye 

The frequency of anxiety disorders in general hospitals Hayriye Elbi, Türkiye 

Pharmacotherapy vs psychotherapy in anxiety disorders? Şebnem Pırıldar, Türkiye 


11.00-12.30 PS-11: Psychotropic drug treatments during pregnancy and lactation 

Co-chairs: Medaim Yanık - Nihat Alpay, Türkiye 

Schizophrenia Bülent Kayahan, Türkiye 

Bipolar disorders Fisun Akdeniz, Türkiye 

OCD Servet Ebrinç, Türkiye 

Depression Gökay Alpak, Türkiye 

Substance dependency Zehra Arıkan, Türkiye 

Panic disorder Faruk Uğuz, Türkiye 

12.30 - 13.30 LUNCH 



14.30-16.00 PS-14: Clinical course of psychiatric disorders associated with trauma and treatment issues 

HALL B 

Co-chairs: Nahit Özmenler - Ümit Başar Semiz, Türkiye 

Trauma and psychotic disorders Selma Bozkurt Zincir, Türkiye 

Trauma and mood disorders Medine Yazıcı Güleç, Türkiye 

Trauma and anxiety disorders Esin Evren Kılıçaslan, Türkiye 

Trauma and personality disorders Barbaros Özdemir, Türkiye 

Trauma and dependencies Taner Öznur, Türkiye 

Trauma and sexual dysfunctions Murat Erdem, Türkiye 


16.30-18.00 JS-03: Hellenic Society for the Advancement of Psychiatry and Related Sciences 

Disorders of sleep and wakefulness and their pharmacological management 

Co-chairs: Constantin Soldatos, Greece - Sunar Birsöz, Türkiye 

Insomnia and the effects of hypnotics on sleep Constantin Soldatos, Greece 

Hypersomnias and the effects of vigilance - promoting compounds Antigone Papavasiliou, Greece 

Depression and the effect of antidepressants on sleep Thomas Paparrigopoulos, Greece 

18.00 - 18.30 COFFEE BREAK


18.30-20.30 PS-16: Marijuana; from mellow to madness 

Co-chairs: Mohamed Husain Habil, Malaysia - Zehra Arıkan, Türkiye 


What is prevalence of cannabis dependence in Türkiye? Hakan Coşkunol, Türkiye 

The effect of cannabis use on cognitive functions Cüneyt Evren, Türkiye 

The differences of marijuana psychosis from other substance induced psychoses Mükerrem Güven, Türkiye 

Pharmacological treatment of cannabis psychosis Ömer Geçici, Türkiye 

Selective serotonin reuptake inhibitors (SSRIs) in the treatment of cannabis dependence Musa Tosun, Türkiye 

Pharmacological drug treatment of substance-induced psychosis, Osman Vırıt, Türkiye 

drug interactions, and considerations 


HALL B

09.00-10.30 PS-10: Will glutamatergic modulators be a target for the future therapy of depression? 

Co-chairs: Cyril Höschl, Czech Republic - Glen Baker, Canada 

HALL C 

Treatment with traditional antidepressants and related problems Ayşegül YIldız, Türkiye 

Glutamatergic system and its importance in the neurobiology of depression Feyza Arıcıoğlu, Türkiye 

Glutamatergic system and genetic markers associated with Hasan Herken, Türkiye 

antidepressant treatment 

Ketamine and other glutamatergic modulators as an antidepressant Serdar Dursun, Canada 

Do atypical antipsychotics have any glutamatergic effect? Kemal Yazıcı, Türkiye 


11.00-12.30 PS-12: Vitamin and mineral supplementation in treatment of childhood psychiatric disorders 

Co-chairs: Tümer Türkbay - Özgür Öner, Türkiye 

Iron supplementation Ayhan Bilgiç, Türkiye 

Zinc supplementation Ebru Kültür Çengel, Türkiye 

Calcium and Vitamin D supplementation Ömer Faruk Akça, Türkiye 

Cholesterol and Omega 3 fatty acids supplementation Sabri Hergüner, Türkiye 

Vitamin B 12 and folate supplementation Burak Doğangün, Türkiye 

Antioxidant vitamin supplementation Betül Mazlum, Türkiye 

12.30 - 13.30 LUNCH 


16.30-18.00 PS-15: Depression and pain 

Chairperson: Selçuk Kırlı, Türkiye 

Epidemiology of pain in depression Saygın Eker, Türkiye 

Clinical characteristics and mechanism of pain in depression Selçuk Kırlı, Türkiye 

Interaction of pain and depression in terms of clinical characteristics Yusuf Sivrioğlu, Türkiye 

and mechanism 

Impact of pain on treatment in depression Cengiz Akkaya, Türkiye 



18.30-20.30 PS-17: Overcoming treatment resistance: An update 

Co-chairs: Orhan Doğan- Sefa Saygılı, Türkiye 


Treatment resistant psychiatric disorders and comorbidities Tunç Alkın, Türkiye 

Treatment resistant psychiatric disorders and trauma history M. Akif Ersoy, Türkiye 

Strategies in treatment resistant psychotic disorders M. Emin Ceylan, Türkiye 

Strategies in treatment resistant depression Selçuk Aslan, Türkiye 

Strategies in treatment resistant panic disorders Erhan Bayraktar, Türkiye 

Psychosocial interventions in resistance to treatment Mustafa Yıldız, Türkiye

14.30-16.00 KC-03: CBT in somatization disorders 

Axel Würz, UK 

20.30-22.30 WS-01: Management of panic disorder 








COURSES 

HALL C 

HALL C 

HALL D 

HALL E 




participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro

09.00-10.30 JS-05: Indian Psychiatric Society 

Current concept of obsessive compulsive disorder (OCD) 

Co-chairs: Manickam Thirunavukarasu, India - Numan Konuk, Türkiye 

Current understanding of the concept of obsessive compulsive disorder Manickam Thirunavukarasu, India 

Biological theories of obsessive compulsive disorder A. Shyam Sundar, India 

Psychopharmacological and somatic interventions in OCD Kandasamy Arun, India 

Psycho-social interventions in OCD Manickam Thirunavukarasu, India 


13.30-15.30 JS-06: Czech NeuroPsychopharmacological Society (CNPS) 

From models of schizophrenia to clinical outcome: A psychopharmacological perspective 

Co-chairs: Cyril Höschl, Czech Republic - Özcan Uzun, Türkiye 

Basic concepts of schizophrenia: Experimental approaches Cyril Höschl, Czech Republic 

Prediction validity in animal models of schizophrenia Tomas Palenicek, Czech Republic 

The ins and outs of human model of schizophrenia Jiri Horacek, Czech Republic 

Safety first, efficacy second? Fear and needs of treatment in the Pavel Mohr, Czech Republic 

absence of controlled data 



16.00-18.00 JS-07: Canadian College of Neuropsychopharmacology 

Advances in psychotropic drug development: Promising novel targets and 

agents for psychiatric disorders 

Co-chairs: Glen Baker, Canada - Mesut Çetin, Türkiye 


HALL A 

11.00-12.30 KL-06: Early intervention in anxiety and depression: What we know, Joseph Zohar, Israel 

what we don’t know and what we should know? 

Chairperson: Oğuz Karamustafalıoğlu, Türkiye 

12.30 - 13.30 LUNCH 

Novel imidazoline compounds as potential new therapies Alan Leslie Hudson, Canada 

for psychiatric disorders 

Advances in antipsychotic targets and drug development Serdar Dursun, Canada 

Advances in antidepressant targets and drug development Glen Baker, Canada 





HALL B 

09.00-10.30 KL-05: Medical marijuana use in psychiatry Tahir Tellioğu, USA 

Chairperson: Ömer Geçici, Türkiye 


11.00-12.30 PS-19: Are the effects of psychopharmacological and other therapeutic approaches 

neuroregenerative or neurodegenerative? Review of recent data 

Co-chairs: Rüstem Aşkın - A. Saffet Gönül, Türkiye 

What is the hippocampal neurogenesis? Çağdaş Eker, Türkiye 

Effects of psychotropics Ömer Aydemir, Türkiye 

Effects of ECT, TMS, and others Alpay Ateş, Türkiye 

Effects of psychotherapies Mine Özmen, Türkiye 

Effects of physical exercise Hakan Balıbey, Türkiye 

12.30 - 13.30 LUNCH 

13.30-15.30 PS-21: Treatment approaches to comorbidities of ADHD 

Co-chairs: Meral Berkem, Türkiye - Rasim Somer Diler, USA 

Treatment approaches to psychiatric comorbidities of ADHD in children Tümer Türkbay, Türkiye 

Treatment approaches to psychiatric comorbidities of ADHD in adolescents Bengi Semerci, Türkiye 

Treatment approaches to psychiatric comorbidities of ADHD in adults İlhan Yargıç, Türkiye 

Treating children with ADHD and comorbid neurological disorders Murat Yüce, Türkiye 

Drug interactions in medications for comorbidities of ADHD Osman Abalı, Türkiye 


16.00-18.00 PS-22: How to fight with bipolar disorder? From guidelines to clinical practice: Myths and realities 

Co-chairs: Haluk Savaş - Erhan Kurt, Türkiye 

How the guidelines are prepared? Are they necessary? Yasin Bez, Türkiye 

How to use them? Their benefits and limitations? 

Manic episode: Treatment recommendations in guidelines and Numan Konuk, Türkiye 

clinical challenges / realities? 

Bipolar depression: Treatment recommendations in guidelines and Haluk Savaş, Türkiye 


Maintenance in bipolar disorder: Treatment recommendations in İbrahim Eren, Türkiye 

guidelines and clinical challenges / realities? 

Mixed episode in bipolar disorder: Treatment recommendations in Ahmet Ünal, Türkiye 

guidelines and clinical challenges / realities? 

Type II bipolar disorder: Treatment recommendations in guidelines and Cengiz Başoğlu, Türkiye 




09.00-10.30 PS-18: Chronobiotics and chronotherapeutics in psychiatry 

Co-chairs: Tunay Karlıdere - Ahmet Korkmaz, Türkiye 


12.30 - 13.30 LUNCH 




HALL C 

Phylogenetic aspects of biological rhythms and behavior Okan Çalıyurt, Türkiye 

Melatonin and mood Ahmet Korkmaz, Türkiye 

A general overview of chronotherapeutics Yavuz Selvi, Türkiye 

Psychotropic drugs affecting biological rhythms (chronobiotics) Elif Oral, Türkiye 

Bright light therapy use in treatment of depressions other than Mustafa Güleç, Türkiye 

seasonal affective disorder 

Sleep deprivation use in treatment of depressive disorders Adem Aydın, Türkiye 

11.00-12.30 PS-20: Controversial topics in eating disorders 

Co-chairs: Atila Erol, Türkiye - Alican Dalkılıç, USA 

Psychopharmacological treatments in eating disorders Alican Dalkılıç, USA 

Night eating syndrome Özlem Orhan, Türkiye 

Efficacy of psychotherapy in bulimia nervosa Başak Yücel, Türkiye 

Body image issues in eating disorders Erdal Vardar, Türkiye 

Obesity and impulsivity Bilge Burçak Annagür, Türkiye 

Comorbidities in eating disorders Atila Erol, Türkiye 

16.00-18.00 PS-23: Individualized medicine: Focus on pharmacogenetics 

Co-chairs: Rüstem Aşkın - Feyza Arıcıoğlu, Türkiye 

Genetics and drugs: From research to clinical studies Turkish perspective Cem Şengül, Türkiye 

Pharmacogenomic biomarkers and individualized medicine in psychiatry Yeşim Aydın Son, Türkiye 

What is the rationale of individualized medicine in psychiatry? Hasan Herken, Türkiye 

Pharmacogenetics: Management of side effects and drug Murat Kuloğlu, Türkiye 

interactions of antipsychotics 

Pharmacogenetics and how individualized medicine can be Çiğdem Aydemir, Türkiye 

applied to the practice of psychiatry? 

Pharmacogenetics: Side effects and drug interactions of Oğuz Karamustafalıoğlu, Türkiye 

antidepressants and their management





18.30-20.30 KC-05: EMDR course 



18.30-20.30 WS-02: Residency and fellowship training and short-term research / clinical observership 

possibilities in psychiatry in USA 

Tahir Tellioğlu, USA - Alican Dalkılıç, USA 


COURSES 

HALL D 

HALL E 

HALL C 

HALL B 




participants each. Registration is required for each course and workhop. Registration fee is 10.-Euro

NOVEMBER 27, 2011 SUNDAY 

09.00-10.30 PS-24: Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety 

Co-chairs: Ali Çayköylü - Mecit Çalışkan, Türkiye 


HALL A 

Psychotropics and other drugs: Sleep and road traffic accidents Mustafa Bilici, Türkiye 

Effects of psychotropics and other drugs on flight and flight safety Muzaffer Çetingüç, Türkiye 

Effects of psychotropics and other drugs on cognitive functions and Serhat Çıtak, Türkiye 

employee security 

Sexual side effects of psychotropic and other drugs Adnan Özçetin, Türkiye 

Their side effects of psychotropics and other drugs on quality of life Ömer Böke, Türkiye 


11.00 - 12.00 CLOSING and AWARDS CEREMONY

Author(s) 

Abstracts of the Invited Speakers 

1 C. R. Cloninger 

2 P. R. Martin 

3 A. L. Hudson, N. Zepeda, A. Perreault 

M. Lalies, G. Baker 

4 R. S. Diler 

5 A. Dalkilic 

6 T. Tellioglu 

7 I. Anderson 

8 I. Kirsch 

9 S. Kırlı 

10 S. Hofmann 

11 N. Kazantzis 

12 M. Z. Sungur 

13 R. A. Rashid, A. K. B. A. Bakar, 

H. B. Zakaria, U. B. Adzlin, M. H. Habil 

14 T. Paparrigopoulos 

15 C. R. Soldatos, T. PaparrigopoulosI 

16 A. Papavasiliou 

17 T. Brueckl, M. Uhr 

18 A. Llerena 

19 I. Cascorbi 

20 M. Thirunavukarasu 

21 A. S. Sundar 

22 K. Arun 

23 M. Thirunavukarasu 

24 P. Mohr, D. Hnidek, D. Seifertova 

25 C. Höschl 

26 J. Horacek, V. B. Valesova, 

T. Palenicek, F. Spaniel, C. Höschl 

27 S. Dursun, G. B. Baker, M. Mackay 

28 G. B Baker, N. D Mitchell, 

J. M. Le Melledo, S. Dursun 

Tit le 

Contents 

The evolution of human brain functions: Implications for psychobiological targets for wellbeing 

Opioid dependence during pregnancy: Balancing risk versus benefit 

l-Benzylpiperazine, a major contaminant of ecstasy, induces marked changes in rat brain 

neurochemistry and behaviour 

Unipolar versus bipolar depression in children: What do we know about the etiology, 

diagnosis, and treatment? 

Transcultural psychiatry: Practice and sample cases in USA and status in Turkiye 

Medical marijuana use in psychiatry 

Antidepressants are useful in the treatment of depression: the case for the motion 

Have clinically significant benefits of antidepressants been demonstrated? 

Antidepressants are useful in the treatment of bipolar disorders 

Recent advances in the treatment of anxiety disorders 

Translating science into practice, collaborative empiricism and engagement in homework 

assignments in cognitive behavior therapy 

CBT as an evidence based treatment approach: Warning signs in therapy and common 

mistakes in daily practice 

A harm minimization program against drug use and HIV problems in Malaysia 

Depression and the effect of antidepressants on sleep 

Insomnia and the effects of hypnotics on sleep 

Hypersomnias and the effects of vigilance-promoting compounds 

Role of polymorphic drug transporter in treatment-resistant depression 

Relationship between pharmacogenetics and personality traits: Relevance for suicide 

Genetic causes of hypersensitivity to antipsychotics – the clozapine story 

Current understanding of the concept of obsessive compulsive disorder 

Biological theories of obsessive compulsive disorder 

Psychopharmacological and somatic interventions for OCD 

Psycho-social interventions for OCD 

Safety first, efficacy second? Fear and the need for treatment in the absence of 

controlled data 

Basic concepts of schizophrenia: Experimental approaches 

The ins and outs of the human model of schizophrenia 

Recent advances in the neurochemistry of schizophrenia and potential targets for 

antipsychotic drug development 

Advances in antidepressant targets and drug development 

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Author(s) 


29 E. Eker 

30 S. Doğan 

31 Ö. Şenormancı 

32 F. Maner 

33 M. Ak 

34 A. Altındağ, G. Elboğa 

35 H. Güleç 

36 K. M. Doksat 

37 R. S. Diler 

38 M. Öztürk 

39 N. Tarhan, G. Hızlı, S. Aydın 

40 B. Bakım 

41 Ayhan Algül 

42 Ş. V. Buturak 

43 M. D. Aydın 

44 N. B. V. Özçelik 

45 D. Ünay 

46 F. Karadağ 

47 E. Taner 

48 E. Özkorumak 

49 Ç. Hocaoğlu 

50 B. Bahçeci 

51 İ. Durukan 

52 M. C. Kaya 

53 H. Elbi 

54 N. E. Özen 

55 H. Günay 

56 S. Dursun, G. Baker, N. Mitchell 

57 F. Arıcıoğlu 

58 F. Uğuz 

59 S. Ebrinç 

Tit le 

Alzheimer’s disease: Genes and/or life style 

From Don Juanism and nymphomania to hypersexual disorders 

Pathological gambling: review of recent data 

Is binge eating a type of addiction? 

Pain and personality 

Contents 

The differences between SSRIs and SNRIs in the treatment of psychiatric pain syndromes 

How does alexithymia lead to painful syndromes? 

Hypnotherapy for painful syndromes in psychiatry 

ADHD and mood disorders in children 

Academic and occupational problems in ADHD 

Concomitant use of qEEG and rTMS in treatment of depressive disorder, new approaches 

What does transcranial magnetic stimulation (TMS) promise in psychiatric disorders other 

than depression? Future perspectives 

Transcranial magnetic stimulation (TMS) as a treatment for depression 

Vagus Nerve Stimulation (VNS) in depression treatment 

Neurophysical basis of neurostimulative psychosurgery: A historical review, new 

perspectives, and future insights 

What is the real meaning of ventricular enlargement in schizophrenia? 

Neuroimaging studies in dementia, psychiatric disorders, drug discovery, and more 

Pharmacogenetics and antipsychotic combinations 

Scientific bases of use of atypical antipsychotics 

Is fish oil promising in the treatment of depression during pregnancy and lactation? 

Can St. John’s Wort be an alternative treatment for depression? 

Complementary medicine alternatives for other psychiatric abnormalities 

(Like insomnia and pain) 

Essential fatty acids in ADHD treatment 

Mechanisms of fish oil (Omega-3 fatty acids), vitamin B12, folate and other add-on 

treatments in psychiatric disorders 

Medical disease and anxiety disorders 

Genetic models in anxiety disorders 

Anxiety models in experimental animals 

Ketamine and other glutamate modulators as potential antidepressants 

The glutamatergic system and its importance in the neurobiology of depression 

Pharmacotherapy of panic disorder during pregnancy and lactation 

Psychotropic drug treatment during pregnancy and lactation in obsessive compulsive disorder 

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Author(s) 


60 Ö. F. Akça 

61 S. E. Ç. Kültür 

62 A. Bilgiç 

63 B. Mazlum 

64 S. Hergüner 

65 M. Uğur 

66 N. Atasoy 

67 T. Turan 

68 E. Deveci 

69 M. Cetin 

70 M. Y. Güleç 

71 S. B. Zincir 

72 M. Erdem 

73 C. Akkaya 

74 S. Kırlı 

75 C. Evren 

76 M. Güven 

77 M. Tosun 

78 S. Aslan 

79 M. A. Ersoy 

80 M. Yıldız 

81 A. Aydın 

82 E. Oral 

83 Y. Selvi 

84 M. Güleç 

85 Ö. Aydemir 

86 M. Özmen 

87 H. Balıbey 

88 A. Erol 

89 A. Dalkilic 

90 B. B. Annagür 

91 B. Yücel 

Tit le 

Contents 

Vitamin and mineral supplementation in treatment of childhood psychiatric disorders – 

Calcium and vitamin D supplementation 

Zinc supplementation in psychiatric disorders of children 

The impacts of iron deficiency on mental health in childhood 

Antioxidant vitamin supplementation therapies in child psychiatry 

Effectiveness of omega fatty acid supplementation for childhood psychiatric disorders 

Melatonin and human behaviour 

Effects of oxytocin on social behaviour 

Thyroid hormones and psychiatric disorders 

Sex steroids and psychiatric disorders 

Insulin and psychiatric disorders 

Trauma and mood disorders 

Trauma and psychotic disorders 

Relationship of sexual dysfunction with trauma 

Impact of pain on treatment in depression 

Clinical characteristics and mechanism of pain in depression 

Effect of cannabis use on cognitive functions 

The differences between marijuana psychosis and other substance induced psychoses 

Selective serotonin reuptake inhibitors in the treatement of cannabis dependence 

Treatment strategies for treatment resistant depression 

Treatment resistant psychiatric disorders and trauma history 

Pyshosocial approaches for treatment resistant symptoms in patients with schizophrenia 

The use of sleep deprivation in the treatment of depressive disorders 

Psychotropic drugs effecting biological rhythm (Chronobiotics) 

A general overview of chronotherapeutics 

Bright light therapy in treatment of depressive disorders other than seasonal affective disorder 

Is the effect of psychotropic drugs neurodegenerative or neuroprotective? 

Effect of psychotherapy on neurogenesis 

Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative 

or neurodegenerative? Review of recent data and effects of physical exercise 

Comorbidities in eating disorders 

Psychopharmacological treatments in eating disorders 

Obesity and impulsivity 

Efficacy of psychotherapy in bulimia nervosa 

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Author(s) 


92 T. Türkbay 

93 B. Semerci 

94 M. Yüce 

95 O. Abalı 

96 A. Ünal 

97 Y. Bez 

98 I. Eren 

99 C. Şengül 

100 Ç. Aydemir 

101 Y. Aydın Son 

102 M. Çetingüç 

103 A. Özçetin 

104 S. Kılıç 

105 A. Würz 

106 K. Ögel 

107 S. Güner 

108 S. Güner 

Abstracts of Oral Presentations 

1 C. Neale, A. Scholey, M. Hughes, 

P. Johnston 

2 C. B. Şengül, M. E. Erdal, C. Şengül, 

Ö. İ. Ay, M. Efe, M. E. Ay, H. Herken 

3 M. C. Pieri 

4 O. Erbas, S. Bora 

5 S. Abolghasemi, G. Mahmodi, M. Zafari 

6 M. M. Abtahi, H. Molavi, J. Moshtaghian, 

K. Askari 

7 J. Shafaie, S. Farjad 

8 M. Allahtavakoli, B. Jarrott 

9 F. Hashemian, M. S. Tabatabayi, 

A. Sharifi, M. Majd 

Tit le 

Treatment approaches to psychiatric comorbidities of ADHD in children 

Treatment approaches to psychiatric comorbidities of ADHD in adolescents 

Treatment of neurological co-morbid disorders in children with ADHD 

Drug interactions of medications for comorbidities of ADHD 

Treatment of mixed episodes of bipolar disorders in manuals. What are the recommendations? 

How are the guidelines prepared? Are they necessary? How to use them? Their benefits and 

limitations? 

Maintenance treatment in bipolar disorder: What do guidelines recommend? 

Genetics and drugs: From research to clinical studies Turkish perspective 

Pharmacogenetics and how individualized medicine can be applied to the practice of psychiatry 

Pharmacogenomics biomarkers and personalized medicine in psychiatry 

The effects of psychotropic and other drugs on flight and flight safety 

Sexual side effects of psychotropic and other drugs 

Basic Biostatistics 

Contents 


Mindfulness and acceptance based therapies 

Eye movement desensitization and reprocessing method [EMDR] Specifically designed for 

Turkish patient population in the Netherlands 

Alternative CBT method of panic disorder treatment for Turkish patients 

Bacopa monniera: Current trends and future directions 

Association of the DRD2 TaqIA, 5-HT1B A-161T, and CNR1 1359 G/A polymorphisms 

with alcohol dependence: A single center study in the Denizli Province of Turkey 

Treating psychotic substance abuse patients with opioid agonist therapy and the atypical 

antipsychotic olanzapine 

A comparison of the effects of typical and atypical antipsychotics on the basolateral 

amygdala of rats using deep brain EEG recordings 

The effect of cognitive-behavioral therapy in reducing the feeling of emotional 

pressure and blood sugar control in patients with type 2 diabetes 

Acute effects of nicotine on working and reference memory in rats using 

a 12-arm radial maze 

The relationship between personality characteristics and internet addiction in adolescents 

The sigma-1 receptor ligand, PRE-084, reduced infarct volume, neurological deficits, 

pro-inflammatory cytokines, and enhanced anti-inflammatory cytokines after embolic 

stroke in rats 

Comparison of the effects of bupropion and fluoxetine on reaction time in adults 

with major depressive disorder in a 4-week, single-blind study 

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Author(s) 


10 O. Bigdeli, F. Hashemian, M. Shohrati, 

A. Mokri, M. Majd 

11 M. Altın, L. Alev, K. Özbek, D. Hobbs, 

J. Karagianis, T. Treuer, J. Raskin 

12 L. Alev, M. Altın, K. Özbek, D. Sheehan, 

A. Meyers, J. Ahl, A. Prakash, 

T. M. M. Oakes 

13 Z. Kechrid, M. Hamdikene 

14 G. R. Kheirabadi, M. Salehi, 

M. R. Maracy, M. Ranjkesh 

15 Serwa Mohamadzadeh Ashna 

16 O. Erbas, V. Evren, S. Bora, 

G. O. Peker 

17 O. Erbas 

Poster Presentation 

1 S. Korkmaz, M. Kuloglu, S. Saglam, 

M. Atmaca 

2 R. Konkan, E. Aydın, O. Güçlü, 

Ö. Şenormancı, M. Z. Sungur 

3 M. Zafari, A. Aghamohammadi 

4 H. Balibey, A. Balikci 

5 R. N. Yuksel, Z. E. Kaya, N. Dilbaz 

6 J. S. Ahn, J. Shin, K. C. Park, S. Min, 

M. H. Kim 

7 H. Yaci, E. K. Koca, Y. Uz, A. Demir, 

A. A. Ozşahin, F. M. Domac 

8 F. Canan, U. Aydınoglu, G. Sinani 

9 Ç. H. Yeloglu, H. Guveli, K. Sarp, 

B. Bahceci, C. Hocaoglu 

10 E. O. Sonmez, N. Kaya 

11 M. Ak, E. Sinici, O. Maden, A. Bozkurt, 

A. Ozsahin 

12 E. Valzdorf 

13 M. Nachnani, S. Beatson 


15 S. Karayılan, A. Erol 

Tit le 

Contents 

A placebo-controlled double-blind add-on study of Ginseng in opioid withdrawal syndrome 

An in vitro analysis of disintegration times of different formulations of orally disintegrating 

olanzapine 

Effect of duloxetine on functional outcomes in patients with major depressive disorder 

Effect of vitamin D on zinc status, carbohydrate metabolism, and activities of some 

enzymes in alloxan-diabetic rats fed on a zinc deficient diet 

Gabapentin in the treatment of opioid withdrawal 

The role of transcranial magnetic stimulation in cognitive processes and treatment of 

psychiatric disorders 

Oxytocin inhibition of pentylenetetrazole-induced convulsions and its identification by 

behavioral measurement and thalamic EEG in the rats 

The effects of metoprolol and diltiazem in the prolonged QTc interval caused by 

ziprasidone injection in rats 

Visual hallucinations induced by bupropion: A case report 

Clinical features of patients with panic disorder in outpatient clinics of a psychiatric training 

and research hospital 

Effect of calcium in treatment of premenstrual syndrome 

Eye movement desensitization and reprocessing (EMDR) treatment in a patient with 

post-traumatic stress disorder: A case report 

Cabergoline induced manic episode: A case report 

Substance use and eating patterns of female adolescent students 

Neuroleptic malignant syndrome: A case report 

Treatment of clozapine induced obsessive compulsive behavior in a schizophrenic patient 

with valproic acid augmentation: A case report 

Treatment of bipolar disorder in adolescents: A case report 

Leukopenia and neutropenia due to venlafaxine use: A case report 

EMDR treatment for a sexual rape victim: A case report 

Influence of family and education factors on the inclination to commit crimes in 

Soviet times and today 

Survey of referral pathways to a crisis team 

Fluanxol and haloperidol efficacy evaluation in treatment of schizophrenic patients 

Anorexia nervosa and cannabis abuse: A case report 

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Author(s) 


16 A. Yucel, M. Gulec, A. Aydin 

17 M. López, P. Dorado, A. Ortega, 

E. P. Lledó, N. Monroy, E. Machín, 

M. E. Alonso, A. Llerena 

18 P. Dorado, E. P. Lledó, E. Machín, 

A. Llerena, E. Terán, L. Beltrán 

19 S. E. Herizchi, I. T. Piri, I. T. Asvadi, 

Z. T. Sanaat, M. T. Golchin, 

R. T. Shabanloui 

20 O. Erbas, S. Bora, S. Demirgoren, 

G. Peker 

21 F. Maner, O. Hisim, O. Sahmelikoglu, 

O. C. Girit, A. Ermis, M. E. Ceylan 

22 Ö. Ç. Girit, F. Maner, E. Kılınç, 

D. İpekçioğlu, M. E. Ceylan 

23 M. Zafari, A. Aghamohammady 

24 M. G. Ayhan, F. Uguz, N. Kaya 

25 M. Altın, L. Alev, T. M. Durell, 

L. A. Adler, D. W. Williams, A. Deldar, 

J. J. Mcgough, P. E. Glaser, R. L. Rubin, 

E. S. Sarkis, T. A. Pigott, B. K. Boardman 

26 R. M. Alowesie 

27 R. Konkan, E. Aydın, O. Güçlü, 


28 N. R. N. Jaafar, N. Mislan, A. Baharudin, 

N. Ibrahim, S. A. Aziz, H. Sidi 

29 B. Tıkır, E. Göka, M. Ç. Aydemir, 

S. Duran 

30 E. A. Sünbül, M. Sünbül, F. F. Cengiz 

31 S. Hergüner, A. Hergüner 

32 J. S. Choi, H. W. Lee, J. Y. Lee, 

H. Y. Jung 

33 S. Kesebir, B. Baykaran, B. Toprak, 

A. E. Tezcan 

34 K. Chichinadze, T. Domianidze, 

T. Matitaishvili, I. Labadze, 

A. Lazarashvili, M. Khananashvili 

35 R. R. Hegazy, H. F. Zaki, O. A. Sharaf, 

I. E. Ismail, S. A. Kenawy 

36 M. İ. Atagün, Ü. Altınok, Ö. D. Balaban, 

Z. Atagün, L. R. Alpkan, K. Öneş 

Tit le 

Contents 

Fluoxetine-induced thrombocytopenia: A case report 

Interethnic differences in UGT1A4 genetic polymorphisms in Mexican and Spanish 

populations 

Influence of CYP2C9 genetic polymorphism on losartan oxidation in an Ecuadorian 

population 

Efficacy of progressive muscle relaxation training on anxiety, depression and quality of life 

in cancer patients under chemotherapy 

Anxiety reducing effects of oxytocin on the basolateral amygdala by using an 

electrophysiological method 

Genital mutilation in a patient with schizophrenia: A case report 

Hoarding and mood disorder: A case report 

Effect of fish oil on treatment of premenstrual syndrome 

Improvement of risperidone-induced hyperprolactinemia with the addition of aripiprazole: 

Case report 

Atomoxetine for the treatment of ADHD in young adults with an assessment of associated 

functional outcomes 

Role of psychopharmacological intervention in cognitive and psychological recovery in 

hemorrhagic brain injury 

Obsessive beliefs in patients with panic disorder 

Erectile dysfunction in patients on methadone maintenance therapy in Malaysia 

Cerebellar contusion presenting with pure psychiatric symptoms and cerebellar cognitive 

affective syndrome: A case report 

Self-perception and anger with chest pain without cardiac etiology 

Mirtazapine treatment for weight loss and insomnia associated with methylphenidate: 

A chart review depression and somatic symptoms 

Rapid-onset hyponatremia induced by duloxetine in a middle-aged male with 

depression and somatic symptoms 

Gender specific metabolic adverse effects in bipolar patients: A comparison between lithium, 

quetiapine and olanzapine 

New model of psychogenic stress-induced depression and antioxidant system of rat brain 

Effects of strawberry leaf and celery seed extracts in terlipressin-induced chronic 

hyponatremia in rats 

Post traumatic stress disorder in patients with spinal cord injury and relevant factors 

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Author(s) 


37 S. Kesebir, F. Akdeniz, A. Demir, 

M. Bilici 

38 S. Ö. Kavzoğlu, A. G. Hariri 

39 F. Canan, G. Sinani, Ü. Aydınoğlu 

40 Ö. Şenormancı, O. G. Güçlü, R. Konkan, 

Y. Altunkaynak, G. Şenormancı 

41 M. Kazemi, S. Karimi, H. Hasankhani, 

S. Kazemi 

42 S. S. A. Hashmi, A. A. A. Sabri, 

N. M. A. Felati 

43 A. Ansari, T. Negahban, A. R. Sayyadi 

44 A. Aydın, P. G. Özdemir, Y. Selvi, F. Uğuz 

45 F. Canan, Ü. Aydınoğlu, G. Sinani 

46 Y. Yang, J. Kim, B. Kim, M. Shin, S. Cho 

47 F. Jan, V. Kennedy 

48 K. Ögel, G. Karadayı, Z. Karaman, 

H. A. Arıcan, N. Kaya, U. Karaman, 

A. M. Altuğ 

49 K. Ögel, C. Koç, B. Karalar, A. Başabak, 

A. Aksoy, M. İşmen, R. Yeroham 

50 K. Ögel, A. Başabak, C. Koç, A. Aksoy, 

G. Karadayı 

51 S. Ulusoy, İ. Alnıak, K. F. Yavuz, T. Kara 

52 C. Neale, S. Benson, C. Stough, A. Scholey 

53 N. Sarp, A. A. Çoban, K. Ögel 

54 F. Yousefi, S. Mohamadzadeh 

55 K. Ögel, F. Karadağ, C. Evren, 

D. T. Gürol 

56 M. A. Abnavi, A. Javadpour, 

S. Mohamadzadeh 

57 A. A. Nasiripour1, G. Mahmodi, 

M. Zafari 

58 N. A. Kumsar, A. Erol 

59 H. A. Döm, M. A. Döke, Y. Y. Tuncel, 

G. Üstünkar, Y. A. Son 

Tit le 

Contents 

A comparison before and after using lamotrigine in long term continued treatment: the effect 

of blood levels 

ICAM, VCAM and E-selectin levels in first episode schizophrenic patients 

Body dysmorphic disorder incidentally treated with bupropion 

Tardive akathisia with aripiprazole: A case report 

Comparing mental disorders between divorced couples and normal couples in a city of Iran 

Suicide rate in Oman in the period between January 2000 and December 2010 

The effect of the recitation of the Quran on depressed patients in the psychiatry department 

of Moradi hospital in Rafsanjan (IRAN) 

Dissociative symptoms associated with piracetam use: a case report 

Reversible normoprolactinemic galactorrhea induced by fluoxetine 

Influence of polymorphism of the norepinephrine transporter gene (SLC6A2) and alpha-2 

adrenergic receptor gene (ADRA2A) on regional cerebral blood flow in a Korean ADHD 

sample: a preliminary study 

Do we need specialist clinics to monitor metabolic side effects on chronic bipolar patients 

in Treatment? – Audit of management of bipolar disorder against NICE guidelines in South 

Staffordshire NHS Trust, UK 

Assessment of risk of absenteeism in elemantary school students 

Effectiveness of an addiction treatment program called SAMBA: A pilot study 

Psychometric properties of different forms of the Addiction Profile Index (BAPI) 

Aripiprazole treatment for the choreoathetoid movements and psychotic symptoms of 

Huntington’s disease: A case report 

Acute effects of Bacopa monnieri on mood in healthy young adults 

Anxiety and depressive symptom levels among adolescents with risk taking behaviour 

The relationship between mental health and academic achievement among Kordestan high 

school students 

Does the profile of addiction change according to the type of the substance used? 

Death anxiety among terminally ill inpatients 

The effective features of access to medical care in Iran 

Smoking behaviour during the course of paroxetine treatment: A case report 

Development of a SNP genotyping panel and a medical decision support algorithm to predict 

drug response in schizophrenia 

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Author(s) 


60 Barış Yılbaş, Murat Gönen 

61 B. E. Cumurcu, R. Karlıdağ, Ş. Kartalcı, 

I. G. Gül, S. Demir, B. Yeşil 

62 U. M. Aksoy, Ş. G. Aksoy, F. Maner 

63 B. Soyer, J. Kenar, K. S. Karataş 

64 A. A. Bilgin, B. Çam 

65 Y. Taner, H. A. Taner 

66 H. Toğul 

67 H. Ünübol, B. Ünübol, J. Güler, A. Ünal 

68 İ. İnanlı, İ. Eren, T. Etli 

69 F. Büyükşahin, J. Güler, B. Ünübol, 

H. Ünübol, A. Ünal 

70 H. Balıbey, T. Türker, Z. Perdeci1, 

N. Bayar, M. B. Evren 

71 A. Aghamohammadi, M. Zafari 

72 T. Kuru, M. E. Karadere, S. Çelenk, 

B. Demirel, K. F. Yavuz 

73 Y. Yılmaz, Ö. Yanartaş, İ. Saygılı, 

Ü. B. Semiz 

74 Ö. Yanartaş, Y. Yılmaz, İ. Saygılı, 

S. B. Zincir, Ü. B. Semiz 

75 F. Arıcıoğlu, T. Utkan 

76 F. F. Cengiz, E. A. Sünbül 

77 A. A. Budaklı, M. A. Ateş, A. Algül 

78 F. Amani, A. Shaker 

79 K. S. Karataş, J. Güler, Ö. B. Topçuoğlu, 

E. D. Bostancı, B. Soyer 

80 S. Gümrü, E. Yarcı, Ö. Şehirli, Y. Yazır, 

T. Utkan, F. Arıcıoğlu 

81 M. C. Kaya, Y. Bez, S. Selek, 

H. A. Savaş, H. Çelik, H. Herken 

82 E. Mutlu, M. E. Ceylan, A. Aydın 

83 M. Ak, A. Bolu, S. Akarsu, D. Sezlev, 

T. Yanık, Ö. Uzun, F. Özgen, A. Özşahin 

84 R. Konkan, Ö. Şenormancı, O. Güçlü, 

E. Aydın, Mehmet Z. Sungur 

Tit le 

Contents 

Basal ganglial hemorrhage induced mania 

Evaluation of cognitive functions in euthymic bipolar patients using mono- and multi- drug 

treatments 

Adult ADHD symptoms in cannabis dependence and the importance of comorbidity 

in Adult ADHD 

Ganser syndrome as a dissociative disorder: A case report 

Escitalopram induced galacthorrea: Phenomenon presentation 

Amisulpride use in treatment of Tourette’s disorder 

Lithium associated glossodynia syndrome: A case report 

Two cases of affective disorder due to immunosuppresive treatment that followed renal 

transplantation 

Varenicline induced psychotic disorders: A case report 

Affective disorders and catatonia: Report of two cases 

The relationship of incarceration, past suicide attempts, depression, anxiety and attention 

deficit hyperactivity disorder in cases of anti-social personality disorder 

Relation between unintended pregnancy and post-partum blues 

Comparison of antipsychotic prescribing in the treatment of schizophrenia between the years 

of 2004-2009 

Valproate-induced hyperammonemic encephalopathy: A case report 

Two cases of tardive dyskinesia associated with the use of paliperidone ER and their 

management 

Effects of agmatine in rats with chronic unpredictable mild stress 

A case of obsessive compulsive disorder with psychotic features that suffered from sexual 

trauma 

Priapism associated with zuclopenthixol treatment: A case report 

Prescribing patterns and inappropriate use of medications in patients referred to doctors in 

Ardabil City of Iran 

Bipolar affective disorder and normal pressure hydrocephaly: A case report 

Agmatine attenuats cognitive impairment and oxidative damage following chronic 

unpredictable mild stress: A behavioral, biochemical, and histological study 

Ceruloplasmin levels before and after treatment in patients with depression: 

A case-control study 

Foetality in schizophrenia 

Metabolic changes in the acute phase with olanzapine treatment 

Do cultural factors effect clinical manifestations of OCD? Clinical features of 

a Turkish sample 

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Author(s) 


85 C. Evren, S. Çelik, R. Aksoy, T. Çetin, 

M. Ülkü, S. Yiğiter, E. Mutlu 

86 C. Evren, S. Çelik, R. Aksoy, T. Çetin, 

S. Yiğiter, M. Ülkü, E. Mutlu 

87 M. Ak, C. Yükselir, A. Bozkurt, 

M. Erdem, A. Özşahin 

88 A. Bolu, S. Akarsu, C. Çelik, 

B. Özdemir, K. N. Özmenler 

89 O. Durmaz, M. A. Ateş, M. Çetin, 

S. Ebrinç, C. Başoğlu, A. Algül 

90 R. Tükel, H. Gürvit, B. Özata, 

B. A. Ertekin, E. Ertekin, B. Baran, 

Ş. A. Kalem, N. Öztürk, G. S. Direskeneli 

91 S. G. Kabak, M. B. Baykaran, S. B. Zincir 

92 R. Konkan, M. Bayrak, O. Güçlü, 


93 A. Aydın, M. E. Ceylan, E. M., 

A. F. Maner 

94 P. G. Özdemir, A. Aydın, M. Güleç, 

E. Füsün A. Çim 

95 F. Karadağ, H. Herken, B. Kaptanoğlu, 

Y. Enli, Ö. Kalkancı, C. B. Şengül, 

H. A. Alaçam 



98 S. Barlak, A. Ateş, C. Başoğlu, S. Ebrinç 


100 Ö. Ö. Sarıkaya, D. G. Öyekçin 

101 F. Hashemian, M. Majd, S. M. Hosseini, 

A. Sharifi, M. V. S. Panahi, O. Bigdeli 

102 S. Karimi, M. Kazemi, H. Hasankhani, 

S. Kazemi 

103 Y. Yılmaz, Ö.Yanartaş, İ. Saygılı, 

A. G. Hariri 

104 P. Dorado, H. Trejo, E. Alonso, 

E. P. Lledó, A. Llerena, M. López 

105 P. Dorado, E. L. Torres, E. M. P. Lledó, 

J. M. Antón, A. Llerena 

106 M. López, E. P. Lledó, H. Trejo, 

P. Dorado, J. Guerrero, M. E. Alonso, 

A. Llerena 

107 A. Karahan, A. Tiryaki, B. İskender, 

E. Özkorumak 

Tit le 

Contents 

Reliability and validity of Turkish version the Brief Fear of Negative Evaluation Scale II 

(BFNE-II) among male patients with alcohol dependency 

Reliability and validity of Turkish versions of the Social Phobia Scale and Social Interaction 

Anxiety Scale among male patients with alcohol dependency 

ECT in treatment of pathological gambling: A case report 

Venlafaxine-mirtazapine combination in the treatment of post traumatic stress disorder 

Efficacy and 3-month follow-up of repetitive transcranial magnetic stimulation (rTMS) in 

treatment resistant depression: Three cases 

The effects of brain-derived neurotrophic factor Val66Met polymorphism on executive 

functioning in patients with obsessive-compulsive disorder 

Diagnostic confusion about OCD and schizophrenia: A case report 

Is vaginismus a specific phobia? 

Are personality traits helpful to predict psychosis? 

Switching to fluoxetine due to sertraline-induced urinary incontinence: A case report 

The relationship between the serum bilirubin levels and metabolic syndrome 

in schizophrenia patients 

Olanzapine abuse: A case report 

Various reasons for self-destructive acts and objects used to commit them in 1991 

Topiramate induced acute psychotic disorder 

Glass-aating behaviour with radiological findings: A pica case 

The use of bupropion in treatment Kleptomania’s: Two cases 

A randomized, double-blind, placebo-controlled trial of celecoxib augmentation of sertraline 

in the treatment of a drug-naïve women with major depression 

To compare marital conflicts, between divorced and normal couples in Sirjan of Iran 

Adult primary enuresis nocturna: A case report 

Major depressive disorder and the 5-HTTLPR in Spanish and Mexican populations 

Phenytoin toxicity in a pediatric epileptic patient and CYP2C9, CYP2C19, and ABCB1 

genetic polymorphisms 

Influence of CYP2D6 genetic polymorphism on fluoxetine and amitriptyline 

clinical response 

Evaluation of insight and functional recovery in patients with schizophrenia 

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Author(s) 


108 O. Özdemir, Y. Selvi, H. Özkol, 

Y. Tülüce, L. Beşiroğlu 

109 C. Neale, A. Scholey, M. Hughes, 

P. Johnston 

110 S. Özdemir, F. A. Özdemir 

111 M. Güleç, Y. Selvi, Ü. Aydınoğlu 

112 S. B. Zincir, Ü. B. Semiz, A. Yenel, 

E. Başoğlu, M. Bilici, C. Tulay 

113 S. B. Zincir, Ü. B. Semiz, A. Demir, 

Y. Yılmaz, S. G. Kabak 

114 S. B. Zincir, A. Yenel, S. Ç. Parlak, 

G. Şimşek, A. Bayrak, D. Bilge, 

Ü. B. Semiz, M. Bilici 

115 M. Akbıyık, O. Karamustafalıoğlu 

116 M. Özten, A. Erol 

117 S. Karayılan, A. Erol 

118 M. Özten, A. Erol 

119 K. S. Karataş, J. Güler, A. Hariri 

120 B. Çam, H. Kurt 

121 H. Özer, A. Erol 

122 O. Kadıoğlu, G. Üstünkar, Y. A. Son 

123 A. Büyükkınacı, D. Ö. Can, G. Silsüpür 

124 Y. Şimşek, G. E. Sarıdoğan, E. Şahan, 

M. Nebioğlu, C. Cerit, M. Çalışkan 

125 O. Yılmaz, M. A. Ateş, G. Meral, 

C. Başoğlu, A. Algül, S. Ebrinç, M. Çetin 

126 E. Özkorumak, H. Hıdıroğlu, A. Tiryaki, 

İ. Ak 

127 M. Güleç, E. Oral, E. F. Aydın 

128 T. Kara, A. Çiftçi 

129 H. A. Altaiar 

Tit le 

Contents 

Comparison of superoxide dismutase, glutathione peroxidase, and adenosine deaminase 

activities between respiratory and nocturnal subtypes of patients with panic disorder 

The neural and cognitive effects of Bacopa Monniera: An fMRI study 

Methlyphenidate induced thrombocytopenia in a pediatric patient with ADHD and stuttering 

Use of mirtazapine and olanzapine in treatment of major depressive disorder with psychotic 

features developed during pregnancy: A case report 

Effects of group musical therapy on inpatients with schizophrenia: A preliminary study 

Clinical correlations of childhood trauma and dissociation in a sample of female inpatients 

diagnosed with schizophrenia spectrum disorders and severe nonpsychotic disorders: the 

preliminary data 

Comparison of neurocognitive skills between generalized anxiety disorder and premenstrual 

dysphoric disorder patients: A controlled study 

Evaluation of olfactory function and olfactory bulb volume in major depressive disorder 

Fluoxetine induced hypomanic shift in a bulimic patient: A case report 

Schizophrenia and Mega Cisterna Magna: A case report 

Congenital hypogonadism and comorbid anorexia nervosa in a male patient: A case report 

Review of diagnosis and treatment of pregnant psychiatric patients in a state hospital 

Peripheral edema associated with mirtazapine: Presentation of a case 

Abuse of tianeptine: A case report 

GWAS with AHP based SNP prioritization approach to identify SNP biomarkers for 

Alzheimer’s disease 

A case report of a relapse in a major depression patient with valsartan/hydrochlorothiazide 

Monosymptomatic hypochondriacal psychosis: A case report 

Amisulpride in the treatment of treatment resistant tic disorder: A case report 

Evaluation of patients with obstructive sleep apnea syndrome referred to the sleep disorders 

unit of a university hospital 

Clozapine use in idiopathic tardive dystonia and paranoid schizophrenia comorbidity: 

A case report 

The clinical use of Buprenorphine-Naloxone in the opioid-dependent patient with Hepatitis C 

The use of z hypnotics in the management of insomnia in forensic psychiatric 

units in Oxford, England 

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4th International 




November 23-27, 2011 



ABSTRACTS OF THE INVITED SPEAKERS



The evolution of human brain functions: Implications for psychobiological targets for well-being 

Claude Robert Cloninger 

Washington University, St. Louis, MO, USA 

E-mail: crcloninger44@gmail.com 

The natural building blocks of human personality are described based on the evolution of human brain functions (Cloninger, 2009; 

Cloninger, 2011). The phylogeny of human beings is traced from early vertebrates through mammals. The functional capacities that 

emerge along this lineage of ancestors are described. Comparative neuroanatomy is reviewed to identify the brain structures and 

networks that emerged coincident with the emergent brain functions. 

Neocortical development in mammals proceeded in 5 major transitions from early mammals to early primates, monkeys and apes, early 

humans, and modern Homo sapiens. These transitions provide the foundation for human self-awareness related to sexuality, materiality, 

emotionality, intellectual communication, and spirituality respectively. 

The evolution of functions in humans is compared to the psychobiological model of temperament and character previously described on 

the basis of individual differences in learning and genetic variation in human beings. The psychobiological model of personality provides 

a natural and thorough description of both the evolution and the development of personality in human beings. 

These evolutionary findings are related to clinical approaches to assessment and treatment of children and adults. Identification of the 

causal processes underlying well-being and ill-being is helpful in improving assessment and treatment in comparison to the frequent 

drop-out relapse rates obtained when diagnosis and treatment are based on symptoms, rather than their causes. Monitoring symptoms 

of illness and past lifestyle behavior has failed to promote change in well-being in a strong and consistent way in either individual care 

or public health. A clinician’s effectiveness in treatment depends substantially on his or her attitude toward, and understanding of, the 

patient as a person endowed with self-awareness and the will to direct his or her own future (Cloninger and Cloninger, 2011a). 

The causes of well-being operate as components of a virtuous circle of reciprocally interactive processes (Cloninger and Cloninger, 2011a) 

which evolved and develop in a stepwise manner. For example, emotions, cognitions, and actions have reciprocal interactions with one 

another. The induction of a positive mood by humor or kindness leads to a broadening of attention to be more inclusive and less defensive 

in thinking, which I have described as an outlook of unity (Cloninger, 2004; Cohn et al., 2009; Fredrickson, 2004; Fredrickson and Losada, 

2005). In turn, an outlook of unity allows a person to cultivate greater self-acceptance, environmental mastery, and creativity, which in 

turn lead to greater health and happiness, thereby completing the self-reinforcing cycle. 

Positive emotional states can be induced by a variety of self-transcendent activities, such as acts of virtues, including cheerful humor, 

generosity, and humility (Cloninger and Cloninger, 2011b). Virtues interact with functional practices of well-being, including working in 

the service of others, letting go of fighting and worrying, and growing in awareness. In turn, virtues and self-regulatory functions interact 

with the body to promote human plasticity. Human beings probably show greater plasticity, and hence variability, than other animal 

species, which has allowed us to adapt to highly variable environmental conditions successfully. 

Key words: Cognition, emotionality, human characteristics, thinking, personality, character, health, happiness, wellness, well-being 

References: 

1. Cloninger, C.R., 2004. Feeling Good: The Science of Well-Being. Oxford University Press, New York. 

2. Cloninger, C.R., 2009. The evolution of human brain functions: the functional structure of human consciousness. Australian and New Zealand Journal of Psychiatry 

43, 994-1006. 

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, 

C.R. (Eds.), The Origins of Cooperation and Altruism. Springer, New York, pp. 63-110. 

4. Cloninger, C.R., Cloninger, K.M., 2011a. Development of instruments and evaluative procedures on contributors to Illness and health. International Journal of 

Person-centered Medicine 1, in press. 

5. Cloninger, C.R., Cloninger, K.M., 2011b. Person-centered Therapeutics. International Journal of Person-centered Medicine 1, in press. 

6. Cloninger, C.R., Zohar, A.H., 2011. Personality and the perception of health and happiness. J Affect Disord 128, 24-32. 

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. 

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. 

9. Fredrickson, B.L., 2004. The broaden-and-build theory of positive emotions. Philos Trans R Soc Lond B Biol Sci 359, 1367-1378. 

10. Fredrickson, B.L., Losada, M.F., 2005. Positive affect and the complex dynamics of human flourishing. Am Psychol 60, 678-686. 

Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S34 

S34 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org

LECTURES 

[KL-01] 

Opioid dependence during pregnancy: Balancing risk versus benefit 

Peter Robert Martin 

Departments of Psychiatry and Pharmacology, Vanderbilt University, Nashville, Tennessee, USA 

E-mail: peter.martin@vanderbilt.edu 

Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org 


Public health consequences of opioid dependence during pregnancy can only be inferred as increasing proportions of opioid-dependent 

women are addicted to non-medically prescribed analgesics and receive obstetrical care without being identified as addicted or treated. 

Because treatment recommendations for management of opioid dependence in pregnancy have primarily derived from studies in heroindependent 

pregnant women, there is a need to characterize and compare the clinical courses and complications of injection drug use 

(IDU) and non-medically prescribed opioids. Intrauterine overdose or withdrawal and the neonatal abstinence syndrome (NAS) may occur 

regardless of the route of opioid administration; whereas other obstetrical complications are likely consequences of poor prenatal care/selfneglect 

typical for IDU. Methadone maintenance compared to active IDU is associated with improved prenatal care, increased fetal growth, 

reduced fetal mortality, decreased risk of HIV infection, decreased risk of pre-eclampsia, decreased NAS and reduced foster care placement; 

however, significant NAS is still observed in >50% of these births. Benefits of methadone maintenance during pregnancy for addiction to nonmedically 

prescribed opioid analgesics may be attributed to support, structure, and prenatal obstetrical oversight compared to the stressful 

and chaotic lifestyle of active addiction. While methadone has been the standard of care for >40 years, the Schedule III (methadone is Schedule 

II) partial opioid agonist buprenorphine merits examination in pregnancy because it has been found highly effective for treatment of opioid 

dependence, is associated with less severe withdrawal and is available in the U.S. under less severe restrictions than methadone. In the MOTHER 

study, maternal and neonatal outcomes of treatment with buprenorphine or methadone throughout pregnancy were compared in pregnant 

opioid-dependent women, in an international multi-center randomized, controlled, double-blind/double-dummy clinical trial (Jones et al., 

N Engl J Med 2010;363:2320-31). Although comparable numbers of methadone-exposed (57%) and buprenorphine-exposed (47%) babies 

required treatment for NAS, buprenorphine-exposed neonates required 89% less morphine to treat NAS; spent 43% less time in the hospital; 

and spent 58% less time in the hospital being medicated for NAS. The safety of opioid maintenance treatment during pregnancy must be 

judged in the context of comprehensive services (other than the administered medication per se) provided to addicted women by treatment 

programs. Buprenorphine is not inferior to methadone but may be preferable in terms of certain fetal outcome measures. Further research is 

needed to implement safe buprenorphine induction procedures in pregnant women, to balance reported teratogenic effects of opioids and 

benefits of opioid maintenance, and to determine the comparative safety and efficacy of methadone and buprenorphine for mother/fetus 

with co-occurring alcohol/benzodiazepine dependence or other psychiatric disorders and the psychoactive medications used to treat them. 

Key words: Opioid dependence, pregnancy, buprenorphine, methadone 


[KL-02] 

l-Benzylpiperazine, a major contaminant of ecstasy, induces marked changes in rat brain 

neurochemistry and behaviour 

Alan Leslie Hudson 1 , Nubia Zepeda 1 , Amanda Perreault 1 , Maggie Lalies 1 , Glen Baker 2 

1 Department of Pharmacology, University of Alberta, Edmonton, Canada 

2 Department of Psychiatry, University of Alberta, Edmonton, Canada 

E-mail: ahudson@pmcol.ualberta.ca 

Ecstasy [(±) -3-4-methylenedioxymethamphetamine, MDMA] is a widely abused drug which in overdose can lead to serotonin syndrome. 

The patient presents with agitation, tremors, and muscle spasms, followed by hyperthermia which can lead to fatal organ failure. Recently 

ecstasy tablets have been found to contain piperazines, particularly 1-benzylpiperazine (BZP). The purpose of cutting ecstasy with BZP is 

to enhance the psychostimulant effects of MDMA. BZP is also marketed as a “legal high” in some countries; therefore some ecstasy tablets 

contain solely BZP. BZP is the active metabolite of an antidepressant drug, trelibet, which failed in clinical trials. There has been little study 

on the pharmacological effects of combining BZP with MDMA so we have investigated the bioavailability, neurochemistry and behavioral 

S35


profile of these drugs administered alone or in combination in rats. We have used the technique of brain microdialysis in rat frontal cortex, 

to monitor extracellular levels of noradrenaline, dopamine and serotonin in response to peripheral administration of BZP and MDMA. We 

were also able to monitor the animals for evidence of rodent serotonin syndrome. BZP (10mg/kg, i.p.) was able to elevate extracellular 

levels of dopamine, noradrenaline and to a lesser extent, extracellular serotonin in rat frontal cortex. MDMA (3mg/kg, i.p.) potently 

elevated extracellular serotonin and noradrenaline and to a lesser extent extracellular dopamine in frontal cortex. These neurochemical 

effects lasted for at least 2 to 3 hours relative to saline treated control animals. Combined BZP and MDMA administration led to markedly 

elevated extracellular levels of all three monoamines indicating the effects of the drugs were additive. BZP (10mg/kg, i.p.) caused marked 

behavioral activation, for example, increased locomotor activity and rearing behavior, whereas MDMA (3mg/kg, i.p.) resulted in flat body 

posture and less rearing. Similar to MDMA (3mg/kg, i.p.), BZP increased grooming, forepaw treading, sniffing and head weaving relative 

to saline injected animals. We also investigated a 5-HT2A receptor antagonist, ketanserin (3mg/kg i.p.), to see if it could attenuate BZPinduced 

behaviors. Ketanserin alone had little effect on rat behavior but when co-administered with BZP, was able to decrease locomotion 

and rearing behavior. Interestingly, ketanserin had little effect on the increased sniffing and head weaving induced by BZP. At the doses 

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 

of BZP and MDMA hence we know bioavailability was not a problem. Overall, these results suggest that BZP and MDMA share certain 

psychopharmacological and neurochemical properties in the rat. Furthermore, combined administration of BZP with MDMA leads to a 

marked elevation of extracellular levels of all three monoamines in the frontal cortex rather than just serotonin which, if translated into 

the clinical setting, may explain the agitation and sympathomimetic toxic syndrome reported in some patients. All animal studies were 

conducted in accordance with the Canadian Council on Animal Care Guidelines and Policies with approval from the Animal Care and Use 

Committee in Health Sciences for the University of Alberta. This work is supported with a grant from Canadian Institute of Health Sciences. 

Key words: Ecstasy, (±) -3-4-methylenedioxymethamphetamine, 1-benzylpiperazine, serotonin syndrome, rat behaviour, brain microdialysis 

Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S35-6 

[KL-03] 

Unipolar versus bipolar depression in children: What do we know about the etiology, 

diagnosis, and treatment? 

Rasim Somer Diler 

Department of Psychiatry, University of Pittsburgh, PA, US 

E-mail: dilerrs@yahoo.com 

Bipolar disorder (BP) is a familial and recurrent illness that significantly affects the child’s normal development. BP is often manifested by periods of 

depression during which the child has significant psychosocial problems and increased risk for suicide. However, most clinical studies have focused 

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, 

depressed youth with BP are more likely to have more severe depression, greater suicidality, and higher rates of comorbidities and functional 

impairment relative to depressed youth with major depressive disorder (MDD or “unipolar depression”). However, it is difficult to clinically 

differentiate the symptoms of BP depression from those of MDD. This issue is very important because youth with BP depression may be treated 

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 

of depression until BP is diagnosed and appropriate treatment is prescribed. Thus, early identification of BP youth, especially during depression, is 

critical not only to improve the long-term prognosis of BP, but also to prevent inappropriate treatments for BP youth. As demonstrated recently in 

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 

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 

depression and agreed that there was insufficient evidence to develop a treatment algorithm for it. Several studies suggest that there are effective 

and well-tolerated treatment options (e.g., lithium, mood stabilizers, second-generation antipsychotics [SGA]) for manic or mixed episodes of BD 

in youth; however, there are no maintenance studies in depressed children and adolescents with BP and available data for depressive episodes 

in BP is limited to one small randomized and two open-label acute treatment studies in adolescents. Management of depression is very different 

in BP depression than in MDD; antidepressants are widely used in MDD, but may exacerbate or induce mania and suicide in depressed BP youth. 

Antidepressant monotherapy is therefore contraindicated for the treatment of BP depression, and studies in depressed BP adults show that 

combining antidepressants with mood stabilizers may also not be effective. In conclusion, early differential diagnosis and treatment of depression 

in youth is a key factor to enable youth to follow a normal developmental path and prevent an unrecoverable loss in their development. 

Key words: Child, bipolar, depression, neuroimaging 



[KL-04] 

Transcultural psychiatry: Practice and sample cases in USA and status in Turkiye 

Alican Dalkilic 

Virginia Commonwealth University, Richmond, VA & SEH, Washington, DC, USA 

E-mail: E-mail: drdalkilic@gmail.com 



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 

attitudes of a group characterize their culture. Culture and people influence and interact with each other reciprocally (1). In clinical practice patient’s 

culture, physician’s culture, and medical culture play a significant role. Adequate and appropriate understanding of cultural dimensions is essential for 

culturally competent practice (1). Also the impact of culture in evaluation and treatment of children and adolescents is significant in psychiatric patients (2). 

Cultural competency is a requirement for medical licensure in most states the US. To prove clinical competency clinicians are required 

demonstrate cultural competency. Clinicians typically work in multicultural and multiethnic societies (1). Ongoing globalization and 

interconnection of economies and rapidly spreading new social media platforms will increase diversity in all communities, but especially 

in developing countries including Turkiye. Therefore cultural competency training should be incorporated into residency training and 

continuous medical education systems especially for mental health clinicians. 

Clinicians should be familiar with culturally relevant relations and interactions of their patients (1), in order to establish therapeutic alliance and 

provide competent care and therapy besides demonstrating cultural sensitivity, knowledge, and empathy. Also most psychotherapies are based 

on Euro-American values of individualistic and egocentric concept, which can be contrasted with more sociocentric, ecocentric, and cosmocentric 

views (3). This issue should be taken into consideration when treating patients from other cultures or subcultures in the US and Europe. 

In this presentation I will review transcultural psychiatry practice in the US, provide and discuss some cases and summarize the status in Turkiye. 

Key words: Transcultural psychiatry, Turkish American cases, transcultural psychiatry in USA 

References: 

1. Focus, winter 2006 Vol. IV. No. 1, 81-89. Introduction: Culture and Psychiatry. Tseng W-S, Streltzer J. 

2. Child Adolesc Psychiatr Clin N Am. 2010 Oct;19(4):661-80. Culture and development in children and youth. Pumariega AJ, Joshi SV. 

3. Transcult Psychiatry. 2007 Jun;44(2):232-57. Psychotherapy and the cultural concept of the person. Kirmayer LJ 


[KL-05] 

Medical marijuana use in psychiatry 

Tahir Tellioglu 

Brown University, Rhode Island Hospital Dept Psychiatry, Providence USA 

E-mail: TTellioglu@Lifespan.org 

Medical marijuana refers to the use of parts of the cannabis plant or synthetic forms of specific cannabinoids as a physician-recommended 

form of medicine. The cannabis plant has been known to have medicinal use as an analgesic, appetite stimulant, antiemetic, muscle 

relaxant and anticonvulsant agent. A number of clinical studies, some disputed, claim that cannabinoids present an interesting 

therapeutic potential as antiemetics, appetite stimulants in debilitating diseases (cancer and AIDS) and analgesics, and in the treatment 

of multiple sclerosis, spinal cord injuries, Tourette’s syndrome, epilepsy and glaucoma. 

Despite its illegality, patients have continued to obtain cannabis on the black market for self-medication for its self reported anti-anxiety 

or antidepressant effects. A survey of 3,000 patients in California from 1993-2000 revealed about 27% of individuals used it primarily for 

psychiatric conditions such as as an antidepressant or anxiolytic. 

Understanding the mechanisms of action of cannabinoids has revived therapeutic interest in these substances. However, clinical studies 

about the use of cannabis for psychiatric conditions are very limited. Further clinical trials, well-designed, carefully executed, and powered 

for efficacy, are essential to clearly define the role of cannabinoids in the treatment of psychiatric conditions. 

Key words: Medical marijuana, cannabis, psychiatric disorders 


S37


DEBATES 

[MD-02] 

Antidepressants are useful in the treatment of depression: the case for the motion 

Ian Anderson 

Neuroscience and Psychiatry Unit, University of Manchester, UK 

E-mail: ian.anderson@manchester.ac.uk 

The group of drugs we call antidepressants have been available for nearly 60 years and are the first available physical treatment for 

depression that became accepted by the public and clinicians alike. However in the last decade, associated with the rise of evidencebased 

medicine and a concern about the medicalisation of distress, there has been a questioning and re-evaluation of their efficacy 

and place in the treatment of depression. This has occurred against the backdrop of increasing distrust of ‘Big Pharma’ and emphasis 

on psychological treatment approaches. I will be addressing some of the main challenges that have been put forward questioning the 

usefulness of antidepressants, ranging from the denial that depression is a disorder that can be treated by physical means, to the argument 

that there is no pharmacological or empirical evidence for a clinically useful benefit over psychologically-mediated placebo effects. To 

do this I will touch on recent developments in the understanding of how antidepressants might directly influence the processing by the 

brain of emotional material, consider the evidence that direct pharmacological effects are necessary to maintain the therapeutic effects of 

antidepressants and review the empirical evidence for clinically important efficacy from treatment trials in depression. I will conclude that 

while antidepressants are certainly not a panacea, denying their place in treating depression is based on prejudice rather than objective 

appraisal of the evidence. 

Key words: Depression, antidepressants, placebo, efficacy 


[MD-02] 

Have clinically significant benefits of antidepressants been demonstrated? 

Irving Kirsch 

Associate Director, Program in Placebo Studies (PiPS) and Lecturer in Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Professor Emeritus of 

Psychology, University of Hull & University of Connecticut 

E-mail: I.Kirsch@hull.ac.uk 

Despite their widespread use, clinically significant benefits of antidepressants have not been demonstrated for most of the patients to 

whom they are prescribed. Meta-analyses of complete data sets consistently show a drug-placebo difference in improvement on the 

Hamilton Rating Scale for Depression (HAMD) of approximately two points, which is well below the 3-point difference set by the National 

Institute for Health and Clinical Excellence (NICE) as a criterion of clinical significance (1). 

Drug placebo differences increase with increasing severity of depression, but reach clinical significance only for 10% of the patients to 

whom they are prescribed (2). Defenders of antidepressants claim that depression scores are inflated by researchers who are anxious to 

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 

these trials are discarded, the absence of negative evidence does not constitute positive evidence of effectiveness. 

Discontinuation studies show a relapse rate of approximately 50% when patients are switched to placebo. However, approximately 

half of the relapses may be due to prior administration of the active agent. In extension trials, in which responders are kept on 

placebo, the relapse rate is only 25% (3). These data suggest that antidepressants might induce a biological vulnerability to relapse. 

Consistent with this hypothesis, a meta-analysis of tryptophan depletion studies indicates that the risk of becoming depressed after 

acute lowering of serotonin levels is greatest between three and six months after discontinuation of an antidepressant (4). It is also 

consistent with the results of the STAR-D trial, which was designed to be more representative than typical clinical trials of what 

happens in clinical practice. Following successful treatment in the STAR-D trial, 93% of patients either relapsed or dropped out of the 

trial within a year (5). Taken together, these data suggest that in the long run, rather than helping depressed people, antidepressants 

may make them worse. 


References: 



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 

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. 

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. 

Journal of the American Medical Association2010;303(1):47-53. 

3. Andrews P, Kornstein S, Halberstadt L, Gardner C, Neale MC. Blue again: Perturbational effects of antidepressants suggest monoaminergic homeostasis in major 

depression. Frontiers in Psychology. [Original Research]. 2011;2. 

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 

studies. Molecular Psychiatry2007;12:331-59. 

5. Pigott HE, Leventhal AM, Alter GS, Boren JJ. Efficacy and Effectiveness of Antidepressants: Current Status of Research Psychotherapy and Psychosomatics2010;70:267-79. 


[MD-03] 

Antidepressants are useful in the treatment of bipolar disorders 

Selçuk Kırlı 

Department of Psychiatry, Uludag University, Bursa, Turkey 

E-mail: kselcuk@uludag.edu.tr 

Using antidepressant drugs in Bipolar Depression (BD) has not been adequately considered or explored. This matter is indeed an area of 

ambiguity which should to be clarified as soon as possible due to the following facts concerning bipolar disorder: 

• It is repetitive and progresses relatively slowly 

• It tends to become chronic 

• It involves a high risk of suicide 

• It causes more disability than the other variations of the disease (1). 

Treatment manuals, expert views and practices do not fully agree with each other on the issue of whether or not it is appropriate to 

use antidepressant (AD) drugs to treat BD. There are also differences in the manuals of various countries although they have similar 

approaches. Americans and Canadians, in particular, strictly oppose the use of ADs in BD. They generally recommend using mood 

stabilizers (MSs) in treating less severe depressions, using ADs alongside these drugs only in severe depressions and discontinuing ADs as 

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 

different approaches, it is a fact that the decision to use antidepressant drugs in BD is not easy. 

The difficulty might stem from a number of reasons including: 

• 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. 

• 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). 

The matters of debate that may clarify this issue can be summarized as follows (2): 

• Transition to mania and rapid cycling are significant phenomena in Bipolar Disorder (BD). 

• The issue of suicide is, in fact, of minimal importance in BD. 

• The efficacy of antidepressants in BD has not been supported by satisfactory evidence. 

• MSs having an AD effect in BD has been supported by satisfactory evidence. 

Here are some brief answers to the matters of debate: 

• Like ADs, MSs have also not been officially approved in the treatment of BD. It is worthwhile to discuss the new generation antipsychotics 

(NGAPs) which have been approved in this context. 

• The data on manic transition and rapid cycling are problematic for the use of tricyclics to a certain extent; the data obtained from modern 

antidepressants have largely removed this issue from being a special problem area. There are also other alternatives to diminish the risk (4). 

• The antidepressant effect is directed towards the syndrome, thus these drugs are also effective in BD, but there are no noteworthy 

positive data on this issue for MSs other than a slight benefit obtained from Lithium. 

• The issues of suicide and chronicity cause a greater risk than all other issues in terms of contribution to a bad result for BD. 

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 

in combination with MSs or NGAPs in the treatment of BD. This approach is already commonly applied in practice. 

Key words: Bipolar disorder, antidepressants, depression 

S39


References: 

1. Gijsman HJ, Geddes JR, Rendell JM, Nolen WA, Goodwinn GM: Antidepressant for bipolar depression: A systematic review of randomized, controlled trials. Am J 

Psychiatry 2004;161:1537-1547. 

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 

Clin Neurosci 2000;250:57-68. 

3. Sachs SG, Nierenberg AA, Calabrese JR, Ketter TA, Marangeli LB, Milowitz DJ, Miyahara MS, Bauer MS: Effectiveness of adjunctive antidepressant treatment for 

bipolar depression. N Eng J Med 2007;356:1711-1722. 

4. Ghaemi SN, Rosenquist KJ, Ko YJ, Baldassano CF, Kontos NJ, Baldessarini RJ: Antidepressant treatment in bipolar versus unipolar depression. Am J 

Psychiatry2004;161:163-165. 


JOINT SYMPOSIA 

[JS-01] 

International Association for Cognitive Psychotherapy (IACP) 

Symposium title: Advances and problems in cognitive behavior therapy (CBT) 

Recent advances in the treatment of anxiety disorders 

Stefan Hofmann 

Department of Psychology, Boston University, Boston, USA 

E-mail: shofmann@bu.edu 

Cognitive behavioral therapy (CBT) is the first-line psychological treatment for anxiety disorders. Although effective, partial or nonresponse 

to treatment remains an all-too-common occurrence, with over half of patients failing to respond fully to first-line cognitive 

behavioral therapy. The same is true for pharmacological interventions for anxiety disorders. Combining CBT with conventional anxiolytic 

medication is typically not more effective than unimodal therapy for treating anxiety disorders. This presentation will examine strategies 

to augment and modify CBT to enhance its efficacy. Recently, the search for new strategies to augment CBT has turned to a unique model 

of combination therapy. Rather than using pharmacotherapy as an anxiolytic in its own right, it is used to augment the core learning 

processes of cognitive-behavior therapy and exposure procedures. Moreover, recent work in emotion research points to new intervention 

strategies for anxiety disorders, such as mindfulness-based therapies and meditation practices. 

The first half of this presentation will review the current literature on conventional and novel combination strategies. A particularly 

successful prototype of a novel augmentation strategy of CBT is the use of d-cycloserine (DCS), a partial agonist at the glycine recognition 

site of the glutametergic N-methyl-D-aspartate receptor, to facilitate extinction learning. The second half the presentation will review 

novel and adaptive emotion regulation strategies, including mindfulness and loving-kindness mediation. 

The efficacy of CBT for anxiety disorders can be enhanced by (1) augmenting the treatment with the cognitive enhancers such as DCS, 

and (2) modifying the intervention using novel emotion regulation strategies. The augmentation strategies are based on the fact that 

exposure-based treatments in humans partly rely on extinction to reduce the fear response in anxiety disorders. In fact, animal studies 

have consistently shown that DCS facilitates extinction learning. Similarly, recent human trials have shown that DCS enhances fear 

reduction during exposure therapy of some anxiety disorders. Positive findings so far have been reported in placebo-controlled trials for 

specific phobia, social anxiety disorder, panic disorder, and obsessive compulsive disorder. The strongest effects were observed in studies 

in which patients receive a small dose of DCS (50 mg) acutely 1 hour before the exposure trials with no more than 5 administrations 

weekly. The modification strategies of CBT have primarily focused on enhancing adaptive emotion regulation strategies, beyond 

traditional reappraisal strategies. Whereas cognitive reappraisal strategies are antecedent focused, these novel strategies are primarily 

emotion response focused. Although these strategies have only recently been studied as treatments for anxiety disorders, they are rooted 

in ancient Eastern and Buddhist practices. CBT is an evolving science that integrates traditional and modern approaches and is in line with 

modern emotion and neuroscience theories. 

Key words: Cognitive behavior therapy, anxiety disorders, combination drug therapy, NMDA, glutamate, mindfulness, meditation, emotion 

regulation 



Translating science into practice, collaborative empiricism and engagement 

in homework assignments in cognitive behavior therapy 

Nikolaos Kazantzis 

La Trobe University, Australia 

E-mail: Nikolaos@NikolaosKazantzis.com 



Cognitive-behavioral therapy is more efficacious when between-session ‘homework’ tasks are included. Although the evidence for the 

effectiveness of homework appears compelling, only limited research is available to guide day-to-day practice. Recently, the search for 

strategies to enhance homework compliance (or engagement) has centered on practitioner competence in developing collaborative and 

empirical therapeutic relationships. Rather than viewing practitioner competence as a “trait”, newer measures are better equipped to 

capture the fluctuations in competence from session-to-session, as well as the relationship between therapist competence and patient 

compliance, and their combined effects on positive treatment outcomes. 

This presentation will use meta-analytic methods to review the empirical data demonstrating the causal and correlational effects of 

CBT homework assignments in enhancing positive treatment outcomes. Positive results have been obtained in the treatment of major 

depressive disorder, social anxiety disorder, panic disorder, and generalized anxiety disorder. Data supporting the development of 

therapeutic relationships characterized by strong patient and therapist involvement in the therapeutic work (collaboration) of identifying 

and evaluating the patients’ belief system (empiricism) will also be covered. A recent study in the treatment of major depressive disorder 

suggests that therapist competence in following a compliance enhancement protocol, which focused on collaborative empiricism, 

enhanced treatment outcomes. In conclusion, the results of these studies suggest that patient engagement with homework assignments 

is an important determinant of positive CBT outcomes, but practitioner competence may enhance the effect when the patient-therapist 

relationship is characterized by collaborative empiricism. 

Key words: Cognitive behavior therapy; homework assignments; therapeutic relationship; treatment outcome 


CBT as an evidence based treatment approach: Warning signs in therapy and common 

mistakes in daily practice 

Mehmet Zihni Sungur 

Medical School of Marmara University, Dept. of Psychiatry, Istanbul, Tukey 

E-mail: mzsungur@superonline.com 

The remarkable results obtained from integration of cognitive and behavioral therapies and the simplicity and straightforward 

approaches of the treatment modality have attracted many therapists to practice cognitive-behavioral psychotherapy today. 

Unfortunately a considerable number of these therapists adhere to guidelines of a textbook-kind of therapy without formal training and 

adequate supervision, and therefore suggest standard package-type treatments with little or no attempt to develop individually tailored 

programmes. There are some crucial points that clinicians need to consider during the practice of CBT to increase positive treatment 

outcomes. This presentation will focus on significant points that should be taken into account during the daily practice of CBT, discuss 

common mistakes made in daily practice and the reasons why psychotherapy is devalued during delivery of psychological services, and 

suggest alternative ways to improve the efficiency of CBT for public care. 

Key words: Cognitive behavioral therapy, evidence based treatment, treatment principles and pitfalls 


S41


[JS-02] 

Malaysian Psychiatric Association 

Symposium title: Malaysian perspective of substance dependence 

A harm minimization program against drug use and HIV problems in Malaysia 

Rusdi Abd. Rashid 1 , Abdul Kadir Bin Abu Bakar 2 , Hazli Bin Zakaria 3 , Umi Binti Adzlin 4 , Mohammad Hussain Habil 5 

1University of Malaya Centre for Addiction Sciences(UMCAS), Kuala Lumpur, Malaysia 

2Hospital Permai, Johor Bharu, Malaysia 

3Dept. of Psychiatry, Hospital Universiti Kebangsaan Malaysia,Kuala Lumpur, Malaysia 

4Dept. of Psychiatry, Kajang Hospital, Selangor, Malaysia 

5Dept of Psychological Medicine,Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia 

E-mail: rusdirashid@gmail.com 

This symposium highlights the drug use and HIV situations in Malaysia from the perspective of the development of a harm minimization 

program, methadone assisted therapy for opiate dependents, and the world’s first integrated Islamic psychospiritual intervention with 

methadone treatment in a mosque setting. 

The speakers will present four topics that related to the drug problems in Malaysia. The first speaker will talk about harm minimization 

and the current drugs and HIV situations in Malaysia. The second speaker will highlight the harm reduction services available emphasizing 

pharmacotherapy options available in Malaysia, the challenges and future directions. The third speaker will focus on psychosocial 

intervention in particular an innovative psychospiritual intervention called the Spiritual Enhancement of Drug Addiction Rehabilitation 

(SEDAR) program in the Malaysian Ar-Rahman mosque. The fourth speaker will discuss Assisted Medication Therapy (AST) from an Islamic 

perspective. 

Harm minimization approaches in Malaysia are promising. However, the program needs large scale implementation and new strategies 

in order to make an impact on HIV/AIDS prevalence. 

New and larger platforms and more aggressive promotions are required to implement more harm minimization programs in the 

community. 

Key words: Addiction, harm minimization, HIV/AIDS, psychospiritual interventions 


[JS-03] 

Hellenic Society for the Advancement of Psychiatry and Related Sciences 

Symposium title: Disorders of sleep and wakefulness and their pharmacological management 

Depression and the effect of antidepressants on sleep 

Thomas Paparrigopoulos 

Athens University Medical School, 1st Department of Psychiatry, Athens, Greece 

E-mail: tpaparrig@med.uoa.gr 

Sleep mechanisms and the pathophysiology of depression are closely interrelated. Monoaminergic and cholinergic neurotransmission 

are heavily involved in both. Therefore, it is not surprising that depression is almost invariably associated with sleep abnormalities. 

Several hypotheses have been advanced to explain their occurrence. One suggests that an increased pressure of REM sleep might be 

responsible. Another proposes that a deficiency in the mechanism responsible for non-REM sleep, as explained by the two-process 

model of sleep regulation, may be implicated. Finally, a third hypothesis suggests that an imbalance between the monoaminergic and 

cholinergic systems in the central nervous system (CNS) could be responsible for the pathophysiology of depression and the observed 

sleep aberrations. 

In principle, most antidepressants increase synaptic levels of norepinephrine, serotonin, and dopamine; yet they may also act on 

muscarinic and histamine (H1) receptors. These effects purportedly underlie their principal therapeutic mode of action, as well as their 

potential mechanism of altering sleep architecture. In this line of thought it has been proposed that central to the therapeutic effect 




of the majority of antidepressants is the observed strong and sustained suppression of REM sleep, without overlooking other factors 

involved in the mechanisms underlying treatment response. Moreover, tryptophan depletion and studies of selective serotonin reutake 

inhibitors (SSRIs) in sleep have shown that increases in serotonin levels could mediate the effect on REM sleep, which is often observed 

during antidepressant treatment. However, changes in non-REM sleep and sleep maintenance may be mediated through the action of 

other neurotransmitter systems. 

Although each antidepressant drug affects sleep architecture differently, there are some common features that characterize the various 

types of antidepressants. Thus, the majority of antidepressant drugs suppress REM sleep. Some, however, with little or no noradrenergic 

or serotoninergic reuptake inhibition, such as amineptine, tianeptine, nefazodone, trazodone, bupropion, and trimipramine, do not 

have clear-cut REM suppressant effects. Sleep continuity and total sleep time are improved with sedative medications, such as most 

tricyclic antidepressants (TCAs) and several antidepressants with 5-HT2c receptor antagonist properties, such as mianserin, mirtazapine, 

nefazodone, and trazodone. On the other hand, most (SSRIs) and clomipramine, show evidence early in treatment of stimulating effects, 

thereby reducing total sleep time and sleep efficiency, and promote wakefulness. However, these effects are fairly short-lived and there 

are few significant differences among drugs after a few weeks of treatment. 

In conclusion, the majority of antidepressant drugs suppress REM sleep and increase REM latency, although this is not always the case. As 

far as sleep efficiency and total sleep time are concerned, antidepressants can be distinguished as either sedative or energizing agents. 

This individualized profiling of antidepressants provides a diversity of therapeutic options in terms of the management of concomitant 

sleep disturbances in depression. 

Key words: Depression, antidepressants, medication, sleep 


Insomnia and the effects of hypnotics on sleep 

Constantin R. Soldatos, Thomas Paparrigopoulos 

Athens University Medical School 

E-mail: egslelabath@hol.gr 

Insomnia is conceived as the subjective complaint of reduced sleep quantity and/or quality and affects a significant proportion of 

the general population. Approximately 10% of the population worldwide meet the full ICD-10 criteria for chronic insomnia. Insomnia 

is the outcome of the interplay of many environmental, biological, and psychological factors; consequently, its treatment should not 

only focus on ameliorating sleeplessness but should also address all those predisposing, precipitating and perpetuating factors that 

cause and maintain insomnia. Insomniacs need an integrative individualized management, which includes sleep hygiene measures, 

psychotherapeutic techniques, and the utilization of sleep-promoting drugs. The focus of treatment should be nighttime symptoms, the 

feeling of non-restorative sleep, and impaired daytime functioning as well. 

Benzodiazepine or benzodiazepine-like hypnotics (z-drugs) are still considered as the drugs of choice for the treatment of insomnia. 

However, due to their abuse potential, their pharmacological properties, and their widespread use (there are estimates that one of 

every four adults in developed countries takes sleeping aids at some time point during the year), it is highly recommended that the 

use of hypnotic drugs is restricted to the initial period of treatment mostly as adjuncts to other psychotherapeutic measures. Both 

types of hypnotics focus primarily on the inhibitory neurotransmitter GABA through binding to GABAA receptors; however, other 

neurotransmitter systems, such as the serotoninergic and histaminergic, are also involved in the regulation of sleep-wakefulness and 

may be targeted by other compounds. The non-benzodiazepine drugs are generally preferred as a result of their improved binding 

selectivity and pharmacokinetic profile. However, their potential adverse effects, such as amnestic symptoms, next day residual 

sedation, and abuse potential, indicate the need for novel pharmacotherapies. In this line, agents acting on the melatonergic system 

and circadian mechanisms have been developed and approved for the treatment of insomnia (melatonin and the melatonin receptor 

agonist, ramelteon). Furthermore, a variety of other compounds targeting several neuroreceptors (i.e., GABAA agonism, melatonergic 

MT1/MT2 agonism, 5-HT2A antagonism, orexin receptor OX1/OX2 antagonism) are under investigation and may be added in the 

psychopharmacological armamentarium in the near future. 


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Hypersomnias and the effects of vigilance-promoting compounds 

Antigone Papavasiliou 

Department of Neurology, Pendeli Children’s Hospital 

E-mail: theon@otenet.gr 

Hypersomnia is characterized by a propensity to fall asleep in situations when one is expected to be awake and alert. It may present with 

prolonged sleep episodes coupled with excessive daytime sleepiness (EDS) and frequent napping. It is described in narcolepsy, a neurological 

disorder characterized by EDS occurring with or without cataplexy; in idiopathic hypersomnia, also of central origin, characterized by EDS 

and episodes of prolonged nocturnal sleep; in recurrent hypersomnias, rare disorders manifesting with recurrent episodes of more or 

less continuous sleep (average duration of 1 week), recurring at highly variable intervals (one to several months), such as, Kleine–Levin 

syndrome and menstrual-related hypersomnia. Chronic sleep loss and/or poor sleep quality may be underlying reasons for EDS; these occur 

in numerous sleep disorders, such as obstructive sleep apnea (OSA) and in psychiatric disorders, particularly depression. Approximately 

80% of depressive states are associated with insomnia; patients do not necessarily have a higher propensity to fall asleep in daytime but 

report subjective sleepiness that differs from the EDS encountered in narcolepsy and OSA. There are also hypersomnias attributable to other 

medical conditions, drugs, or substances, as well as behaviorally induced hypersomnia caused by insufficient time to sleep. 

Transition between sleep and wakefulness is simply described as oscillations between two opponent processes, one promoting sleep, 

another promoting wakefulness. The complex neurobiological mechanisms and the neurotransmitters and neuromodulators underlying 

these processes, including noradrenergic, serotonergic, cholinergic, adenosinergic, and histaminergic systems and more recently, the 

hypocretin/orexin and dopamine systems, have been established. The mechanisms of action of some vigilance-promoting agents are as 

follows: psychostimulants act through enhanced dopamine action (amphetamines, methylphenidate) or acetylcholine action (caffeine); 

modafinil may act through enhanced central histamine, hypocretin, and possibly dopamine action; γ -hydroxybutyrate (GHB), acts on GABA 

and GHB receptors. EDS in narcolepsy is traditionally treated with psychostimulants; these are rarely effective in idiopathic hypersomnia, 

although this was not examined through randomized controlled trials. Modafinil, a first-line wakefulness-promoting medication, is a 

useful alternative to psychostimulants for EDS in narcolepsy (Level I evidence). It may be effective for EDS due to idiopathic hypersomnia 

(one Level IV study and expert consensus). It is not associated with rebound hypersomnolence, cardiovascular problems, or abuse 

potential, as may be seen with amphetamines. Modafinil alleviates sleepiness and fatigue in shift work disorders, residual sleepiness in 

treated sleep apnea syndrome, multiple sclerosis, Parkinson’s disease and depression. It is promising as an alternative to psychostimulants 

for excessive fatigue associated with medical and psychiatric disorders and as an augmentation medication for treatment-resistant 

depression. Due to rare serious complications (allergic and psychiatric), the EMA concluded that its benefit/risk balance was positive for 

narcolepsy but negative for other sleep disorders and neurological diseases, including idiopathic hypersomnia. The FDA has approved it 

for EDS in narcolepsy, shift work sleep disorder, and OSA. In narcolepsy, GHB at bedtime reduces nocturnal awakenings, increases stage 

3 and 4 sleep, and consolidates REM sleep periods; these effects coincide with improvement in daytime symptoms, including cataplexy. 

Key words: Vigilance-promoting agents, hypersomnia, psychostimulants, modafinil, γ -hydroxybutyrate 


[JS-04] 

The International Union of Basic and Clinical Pharmacology (IUPHAR) 

Symposium title: Pharmacogenomics of psychoactive drugs 

Role of polymorphic drug transporter in treatment-resistant depression 

Tanja Brueckl, M. Uhr 

Max Planck Institute of Psychiatry, Germany 

E-mail: brueckl@mpipsykl.mpg.de 

To be effective antidepressants and other centrally acting drugs have to penetrate the blood-brain barrier. Transport proteins such as 

p-glycoprotein that are located at the BBB do not only transport toxic substances but also many drugs back into the blood. In preclinical 

animal models and a study examining more than 400 patients, the relationship between polymorphisms in the ABCB1 gene coding 

for p-glycoprotein and the clinical efficacy of antidepressants could be demonstrated. With respect to those antidepressants that are 




substrates of p-glycoprotein there is a significant statistical relationship between polymorphism and remission rate after 4 to 6 weeks. 

Clinically, genetic analysis of ABCB1 polymorphisms may be used to predict how likely it is that a patient will respond to therapy with 

antidepressants or other centrally acting drugs. This in turn will help to select the right drug and/or dosage (Neuron 2008, 57:203-209). 

Further data from a preliminary pilot study suggest that the treatment of depression could be optimized by a routine application of 

an ABCB1 gene test. Patients carrying the less favourable ABCB1 genotype with respect to the clinical efficacy of antidepressants may 

especially benefit from a dosage increase. 

P-glycoprotein in the membrane of vascular cells causes centrally acting drugs such as citalopram, paroxetine, venlafaxine and others to be 

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 

the brain. Depending on changes (polymorphisms) in the ABCB1 gene, p-glycoprotein allows varying amounts of a drug to pass into the CNS. 


Relationship between pharmacogenetics and personality traits: Relevance for suicide 

Adrián Llerena 

International Union of Basic and Clinical Pharmacology (IUPHAR), Extremadura University Hospital 

E-mail: allerena@unex.es 

CYP2D6 genetic polymorphism is related to variability of the enzyme’s hydroxylation capacity. Subjects carrying zero CYP2D6 active 

genes are classified as Poor Metabolizers (PMs). The rest are Extensive Metabolizers (EMs) with one or two active genes, including a group 

of Ultra-rapid Metabolizers (UMs) with more than two active alleles. UMs have a hydroxylation capacity more than 100 times higher than 

PMs. The frequency of PMs and UMs in Spain is 7-10% and 4.9%, respectively (Llerena et al., 2009). 

A higher frequency of UMs has been found among individuals who committed suicide vs. those who died from natural causes (Zackrisson 

et al, 2010). One explanation for this relationship could be treatment failure with antidepressant drugs metabolized by CYP2D6 

(fluoxetine, paroxetine, fluvoxamine, venlafaxine, citalopram, etc.) (Llerena et al., 2004; Llerena et al., 2009) widely used to prevent suicide 

or to treat mood disorders. A complementary explanation could be via the implication of the polymorphic CYP2D6 in the endogenous 

metabolism. Since we found an association between this drug metabolizing enzyme and psychological functioning, CYP2D6 has been 

associated with behavioral and clinical risk factors such as personality and vulnerability to psychopathology (Llerena et al., 1993; Llerena 

et al., 2007; Gonzalez et al., 2008; Peñas-Lledó et al., 2009, Peñas-LLedó et al., 2010). These two hypotheses could explain the relationship 

found between CYP2D6 and suicide (Peñas-LLedón et al 2011, in press) 

The biotransformation of several antidepressants and antipsychotic drugs is mainly determined by genetic factors mediating the 

CYP2D6 gene polymorphism. Additionally, the potential interaction between CYP2D6 and endogenous metabolism must be taken into 

consideration due to its potential implication for personality traits (LLerena et al 1993; Gonzalez et al 2008) and functioning, such as: 

neurocognition (Peñas-Lledó et al 2009) and psychopathology, eating disorders (Peñas-LLedó et al., 2010) and suicide (Peñas-Lledó et al., 

2011). In summary, the pharmacogenetics of CYP2D6 may be a useful tool to predict unexpected side-effects, interactions, or therapeutic 

failures of many relevant drugs and may explain the interethnic differences oberserved in the response to psychotropic drugs, but also 

vulnerability to psychopathology including suicide. 


Genetic causes of hypersensitivity to antipsychotics – the clozapine story 

Ingolf Cascorbi 

Institute of Experimental and Clinical Pharmacology, University of Kiel, Germany 

E-mail: cascorbi@pharmakologie.uni-kiel.de 

Clozapine is considered to be the most efficacious drug to treat schizophrenia, but despite these benefits, clozapine prescriptions 

comprise only 2-10% of the total antipsychotic market for schizophrenia in the United States. It was introduced on the market in 1971 but 

was withdrawn in 1975 after reports of clozapine-induced agranulocytosis (CIA) in Finland. Due to its high efficacy in treatment-resistant 

schizophrenia, it was reapproved in 1990 by the FDA and health authorities in most other countries; however, regular hematological 

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monitoring was required. The implementation of this monitoring system has successfully reduced the incidence of CIA from 1.3% to 0.4%. 

Currently 239 cases of agranulocytosis are registered at the FDA adverse drug reaction data bank. 

There have been certain attempts to predict agranulocytosis by genetic association studies in particular in the NADPH myeloperoxidase 

complex (1) and FC-gamma receptors (2). We could identify an association to the polymorphic myeloperoxidase, responsible for oxidative 

reaction in neutrophils. More recently, confirmatory studies in two independent cohorts of 33 and 49 CIA cases and 54 and 78 controls 

indicated that markers in the HLA system are highly significantly associated with the risk of CIA. HLA-DQB1 6672G>C was associated with 

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 

defined cases of CIA in order to allow genome-wide association studies. 

Key words: Clozapine, agranulocytosis, NADPH-oxidase, myeloperoxidase, HLA-system, genetic association 

References: 

1. Mosyagin I, Cascorbi I, Schaub R, Krüger T, Dettling M. Drug-induced agranulocytosis: impact of different fcgamma receptor polymorphisms? J Clin 

Psychopharmacol. 2005;25:435-40. 

2. Mosyagin I, Dettling M, Roots I, Mueller-Oerlinghausen B, Cascorbi I.. Impact of myeloperoxidase and NADPH-oxidase polymorphisms in drug-induced 

agranulocytosis. J Clin Psychopharmacol. 2004;24:613-7. 

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 

analysis identifies a polymorphism in HLA-DQB1 associated with clozapine-induced agranulocytosis. J Clin Psychiatry. 2011;72:458-63. 


[JS-05] 

Indian Psychiatric Society 

Symposium title: Current concept of obsessive compulsive disorder (OCD) 

Current understanding of the concept of obsessive compulsive disorder 

Manickam Thirunavukarasu 

Professor & Head, Department of Psychiatry, SRM MC & RC, Kattankulathur, 603203, India 

E-mail: arasueshwar@gmail.com 

Obsessive-compulsive disorder (OCD) is a relatively common disorder, occurring in around 2-3% of general population. In the past 

century, the understanding of the disorder has improved and has been clearly delineated as a valid nosological entity. The heterogeneity 

of the disorder has been explained based on various phenotypic subtypes. Factor analytic studies have provided consistent evidence that 

distinct obsessive-compulsive symptom dimensions exist, including obsessions/checking, contamination/washing, symmetry/ordering, 

and hoarding. It has been hypothesized that each symptom dimension may be underpinned by a distinctive set of bio-behavioral 

mechanisms. There has been a good deal of interest recently in the disorders characterised by similar phenomenology and psychobiology 

called obsessive compulsive spectrum disorder (OCSD). These include tic disorder, body dysmorphic disorder, impulse control and eating 

disorders. In view of all these changes in understanding and newer conceptualisation, OC(S)D might find a separate place for itself in the 

DSM V and ICD 11, rather than being classified under anxiety / neurotic spectrum disorders. 


Biological theories of obsessive compulsive disorder 

A. Shyam Sundar 

Assistant Professor, Department of Psychiatry, SRM Medical College Hospital and Research Centre, Kattankulathur, 603203, India 

E-mail: a.shyamsundar@gmail.com 

Although the pathophysiology of OCD is still far from resolved, the existence of a biological basis for OCD has been clearly established. 

Twin, family, segregation and linkage studies have demonstrated that genetic factors contribute to the pathogenesis of OCD. There 




is a general consensus that fronto-striato-thalamo-cortical dysfunction is the neuronal basis of obsessive-compulsive disorder. The 

differential response of OCD to clomipramine and SSRIs, compared to other antidepressants, has led to the primacy of the serotonin (5HT) 

hypothesis of OCD. Currently serotonin has also been implicated in the pathophysiology of other OC spectrum disorders. However, several 

lines of research suggest that the dopamine system, with which 5HT interacts, may play a major role in the expression of OC symptoms. 

Recent genetic and neurochemical studies also implicate glutamate in the pathophysiology of OCD. The recognition of PANDAS (Pediatric 

autoimmune neuropsychiatric disorders associated with streptococcal infection) has increased the interest in the possibility of an 

immune-mediated pathophysiology of obsessive-compulsive disorder. In this presentation, these recent advances in biological models 

of OCD will be discussed. 


Psychopharmacological and somatic interventions for OCD 

Kandasamy Arun 

Assistant professor, Department of Psychiatry, SRM Medical College & Research Center, Kattankulathur, 603203, India 

E-mail: arunnimhans05@gmail.com 

OCD was initially thought to be unresponsive to treatment but subsequently, a range of effective treatments has been developed on the 

basis of two approaches, pharmacological and psychosocial. Pharmacological agents such as Selective Serotonin Reuptake Inhibitors 

(SSRIs) and clomipramine have changed the face of OCD management. Around 50–60 % of patients showed remission after treatment. In 

treatment resistant cases, augmenting agents like clonazepam, risperidone and buspirone are used. Intravenous clomipramine is another 

option. Other strategies which are currently under study include riluzole and other drugs which act on the glutaminergic system, opioid 

agonists and inositol augmentation. Immunomodulatory therapies have also been studied especially in PANDAS. Development of newer 

somatic methods of treatment like repetitive trans-cranial stimulation (rTMS) and Deep Brain Stimulation (DBS) are promising in targeting 

the fronto-striato-pallido-thalamo-cortical circuits for treatment resistant OCD. Although controversial, stereotactic and gamma knife 

assisted neurosurgical procedures such as cingulotomy and anterior capsulotomy are also possible treatments for resistant cases. 


Psycho-social interventions for OCD 

Manickam Thirunavukarasu 

Professor & Head, Department of Psychiatry, SRM MC & RC, Kattankulathur, 603203, India 

E-mail: arasueshwar@gmail.com 

We will review recent advances in the psychological treatments for obsessive compulsive disorder. In the early 20th century, psychological 

treatment for OCD consisted largely of psychodynamic psychotherapy. The general consensus of that era was that OCD was an 

unmanageable condition with a poor prognosis. Starting from the 1950s, laboratory studies on extinction of conditioned responses 

followed by clinical research led to the formulation of Exposure and Response Prevention (ERP) for OCD.We have developed a model 

combining ERP and CBT. This behavioral approach currently is the first-line intervention for adult obsessive-compulsive disorder. Recently 

predominantly cognitive approaches have been evaluated to overcome the shortcomings of ERP. Methodologically rigorous controlled 

trials have suggested that the benefits from CBT exceed those from placebo and attention-control conditions and have similar or greater 

efficacy than serotonergic monotherapy. The clinical predictors for response to CBT include symptom severity, symptom subtype, severe 

depression, the presence of comorbid personality disorders, family dysfunction and the therapeutic alliance. Combination treatment with 

pharmacotherapy has generally revealed promising results. Nevertheless, more studies are still needed in certain areas. We will explain in 

detail how we practice in our patients and the results. 


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[JS-06] 

Czech NeuroPsychopharmacological Society (CNPS) 

Symposium title: From models of schizophrenia to clinical outcome: A psychopharmacological perspective 

Safety first, efficacy second? Fear and the need for treatment in the absence of controlled data 

Pavel Mohr, David Hnidek, Dagmar Seifertova 

Prague Psychiatric Center, Czech Republic 

E-mail: mohr@pcp.lf3.cuni.cz 

In clinical practice, physicians are routinely asked to make decisions about whether to initiate or continue antidepressant treatment in 

a situation where no safety data are available. Pregnancy and breast-feeding can serve as an example, where controlled clinical trials 

provide little guidance. Females of fertile age are rarely included in the early phases of clinical testing, indeed, Phase IIb and III trials have 

a standard provision to use a reliable method of contraception. Pregnancy during a drug trial is considered as a ‘serious adverse event’ 

with subsequent study discontinuation. The reasons are not just ethical and legal but also marketing, including the drug manufacturers’ 

fear of having their products associated with potentially grave side effects, such as malformations. Drug treatment in pregnancy and 

lactation thus pose a highly relevant clinical problem that cannot be addressed in controlled trials. Excessive concerns of negative 

consequences could erroneously result in a generalized recommendation to not get pregnant or to abort an existing pregnancy. However, 

the fetus may already have been exposed to drugs early in the first trimester during frequently unplanned pregnancies; in addition, recent 

epidemiological data indicate increasing consumption of psychotropics, including antidepressants, by pregnant women. Psychiatrists 

have to weigh the known risks of treatment discontinuation versus the potential risks for the fetus and infant. They should also consider 

whether alternative non-pharmacological interventions (psychotherapy, ECT, rTMS) are accessible or effective. The only available safety 

data on antidepressants come from animal studies, epidemiological trials, drug registries, case series, anecdotal case vignettes and clinical 

observations. 

Moreover, published findings have to be viewed with caution and interpreted correctly. For example, recent data suggested an increased 

teratogenic risk for the antidepressant paroxetine. While it is true that a meta-analysis confirmed an increased relative incidence of 

malformations, the absolute risk was raised from 3% to 4% for all congenital malformations and from 1% to 2% for cardiac malformations. 

In 2005 the Prague Psychiatric Center established a specialized consultation outpatient center for pharmacotherapy in pregnancy and 

breastfeeding. The center provides services and information on safety and treatment recommendations directly to patients, their treating 

psychiatrists and other physicians as well. The database consists of patients records, data on their illness, treatment and pregnancy 

outcome. Currently, a prospective study for the longitudinal follow-up of offspring exposed in utero to psychotropics has been designed. 

The focus is on their developmental milestones, physical health, neuropsychological performance and general well-being. 

Key words: Psychotropic drugs, pregnancy, lactation, drug safety, psychiatric disorders 


Basic concepts of schizophrenia: Experimental approaches 

Cyril Höschl 1 

1Prague psychiatric centre, Centre of neuropsychiatric studies, 

3rd Medical faculty, Charles University, Prague, Czech Rep. 

E-mail: hoschl@pcp.lf3.cuni.cz 

One of the crucial questions in the study of schizophrenia is, whether the diagnosis of the disease represents one entity or a group of 

disorders (“Gruppe der Schizophrenien”). Nancy Andreasen suggests the term “lathomenology” for a bottleneck on the pathogenetic way 

from various possible etiological factors to diverse phenomenological expressions (symptoms) (Arch Gen Psych 1999;56:781-787). In the 

background of this common denominator, there is an anatomical and functional disruption in neuronal connectivity and communication, 

which can be a consequence of incomplete or erroneous neuron formation, migration, synaptogenesis or pruning during ontogenesis. 

Also apoptosis and activity dependent changes might play a role in this development. This all can happen from conception to early 

adulthood and can lead to the impairment in fundamental cognitive functions. This leads to the development of clinical symptoms, 

either positive or negative. Schizophrenia can be regarded as a “disconnection” or “information processing disorder”. There are many 




neural circuits, where the clinical impact of the disconnection or misconnection is worthy of study. One of them is the fronto-thalamocerebellar 

circuit with the special role of the cerebellum not only in the synchronization of motor processes, but also in the coordination 

of motor-cognitive sequences. The disconnection of these circuits leads to “cognitive dysmetria”. Mezo-cortical pathways also represent 

a crucial pathogenetic point. Dopaminergic fibers from the ventral tegmental area to the pre-frontal cortex are under serotonergic 

inhibition via 5-HT2 receptors. This configuration can help in the understanding of the dual mode of action of novel antipsychotic agents, 

which are effective in both positive (hyperdopaminergic state in mezo-limbic areas) and negative (hypodopaminergic state in prefrontal 

cortex) symptoms. Disconnection can play a role also in circuits involved in executive functions (fronto-parieto-temporo-cingulate). 

On the neurochemical level, many imbalances in information processing can be explained by the framework of Carlsson’s scheme of 

psychotogenic pathways. The crucial mechanism involves striato-thalamic GABA-ergic control of gating, which is under glutamatergic 

control from cortex. The scheme can also explain the amphetamine model of psychosis, the dopamine hypothesis of schizophrenia, the 

glutamatergic model of schizophrenia and the psychotogenic effects of hallucinogens (LSD), atropine, phencyclidine etc. Our own study 

on the role of serotonin regulation of psychotogenic pathways will be reported (Bubeníková et al., The effect of tryptophan depletion on 

the action of haloperidol in MK-801 treated rats. Eur J Pharmacol, 2004; 502, 1-2:109-116). 

The background of disconnection may involve gene-environment interaction including early neuroinfection (inflammatory process). 

The classical antipsychotic drugs exert primarily antidopaminergic properties, which are responsible also for their side-effects such 

as hyperprolactinemia and extrapyramidal syndrome. Nevertheless, psychotogenic pathways in the brain involve several different 

mechanisms, which could serve as targets of antipsychotic modalities, e.g., facilitation of glutamatergic neurotransmission, blockade of 

serotonin 5-HT2A receptors, expression of BDNF and bcl2, inhibition of GSK-3β phosphorylation and thus apoptosis etc. 

Key words: Schizophrenia, glutamate, dopamine, serotonin, information processing disorder, gating 


The ins and outs of the human model of schizophrenia 

Jiri Horacek 1 , Vera Bubenikova Valesova 1 , Tomas Palenicek 1 , Filip Spaniel 2 , Cyril Höschl 1 

1Prague Psychiatric Center, Prague, Czech Rep. 

2 rd 3 Medical Faculty of Charles University, Prague, Czech Rep. 

E-mail: horacek@pcp.lf3.cuni.cz 

The experimental models of schizophrenia are based on morphological, biochemical and genetic findings in the clinical population. These 

models serve as an important tool for the research of etiology and pathophysiology, and for testing novel potential treatment methods. 

The experimental models of schizophrenia are divided into neurodevelopmental, pharmacological and genetic. Only the pharmacological 

model is useful in humans. 

An important role of the glutamatergic neurotransmitter system in the pathogenesis of schizophrenia has been supported by findings 

on various levels from molecular interactions up to the structural layout of the neuronal network in the human brain. The research of 

the glutamatergic system in schizophrenia has advanced with the use of non-competitive antagonists of glutamate NMDA receptors 

(phencyclidine, ketamine, and dizocilpine). These compounds change both human and animal behavior and induce schizophrenia-like 

manifestations in the field of different neurobiological modalities and markers. 

The models based on both acute and chronic administration of non-competitive antagonists of glutamate NMDA receptors in humans 

and rats show phenomenological validity and are suitable for searching for new substances with antipsychotic effects. In particular, the 

human model of schizophrenia based on infusion of ketamine exerts high face validity in term of induction both positive and negative 

symptoms, and characteristic cognitive, electrophysiological (qEEG) and metabolic (PET) changes. 

Nevertheless, the pathophysiology of schizophrenia remains unexplained. In the light of the neurodevelopmental model of schizophrenia 

based on the early administration of NMDA receptor antagonists, it seems that increased cellular destruction by apoptosis or changes 

in function of glutamatergic NMDA receptors in the early development of the central nervous system are decisive for subsequent 

development of psychosis, which often does not manifest itself until adulthood. Chronic administration of NMDA (not applicable 

in humans) antagonists initializes a number of adaptation mechanisms, which correlate with findings obtained in patients with 

schizophrenia; therefore, this animal model is necessary for research into the pathophysiology of this disease. 

This work was supported by project 1M0517 from the MEYS Czech Republic 

Key words: Schizophrenia, models, NMDA receptors, ketamine, glutamate, neurodevelopment 


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[JS-07] 

Canadian College of Neuropsychopharmacology 

Symposium title: Advances in psychotropic drug development: Promising novel targets and agents for psychiatric disorders 

Recent advances in the neurochemistry of schizophrenia and potential targets for 

antipsychotic drug development 

Serdar Dursun, Glen Baker, Marnie Mackay 

Neurochemical Research Unit, University of Alberta, Edmonton, Canada 

E-mail: Dursun@ualberta.ca 

The dopamine hypothesis of schizophrenia has been a major influence for many years in stimulating research in schizophrenia 

and in assisting in the development of antipsychotic drugs. However, it has become obvious that other neurotransmitters and/or 

neuromodulators must also be involved. The antipsychotic drugs currently available are far from ideal and there is an urgent need to 

continue to search for new targets for potential antipsychotics. 

Much of the recent research on non-dopaminergic systems has focused on the amino acids glutamate and GABA, with the bulk of 

the results suggesting hypofunction of both in schizophrenia. Glutamate does not pass the blood-brain barrier readily and studies 

conducted to develop drugs that act at one or more of its multiple receptors have not, to our knowledge, yet produced potential new 

effective antipsychotics. Two other amino acids, glycine and D-serine, co-agonists at the NMDA glutamate receptor, have received 

considerable attention, and administration of these amino acids, usually in conjunction with currently available antipsychotics, have 

been reported in some studies to result in improvement of some symptoms of schizophrenia. However, these amino acids have to 

be administered in relatively high doses which may result in side effects such as peripheral neuropathies. There is now a great deal of 

interest in testing drugs that inhibit their uptake by neurons and/or glial cells (astrocytes and activated microglia), thus making increased 

levels of these amino acids available to interact with the NMDA receptor or, particularly in the case of D-serine, altering metabolism 

of the amino acid. This research also emphasizes the importance of glial cells. Microglia are also involved in immune responses and 

when activated release a number of proinflammatory cytokines that can result in some behavioural, cognitive, and neuroendocrine 

changes characteristic of schizophrenia. It is also of interest that there is now research indicating that there may be a dysfunction of 

oligodendrocytes and myelination problems in schizophrenia. Another exciting area of research with regard to schizophrenia is in 

the study of neuroactive steroids, rapid acting steroids which can act as positive or negative allosteric modulators at several types of 

neurotransmitter receptors, most notably GABA-A receptors and NMDA receptors. Plasma levels of several of these steroids are altered 

in a number of psychiatric disorders, including schizophrenia and some clinical studies suggest that pregnenolone may be a useful 

adjunctive agent in schizophrenia. Brain levels of some of these steroids have also been reported to be altered in laboratory animals 

following administration of currently available antipsychotics. 

In addition to the compounds mentioned above, potential interventions which may be added to the usual antipsychotic treatments 

include lamotrigine and minocycline. Furthermore, modulation of the nitric oxide pathway continues to gain considerable interest as a 

possible therapeutic target in the treatment of schizophrenia. We will report the results of an RCT double-blind crossover study on the 

addition of L-arginine, the precursor amino acid for nitric oxide, to usual treatment with antipsychotics in schizophrenic patients. 

Key words: Schizophrenia, antipsychotic development, glutamate, nitric oxide, D-serine, glycine, glia, neuroactive steroids 


Advances in antidepressant targets and drug development 

Glen B. Baker, Nicholas D. Mitchell, Jean Michel Le Melledo, Serdar Dursun 

Department of Psychiatry, University of Alberta, Edmonton, AB, Canada 

E-mail: glen.baker@ualberta.ca 

The biogenic amine hypothesis of depression, which suggests that depression is the result of a functional deficiency of noradrenaline 

(NA) and/or serotonin (5-hydroxytryptamine, 5-HT) at certain synapses in the brain, has had a major influence on research into the 

neurochemistry of depression for over fifty years, and most of the antidepressants currently available have an effect on one or both of 

these biogenic amines. However, it was obvious early on that other neurotransmitters or neuromodulators must also be involved, and the 




search continues for other targets that may give clues for the development of future antidepressant drugs that are effective in a greater 

number of depressed patients, are faster acting and have an improved side effect profile over those currently available. Some of those 

targets will be discussed in this overview. 

The amino acids γ-aminobutyric acid (GABA) and glutamate are major inhibitory and excitatory neurotransmitters, respectively in the 

brain, and a delicate balance between them must be maintained for normal brain function. Research on GABA at the animal model and 

clinical levels implies a GABAergic deficit in depression, and animal studies and the rapid antidepressant action of intravenous ketamine 

in human subjects suggest hyperglutamatergia in depression, although the results of some neuroimaging studies to date do not seem 

to support these ideas. In recent years, there has been a great deal of interest in the possible roles of neuroactive steroids (rapid acting 

neurosteroids which can act as positive or negative modulators of a number of neurotransmitter receptors, most notably GABA-A and 

NMDA glutamate receptors) in the etiology and pharmacotherapy of depression. Allopregnanolone has received particular attention 

in this regard. Several researchers have proposed that the hypothalamic-pituitary-adrenal (HPA) axis plays a central role in the etiology 

of depression and there has been considerable interest in corticotropin-releasing hormone (CRH) receptor antagonists as potential 

antidepressants. The peptide substance P acts on neurokinin 1 (NK1) receptors, and there is ongoing interest in NK1 receptor antagonists 

as potential antidepressants. The role of the immune system in depression has been the focus of considerable research and it has been 

proposed that excessive proinflammatory cytokines (which are released by activated microglia) may result in depressive symptoms; it 

is of interest that such cytokines can activate CRH release and reduce levels of 5-HT in the brain. Although there are some contradictory 

results, several studies suggest that antidepressants increase expression of cyclic AMP-regulated element-binding protein (CREB) and 

brain-derived neurotrophic factor (BDNF). Dysfunction of melatonin secretion in depression has been suggested and this may account, 

at least in part, for sleep disorders experienced by many depressed subjects. Agomelatine, a melatonin receptor agonist and 5-HT2C 

receptor antagonist, is now marketed as an antidepressant. The potential interactions of several of the targets mentioned above will be 

discussed. 

Acknowledgements: The authors are grateful to the Canadian Institutes of Health Research (CIHR), the Canada Research Chairs program 

and the University of Alberta for Funding. 

Key words: Antidepressants, biogenic amines, GABA, glutamate, HPA axis, CRH, substance P, neuroactive steroids, glia 


SYMPOSIA 

[PS-01] 

Symposium Title: Epigenetics or genetics: Gene-environment interactions over the life - span 

Alzheimer’s disease: Genes and/or life style 

Engin Eker 

Istanbul University, Cerrahpaşa School of Medicine, Department of Psychiatry 

E-mail: enginekertr@yahoo.com 

A number of genetic risk factors have been identified, but only a small proportion of Alzheimer’s disease (AD) cases can be explained by 

specific gene mutations. Several genetic risk factors have been linked to AD. Mutations in APP, PS1, and PS2 genes have consistently been 

associated with early-onset familial Alzheimer’s disease (FAD). A majority of AD cases manifest as sporadic late onset form (LOAD) typically 

with onset above the age of 65 years. Most people who develop Alzheimer’s are diagnosed after age 80. More recently a large number 

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 

for the APOE4 allele or loci in the clusterin (CLU), phosphatidylinositol binding clathrin assembly protein (PICALM), and complement 

receptor1 (CR1). 

Most diseases of aging are influenced by gene-environment interactions. AD has both genetic and environmental risk factors. The genetic 

susceptibility influenced by genes like ApoE4 are factors to be aware of, but perhaps more important are the environmental risk factors. 

Environmental risk factors can act as triggers in the expression of gene potential. Numerous studies indicate that ApoE4 carriers may be 

more vulnerable to environmental factors. 

Recent studies have shown that dietary factors, such as exposure to a Mediterranean diet, fish and high omega-3 diets, cigarette 

smoking, head trauma, infections, systemic inflammation, and metal exposure can significantly alter an individual’s risk of developing 

AD. On the other hand psychosocial factors such as education, social network, leisure activities and physical activity, chronic stress, and 

S51


depression also seem to be connected to the risk of developing AD. There are some somatic factors that are under the direct influence of 

environmental exposures, such as blood pressure, obesity, diabetes mellitus, cardio- and cerebrovascular diseases, and hyperlipidemia, 

have additionally been implicated in AD etiology. 

Key words: Alzheimer’s disease, genes, environmental risk 


[PS-02] 

Symposium Title: Behavioral addictions and treatments: Review of recent data 

From Don Juanism and nymphomania to hypersexual disorders 

Sultan Doğan 

Namik Kemal University, School of Medicine, Department of Psychiatry 

E-mail: sultandogan@yahoo.com 

Hypersexual Disorder is proposed as a new psychiatric disorder for consideration in the sexual disorders section of the DSM-V. Historically, 

excessive sexual behaviors were clinically documented by diverse clinicians such as the 19th century Western European pioneer sexologists 

Richard von Krafft-Ebing (1840–1902), Havelock Ellis (1859–1939), and Magnus Hirshfeld (1868–1935). Benjamin Rush(1745–1813), a 

physician and founding father of the United States (Rush, 1746-1813) also studied the same subject. These clinicians and investigators 

described a frame of persistent socially deviant sexual behaviors as well as clinical examples of males and females whose nonparaphilic 

(i.e., normophilic) sexual appetite was excessive and maladaptive. The clinical examples of such appetitive behaviors described by these 

investigators were precursors to the 20th century characterization of protracted promiscuity as Don Juanism (Stoller, 1975) or satyriasis 

(Allen, 1969) in males and nymphomania (Ellis & Sagarin, 1965) in females. The DSM-II (American Psychiatric Association, 1968) recognized 

sexual deviations as personality disorders but there was no mention of excessive or maladaptive nonparaphilic sexual behavior disorders. 

By 1980, the DSM-III (American Psychiatric Association, 1980) classified paraphilic disorders as distinct pathologies (Psychosexual 

Disorders) and a residual diagnostic category, Psychosexual Disorder Not Otherwise Specified included ‘‘distress about a pattern of 

repeated sexual conquests with a succession of individuals who exist only as things to be used (Don Juanism and nymphomania)’’. In the 

DSM-IV (American Psychiatric Association, 1994) and its text revision, DSM-IV-TR (American Psychiatric Association, 2000), the original 

DSM-III characterization of these behaviors was reestablished. Sexual Disorders Not Otherwise Specified (302.9) included a condition 

characterized by: ‘‘distress about a pattern of repeated sexual relationships involving a succession of lovers who are experienced by 

the individual only as things to be used’’. Until recently, authors have used different terms for hypersexual disorders, such as “sexual 

addiction” (Carnes), “paraphilia-related disorders and non-paraphilic hypersexuality” (Kafka), “excessive sexual desire disorders” (Marshal), 

“problematic hypersexuality” (Finlayson) and “compulsive sexual bahavior” (Cooper and Coleman). These disorders were described as 

markedly increased expressions of culturally normative sexual desire (fantasies, urges, and behaviors) persisting for a minimum duration 

of 6 months and associated with clinically significant personal distress, impairment in reciprocal romantic relationships or other adverse 

psychosocial consequences. Thera are several form of hypersexual disorders such as compulsive masturbation, pornography dependence, 

telephone sex dependence, cybersex, severe sexual desire incompatibility, anonymous sex and multiple sexual partners (Coleman 1995, 

Carnes 2007, Kafka 2000, Kafka 2007, Cooper 2002, Cooper 2003). 

There are significant gaps in the current scientific knowledge base regarding the clinical course, developmental risk factors, family history, 

neurobiology, and neuropsychology of hypersexual disorder. As is true of so many psychiatric disorders, the comment that ‘‘more research 

is needed’’ is certainly applicable to these conditions. Although there are significant shortcomings in the state of our current empirical 

knowledge, there is little doubt that patients with such conditions commonly present to clinicians as well as to specialized treatment 

programs. 

Key words: Don Juanism, nymphomania, hypersexual disorders 



Pathological gambling: review of recent data 

Ömer Şenormancı 

Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

E-mail: senorman_7@hotmail.com 



Gambling, which could also be defined as risking one’s chances for a possible outcome, is a cultural phenomenon as old as humanity. While 

gambling is a form of entertainment without any drawbacks for the great majority, pathological gambling develops in a small minority. 

The prevalence (0.2%- 5.3%) in the adult population is gradually increasing due to the ease of accessibility such as Internet gambling. This 

increase and the accessibility of gambling becoming easier, have led to some sociodemographic changes in the population who have 

trouble with gambling. Recent studies have shown pathological gambling to be higher in the psychiatric patient population compared 

to the normal population (with no assigned psychiatric diagnosis) and that it is necessary to be included as part of the questioning in a 

psychiatric evaluation. 

Some drugs once thought to be a new hope in the pharmacological treatment of pathological gambling, have been proven ineffective 

in recent randomized, double-blind, and placebo-controlled studies. Current studies are testing GABAergic and antiglutamatergic drugs, 

that are thought to be effective in chemical and behavioral addictions, in the treatment of pathological gambling. 

Two large meta-analysis studies have reported that non-pharmacological therapy approaches are more effective in the treatment 

of pathological gambling. Behavioral therapy, cognitive behavioral therapy and short, motivational, individualized approaches are 

demonstrated to be effective. Although it is suggested that behaviorial therapy + cognitive behavioral therapy and short, motivational, 

and individualized approaches are equally effective, combining the two may improve the efficacy of the treatment. This presentation aims 

to describe pathological gambling accompanied by contemporary information with respect to treatment. 

Key words: Pathological gambling, impulse control disorder, pharmacotherapy, psychotherapy 


Is binge eating a type of addiction? 

Fulya Maner 

Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

E-mail: fmaner@ttmail.com 

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 

people would eat in a similar time period under similar circumstances. There is a sense of lack of control over eating during the episode. 

Eating is much more rapid than normal and one eats until feeling uncomfortably full. After overeating one feels disgusted, depressed or 

guilty. Binge eating disorder is included in eating disorders not elsewhere specified in the DSM-IV and is a symptom of bulimia nervosa 

and anorexia nervosa. 

Research has shown that patients with eating disorders have high rates of co-occuring substance use disorders. The substance of abuse 

and food appear to compete for sites in the brain and abstinence from substance use causes craving for the substance and also for food. 

Addictions involving food and substances share similar etiologies and behavioral symptoms. Individuals suffering from binge eating 

disorder are more likely to have first degree relatives with a substance abuse disorder. According to retrospective reports of patients, 

the initiation of disordered eating usually began before substance abuse. The general reward pathway includes the ventral tegmental 

area and basal forebrain. Substance abuse has been shown to change the neural processes around these connections. The mesolimbic 

dopamine system connects the ventral tegmental area to the basal forebrain and is critical for the self-administration of psychomotor 

stimulants. Dopamine deficiency has been suggested to be a common characteristic of individuals who are prone to substance or food 

addiction. Striatal dopamine receptor (DRD2) availability is significantly lower in obese individuals than in controls. Body mass index is 

shown to correlate inversely with measures of D2 receptors. 

Functional neuroimaging studies have revealed that pleasant smelling, looking, and tasting food has reinforcing characteristics similar 

to drugs of abuse. Many of the brain changes reported for hedonistic eating are also seen in various types of addiction. Overeating may 

have an acquired drive similar to drug addiction with respect to motivation and incentive craving. In both cases, the desire and continued 

satisfaction occur after early and repeated exposure to stimuli. 

Addictive behavior manifests itself in permanent preoccupation with food and eating, withdrawal symptoms, continuation of disturbed 

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eating behavior in spite of negative consequences, loss of control, and frequent relapse. 

Human and animal studies have demonstrated that in some brains the consumption of sugar-rich foods or drinks primes the release of 

euphoric endorphins and dopamine within the nucleus accumbens, in a manner similar to some drugs of abuse. The neurobiological 

pathways of drug and “sugar addiction” involve similar neural receptors, neurotransmitters, and hedonistic regions in the brain. Craving, 

tolerance, withdrawal, and sensitization have been documented in both human and animal studies. In addition, there appears to be cross 

sensitization between sugar addiction and narcotic dependence in some individuals There also appears to be some common genetic 

markers between alcohol dependence, bulimia, and obesity, such as the A1 allele gene and the dopamine 2 receptor gene. 

Key words: Binge eating, eating disorder, addiction 


[PS-03] 

Symposium Title: Painful syndromes in psychiatry and their managements 

Pain and personality 

Mehmet Ak 

Department of Psychiatry, Gulhane School of Medicine, Ankara, Turkey 

E-mail: drmehmetak@gmail.com 

There is a dynamic two-way interaction between pain and personality and the psychophysiology and anatomy of this relationship are 

not elucidated fully. Is there a specific personality type of pain or do some people perceive and express pain more than others? Probably 

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 

Temperament and Character Inventory. A relationship has been demonstrated between some personality traits and pain. In studies that 

reported the prevalence of personality disorders, associations with chronic pain vary between 31% to 81%. The most frequently identified 

personality trait is one with paranoid features. 

Today I will talk mainly about studies using Cloninger’s model, because Cloninger’s integrative psychobiological approach provides a 

flexible framework for both clinical assessment and treatment planning. The most significant and consistent result of these studies was 

elevated harm avoidance scores. Harm avoidance scores still remain high even after controlling for the effect of depression and anxiety. 

Thus this temperament dimension is possibly an important state and trait feature for development of psychosomatic illnesses. These 

findings also confirmed that serotonergic systems are involved in the process of psychosomatic organization. Cloninger described that 

people with chronic anxiety, avoid harm that is characterized by more pain, are difficult to calm, tire easily, and display specific signs 

based on specific anticipatory anxiety. Harm avoidance refers to an inherited tendency to block the behavior in the answers given to the 

blocking, non-rewarding, and punishment signals. High harm avoidance behavior is observed in the form of social withdrawal, becoming 

tired easily, staying away from strangers, fear of uncertainty, and being pessimistic that there would be some problems in a situation even 

when others do not worry.. These people are timid, passive, insecure, and pessimistic individuals. 

Looking at the size of the character, it is seen that low self-directedness scores are the most common finding. The original meaning of 

self-directedness is in accordance with choosing goals and values of the individual, optimization of the behavior to maintain a situation, 

editing capabilities, and being strong-willed. 

Individuals with low self-directedness do not expect to be able to control and positively influence an aversive situation and overcome 

obstacles. Self-directedness is closely related to the concept of self-efficacy. Self-efficacy is defined as the personal conviction that one 

can successfully show problem-solving behavior in a given situation. There is much evidence which suggests that low self-efficacy plays 

an important role in pain control, coping with disability, and treatment outcome. Our clinical experiences show that pain can sometimes 

be the symbol of help, sometimes the quest for attention, and other times problems that can not be expressed. Emotions that are not 

expressed can mean pain and unexpressed emotions can be the cause of pain for some people that do not heal. In order to understand 

and to treat these people, employing a holistic assessment and approach are very important. 

Key words: Character, pain, temperament 





The differences between SSRIs and SNRIs in the treatment of psychiatric pain syndromes 

Abdurrahman Altındağ, Gülçin Elboğa 

Gaziantep University, Medical School, Department of Psychiatry, Gaziantep, Turkey 

E-mail: draltindag@yahoo.com, aaltindag@yahoo.com 

The occurrence of depression with physical symptoms and pain is common. On the other hand, comorbid depression is also common 

in chronic pain syndromes. Antidepressants are effective in the treatment of psychological and physical symptoms of depression and 

chronic pain symptoms of non-depressed patients. 

It is not well described how antidepressants relieve the pain. However, it is suggested that this effect is related to serotonin and 

noradrenaline. Analgesic effects of antidepressants are independent from their effects on the mood. Antidepressants which have effects 

on both serotonin and noradrenaline are more effective than those with effects on one of these neurotransmitters in the treatment of 

depression and comorbid pain syndromes. Tricylic antidepressants (TCAs) have serotoninergic and noradrenergic effects. Therefore, they 

are superior to monoaminergic antidepressants, such as SSRIs, with regard to analgesic and antidepressant effects. The usage of TCAs is 

limited because of their safety profile and side effects. SNRIs have similar analgesic effects to TCAs. On the other hand they have lower 

side effects and a better safety profile. Additionally, SNRIs are more effective than SSRIs in the treatment of physical pain syndromes. SNRIs 

have a similar safety profile to SSRIs and almost similar costs to the older agents. 

Better diagnosis and treatment of pain symptoms, which are strong indicator of depressive relapses, will provide better quality of life and 

productivity in patients with depressive disorders. 

Key words: SSRI, SNRI, pain 


How does alexithymia lead to painful syndromes? 

Hüseyin Güleç 

Erenkoy Psychiatry Hospital, Istanbul, Turkey 

E-mail: huseyingulec@yahoo.com 

Several studies have focussed on defining the network of brain structures involved in pain. Pain perception (sensory discriminative, 

affective/emotional, cognitive/evaluative) has been shown to depend on different areas of the brain. Modern neuroimaging methods 

have been used to determine whether different pain symptoms involve similar brain structures. These studies indicated that acute 

physiological pain and neuropathic pain have distinct although overlapping brain activation patterns, but that there is no unique pain 

matrix/allodynia network. 

Several contemporary neuroscientists and cognitive scientists make a similar distinction between emotions as bodily events and feelings 

as mental events and regard symbolization as an important element in the cognitive processing of emotions. Awareness of feelings, 

together with the thoughts, fantasies, and memories that they elicit, facilitates modulation of the emotional arousal induced by stressful 

events. Feelings are attributed to the symbolic representation in working memory of the activity of unconsciously operating subsymbolic 

systems that generate the brain states and bodily responses which comprise emotions. These representations become integrated with 

representations of past experiences and representations of the self. Attributing the feeling of specific basic emotions to ‘viscerosomatic 

self-representations’ in the lower levels of the brain, attributing reflective awareness and the capacity for experiencing higher-order 

feelings to linguistic symbolizations and an ability to think in perceptual images is important for the parsing and regulation of emotional 

states. 

According to Lumley alexithymia is associated with tonic physiological hyperarousal, certain types of unhealthy behavior, and a biased 

perception and reporting of somatic sensations and symptoms. Alexithymia probably influences illness behavior, but there is little 

support for the hypothesis that alexithymia leads to chronic organic disease. Alexithymia links with physical illness due to four possible 

pathways: a) alexithymia leads to organic disease through physiological or behavioral mechanisms, b) alexithymia leads to illness behavior 

through cognitive or social mechanisms, c) physical illness leads to alexithymia, and d) both alexithymia and physical illness result from 

sociocultural or biological factors. Research on the effects of emotional trauma resulted in the hypothesis that traumatic experiences in 

childhood or adult life may have adverse consequences for physical health. It has been shown that there is evidence of a correlational 

association between childhood trauma and somatization in adulthood, and several retrospective studies with very large samples have 

S55


demonstrated an association between childhood trauma and the development of somatic disease in adult life. An unanswered question 

is: what are the psychological/biological mechanisms that might render trauma in earlier years a risk factor for the development of disease 

later in life? The associations between alexithymia, somatization, dissociation and trauma, have led to the suggestion that dissociation 

acts as a defense against emotionally distressing memories that are associated with the traumatic avents. Attachment insecurity and 

associated deficits in affect development and affect regulation are linked not only to the experience of being raised by parents with 

impaired capacities for mentalization, but sometimes also to more severe developmental traumas. Dissociation within emotion schemas 

is initially an adaptive response to external danger arousal and is especially severe when the child experiences the parent as a threat, for 

then there is no safe place to be. 

Key words: Alexithymia, cognitive processing of emotions, trauma, attachment, mentalizing, somatization 


Hypnotherapy for painful syndromes in psychiatry 

Kerem M. Doksat 

MD, Professor of Psychiatry, POLIMED Psychiatric Center 

E-mail: doksat@tnn.net, doksatster@gmail.com, doksat@superonline.com 

Hypnosis is a misnomer first used by Scottish Surgeon James Braid for a phenomenon probably as ancient as mammalian history. After the 

Austrian Neuropsychiatrist Sigmund Freud has fouled hypnosis in order to glorify his own theory, especially American Psychiatrist Milton 

Hyland Erickson rebuilt the reputation of hypnosis (1). 

In 1846, James Esdaile successfully performed 345 major operations by using mesmeric method in India. English surgeon John Ellitson 

mentioned similar success in many operations in 1843. With the introduction of ether in 1846 and chloroform in 1847, the mesmeric 

method, which has already serious oppositions, was forgotten. Hypnosis may be used alone or in combination with other methods. Its 

use in cancer pain, especially during the terminal phase, may reduce the requirement for opioids, or even totally eliminate them. Hypnosis 

may help the patients to experience with their consciousness fully open and free from side-effects like grogginess of the opioids during 

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’ 

chair phobia, and getting rid of gag reflex. It is effective in 30 to 50 percent of phantom limb pain cases. 

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 

of anecdotal evidence. The approach should be adjusted for the patient; the skill and experience of the hypnotist, his or her relationship 

with the patient and the patient’s personal characteristics and preferences must be adjusted according to all of these. Indeed, hypnotic 

procedures may help people who are not much hypnotizable. For example, in cases experiencing both pain and tension intensively, even 

induction of relaxation reduces pain and in many of the hypnotic procedures, relaxation is utilized. If the patients cooperate well and 

accepts the procedure seriously, even if they are not hypnotizable, they may practice the hypnotist’s relaxation suggestions with success 

while sitting or lying comfortably (2). 

The principal techniques are (2,3): 1) Direct suggestion, 2) Utterance of neurophysiological metaphors, 3) Glove anesthesia replacement 

technique, 4) Replacement pain symptom’s site or differentiating the pain symptom, 5) Dissociation by using the imagination, 6) 

Technique of different interpretation of pain, 7) Auto-hypnosis (self-hypnosis). 

As a summary, the effect of hypnosis on pain is mediated by two mechanisms: 

1) Muscle relaxation, 

2) Change in perception and cognitive distraction. 

Hypnotherapy can be effective in many painful syndromes if suitable patients are chosen. Group psychotherapy and hypnosis can be 

effective in the treatment of cancer patients’ pain (4). 

References: 

1. Doksat R. Tatbikatı ve Nazariyatı ile Hipnotizma. İstanbul: Kader Basımevi, 1962. 253-281. 

2. Doksat MK. Ağrı ve Psikiyatri. Bursa: Psikiyatri ve Sanat Yayın Evi, 2003. 165-172. 

3. Arred Barabasz, Johnn G Watkins Hypnotherapeutic Techniques 2E. New York: Brunner-Routledge. 2005. 219-239. 

4. Porter LS, Keefe FJ. Psychosocial issues in cancer pain. Curr Pain Headache Rep. 2011 Aug;15(4):263-70. 



[PS-04] 

Symposium Title: Adult attention - deficit hyperactivity disorder (ADHD) and comorbidity 

ADHD and mood disorders in children 

Rasim Somer Diler 

Department of Psychiatry, University of Pittsburgh, PA, US 

E-mail: dilerrs@yahoo.com 



Five to 40% of children and adolescents with attention deficit hyperactive disorder (ADHD) also have comorbid major depressive disorders 

(MDD). Moreover, youths with ADHD have up to a 4 times higher risk of developing depressive disorders than the general adolescent population. 

Comorbidity with MDD has been associated with elevated impairment and higher rates of hospitalization versus ADHD alone. However, 

depression in youths with ADHD may be more difficult to diagnose, given that some symptoms overlap between the two disorders. Moreover, 

many of the medications used to treat ADHD cause side effects resembling symptoms of MDD. Available studies suggest the particular 

importance of anhedonia, social withdrawal, psychomotor retardation, negative views of self and future, and suicidal thoughts as symptoms that 

distinguish MDD in youths who have ADHD. Despite ongoing controversy, the view that pediatric bipolar disorder (PBD) is rare or non-existent 

has been increasingly challenged not only by case reports but also by systematic research; however, a significant portion of bipolar youth, 

especially children, have high comorbidity with ADHD. Significant debate exists on whether early onset bipolar disorder is mistakenly attributed 

to attention deficit hyperactivity disorder (ADHD), or whether ADHD is frequently misdiagnosed as mania. Among pediatric-onset cases of 

bipolar disorder, comorbid ADHD is frequently seen, and there is strong evidence to suggest that this pattern has a familial and genetic basis. 

Differentiating bipolarity in children with ADHD is not an academic discussion but also a great concern because of the associated complication of 

the treatment of these disorders. It is suggested that manic symptoms should represent a distinct change from a child’s usual level of functioning 

(e.g., change or worsening of distractibility during a mood episode in children with ADHD). There are some symptoms that mainly occur in BD 

youth as compared to other disorders (e.g., ADHD) and may help to differentiate between BD and these disorders, such as clinically relevant 

euphoria, grandiosity, decreased need for sleep, hypersexuality (without history of sexual abuse or exposure to sex), and hallucinations. We need 

larger longitudinal studies to better understand the risks and resilience factors of developing BP in ADHD youth. 

Key words: ADHD, depression, bipolar, child 


Academic and occupational problems in ADHD 

Mücahit Öztürk 

PEDAM Psikiyatri Merkezi, İstanbul, Turkey 

E-mail: mozturkpdm@gmail.com 

Attention Deficit Hyperactivity Disorder (ADHD) is a syndrome of inattention, hyperactivity, impulsiveness and other deficits of 

executive functions. It’s now well known that ADHD often continues into adulthood (1, 2). ADHD is a chronic disorder which leads to a 

negative impact on functioning throughout the life cycle (3). Children with ADHD are at significant risk of multiple forms of adolescent 

maladjustment. Approximately up to 60% of childhood cases continue symptomatic into adulthood. In the remaining 40 percent 

symptoms may remit in early adulthood (4). The manifestation of ADHD changes over the course of life. In some cases the hyperactivity 

may disappear but decreased attention span and impulse control problems persist (5). 

Approximately 1 in 25 adults have ADHD, 90% of whom may be currently untreated, with a potentially negative impact on the lives of 

patients and their families (6). Significant legal, academic, social, and occupational problems have been observed in adults with ADHD (7). 

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 

risk of negative academic outcomes. ADHD and similar problems entail a risk of underachievement at school. The results indicate that 

students with ADHD underachieve in the school situation in relation to their optimal cognitive capacity (3). 

Adolescents with ADHD complete less education by 2-3 years and demonstrate lower occupational performance at the age of 25 years. Adults 

with ADHD may struggle with frequent job changes, frequent partner changes, higher rates of divorce, increased motor vehicle accidents, 

poor money management and higher rates of unwed pregnancy (8). Although their educational performance is lower than people without 

ADHD, their early employment histories don’t differ from those people with similar education (5). Adolescents with ADHD were more likely 

to smoke cigarettes and use illicit drugs. Their academic attainment was below age norms with more than one fourth repeating grades (9). 

S57


Studies show that effective treatment significantly improves quality of life (3). Severity of childhood ADHD and treatment significantly 

predict the persistence of ADHD into adulthood (5). As previously shown by some research for children and adolescents, stimulant 

medications alone did not eliminate the academic achievement deficit of ADHD undergraduates. ADHD patients who were treated with 

stimulants were significantly less likely to subsequently develop depressive and anxiety disorders and disruptive behavior and less likely to 

repeat a grade compared with participants with ADHD who were not treated. Adolescents with ADHD were also significantly more likely 

to be absent during the academic year, and they were over eight times more likely than adolescents without ADHD to drop out of high 

school. These findings demonstrate that children with ADHD continue to experience severe academic impairment into high school (10). 

Key words: Attention deficit hyperactivity, academic performance, occupation 

References: 

1. Barkley RA. Major life activity and health outcomes associated with attention-deficit / hyperactivity disorder. J. Clin Psychiatry 2002;63 12:10-15. 

2. Weiss G, Hechtman L. Hyperactive Children Grown Up: ADHD in Children, Adolescents, and Adults. New York, NY: Guilford Press; 1993 

3. Cheng K, Myers KM, Stubble DE. Attention deficit hyperactivity disorder Child and Adolescent Psychiatry The Essentials Lippincott Williams &Wilkins 

4. Biederman J, Mick E, Faraone SV. Age dependent decline of symptoms of attention deficit hyperactivity disorder: Impact of remission definition and symptoms 

type. Am J Psychiatry 2000 157:816-818 

5. Sadock BJ, Sadock VA. Textbook of Child and Adolescent Psychiatry. 2009 Lippincott Williams &Wilkins 

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 

Literature Prim Care Companion J Clin Psychiatry 2010 v. 12(6); 

7. McCann BS, Roy-Byrne P Attention-deficit/hyperactivity disorder and learning disabilities in adults. Semin Clin Neuropsychiatry. 2000 Jul;5(3):191-7. 

8. Spetie L, Arnold EL. Attention deficit hyperactivity disorder in Lewis Child and Adolescent Psychiatry A Comprehensive Textbook 2007 Lippincott Williams &Wilkins 

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. 

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 

students with ADHD.Pediatrics. 2009 Jul;124(1):71-8. 


[PS-05] 

Symposium Title: Brain mapping, TMS, NVS, biofeedback and deep brain stimulation in treatment of psychiatric disorders 

Concomitant use of qEEG and rTMS in treatment of depressive disorder, new approaches 

Nevzat Tarhan, Gökben Hızlı, Serap Aydın 

Üsküdar University, Neuropsychiatry Istanbul Hospital, Istanbul, Turkey 

E-mail: ntarhan@uskudar.edu.tr, ntarhan@gmail.com 

Repetitive transcranial magnetic stimulation (rTMS) therapy has been approved for treatment of depression by the FDA in 2008, and was 

included in APA Guidelines as published in October, 2010 issue of American Journal of Psychiatry. Although its efficacy is not as high as 

the efficacy of ECT, rTMS is safer in the treatment of depression in older patients. Especially the absence of common treatment side effects 

of ECT, such as confusion and memory problems, makes rTMS treatment more valuable in patients with high side effect risk. 

This study was performed by the quantitative EEG (qEEG) monitoring before and after rTMS treatment. The aim was to examine the 

predictive value of qEEG as a biological indicator of response to rTMS treatment. 

In Neuropsychiatry Istanbul Hospital, between dates of 2006-2010, rTMS had been applied to 1283 patients with a diagnosis of treatmentresistant 

depressive disorder. The patients discontinued the psychotropic medications 12 hours before the qEEG monitoring. qEEG records were 

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. 

The patients with a medical history of epilepsy were excluded. The cases with no history of seizures, but with suspicious epileptical 

abnormality in pre-treatment EEG were included with special medical caution. rTMS treatment was performed at left DLPFC, as 25 hz. and 

1000 pulse, one session on each day, a total of 15-20 sessions, with Magstim Rapid. 

From 1283 cases, one patient had epileptic seizure as an adverse effect. Due to contraction of facial muscles, one patient had a broken 

tooth. In 3 patients suffering from tinnitus occurred, but later tinnitus decreased significantly. 

The statistical analyses of the cases are ongoing. The initial results with remission and response rates will be presented. qEEG power 

spectrum changes and changes in the activation compared to normative data base in LORETA will be evaluated. 

Key words: Repetitive transcranial magnetic stimulation (rTMS) therapy, quantitative EEG, depression treatment 





What does transcranial magnetic stimulation (TMS) promise in psychiatric disorders other than 

depression? Future perspectives 

Bahadır Bakım 

Sisli Etfal Research and Teaching Hospital, Psychiatry Clinic, Istanbul, Turkey 

E-mail: bbakim@yahoo.com 

Up to 40% of OCD patients fail to respond satisfactorily to generally adequate treatment options, and 10% cannot be helped at all. Because OCD 

may be related to increased neural activity in prefrontal subcortical circuits, the inhibitory effect of rTMS was hypothesized to be beneficial in OCD 

treatment. rTMS has recently demonstrated remote effects, with left prefrontal stimulation inducing changes in cerebral perfusion in the bilateral 

anterior cingulate and orbitofrontal cortex. In conclusion, in open-label studies, high-frequency rTMS of the right and/or left DLPFC appears to 

be effective in reducing obsessive-compulsive symptoms. However, this could not be replicated in double-blind, sham-controlled studies. As the 

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 

in OCD are needed to clarify the specific stimulation region of rTMS. Otherwise, as the improvement of symptoms is often noted in sham settings, 

it would be interesting to investigate the neural underpinnings of the placebo effect caused by sham rTMS. 

Several initial studies on negative symptoms of schizophrenia have suggested that the condition seems to respond to high frequency (20 Hz, 10 Hz) 

repetitive transcranial magnetic stimulation (rTMS). Low frequency rTMS (


of patients with medication-refractory unipolar depression who have failed one good (but not more than one) pharmacological trial. 

Key words: Transcranial magnetic stimulation, depression, rTMS 

References: 

1. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimulation of human motor cortex. Lancet1985;1(8437):1106-7. 

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 

Affect Disord 2011; 129(1-3):14-26. 

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- 

Resistant Depression. Neuropsychopharmacology 2009; 34(5):1255-62. 


Vagus Nerve Stimulation (VNS) in depression treatment 

Şadiye Visal Buturak 

Department of Psychiatry, Kırıkkale University, Faculty of Medicine, Kırıkkale, Turkey 

E-mail: visalbuturak@hotmail.com 

Major Depressive Disorder (MDD) is a prevalent, chronic, recurrent and disabling disorder and it is predicted that MDD will be the second most common 

cause of incapacitating disease in 2020 (1). Although a broad range of effective treatments is available, a considerable proportion of patients do not 

respond adequately (2). Patients who have already experienced recurrent depressive episodes often relapse and do not achieve full remission despite 

treatment with conventional therapies (3). A need for the development of alternative treatments for treatment resistant depression (TRD) that are 

effective, have fewer side-effects or have longer-lasting antidepressant effects has been identified. Vagus nerve stimulation (VNS) therapy is a type of 

treatment where a small electrical pulse is administered through an implanted neurostimulator to a bipolar lead attached to the left vagus nerve (4). 

VNS was approved by the US Food and Drug Administration in 2005 for the adjunctive long-term treatment of chronic or recurrent depression for 

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 

antidepressant treatments. The mechanism of action of VNS is not fully understood although emerging data suggest that VNS therapy modulates the 

function of neural structures implicated in depression and also influences monoaminergic neurotransmission (5). In a randomized sham-controlled 

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 

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 

al. examined the effect of VNS in adult outpatients with nonpsychotic, treatment-resistant major depressive or bipolar I or II (depressed phase) disorders. 

Response rates were 40% for the Hamilton Depression Rating Scale (HDRS) (7). In an open pilot study of VNS in outpatients with treatment-resistant 

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 

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 

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



with the determination of disordered brain structures at the levels of neurons and neuronal populations in brain mapping by creating 

mathematical formulations and treatment. Psychosurgery aims to regain systematic and comprehensive brain functions via minimally 

invasive nondestructive neurosurgical applications. Psychosurgery is indicated for treatment-refractory major mental illnesses such as 

depression, obsessive compulsive disorder, schizophrenia and others. Neurostimulative methods are preferred to neuroablative methods. 

Neurons have highly complex morphological, electrophysiological, and biochemical properties as reflected in many psychomotor 

functions, continuation of mental homeostasis, repertoire of activity patterns and multiple signaling pathways. Morphologically, 

neurochemically and electrophysiologically heterogeneous neuron groups project to the cerebral cortex, deep brain structures, brain 

stem, spinal cord and autonomous ganglia. These highly complex ascending and descending pathways participate in different functions, 

including cognition, motivation, emotion, speech, calculation, memory and autonomic regulation. 

Disorders of neuronal populations can cause neuropsychiatric illnesses. Neurostimulative applications are the most useful treatment 

methods for intractable cases. However, in experimental studies, stem cells and teacher neurons specifically educated by computerised 

mediums have begun to be implantated into the brain for education and stimulation of dysfunctional neuron groups. 

Psychosurgery has been directed to neurocomputer interfacing technologies. Hybride neuroelectric devices, neuromimetic protheses, 

sonic and photonic multichip modules, biotic-abiotic neuromodulators, bio-robotics and reconfigurable neural nanodevices have shown 

promise for future excellent treatment strategies for mental illnesses. 

Key words: Psychosurgery, deep brain stimulation 


[PS-06] 

Symposium Title: Neuroimaging in psychopharmacology: An update 

What is the real meaning of ventricular enlargement in schizophrenia? 

Nazlı Buğçe Vedin Özçelik 

Department of Psychiatry, Ege University, Izmir, Turkey 

E-mail: bugcevedin@gmail.com 

Schizophrenia usually starts during adolescence or young adulthood but tends to persist throughout life. Even at the time that the 

concept of schizophrenia was first defined, it was thought to be a brain disease. Before the development of brain imaging techniques, 

post-mortem brain examinations were performed. It was reported that patients had frontal atrophy and less brain weight than the normal 

population. After the development of computed tomography and magnetic resonance imaging techniques, the number of the studies 

in this field increased. 

Structural MRI imaging studies indicated that brain abnormalities were present at the onset of the disease. One strong piece of evidence 

indicating that schizophrenia is a neurodevelopmental disorder derives from the fact that many types of brain abnormalities are present 

at the time of the first episode off illness. These include decreased cerebral size, decreased frontal and temporal lobe sizes, decreased 

thalamic size, decreases in gray matter and white matter volumes and enlargement of the ventricles. These findings support the likelihood 

that this illness arises because of aberrations in the complex neurodevelopmantal processes that modulate brain maturation during the 

adolescent and young adult period. 

Lateral ventricular enlargement is one of the most consistent findings in patients with schizophrenia. However whether progressive 

ventricular dilatation occurs during the course of the illness has been controversial. Some findings suggest that there is progressive 

ventricular enlargement with no significant effect of age of onset, duration of illness or age at the baseline scan. In some longitudinal 

studies there was evidence that negative symptoms have an association with increases in total CSF volume and in the ventricles as 

indicated by the ventricular–brain ratio. Patients who achieve longer periods of remission have less expansion of the CSF, although, some 

findings support the premise that there is a subgroup of patients with neuroprogression. 

Key words: Schizophrenia, magnetic resonance imaging, lateral ventricle 


S61


Neuroimaging studies in dementia, psychiatric disorders, drug discovery, and more 

Devrim Ünay 

Department of Electrical-Electronics Engineering, Bahcesehir University, Istanbul, Turkey 

E-mail: devrim.unay@bahcesehir.edu.tr 

The continuous progress achieved in medical imaging technology in the past decades has led to considerable improvement in patient 

care. In consequence of this progress, neuroimaging (imaging the structure or function of the brain) has gained an increasingly important 

role in research and clinical practice. 

Dementia, a psychiatric/mental disorder defined as progressive loss in cognitive skills such as learning, memory, orientation and 

language, is a devastating and irreversible brain syndrome. Due to its increasing prevalence (especially in aging populations), long 

duration, caregiver burden and high financial cost of care, dementia has emerged as one of our major public health problems affecting 

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 

neuroimaging in improving the diagnostic process is becoming widely accepted. 

Neuroimaging assessments may aid in the diagnosis of neurodegeneration as opposed to healthy aging, improve differential diagnosis, 

assist in the prediction of conversion to dementia in individuals at a higher risk of developing the disorder, improve the tracking of disease 

progression and finally may serve as an outcome measure for assessing drug efficacy. Hence, in clinical settings the diagnosis of dementia 

is increasingly taken based on combined analysis of data such as the patient’s cognitive skills, demographic status, family history of 

dementia and neuroimaging findings (such as the degree and distribution of atrophy). 

In addition to the improvement in patient care, recent advances in neuroimaging technology also have increased the need for tools to 

analyze and interpret the growing amount of neuroimaging data acquired. Accordingly, various semi-/fully automatic tools for analysis 

and interpretation of such data are made available by research centers as well as medical imaging companies. 

In view of the above, this work aims to provide a non-exhaustive summary of neuroimaging studies in psychiatric disorders with special 

emphasis on dementia and drug discovery. State of the art studies employing both structural (CT, MRI, etc.) and functional (fMRI, PET, 

SPECT, etc.) neuroimaging techniques and their potential contribution to diagnostic research as well as to drug discovery will be discussed. 

The work will also include a brief introduction on the related advances and open questions from an image processing standpoint, and 

finally present our recent research effort on computer-based measurement of dementia-related neuroimaging findings as compared with 

experts’ visual assessments for improved disease understanding, diagnosis, prognosis, and therapy planning. 

Key words: Dementia, drug discovery, fMRI, MRI, neuroimaging, PET, psychiatric disorders, SPECT 


[PS-07] 

Symposium Title: The rationale of antipsychotic combinations in schizophrenia: Epidemiological and clinical evidences 

Pharmacogenetics and antipsychotic combinations 

Filiz Karadağ 

Pamukkale University Medical Faculty, Psychiatry Department, Denizli, Turkey 

E-mail: filizlal@yahoo.com 

Pharmacogenetic studies in schizophrenia aim to use genetic information as a guide to establish individualized treatment options and to 

optimize the effectiveness of treatment. The heterogeneity of response to antipsychotics results in polypharmacy along and combination 

therapy into clinical practice, which lead to an increase in drug-related side effects and non-adherence to treatment. 

Dopamine and serotonin systems may provide some of the genetic polymorphisms and have been proposed to predict the efficacity 

of antipsychotic drugs. Affecting the intensity of the D2 receptors in the striatum, the DRD2- 141C Ins/Del polymorphism has been 

associated with unresponsiveness to clozapine in treatment-resistant patients and a longer response time to olanzapine and risperidone 

in first-episode patients. The D3 receptor DRD3 Ser9Gly polymorphism has been associated with unresponsiveness to clozapine and good 

response to first generation antipsychotics. 

The 5-HT2A receptor gene HTR2A-A-1438G and T102C polymorphisms may cause lower promoter activities and decreased 2A receptor 

density in some brain regions. A-1438G G/G carriers have been found to be less likely to respond to clozapine, olanzapine, and aripiprazole. 




The T102C SNP C/C genotype has been associated with no response to clozapine and good response to risperidone and aripiprazole. 

The long allele of the serotonin transporter gene has been reported to be associated with better response to antidepressants, but 

there are only a few studieson schizophrenic patients. The effectiveness of pharmacogenetics-based combination therapies in patients 

unresponsive to treatment has not been studied yet; the DRD2 and DRD3 genes may be candidates for study. 

Antipsychotic metabolism: The Met/Met genotype of the COMT gene causes a 3- to 4-fold lower enzyme activity. The met allele carriers 

were more likely to respond to clozapine, especially showing improvement in cognitive functions. This polymorphism, seems to deserve 

assessment of the effectiveness of combination therapies in dealing with cognitive symptoms. 

The CYP2D6 enzyme plays an important role in the metabolism of antipsychotic drugs. Individuals carrying duplicate or multiple 

copies of the CYP2D6 gene are known as ultrarapid metabolizers. In ultrarapid metabolizers, due to the decrease in therapeutic efficacy 

of antipsychotic drugs, a combination of drugs that are metabolized by the same cytochrome enzyme would not provide further 

improvement in drug response. 

Antipsychotic-induced side effects: The DRD2 A2 allele of SNP Taq1A, the DRD3 Ser9 Gly Gly allele genetic polymorphisms related to 

D2 and D3 receptors, the COMT Val allele and the CYP2D6 gene variants have been reported to be associated with an increased risk of 

tardive dyskinesia. 

CYP2D6 poor and intermediate metabolizers may be more sensitive to the extrapyramidal side effects of antipsychotics. The 5HT2C gene 

(759T SNP) and the leptin gene are the most studied polymorphisms for antipsychotic-induced weight gain. All of the aforementioned 

polymorphisms may have implications for choice of rational antipsychotic combinations. 

Pharmaco-genetics-based rational antipsychotic combinations may yield promising results for cytochrome enzyme and COMT genes 

and the genes associated with side effects in schizophrenia. However, this issue should be supported and confirmed by clinical 

pharmacogenetics studies. 

Key words: Pharmacogenetics, schizophrenia, antipsychotics, side effects, dopamine, serotonin, polymorphism 


Scientific bases of use of atypical antipsychotics 

Ender Taner 

Department of Psychiatry, Gazi University Faculty of Medicine, Ankara, Turkey 

E-mail: tanerender@yahoo.com 

The predominant hypothesis regarding the pathophysiology of schizophrenia is that it is associated with impaired dopamine 

neurotransmission. The mesolimbic pathway originates from the midbrain ventral tegmental area and innervates the ventral striatum 

(nucleus accumbens), olfactory tubercle, and parts of the limbic system. The mesocortical pathway, also originating from the midbrain 

ventral tegmental area, innervates areas of the frontal cortex and has been implicated in learning and memory. Overactivity of the 

mesolimbic pathway has been implicated in the development of the positive symptoms of schizophrenia. The negative and some cognitive 

symptoms have been associated with a reduction of dopamine activity in the mesocortical pathways together with a hypostimulation 

of dopamine receptors in the prefrontal cortex. There are 2 overall goals of treatment: (1) to reduce the activity of hyperactive pathways 

mediating psychosis and (2) to increase the activity of hypoactive pathways that seem to mediate negative and cognitive symptoms, 

while simultaneously preserving the activity of the pathways that regulate motor movement and prolactin secretion. There is also a 

putative interrelationship between N-methyl-D-aspartate (NMDA) hypofunction and dopamine (DA) dysregulation and these processes 

may be linked to the pathogenesis of schizophrenia. It has been postulated that NMDA hypofunction in the prefrontal cortex and its 

connections may result in a pattern of dopamine dysregulation. In the prefrontal area, this pattern consists of a dopamine deficit and 

a hypostimulation of D1 receptors that are linked to the appearance of negative symptoms and cognitive impairment. However, at the 

subcortical level, NMDA hypofunction results in dopamine excess, hyperstimulation of D2 receptors, and the appearance of positive 

symptoms. It has also been suggested that the prefrontal dopamine deficit and the subcortical dopamine excess feed back, in turn, to the 

NMDA circuitry. In addition there is evidence that the deficit in cortical dopamine may also be linked to the generation of a subcortical 

dopamine excess. There is a complex modulation of dopamine by different serotonergic receptor systems as well as by nicotinic receptors. 

These may be additional sites for effects of antipsychotics. This conference tries to underline the current possible scientific basis for the 

use of atypical antipsychotics. 

Key words: Atypical antipsychotics, schizophrenia, mechanism of action, scientific basis 


S63


Is fish oil promising in the treatment of depression during pregnancy and lactation? 

Evrim Özkorumak 

Karadeniz Technical University, Psychiatry Department, Trabzon, Turkey 

E-mail: evrimozkorumak@yahoo.com 

Increasing concerns about neonatal syndromes following antidepressant use in the late phase of pregnancy(1) have caused more 

hesitation about their use. Although inadequate data about in utero exposure of antidepressants may present risks, the risks of untreated 

maternal depression must be considered as well. One candidate as an antidepressant is fish oil, in light of its omega-3 constituent. 

Omega-3 fatty acids are long-chain, polyunsaturated fatty acids found in plant and marine sources and helpful in treating various medical 

conditions (2). Omega-3 fatty acids may prove to be efficacious in a number of psychiatric disorders. Evidence suggests that omega-3 

fatty acids may have beneficial effects in mood disorders, including bothmajor depression and bipolar disorder, schizophrenia and 

dementia. Furthermore, omega-3 fatty acids may prove to be a safe and efficacious treatment for psychiatric disorders during pregnancy 

and breastfeeding (2). 

Major depressive disorder (MDD) is prevalent among women of childbearing age. Approximately 15% of women experience an episode 

of perinatal depression (PND), antenatally and/or postnatally (3). Because there are increasing concerns about possible adverse effects 

of antidepressant medication use during pregnancy and in breastfeeding mothers (4), it is important to investigate possible alternative 

treatments. Main dietary risk factors of postnatal depression are low riboflavin, low folate, low docosahexaenoic acid, low eicosapantaenoic 

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) 

and docosahexaenoic acid (DHA) (5). Evidence indicates that these fatty acids may be involved in the synthesis and regulation of brain 

neurotransmitters (dopamine, monoamine and serotonin), which are thought to be reduced in cases with depressive symptoms (6). More 

specifically, it is thought that high concentrations of DHA located in non-myelin cell membranes of the central nervous system may help 

support synaptic transmissions (7). Different human studies were identified investigating dietary and/or supplemental sources of n-3 

in relation to the development of postnatal depression. Only two of these trials were randomised controlled trials (8,9). Among others, 

three studies support the theory that dietary and supplemental sources of n-3 are associated with fewer postnatal depression symptoms 

(8,10,11) and five studies contest this theory (12,13,14). 

Key words: Omega-3 fatty acids, depression, perinatal depression 


[PS-08] 

Symposium Title: Advances in complementary alternative psychotropic drugs: Fish oil (omega-3 fatty acids), vitamine B12, folate 

ve other add-on therapies in psychiatric disorders 

Can St. John’s Wort be an alternative treatment for depression? 

Çiçek Hocaoğlu 

Rize University, Medical School, Department of Psychiatry, Rize, Turkey 

E-mail: chocaoglu@superonline.com 

The herb St. John’s Wort (Hypericum perforatum) has been used for centuries to treat a variety of medical illnesses. In certain areas of 

Europe, St. John’s Wort has been a commonly prescribed treatment for depression. In some countries extracts of the plant Hypericum 

perforatum L. (popularly called St. John’s Wort) are widely used for treating patients with depressive symptoms. Extracts of the plant 

Hypericum perforatum have been used in folk medicine for a long time for a range of indications including depressive disorders. Some 

researchers believe that specific chemical constituents of St. John’s Wort produce changes in depression in a manner similar to that of 

antidepressant medications, yet this hypothesis is problematic. In addition, studies that support the efficacy of St. John’s Wwort in patients 

with mild-to-moderate depression have limitations that may affect the accuracy of their conclusions. Studies measuring the effect of St. 

John’s Wort in major depression have reported conflicting results and need to be reexamined. In patients who meet the criteria for major 

depression, several recent placebo-controlled trials suggest that the tested hypericum extracts have minimal beneficial effects while 

other trials suggest that hypericum and standard antidepressants have similar beneficial effects. Preliminary data suggest that hypericum 

extract is effective in atypical depression based on the reported outcome of an 8-week double-blind, placebo-controlled, randomized 




trial (positive results in patients with vegetative features of atypical depression, i.e. hyperphagia or hypersomnia). The study supports the 

beneficial effect of St. John’s Wort in depression with atypical features and the validity of the definition of atypical depression on the basis 

of reversed vegetative signs. 

Consequently, St. John’s Wort is considered by some to be an alternative to conventional therapies but, clinicians need to know whether 

it is an effective and safe treatment for different levels of severity of depression. Current evidence does not support its use and because 

of potential drug interactions, St. John’s Wort is not a benign treatment. 

Key words: St. John’s Wort, depression 

References: 

1. Shelton RC. St John’s wort (Hypericum perforatum) in major depression. J Clin Psychiatry. 2009;70 Suppl 5:23-7. 

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, 

and placebo-controlled trial. J Psychiatr Res. 2010 Sep;44(12):760-7. Epub 2010 Feb 23. 

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 

of data from controlled clinical trials. Eur Arch Psychiatry Clin Neurosci. 2008 Feb;258(1):59-63. Epub 2007 Dec 14. 

4. Trautmann-Sponsel RD, Dienel A. Safety of Hypericum extract in mildly to moderately depressed outpatients: a review based on data from three randomized, 

placebo-controlled trials. Affect Disord. 2004 Oct 15;82(2):303-7. 

5. Linde K, Mulrow CD, Berner M, Egger M. St John’s wort for depression. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD000448. 


Complementary medicine alternatives for other psychiatric abnormalities 

(Like insomnia and pain) 

Bülent Bahçeci 

Department of Psychiatry, Rize Üniversity, Rize,Turkey 

E-mail: bulentbahceci@hotmail.com 

Complementary and alternative medicine have been used for the treatment of a variety of diseases for a long time. Since the applications 

of these two branches of medicine have been increasingly spreading globally and have been accompanied by inadequate scientific 

studies in the literature, the NIH has established the National Centre for Complementary and Alternative Medicine (NCCAM). The aims of 

the centre are to investigate the safety/reliability and efficacy of complementary and alternative medicine applications, and to integrate 

those that are scientifically proven to be effective into conventional therapies. All health protection and medical applications/practices 

outside of conventional medicine are referred to as complementary and alternative medicine (CAM). 

CAM applications are becoming widespread in Turkey, as well, and are sought by 34-77% of sufferers as the first choice for therapy. 

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 

treatment of chronic pain, eating and sleeping abnormalities, alcohol and substance addiction, Alzheimer’s disease and delirium has 

yielded contradictory results in the national and international literature. Therefore, it has been reported that CAM methods require further 

evidence-based studies. 

Taking into consideration the widespread use and popularity of CAM, it is evident that these methods must be investigated further for 

their side effects, dosages, indications, interactions with other drugs, and standardisations. In addition, the regulations concerning their 

use must be redrawn and physicians must follow the relevant literature in order to prevent possible harm to their patients before initiating 

CAM treatments. 

Key words: Complementary and alternative medicine, psychiatry, education 


S65


Essential fatty acids in ADHD treatment 

İbrahim Durukan 

Deparment of Child and Adolescent Psychiatry, Gülhane Military Medical School, Ankara, Turkey 

E-mail: idurukan2003@yahoo.com 

Attention deficit hyperactivity disorder (ADHD) is characterized by problems with attention, hyperactivity and impulsivity. These problems 

often severely affect families, relationships and school performance. Although stimulants and atomoxetine are efficacious in many 

children, these medications can have side effects such as insomnia, decreased appetite, irritability and impaired growth. The etiology 

of ADHD is generally accepted to be complex and multifactorial. Little progress has been made in elucidating predisposing biological 

factors. Related contributory factors for ADHD etiology are diet, nutrition and particular abnormalities in the metabolism of the longchain 

polyunsaturated fatty acids (LCPUFAs). 

Essential fatty acids (EFAs) as a complementary or alternative treatment for ADHD have been used as both a primary and an adjunctive 

treatment in many countries. Humans are unable to synthesize linoleic acid (an omega-6 fatty acid), and a-linolenic acid (ALA), an omega- 

3 fatty acid. The main dietary sources of linoleic acid and ALA are vegetable oils and their seeds. 

Both omega-3 and omega-6 LCPUFAs have critical importance for normal brain development and function. Large amounts of both omega- 

6 and omega-3 LCPUFAs are deposited in the central nervous system during fetal life. During infancy, dietary intake of both omega-3 and 

omega-6 LCPUFAs continues to be essential for neuronal development. LCPUFAs and their derivates work as facilitators of dopamine, 

serotonin and norepinephrine release, as regulators of gene transcription, as modulators of Na+ -K+ ATPase channel function and as the 

precursors of pro-inflammatory and anti-inflammatory molecular families. The most abundant LCPUFA in the brain is DHA from the omega- 

3 series, which is concentrated at nerve cell synapses and is important for neural cell signalling and neurotransmitter processes. 

There is increasing evidence that omega-3 LCPUFAs play a part in many neurodevelopmental and psychiatric disorders. ADHD, dyslexia, 

developmental coordination disorder and autistic spectrum disorder are suggested to be related to the omega-6/omega-3 spectrum of 

disturbances. Several studies of LCPUFA supplementation in children with ADHD symptoms have been conducted. Open-label EFA trials 

in ADHD demonstrate that ADHD symptoms are responsive to EFA supplementation. Despite successful open-label trials, randomized 

controlled trials of EFA in ADHD have generally been unsuccessful in demonstrating treatment effects and some of them even displayed 

better results for the placebo group. There are three studies with partial positive results but these studies represent a small minority and 

two of them have several methodological limitations. 

The side effects of EFA are generally related to the gastrointestinal system and usually include diarrhea, nausea, fishy aftertaste, belching 

and indigestion. These side effects seem to be mild, transient and infrequent, and also appear in the placebo groups. 

Current findings from randomized clinical trials of EFA in children with ADHD are not promising. Most randomized trials have clearly 

demonstrated lack of superiority compared to placebo. Moreover, the studies that showed positive findings did not use children properly 

diagnosed with ADHD and none of them demonstrated clinical improvement in more than one setting. This delineation does not support 

the use of EFA supplements as a treatment for children with ADHD. Future studies should be planned to consider methodological issues 

such as proper ADHD diagnosis, blinded controls, adequate sample size and behavioral assessment in more than one setting. 

Key words: ADHD, essential fatty acids 


Mechanisms of fish oil (Omega-3 fatty acids), vitamin B12, folate and other add-on treatments 

in psychiatric disorders 

Mehmet Cemal Kaya 

Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey 

E-mail: mcemalkaya@yahoo.com 

The need for new treatments has led several investigators to examine the potential role of omega-3 fatty acids, found in marine and plant 

sources, in the treatment of psychiatric disorders. Omega-3 fatty acids are associated with normal brain development, neuronal plasticity, 

and function (1). Cell biology and molecular studies suggest that omega-3 fatty acids modulate membrane fluidity and dopaminergic 

and serotonergic neurotransmission (2). It has been observed that omega-3 fatty acids have effects on the phospholipid cell membrane 

and the secondary messenger system similar to mood stabilizing drugs like lithium (3). It has been also demonstrated by recent studies 




that add-on treatments with omega-3 fatty acids in mood disorders significantly improved the symptoms. Another way to investigate the 

effects of omega-3 fatty acids is by estimating the regional brain concentrations of various metabolites with proton magnetic resonance 

spectroscopy (PMRS). In a study that used this method in a population with first-episode psychosis, improvement of the negative 

symptoms of the patients were observed parallel to the increase in glutathione availability and modulation of the glutamine/glutamate 

cycle with ethyl-eicosapenthaenoic acid augmentation treatment (4). Post-mortem polyunsaturated fatty acid concentrations in the 

prefrontal areas of antipsychotic-naive schizophrenia patients were found to be lower than those of schizophrenia patients treated with 

atypical antipsychotics. Additionally, in an animal study, increases in the omega-3 fatty acid concentration in erythrocytes and prefrontal 

cortex were observed after long-term treatment with risperidone. 

One of the earliest reports about the possible psychiatric effects of vitamin B12 deficiency belongs to Langdon in 1905. Vitamin B12 

together with folate are essential for conversion of homocysteine to methionine and synthesis of adenosyl-methionine. S-adenosylmethionine 

is responsible for methylation in the metabolism of neurotransmitters (5). There are various studies that showed associations 

of depression, dementia and schizophrenia with deficiencies of folate and vitamin B12. Some studies have focussed on folate rather 

than vitamin B12 and have suggested a stronger role for folate in depression. Independent from serum levels of folate and vitamin 

B12, augmention with these vitamins may be beneficial to patients who have predominantly cognitive symptoms, who are resistant to 

treatment, pregnantor use lithium (6). 

Consequently, augmentation with omega-3 fatty acids, folate and vitamin B12 may have some clinical benefits in the treatment of some 

psychiatric disorders. However, mechanisms of their actions still need to be further elucidated. 

Key words: Omega-3 fatty acids, vitamin B12, folate, psychiatric disorders 

References: 

1. Bazan NG. Lipid signaling in neural plasticity, brain repair, and neuroprotection. Mol Neurobiol 2005; 32: 89–103 

2. Yao JK, Leonard S, Reddy R. Altered glutathione redox state in schizophrenia. Dis Markers 2006; 22: 83–93 

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 

bipolar disorder. J Psychopharmacol 2007; 21: 435-439 

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 

psychosis. A 1H-MRS study. Neuropsychopharmacology 2008; 33: 2467-2473 

5. Bottiglieri T. Folate, vitamin B12, and neuropsychiatric disorders. Nutr Rev 1996; 54:382-390 

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 

health survey: Correlations with cognitive and affective functions. J Am Coll Nutr 2000; 19: 68-76 


[PS-09] 

Symposium Title: From preclinical studies to clinical practice in anxiety disorders 

Medical disease and anxiety disorders 

Hayriye Elbi 

Ege University, School of Medicine, Dept. of Psychiatry, İzmir, Turkey 

E-mail: hayriye.elbi@yahoo.com;hayriye@ege.edu.tr;hayriye.elbi@med.ege.edu.tr 

Chronic medical illness causes us to face our vulnerabilities and is a significant risk factor for the development of an anxiety disorder. 

The vulnerability could be associated with the stress of illness and coping with the limitations of illness. Anxiety disorders may also 

develop secondary to predisposing biological mechanisms (as in diabetes or thyroid disorders) or may be related to a patient’s specific 

medications. 

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 

treatments. Drug interactions are very important in medical comorbidity cases. Every disorder comes with a new life style and necessity 

for new adaptations. The uncertainty and barriers to daily life worsen the situation. I will review the anxiety associated with medical 

diseases and the current treatments for it. 

Key words: Medical diseases, anxiety disorders 


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Genetic models in anxiety disorders 

Nurper Erberk Özen 

Department of Psychiatry, Ufuk University, Ankara, Turkey 

E-mail: nerberk@superonline.com 

Animal models are key to our understanding of many human diseases and psychiatric disorders are no exception. Animal models have 

provided insight into the neurotransmitter systems and brain circuitry underlying psychiatric illnesses that have enabled the screening 

of potential psychiatric medications for efficacy and guided the search for new pharmacotherapies. However, modeling complex 

psychiatric disorders in animals presents distinct challenges. Modeling psychiatric disorders in animals is difficult due to the complexity 

of human thoughts, emotions, and behavior; the heterogeneity of many psychiatric disorders; and the requirement of self-reporting of 

internal state for diagnosis. According to the DSM-IV, most psychiatric diagnoses are made when a patient displays a certain number of 

diagnostic criteria. However, patients with the same diagnosis can differ significantly in specific symptoms, perhaps implying differences 

in the underlying etiology of their disorders and explaining the heterogeneity of response to pharmacotherapy. Many symptoms are 

identified by the patient’s report of internal state (e.g., obsessive obtrusive thoughts or ruminations). This leads to questions of how we 

can best model disorders in animals that are, by definition, both heterogeneous and dependent on report of internal state. Rather than 

attempting to model a psychiatric disorder in its entirety, most neuroscientists focus on individual aspects or dimensions of a disorder 

and use physical manifestations and measurable behaviors when modeling a particular aspect. 

Inferences from experiments with animal models have the potential to impact clinical practice; therefore, stringently validating such 

models is of utmost importance. The strengths and weaknesses of a model can be conceptualized with different types of validity. 

Three important types of validity are suggested as predictive, face, and construct validity. In the first one, the animal should display 

reduced anxiety when treated with anxiolytics (predictive validity). In the second type, the behavioral response of an animal model to 

a threatening stimulus should be comparable to the response known for humans (face validity). Finally, in the third type of validity, the 

mechanisms underlying anxiety as well as the psychological causes should be identical (construct validity). In the meantime there is no 

consensus about which type of validity is superior. Some authors argue that predictive validity is most essential but the others suggest 

that constructive validity is the most crucial. On the other hand, these three requirements are difficult to achieve in any animal model for 

each anxiety disorder. Moreover, in the related literature, the term“animal model of anxiety” is used for animals that are altered in their 

anxiety-related behavior, as well as for test assays conceptualized to assess anxiety-related behavior in animals. 

Key words: Anxiety disorders, genetic, rat, transgenic 


Anxiety models in experimental animals 

Hüseyin Günay 

Etimesgut Military Hospital, Psychiatry Clinic, Ankara, Turkey 

E-mail: huseyingunaydr@yahoo.com 

The basic measure in testing validity of an animal model is its prediction validity, which means making true assumptions for a disorder 

in humans. The necessary features of an animal model are analogy to a disorder in humans, objective testing, effective interventions in 

humans and the capability of retesting. Structural validity is the capability to retest of the target condition and first sight validity is the 

measurement of phenomenological similarity. First sight validity points to the surface similarity between the model and the disease and 

structural validity points to the underlying mechanisms. Anxiety models are mainly used in understanding causes and mechanisms and 

also determining drug effects. Anxiety in animals, which is similar to humans, can be developed with different environmental conditions. 

These situations can help to understand and intervene to treat anxiety. Three ways are used in the development of anxiety models: using 

a new environment, reward and punishment applications, and punishment procedures. 

Anxiety models using new environment: 

These are the methods for establishing and evaluating anxiety models in a new environment, such as elevated plus maze and derivers, 

elevated T-maze, open field, staircase test, social isolation, novelty suppressed feeding, social interaction, holeboard, predatory odor, 

operant conflict tests for reward-punishment applications and experiments with punishment procedures such as defensive burying, 

passive avoidance, foot shock, hot plate and four plate tests. 




The purpose of this study is to show the usefulness of the tests in the literature and to compare the advantages and disadvantages in 

terms of structural validity and first sight validity. 

Key words: Anxiety, anxiety models 


[PS-10] 

Symposium Title: Will glutamatergic modulators be a target for the future therapy of depression? 

Ketamine and other glutamate modulators as potential antidepressants 

Serdar Dursun, Glen Baker, Nick Mitchell 

Neurochemical Research Unit, University of Alberta, Edmonton, Canada 

E-mail: Dursun@ualberta.ca 

Depression is seen as a complex neuropsychiatric disorder affecting integrated pathways connecting discrete cortical, subcortical, and 

limbic regions and their associated neurotransmitter and molecular mediators. One episode of major depression is a strong predictor of 

future episodes, and more than 50% of individuals who have an episode of major depression experience a recurrence. 

Unfortunately, currently approved pharmacological treatments for depression require several weeks for onset of efficacy. Despite 

advances in the understanding of the psychopharmacology of depression and the introduction of several novel classes of antidepressants 

in the last 3-4 decades, patient response to any given pharmacological approach continues to be unsatisfactory. 

Although almost all of the prescription drugs currently available as antidepressants have effects on noradrenaline (NA) and/or 

5-hydroxytryptamine (5-HT), it is obvious that other factors are also important in the etiology and pharmacotherapy of depression and 

that the monoamines cannot be considered in isolation. Perhaps the most exciting system and that for which there is now substantial 

translational evidence for a role in depression is that involving glutamate. Ample evidence indicates that glutamate homeostasis and 

neurotransmission are disrupted in major depressive disorder but the nature of these disruptions and the mechanisms by which they 

contribute to the syndrome are unclear. Likewise, the specific effects of existing antidepressants on glutamate are unclear, as is the 

potential of drugs directly targeting glutamatergic neurotransmission to act as novel antidepressant medications. However, these are 

areas of active research and some exciting results have been obtained. 

This presentation will review the current knowledge of the contribution of the N-methyl-D-aspartate (NMDA) receptor, one of the several 

types of glutamate receptors, to depression and its treatment. Several lines of evidence, in humans and in animal models, support 

the contention that neurotransmission via the NMDA receptor is dysregulated in depression. Drugs targeting the NMDA receptor as 

antagonists have shown antidepressant properties in both clinical and preclinical studies. Nevertheless, other effects of such medications, 

including both cognitive side effects and their psychotomimetic properties, complicate such an application and represent a challenge to 

the development of clinically useful agents. 

There is a recent hypothesis that the therapeutic effects of monoaminergic antidepressants and the NMDA receptor antagonist ketamine 

may be mediated by increased alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-to-NMDA glutamate receptor activity 

in critical neuronal circuits. It has been hypothesized that ketamine directly mediates this receptor activity, whereas monoaminergic 

antidepressants work indirectly and gradually; this may explain, in part, the lag of onset of clinical improvement of several weeks that 

is observed with traditional antidepressants. Ketamine (intravenous) is the first medication reported to produce rapid, relatively longlasting 

antidepressant efficacy. Although the precise antidepressant mechanisms of action of ketamine remain unclear, there is preclinical 

evidence to suggest that both AMPA and NMDA receptor subtypes are involved. In terms of neuroanatomical sites of action, it has been 

shown that the subgenual cingulate cortex (Sg CG) is overactive in depression while the dorsal frontal regions and posterior cingulate are 

underactive and that successful treatment normalizes the pattern. There is also evidence from functional magnetic resonance imaging 

(fMRI), which has demonstrated that the effect of ketamine resembles the pattern of normalisation after successful antidepressant 

treatment, i.e., in healthy volunteers there is decreased orbitofrontal cortex (OFC)–Sg CG blood oxygen level-dependent (BOLD) signal 

response and increased BOLD signal response in the dorsolateral prefrontal cortex (PFC) (Brodmann area 8) and the posterior cingulate 

region. These findings suggest that an overactive Sg CG may be the dysfunctional organising region in depression. 

Key words: Ketamine, rapid antidepressant efficacy, glutamate, NMDA receptor 


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The glutamatergic system and its importance in the neurobiology of depression 

Feyza Arıcıoğlu 

Department of Pharmacology, Marmara University, Istanbul, Turkey 

E-mail: feyza.aricioglu@gmail.com 

Recent advances in research on depression have confirmed that it is common, recurrent and disabling mental disorder affecting millions 

of individuals worldwide. Current medications for the treatment of depression have limited efficacy and delayed onset of therapeutic 

action. Existing antidepressants used to treat these disorders are insufficient for many. Patients continue to have low remission rates, 

delayed onset of action, residual subsyndromal symptoms, and relapses. New therapeutic agents able to exert faster and more sustained 

antidepressant effects are urgently needed to treat these disorders. Multiple lines of evidence suggest that inflammation and glutamate 

dysfunction contribute to the pathophysiology of depression. Excess levels of inflammatory mediators occur in a subgroup of depressed 

patients. Patients with depression have been found to exhibit increased blood inflammatory biomarkers, including inflammatory cytokines, 

which have been shown to be involved in depression. Activation of inflammatory pathways is believed to contribute to a confluence of 

decreased neurotrophic support and altered glutamate release/reuptake, as well as oxidative stress, leading to excitotoxicity and loss of 

glial elements, consistent with findings that characterize depressive disorders. Neurotrophic factors such as brain-derived neurotrophic 

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 

BDNF levels are decreased in patients with depressive disorder and antidepressant treatment induces BDNF expression. In this context, 

the glutamatergic system has been implicated in the pathophysiology of depression in unique clinical and neurobiological ways. The data 

from depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood 

and increase treatment response to conventional antidepressant medication. The past decade of efforts to find improved treatment for 

depression has been dominated by genome-driven programs of rational drug discovery directed toward highly selective ligands for 

nonmonoaminergic agents. To date, the monoaminergic systems (serotonin, norepinephrine, and dopamine) have received the most 

attention in the neurobiology of depression, and all classes of antidepressants target these monoaminergic systems. Accumulating 

evidence suggests that the glutamatergic system plays an important role in the neurobiology and treatment of depression. Many 

reports have highlighted alterations in glutamate signaling as well as changes in the expression of AMPA or NMDA receptor subunits 

in depression. In parallel, there is growing interest in the non-competitive NMDA receptor antagonist, ketamine, which produces a 

rapid and sustained antidepressant response in patients with treatment-resistant depression. Importantly, such effects of ketamine are 

seen at subpsychomimetic doses of the drug. Moreover, ketamine produces a profound reduction in suicidality. Based on findings with 

ketamine, there is interest in developing subtype-selective NMDA antagonists, particularly those that act through allosteric mechanisms. 

A final glutamatergic strategy for treating depression may be through modulating metabotropic (G protein-coupled) glutamate (mGlu) 

receptors. During the last 10 years, several selective mGlu receptor competitive antagonists and potentiators have been discovered. 

Selective mGlu receptor antagonists are among the most promising agents under development for the treatment of depression. Overall, 

this system holds considerable promise for developing the next generation of therapeutics for the treatment of depression. 

Key words: Glutamate, depression, cytokines, neurotrophic factors, NMDA, mGLU receptors 


[PS-11] 

Symposium Title: Psychotropic drug treatments during pregnancy and lactation 

Pharmacotherapy of panic disorder during pregnancy and lactation 

Faruk Uğuz 

Selcuk University, Meram Faculty of Medicine, Department of Psychiatry 

E-mail: farukuguz@gmail.com;farukuguz@hotmail.com 

Panic disorder is one of important psychiatric problems during pregnancy and lactation. The prevalence rate of this disorder has been 

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. 

Although pharmacotherapy of panic disorder is well known, data on treatment of this disorder during pregnancy and lactation are very 

limited. It is difficult to decide about pharmacotherapy of panic disorder during the perinatal period, particularly during pregnancy, 




because both effective pharmacological agents and untreated maternal anxiety seem to be associated with several negative outcomes 

on the course of pregnancy and the fetus. Despite the absence of practical guidelines for pharmacological management of panic disorder 

during pregnancy and lactation, some general points about pharmacological treatment include the following: (1) Pharmacotherapy 

should be preferred when the potential impact of untreated maternal panic disorder is higher than the impact of the pharmacological 

agent on the fetus or new mother. (2) The patient and relatives should be informed about the benefits and risks of pharmacological 

treatment or nontreatment of the current maternal psychiatric picture and written informed consent forms should be obtained. (3) 

Selective serotonin reuptake inhibitors except paroxetine and low dose imipramine may be preferred during pregnancy. (4) Sertraline, 

paroxetine, orlow doses of imipramine or clomipramine appear to be appropriate pharmacological agents during the lactation period. 

Key words: Panic disorder, pregnancy, lactation 


Psychotropic drug treatment during pregnancy and lactation in obsessive compulsive disorder 

Servet Ebrinç 

GATA Haydarpasa Training Hospital, Clinic of Psychiatry, Istanbul, Turkey 

E-mail: sebrinc1@gmail.com 

According to recent studies, obsessive compulsive disorder(OCD) is one of the leading cause of disability and the prevalence of OCD is 

found to be 0.2-3.5% in pregnancy and 2.7-9% in the postpartum period. 

The efficacy and tolerability of SSRIs and SNRIs in the treatment of OCD are well-determined in many double-blind randomized controlled 

trials. Despite the fact that it is well known that OCD patients may benefit from antiobsessional therapy during pregnancy and the 

postpartum period, very little data are available about the efficacy of the treatment and no evidence suggests that patients would react 

differently to these drugs. Hence, OCD women who are pregnant and in the postpartum period might be treated using standardized 

treatment approaches. 

During pregnancy and the postpartum period, the treatment of OCD should clinically take the risks and benefits of several treatment 

modalities and the expectations of the patient into account. While cognitive-behavioral therapy (CBT) is the leading choice in nonpharmacological 

treatment of OCD, pharmacoterapy might be used if necessary. 

If CBT is inadequate and pharmacotherapy is needed, during pregnancy, fluoxetine, and during the lactation period, paroxetine, are 

proposed to be the first line treatments. Although evidence is limited, other SSRIs are acceptable as alternative treatment options. 

All of the antidepressant drugs are transferred to the nursing infant during breastfeeding. The American Academy of Pediatrics classifies 

psychotropic drugs as “drugs whose effects are unknown, but may be of concern.” The best way of determining the exposure to the drug is 

measuring the drug concentration in the plasma of the baby. Clinical evaluation is important to identify any side effects while monitoring the baby. 

There is no evidence indicating an increase in the rates of intrauterine death or malformation in the case of exposure to tricyclics or 

SSRIs. Whether exposure to SSRIs causes a decrease in birth weight or an increase in premature births is not certain and the evidence is 

controversial. Nonetheless, The Food and Drug Administration (FDA) has determined that first trimester exposure to paroxetine might 

cause an increase in the risk for congenital malformations particularly cardiac defects. Therefore, the FDA has changed paroxetine’s 

pregnancy category from C (risk can not be ruled out) to D (positive evidence of human fetal risk). 

A “withdrawal syndrome,” consisting of symptoms in the locomotor, central nervous, respiratory and gastrointestinal systems may occur 

in newborns exposed to SSRIs in the third trimester. Although monitoring is required in an exposed newborn, this syndrome is relatively 

mild, can be managed with supportive therapy and diminishes within 2 weeks. Some evidence points out an increase in the rates of 

persistent pulmonary hypertension in infants exposed to SSRIs during the third trimester. Before delivery, lowering the dosage of the 

mother’s drugs that might have been augmented due to the symptom severity of OCD, is recommended. 

Key words: lactation, obsessive-compulsive disorder (OCD), psychopharmacotherapy, pregnancy 

References: 

1. Clinical Management Guidelines for Obstetrician-Gynecologists Use of Psychiatric Medications During Pregnancy and Lactation. ACOG Practice Bulletin, 

(Reprinted with permission from Obstetrics & Gynecology 2008; 111:1001–1020) 

2. Brandes M, Soares CN, Cohen LS. Postpartum onset obsessive-compulsive disorder: diagnosis and management. Arch Womens Ment Health 2004; 7:99–110 

3. Use of Psychoactive Medication During Pregnancy and Possible Effects on the Fetus and Newborn Amerikan Academy of Pediatrics Committee on Drugs Pediatrics 

2000; 105; 880-887 

4. Koran LM, Hanna GL, Hollander E et al. Practice Guidline for theTreatment of Patients with Obsessive-Compulsive Disorder. Copyright 2010, American Psychiatric 

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Association. 

5. McGuinness M. OCD in the Perinatal Period: Is Postpartum OCD (ppOCD) a Distinct Subtype? A Review of the Literature. Behavioural and Cognitive Psychotherapy 

2011, 39, 285–310 


[PS-12] 

Symposium Title: Vitamin and mineral supplementation in treatment of childhood psychiatric disorders 

Vitamin and mineral supplementation in treatment of childhood psychiatric disorders – Calcium and 

vitamin D supplementation 

Ömer Faruk Akça 

Samsun Psychiatry Hospital, Child and Adolescent Psychiatry Clinic, Samsun, Turkey 

E-mail: dromerakca@gmail.com 

Vitamin D has significant roles in cell proliferation, the immune system and the nervous system as well as in bone development. Adult 

studies indicate that vitamin D deficiency may be related to some neurological and psychiatric disorders like Parkinson’s disease, 

Alzheimer’s disease and depression (1). Childhood studies on this subject are mainly related to the impact of vitamin D deficiency on the 

development of autism. Because vitamin D has an essential role in the development of the nervous system, some investigators suggest 

that vitamin D deficiency during pregnancy may contribute to the development of autism. Autism is stated to be more frequent in people 

with dark skin and people who live in countries at higher latitudes. Additionally, children of mothers who consume more vitamin D in 

pregnancy have better mental development and present with fewer autistic signs. This knowledge indicates that vitamin D may be a 

mediator in the emergence of autism for genetically vulnerable people (2). Autism frequency has increased in recent years and this increase 

has occurred at the same time as the suggestions on the avoidance of sunlight have arisen. This coincidence is claimed to be supportive 

of the autism-vitamin D hypothesis (2,3). This hypothesis suggests two possible mechanisms: 1) vitamin D deficiency during pregnancy 

may cause inappropriate development of the fetal brain and then autistic signs may emerge, 2) in light of the hypotheses that autism 

is an autoimmune disorder and vitamin D is important for immune system functions, it may be assumed that vitamin D deficiency may 

cause autistic signs in vulnerable individuals (4). Some studies have stated that autism is more frequent in children of winter pregnancies 

and people of higher latitude countries (4). Additionally, it is stated that autistic patients have the lowest vitamin D levels among all kinds 

of psychiatric disorders in a psychiatry inpatient clinic (5). In another recent study, autistic children have lower 25-hydroxy vitamin D, 

1,25-hydroxy vitamin D and calcium levels in comparison with healthy children (6). These findings are supportive of this hypothesis. 

According to this hypothesis, it can be estimated that children with rickets would have more autistic symptoms. There is no recent study 

on this assumption. However, in past studies it has been stated that these children had more mental disorders, which disappeared after 

treatment (7). 

On the other hand, because children with autism may have food selectivity, vitamin D and calcium deficiency may occur in these children 

more frequently. Some investigations were made on this subject and many of them found supportive findings (8,9). 

We may conclude that autism-vitamin D relationship needs to be investigated more with larger sample studies. 

Key words: Autism, vitamin D, calcium 

References: 

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. 

2. Cannell JJ. Autism and Vitamin D. Med Hypotheses 2008; 70: 750-759 

3. Cannell JJ, Hollis BW. Use of Vitamin D in Clinical Practice. Altern Med Rev 2008; 13:6-20. 

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. 

Dermatoendocrinol 2009; 1:223-228. 

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, 

ethnic origin and psychiatric diagnosis. J Steroid Biochem Mol Biol 2010;121:467-470. 

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 

Complement Med 2010; 16:641-645. 

7. Cannell JJ. On the aetiology of autism. Acta Paediatr 2010; 99:1128–1130. 

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 


Dev Disord. 2011 Article in press. 



9. Emond A, Emmett P, Steer C, Golding J. Feeding Symptoms, Dietary Patterns, and Growth in Young Children With Autism Spectrum Disorders Pediatrics 2010; 

126:337-342. 


Zinc supplementation in psychiatric disorders of children 

Sadriye Ebru Çengel Kültür 

Department of Child and Adolescent Psychiatry, Hacettepe University, Ankara, Turkey 

E-mail: ebru.kultur@gmail.com;ecengel@softhome.net 

Micronutrient supplementation is considered as a useful intervention in many cases. Zinc is one of these micronutrients and an essential cofactor 

for over 100 enzymes, both metalloenzymes and metal-enzyme complexes that are required in the metabolism of carbohydrates, fatty acids, 

proteins and nucleic acids. Zinc is considered as an essential element in neuronal development, synaptogenesis and synaptic transmission. 

In experimental animal studies, zinc deficiency during early brain development is mainly related with malformations. In humans, 

neuropsychological and neurobehavioral effects of zinc deficiency are largely studied in severely zinc deficient groups or cases exposed to 

deficiency during early developmental stages. In addition zinc supplementation studies mainly occur in the gestational period or infancy 

and use zinc doses higher than the protective dosage. Limited numbers of interventional trials have been performed to demonstrate 

the effects of zinc supplementation on behavioral, cognitive and neuropsychological functioning in school-aged children. Some of these 

studies showed no significant effects on average attention span and short-term memory. On the other hand some found improvement 

in neuropsychological performance and decrease in the number of children with clinically significant parents’ scores for attention deficit 

and hyperactivity. When searched for internalizing symptoms, no significant effect was revealed in parent-teacher rated scales. 

In clinical cases with attention deficit hyperactivity disorder (ADHD) and autism low serum zinc levels were reported. Zinc supplementation 

studies in ADHD cases showed significant improvement reported in parents’ and teachers’ ratings of hyperactivity, impulsivity and 

socialization scores. Furthermore, one study found that improvement was mainly in parent-teacher-rated inattentive symptoms in ADHD 

cases. In a placebo controlled study, zinc supplementation in addition to ADHD treatment revealed a 37% reduction in d-amphetamine 

dose compared to placebo, though no significant superiority of zinc supplementation for ADHD symptoms was observed. 

In conclusion, zinc supplementation studies suggest a special relationship to ADHD diagnosis. However it is not possible to establish 

either an etiological relation or an alternative treatment approach in ADHD. 

Key words: Zinc supplementation, ADHD 


The impacts of iron deficiency on mental health in childhood 

Ayhan Bilgiç 

Department of Child and Adolescent Psychiatry, Meram Faculty of Medicine, Selcuk University, Konya, Turkey 

E-mail: bilgicayhan@yahoo.com 

Numerous studies have found associations between iron deficiency (ID) and iron deficiency anemia (IDA) and poor cognitive and motor 

development in infancy and early childhood. In addition, it has been reported that there are associations between ID/IDA and some 

childhood neuropsychiatric disorders including attention deficit hyperactivity disorder, conduct disorders, autism spectrum disorders, 

restless leg syndrome, sleep disturbance and Tourette’s syndrome. Iron is required for proper function of some enzymes that are engaged 

in the myelinization process and in monoamine neurotransmitter synthesis. Therefore, it has been considered that these negative effects 

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 

sufficient for occurrence of functional disturbances, although exceptions exist. There are studies which considered that, especially early 

in life, the negative impacts of ID on psychomotor and neurological development do not seem to be reversible by iron supplementation 

and ID may cause permanent hazards in the brain. However, some studies have reported that iron supplementation resolved the effects 

of ID including cognitive and motor development problems in children and the development of psychiatric disorders. Despite there being 

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large amounts of data, the possible confounding effects of poor socioeconomic backgrounds prevent causal inferences. Even nowadays, 

it is still not clear whether poor development of iron-deficient children is related to poor social backgrounds or irreversible damage due 

to ID and if it is remediable with iron treatment. 

Key words: Iron deficiency, children, development, psychiatric disorders 


Antioxidant vitamin supplementation therapies in child psychiatry 

Betül Mazlum 

İstanbul University, Institute of Experimental Medicine, Department of Neuroscience, İstanbul, Turkey 

E-mail: drbakkaloglu@yahoo.com 

Oxidative stress can be defined as an imbalance between pro-oxidant molecules produced by the body during metabolism and members 

of the antioxidant system, in favor of the former. Antioxidant defense mechanisms include antioxidant enzyme systems and molecules 

(vitamins, minerals, etc.) which have the ability to detoxify free oxygen radicals. 

The brain is highly vulnerable to oxidative stress since it has limited antioxidant capacity, high energy demand and high lipid content. 

Moreover, each brain region may have a genetically determined different vulnerability levels to oxidative stress. 

Oxidative stress, which is included in the pathogenesis of cancer, aging, cardiovascular and neurodegenerative disorders, is also 

considered for pathogenetic mechanisms underlying psychiatric disorders including schizophrenia, bipolar disorder, depression, autism 

and attention deficit hyperactivity disorder. There are accumulating data about increased oxidative stress particularly in childhood autism 

and therefore antioxidant therapies are considered as an alternative treatment option. In addition, vitamin and mineral supplementation 

are recommended to compensate low intake when children with autism have feeding problems. The data about the effects of antioxidant 

therapies in autism are restricted but promising. Since oxidative stress is a common finding in the pathogenesis of different disorders, it can 

be suggested that individual differences, including single nucleotide polymorphisms of the genes coding for members of the antioxidant 

defense system, might determine the vulnerability level to oxidative stress. Individual genetic differences might also be the determinant 

of the level of benefit from antioxidant vitamin therapies. Not only the factors related to the biochemistry of leading antioxidant vitamins 

(vitamin A, C and E) but also the disease and patient related differences might be acting on the response to supplementation with these 

vitamins. These two groups of factors might determine the details of supplementation therapies with antioxidant vitamins in the future: 

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 

brain areas to oxidative stress, accompanying diseases and possible effects of antioxidant vitamin supplementation on the pathogenesis 

of these comorbid diseases; 2) Factors related to the biochemistry of the antioxidant vitamins in the body, i.e., polymorphisms of 

molecules mediating intestinal absorption and blood-brain transfer of vitamins, important effects of these vitamins on specific gene 

regulation and effects of vitamins on brain mechanisms. 

Antioxidant vitamin supplementation is a promising alternative therapy in psychiatry, but it should be kept in mind that these vitamins 

might also have undesirable results through their effects on other biological processes. This part of the panel will focus on the study 

results of antioxidant vitamin supplementation therapies in child psychiatry and molecular data about the genetic and biochemical 

processes of antioxidant vitamins in the body. 

Key words: Antioxidant vitamins, psychiatry 


Effectiveness of omega fatty acid supplementation for childhood psychiatric disorders 

Sabri Hergüner 

Selcuk University, Meram Faculty of Medicine, Department of Child and Adolescent Psychiatry, Konya, Turkey 

E-mail: herguners@yahoo.com 

Neuronal membranes are composed of phospholipids containing large amounts of polyunsaturated fatty acids (PUFA), especially the 

omega-3 and omega-6 acids. Because humans cannot manufacture these de novo, they are “essential” in the diet. Membrane stability is 




essential for neuronal maturation as well as for advanced integrated central system activities including attention, alertness and motor 

coordination. PUFA are critically important for normal brain development and functioning. During fetal life, large amounts of PUFA are 

deposited in the central nervous system. During infancy, dietary intake of PUFA, both omega-3 and omega-6 acids, continues to be 

essential for neural development. 

PUFA are metabolized to prostaglandins and other eicosanoids, which modify many metabolic processes and immune functions. They 

moderate dopamine, serotonin and norepinephrine release, regulate gene transcription and Na-K-ATPase channel function. There is 

increasing evidence that omega acids play a part in many neurodevelopmental and psychiatric disorders including attention deficit 

hyperactivity, dyslexia, developmental coordination disorder and autism spectrum disorders. 

The focus of this speech will be on the effects of PUFA supplementation on pediatric neurodevelopmental disorders. 

Key words: Children, neurodevelopmental disorders, omega fatty acids 


[PS-13] 

Symposium Title: Hormones and psychiatric disorders 

Melatonin and human behaviour 

Müfit Uğur 

İstanbul Üniversitesi, Cerrahpaşa Tıp Fakültesi, Psikiyatri AD, Cerrahpaşa, İstanbul, Turkey 

E-mail: mugur52@hotmail.com 

Melatonin is secreted from the pineal gland and regulates the sleep wake cycle, core body temperature, ovulation, and sexual behavior 

in females, as well as immune and cardiovascular functions. It also has antioxidant, antiinflammatory, and glucose regulatory properties. 

Melatonin also changes behavior especially in depressed patients or patients who are prone to a psychiatric illness. 

External noradrenergic stimuli act on the suprachiasmatıc nuclei and control melatonin secretion, which in turn regulates autonomic 

functions and daily behaviors by acting as an endogenous synchronizer. 

Melatonin, which manages body core temperature, the sleep wake cycle, and gonadal sex steroids, also causes some behavioral problems 

in case of depression. In bipolar manic patients nocturnal melatonin is found to be higher than in depressed patients because of 

noradrenergic stimulation. 

Melatonin secretion and body core temperature are also closely related. Core body temperature is the lowest when the nocturnal melatonin 

secretion is high. By controlling core body temperature, melatonin also helps to regulate the body metabolism and glucose utilization. 

Ovulation in females is under the control of melatonin. When melatonin is the lowest nocturnally, which causes high core body 

temperature, it is time for ovulation in females. High core body temperature and low nocturnal melatonin secretion return to normal 

after the ovulation occurs. It also controls the secretion of sex steroids by its suppressive effect on the gonads. Nowadays some research 

is working on using it as an oral contraceptive agent. 

It also regulates immune functions by acting on T lymphocytes and help organisms to have a high defense against infections, supplying 

an anti-inflammatory effect and serving as an antitumor agent. 

Today it is used specifically for the treatment of sleep disorders such as: 

-Advanced sleep phase syndrome 

-Delayed sleep phase syndrome 

-Circadian rhythm disorders 

-Insomnia 

-Irregular sleep wake cycle 

-Jet-Lag 

-Seasonal affective disorders 

-REM related behavior disorders 

Key words: Melatonin 


S75


Effects of oxytocin on social behaviour 

Nuray Atasoy 

Zonguldak Karaelmas University, Faculty of Medicine, Psychiatry Department, Zonguldak, Turkey 

E-mail: nurayulus@yahoo.com 

Oxytocin (OXT) is traditionally viewed as a female hormone that is primarily associated with labor and it has a very special affect on 

mothering. In mothers it increases their attachment to their infant, promoting the feeling of love, and makes her infant more valuable 

to her. Oxytocin has been called the love and bonding hormone. Furthermore, oxytocin mediates attachment behavior over the course 

of development, with lower urinary concentrations of oxytocin found in maltreated children and in adult males with a history of early 

separation. Psychologically, oxytocin promotes a feeling of well being and tranquility. It also suppresses the fear that would normally 

cause a mother to back off from a threat. In humans, based on the animal literature, it has been postulated that beyond these peripheral 

actions, central OXT modulates cognition in the context of social interactions, thus promoting positive sociality. 

In particular, recent experiments have shown that OXT promotes trusting behavior, enhances facial emotion recognition and memory 

for positive social information, reduces social stress, improves social cognition in socially impaired individuals with autism, and alters 

dysfunctional cognition in social phobia. 

Functional imaging studies have just begun to elucidate the underlying neural correlates of these pro-social effects. A number of studies 

have provided evidence that the amygdala might be a key structure for the mediation of the social cognitive effects of OXT. Several studies 

have shown that a single dose of OXT reduced amygdala reactivity to pictures of aversive scenes and faces with negative valence. 

While studies of oxytocin and monogamous behavior in humans have not been conducted to date, one study found that in co-habiting 

couples, greater partner support is associated with higher plasma oxytocin in both men and women before and after a period of warm 

partner contact. 

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 

receptor affinity, appears to be modulated by gonadal steroids such as estradiol and progesterone. It has been shown, in a study on 

prairie voles, that female parenting behavior is more dependent on OXT, whereas male parenting behavior is associated with vasopressin. 

Another study demonstrated that aggression is associated with OXT in females, but not in males. However, the hypothesis of homology 

between paternal and maternal behavior has not yet been adequately tested and it is possible that different neuroendocrine circuits could 

lead to the same behavior in males and females. Future studies should include both sexes to determine a possible sexual dimorphism in 

the neural effects of OXT, considering gonadal steroids and OXT receptor affinity. 

Key words: Oxytocin, social behaviour 


Thyroid hormones and psychiatric disorders 

Tayfun Turan 

Department of Psychiatry, Erciyes University, Kayseri, Turkey 

E-mail: mtturan@erciyes.edu.tr 

The role of the hypothalamic-pituitary-thyroid (HPT) axis in psychiatric symptoms and disorders has been stressed in many studies. 

Secretion of thyroid hormones is controlled by this axis. Hypothalamic thyrotropin releasing hormone (TRH) stimulates pituitary 

thytrotropin-stimulating hormone (TSH) and the latter controls the secretion of thyroid hormones. Serum thyroid hormones regulate the 

HPT axis by a negative feedback system. The main secretion of the thyroid gland is thyroxine (T4). T4 is converted into triiodothyronine (T3) 

in various tissues, especially in brain, by enzymes called “deiodinases”. Transthyretin, a hormone transporter, transports T4 into the brain (1). 

Thyroid hormones play a critical role in the developing and functioning of the brain (2). In this regard, it is suggested that interactions 

between thyroid hormones and neurotransmitter systems, especially serotonin (5-HT), norepinephrine (NE) and acetyl choline (Ach), 

probably contribute to the regulation of mood and behaviour (1). T3 enhances the effects of NE, 5-HT and γ-aminobutyric acid, which are 

thought to be involved in the etiology of some psychiatric conditions (3). 

In the literature there are many case reports and studies indicating probable relationships between clinical or subclinical thyroid diseases 

and psychiatric disorders. So far, many cases have been reported of hypothyrodism or hyperthyroidism associated with psychiatric 

disorders, including mania, depression, schizophreniform psychosis, paranoid psychosis, cognitive disturbances, delirium and anxiety 




(4-9). One percent of thyrotoxic patients are suggested to have been first diagnosed with a psychiatric disease (5). Interestingly, it 

seems that both hyperthyroism and hypothyroidism could lead to mania, anxiety or schizophrenic symptoms. The underlying reason 

for the co-occurrence of thyroid diseases and psychiatric disorders is not yet known. However, in these cases, combined hormonal and 

psychotropic interventions may improve symptoms. 

Several studies have assessed HPT axis activity in various psychiatric disorders, especially mood disorders and anxiety disorders. Up 

to 45% of the euthyroid patients with major depression showed blunted TSH response to TRH stimulation (10). Moreover, thyroid 

hormones accelerate the antidepressant effect of tricyclic antidepressants (11). HPT axis alterations may play an important role in the 

pathophysiology of bipolar disorder, but this area has received much less attention than major depressive disorder. However, it seems 

that abnormalities of this axis are not uncommon among bipolar patients, especially among the rapid cycling subgroup. So far, thyroid 

dysfunctions such as hypothyroidism and exaggerated TSH response to TRH have been found in rapid cycling patients (12,13). In some 

bipolar patients, latent thyroid dysfunction becomes overt by lithium treatment. Moreover, it has been suggested in a recent study that 

bipolar disorder itself may cause increased thyroid volumes and decreased thyroid hormones as well as lithium treatment in patients (14). 

Few studies have investigated possible thyroid dysfunctions in psychotic patients. In a study, schizophrenic patients showed increased 

serum T4 levels, which normalized after antipsychotic treatment. Elevated serum T4 levels in schizophrenic patients may suggest an 

impairment of T4 metabolism in the brain (4). 

A few studies of panic disorder have demonstrated evidence of a blunted TSH response to TRH. A previous study showed higher TSH 

levels in non-medicated patients with severe panic attacks (7). Increased TSH levels seen in patients with panic disorder might be due to 

reduced intracerebral 5-HT concentrations (15). 

Eletroconvulsive therapy (ECT) itself may affect the HPT axis as do psychotropic drugs. In a previous study, elevated TSH levels were found 

following ECT in depressed patients. This response might contribute to the therapeutic effect of ECT (16). 

In conclusion, the HPT axis and thyroid hormones play an important role in the pathophysiology of many psychiatric disorders. However, 

further well-designed studies are needed to clarify the confusion in this field. 

Key words: Hypothalamic-pituitary-thyroid axis, thyroid hormones, psychiatric disorders 


Sex steroids and psychiatric disorders 

Erdem Deveci 

Regional Training and Research Hospital, Department of Psychiatry, Erzurum, Turkey 

E-mail: erdemdeveci@gmail.com 

Sex steroids play very important roles in the development and function of the central nervous system and have long been known to 

exert powerful effects on brain differentiation, neural plasticity, central neurotransmission and behavior. Estrogens, progestins, and 

androgens are able to induce several effects in brain areas of the central nervous system, through binding with specific receptors (1). 

Sex steroid hormones act through genomic mechanisms, modulating synthesis, release and metabolism of many neuropeptides and 

neurotransmitters, and through non-genomic mechanisms, influencing electrical excitability, synaptic function, morphological features 

and neuron-glia interactions (2). 

Animal research has shown that estrogens, progesterone and testosterone are critically involved in myelination, forming the basis of white 

matter connectivity in the central nervous system. Animal studies have also provided evidence that estrogen modulates dopaminergic 

activity and affects dopamine related behaviors in animals in a variety of ways. 

Clinical observations suggest that sex steroids have potent effects on mood, mental state and cognitive functions. Data also suggest 

that estrogen has a pivotal role in modulating other neurotransmitter systems such as serotonergic and glutamatergic systems that 

have implications for schizophrenia and mood disorders (3,4). Sex steroid deficiency causes many neuroendocrine changes. At the 

hypothalamic level, estrogen withdrawal gives rise to vasomotor symptoms, eating behavior disorders, and altered blood pressure 

control. On the other hand, at the limbic level, the changes in serotoninergic, noradrenergic and opioidergic tones contribute to 

modifications in mood, behavior and nociception. 

Studies of testosterone concentrations in depression have yielded inconsistent results reporting low as well as high testosterone levels 

associated with depression (5). On the other hand anabolic steroid use has increased in prevalence in many countries over the past 

decade, and it can lead to aggression, depression, mania and psychosis, in addition to a range of physical complications which seem to 

be important in clinical practice (6). 

Key words: Depression, estrogen, mood disorders, progesterone, schizophrenia, testosterone 

S77


References: 

1. McEwen BS Steroid hormones are multifunctional messengers to the brain. Horm Res. 1992; 37(Suppl 3):1-10. 

2. Genazzani A.R. et al. Endocrinology of Menopausal Transition and Its Brain Implications CNS Spectr. 2005 Jun;10(6):449-57. 

3. Janice R, Stevens MD Schizophrenia: reproductive hormones and the brain. Am J Psychiatry 2002; 159:713-719. 

4. Seeman MV. The role of estrogen in schizophrenia. J Psychiatry Neurosci 1996; 21:123-125. 

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. 

6. Hall, R. C. W., Hall, R. C. W. & Chapman, M. J. Psychiatric complications of anabolic steroid use. Psychosomatics, 2005; 46- 285. 


Insulin and psychiatric disorders 

Mesut Cetin 

Department of Psychiatry, GATA Haydarpasa Training Hospital, Uskudar, Istanbul, Turkey 

E-mail: mesutcetin@yahoo.com 

Insulin is a hormone central to regulating carbohydrate and fat metabolism in the body. Insulin also influences other body functions, such 

as enhancing acute thermoregulatory and glucoregulatory responses to food intake. It is also a neuropeptide transmitter and enhances 

learning and memory. 

Hypoglycemia is a lack of sufficient glucose and a scarcity of the sources of glucose, which can dramatically manifest itself with impaired 

functioning of the central nervous system and can cause dizziness, speech problems, and even loss of consciousness. While producing 

those symptoms, hypoglycemia also provokes a rapid increase in epinephrine secretion, which leads to tremulousness, lightheadedness, 

perspiration, anxiety, hunger, nausea, and tachycardia. These symptoms present like a panic attack, suggesting that if hypoglycemia does 

provoke anxiety attacks it may be through its action as a nonspecific stressor, perhaps by interacting with an underlying CNS disorder 

that predisposes to panic. The fear of hypoglycemia-induced bodily symptoms of arousal has been implicated in the pathogenesis of 

both spontaneously occurring and experimentally provoked panic attacks. The fear of bodily symptoms may be a characteristic of panic 

disorder and is hypothesized to predict state anxiety and panic frequency during experimentally induced peripheral arousal. 

Insulin resistance and metabolic syndrome (MS) have become worldwide problems. MS is a cluster of risk factors associated with 

increased risk of cardiovascular diseases and type 2 diabetes. Based on research data from 2004, 40% of adults in Turkey meet the criteria 

for diagnosis of metabolic syndrome. The use of certain medications, such as atypical antipsychotics, may increase insulin resistance and 

the risk of the metabolic syndrome. 

Key words: Insulin, panic disorder, insulin resistance, hypoglycemia, depression 


[PS-14] 

Symposium Title: Clinical course of psychiatric disorders associated with trauma and treatment issues 

Trauma and mood disorders 

Medine Yazıcı Güleç 

Erenkoy Mental Research and Training Hospital, Istanbul, Turkey 

E-mail: drmedineyazici@yahoo.com, medineyazici@hotmail.com 

There is increasing evidence for the role of adverse childhood experiences in the occurence of mood disorders (MD). A great number of 

studies have shown that there is a correlation between MD and parental indifference, neglect and sexual and physical abuse. Angst et 

al., in a 20-year longitudinal study, suggested that childhood family issues have a robust correlation with the chronicity of bipolar and 

unipolar MD, and adverse childhood experiences give rise to low self-esteem and anxious personality. The presence of childhood trauma 

(CT) has found to be associated with increases in rates of substance abuse, early age of onset, rapid cycling, and suicide. There is severe 

CT in half (49%) of bipolar MD patients. 




Individuals with CT have both an overall increased risk for depression and a substantially increased sensitivity to the depressogenic 

effects of stressful life events. The relation between CT and stressful life events is dose dependent and correlated with the intensity of the 

neuroticism. It has been shown that the severity of CT predicts an early age of onset and the number of life time depressive episodes, 

and that it is associated with more comorbidity. Increased rates of emotional CT, depressive symptoms and anxiety have been reported 

in treatment resistant group of patients. 

Childhood adverse life events are associated with various neuroendocrine and neuroanotomical changes. There is a 6 times larger ACTH 

response to stress in depressive female patients who reported CT. These patients also have an increased cortisol response and heart 

rate response to psychosocial stress. Women, who have reported CT but were not depressed, have exhibited normal cortisol responses, 

despite having increased an ACTH response. This can be interpreted as resilience against depression, an adrenal adaptation to central 

sensitization. It has been reported that decreased hippocampal volume (18%) in depression is related to CT and that the hippocampal 

volumes of depresssive patiens who did not report CT were equal to those of the control group. Repeated bursts of CRF in response to 

stress during development and increased cortisol reactivity over the course of time may contribute to smaller hippocampi after childhood 

trauma exposure, leading to further sensitization of the stress responses. These results would suggest that there are biologically distinct 

subtypes of depression as a function of childhood trauma. 

The effect of CT on predisposition to illness is associated with genotype. The s/s allele of the serotonin transporter gene, the gene 

polymorphism of BDNF and the CRF-1 gene have been shown to be related to vulnerability to trauma effects. 

CT is associated to decreased response to pharmacological treatment. Among chronically depressed patients with no history of early 

trauma, combination treatment was most effective in attaining remission compared to pharmacotherapy and psychotherapy. In contrast, 

in chronically depressed patients with early-life trauma, remission rates were significantly higher for psychotherapy alone versus 

pharmacotherapy. Combination treatment did not have any further advantage over psychotherapy alone. Improved effects of cognitive 

and behavioral therapies, group therapies and EMDR have been reported in various studies. Questioning about CT in MD patients seems 

to be important for treatment planning, assessment of risks and prophylactic interventions. 

Key words: Childhood trauma, mood disorders 


Trauma and psychotic disorders 

Selma Bozkurt Zincir 

Erenkoy Mental Health and Diseases Training and Research Hospital, Istanbul, Turkey 

E-mail: sbozkurtzincir@yahoo.com 

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 

is growing literature to indicate that trauma is also linked with more severe psychiatric disturbances, including symptoms indicative of 

psychosis in general and schizophrenia in particular. Several lines of evidence suggest an association between trauma and psychosis with 

a dose-response effect. First, studies have demonstrated a high incidence of trauma in the lifetimes of patients with psychosis. Abused 

patients are particularly likely to experience positive symptoms, such as paranoid ideation, thought insertion, visual hallucinations, ideas 

of reading someone else’s mind, ideas of reference, and hearing voices making comments. Secondly, it has been suggested that of all 

diagnostic categories, psychosis displays the strongest association with child abuse. Thirdly, according to some researchers childhood 

sexual abuse is the most powerful predictor of later psychiatric symptoms and disorders after controlling for significant demographic 

variables. 

It has been suggested that the experience of abuse may create a biological or psychological vulnerability for the development of 

psychotic symptoms, including sub-clinical psychotic experiences such as low-grade delusional ideation, suicidal thinking and isolated 

auditory hallucinations. Exposure to psychological trauma worsens the prognosis of expression of psychosis, in terms of greater likelihood 

of transition to a more severe psychotic state. According to recent cognitive models of psychosis early adverse experiences such as 

social marginalization, childhood loss or severe childhood trauma may create an enduring cognitive vulnerability characterized by less 

subjective control over these experiences, negative schematic models of the self and a world that facilitates external attributions. This 

tendency to externally attribute events may lie beneath paranoid ideation. 

Current ideas about biological consequences of early adversities lend even more credibility to the notion of an enduring psychological 

vulnerability. It has been suggested that adverse life events or significant losses might be able to mould the neurodevelopmental 

abnormalities that underlie sensitivity to stressors, if they occur early enough or are sufficiently severe. Thus abnormal neurodevelopmental 

processes may originate from traumatic events in childhood. Specifically, when exposure to stressors persists and heightened stress- 

S79


induced glucocorticoid release is chronic, permanent changes in the hypothalamic-pituitary-adrenal (HPA) axis may ensue. This may 

account for the dopaminergic abnormalities considered central to biological accounts of psychosis. Other researchers are also examining 

the role of dissociative processes, attachment styles, and trauma related cognitive biases to try to better understand precisely how 

childhood trauma can lead to psychosis later in life. 

Clinically it is imperative to routinely enquire about traumatic experiences to respond appropriately and to offer psychosocial treatments 

to those who report traumatic life events in the context of psychotic experiences. 

Key words: Trauma, psychotic disorders, schizophrenia 


Relationship of sexual dysfunction with trauma 

Murat Erdem 

Gulhane Military Medical Faculty, Psychiatry Department, Ankara, Turkey 

E-mail: drmerdem@yahoo.com 

Exposure to sexual trauma in adulthood is perceived as helplessness and loss of control even if sexuality has been defined as a pleasant 

event before trauma. Feelings of guilt and shame occurring after trauma as well as secondary clinical pictures such as depression, 

post traumatic stress disorder, and alcoholism are major causes of sexual dysfunction. Also sexual abuse in childhood raises a sense of 

weakness and perception of inadequacy. These individuals are at risk of developing inappropriate sexual behaviors over time. Indulging 

in sexual behaviors and thoughts that are evaluate sexuality as a gift or privilege are precursors for these inappropriate behaviors. In 

addition, the stigmatization caused by feelings of shame and guilt in these children is another cause of sexual problems in the future. 

Childhood sexual trauma is associated with negative attitudes about sexuality, lack of sexual satisfaction, orgasmic failure, need for sexual 

therapy and low self-esteem about sexual attractiveness. Chronic pelvic pain is a significant clinical entity which causes sexual dysfunction 

in many ways. In studies, the rate of traumatic childhood sexual experiences was found to be over 60% in these patients (N. Leithner, 

2006). The difference between patients with chronic pelvic pain and a healthy control group was found to be even greater in terms of the 

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% 

of cases and deficiencies in sexual function were found to be associated with the level of depression in these patients (ME Randolph, 

2006). 

There are several studies that show that physical and sexual trauma plays a role in the etiology of vaginismus. In a study comparing the 

childhood and adolescent sexual traumas of patients with vaginismus and dyspareunia and control groups -(each group consisting of 

29 patients) childhood sexual trauma was found to be twice as high as the control group in the vaginismus group (Reissing ED, 2003). 

In the literature there are case reports suggesting that EMDR is effective in cases of vaginismus resulting from childhood sexual trauma. 

In studies evaluating the relationship between childhood sexual traumas and a specific sexual dysfunction, aand in studies examining 

sexual functioning in general, a strong relationship has been found between these two situations. Structural vulnerability and the severity 

of sexual trauma were also reported to affect this relationship. While childhood sexual trauma is associated with sexual stimulation 

disorder, orgasmic disorder, vaginismus, dyspareunia and emotional problems about sexuality (sexual guilt, sexual anxiety etc.) in most 

individuals, high-risk sexual behaviors, characterized by extreme preoccupation with sexuality and uncontrolled sexual relationships, are 

seen in fewer individuals. 

Sexual childhood trauma in men is being reported, recognized and treated less frequently than the actual prevalence. Sexual dysfunction 

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 

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 

sexes, especially in women, an association between the presence of childhood sexual trauma and sexual dysfunction has been identified 

(Najma JM, 2005). Leonard et al. found that problems associated with orgasm are the most frequent sexual problems seen in individuals 

who were exposed to a childhood sexual trauma (2008). 

Key words: Trauma, sexual dysfunction 



[PS-15] 

Symposium Title: Depression and pain 

Impact of pain on treatment in depression 

Cengiz Akkaya 

Departments of Psychiatry, Uludag University, Bursa, Turkey 

E-mail: cakkaya@uludag.edu.tr 



Major depressive disorder (MDD) is a chronic, disabling condition with a wide range of symptoms, including core mood symptoms of 

depression and anxiety, cognitive and behavioral deficits, and somatic/physical disturbances. Approximately two-thirds of patients with 

depression experience physical pain symptoms (e.g. headache, neck and back pain, abdominal pain, diffuse musculoskeletal pain). Pain 

as a symptom of depression, often has a negative impact upon other depressive symptoms (for example, it may induce or exacerbate 

low energy, sleep disturbance, and anxiety), adherence to medication, and obtaining adequate therapy. Therefore, pain influences both 

the course of depressive illness and the treatment outcome. Also the severity of pain is found to be a strong predictor of poor response 

and health-related quality of life. Impairments in social and occupational functioning may increase when depression and pain coexist. 

Patients who fail to achieve remission after antidepressant therapy are more likely to suffer residual pain and other physical symptoms 

compared with remitted patients. 

The close relationship between pain and depression, and the growing evidence of a connection between treatment outcomes in these 

conditions, suggests that maximal patient benefit may result from treatments which effectively address both emotional and physical 

symptom domains. Therefore, treatments that address both depression and pain are highly desirable. Neurobiological evidence suggests 

that mood and chronic pain are connected via serotonin and noradrenaline neurotransmitter pathways. Serotonin and norepinephrine 

play a key modulating role in pain mechanisms in the central nervous system. Serotonin modulates both descending inhibitory and 

facilitatory pathways and thus exerts both an antinociceptive and a pronociceptive effect. Noradrenaline, however, typically acts centrally 

in an antinociceptive manner, exerting its effects via a-2-adrenoreceptors in the descending antinociceptive pathways. 

Efficacy for treating pain is best established for tricyclic antidepressants. But through the last decade, antidepressant medications, 

particularly selective serotonin reuptake inhibitors (SSRIs) and selective serotonin and norepinephrine reuptake inhibitors (SNRIs), are 

widely used in the management of MDD. SSRIs are often favored in practice because of their tolerability and safety. However, their efficacy 

in pain is thought to be relatively weak. On the other hand the mechanism of SNRIs has been hypothesized to confer analgesic effects 

independent of antidepressant action. Evidence suggests that potentiation of both serotonin and norepinephrine is required for effective 

analgesia; drugs that inhibit only one of these systems (particularly serotonin) appear to have a limited effect. Whether antidepressants 

relieve pain through direct analgesic effects or indirectly through antidepressant action is still under discussion. There may be a close 

association between analgesic and antidepressant effects and pain relief may be secondary to mood improvement. 

Key words: Pain, depression, antidepressant 


Clinical characteristics and mechanism of pain in depression 

Selçuk Kırlı 

Department of Psychiatry, Uludag University, Bursa, Turkey 

E-mail: kselcuk@uludag.edu.tr 

Although there is a large amount of data indicating that depression and pain symptoms are closely interrelated, they are not included in 

depression symptoms in the classification systems. Even so, new developments in neuroscience have carried the data on this interrelation 

and co-occurrence beyond the epidemiological dimension to the awareness of a common underlying mechanism (1,2). 

Although such a co-occurrence and the mechanisms that influence it are being discussed more and more, pain symptoms still cannot 

be well assessed or monitored and they are usually described by terms such as ‘medically unexplainable’, ‘functional’ or ‘psychosomatic’. 

The following statements may be made about the clinical characteristics of the symptoms (1): 

• They do not conform to the anatomic localizations which would help explain their causes. 

• They may vary in severity and location. 

S81


• Pain symptoms occur in 1/5 – 1/3 of patients with depression. These ratios are approximately 4 times higher than the ratios of those 

with no depression. The ratios in the literature about pain symptoms in patients with depression are approximately 65% on average (3). 

• Chronic pain is a significant individual risk factor for suicide and self-injury. 

• Chronic pain results in increases in treatment costs and a poorer outcome. 

• The presence of pain as a residual symptom is the strongest predictor of recurrence. 

It should be kept in mind that chronic pain, which is considered as being ‘functional’ in terms of the mechanisms involved in having pain 

during depression, is medically unexpected, self-generated and associated with vulnerability to pain. Therefore, central factors should 

play a leading role in experiencing it (4). Living with pain causes negative emotions, but beyond that, continuous pain is a physical 

symptom of depression. A neurobiological explanation of experiencing these two situations concurrently is not all that difficult when the 

broadness and diversity of the mechanisms involved in experiencing depression are taken into consideration (5). 

The mechanisms involved in this co-occurrence may be summarized as follows: 

• The connection between the emotional and somatic (e.g. pain) symptoms of depression is probably set up through the HPA axis. This 

system plays an important function in vulnerability to stress. 

• 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 

pain pathophysiology (6). Monoamines regulate both mood symptoms and sensations of pain. 

• Pain stimuli are carried from the periphery to the CNS by primary afferent fibers and are regulated by stimulating glutamate and 

suppressor GABA. 

• The sub-cortical areas involved are the hypothalamus, periaqueductal gray matter, raphe dorsalis and locus coeruleus. These areas are 

also regulated by 5HT and NA. 

• Cortical processing of a pain sensation is carried out in the relevant areas of the cortex. 

In conclusion, it is obvious that common pathophysiological processes underlie the co-occurrence of depression and somatic pain 

symptoms seen in this picture and it is important to take such pain symptoms into consideration in a comprehensive treatment approach. 

Key words: Pain, depression, clinical characteristics 

References: 

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. 

2. Von Knorring L, Ekselius L: Idiopatic pain and depression. Quality of Life Research 1994;3:557-568. 

3. Bair MJ, Robinson RL, Katon W, Kroenke K: Depression and pain comorbidity. A literatüre rewiev. Arch Gen Psychiatry 2003;163:2433-2445. 

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 

Danubina 2010;22:4-13. 

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. 

6. Wise TN, Fishbain DA, Holder-Perkins V: Painfull physical symptoms in depression: a clinical challenge. Pain Med 2007;8 (suppl. 2):75-82. 


[PS-16] 

Symposium Title: Marijuana; from mellow to madness 

Effect of cannabis use on cognitive functions 

Cüneyt Evren 

Bakirköy Training and Research Hospital for Psychiatry, Neurology, and Neurosurgery AMATEM, İstanbul, Turkey 

E-mail: cuneytevren@yahoo.com 

If we look at the data of recent years, probation admissions to AMATEM Istanbul, which are mostly related to cannabis use, have increased 

significantly; the number of first admissions/number of control admissions for 2008, 2009 and 2010 are 2318/24261, 3759/31862 and 

5639/30959, respectively. As for other psychoactive substances, the negative effects of cannabis use on cognitive functions are well 

known. Some cannabis-related cognitive function deficits improve after cessation of cannabis use, but growing evidence also suggests 

that other deficits persist after cannabis is discontinued and may hinder an individual’s ability to make the best use of behavioral 

therapies, putting him or her at greater risk for relapse of cannabis use (1). 

Cannabis seems to continue to exert impairing effects in executive functions even after 3 weeks of abstinence and beyond. Although 

basic attentional and working memory abilities are largely restored, most enduring and detectable deficits are seen in decision-making, 




concept formation, and planning. Those subjects reporting chronic, heavy cannabis use show the most enduring deficits (2). One can 

suggest that some of these impairments are not completely reversible upon cessation of cannabis use and moreover may interfere with 

the treatment of cannabis addiction. Therefore, targeting cognitive impairment associated with chronic cannabis use may be a promising 

novel strategy for the treatment of cannabis addiction (3). 

While acute administration of cannabis to patients with schizophrenia exacerbates symptoms and cognitive impairments and may have 

enduring effects, cannabis has also been found to have some beneficial effects on cognition, at least in certain subgroups of patients (4). 

Cannabis using patients had better attention and executive functions than non-cannabis using patients at baseline and after one year of 

treatment in a representative sample of first-episode schizophrenia patients. Cannabis using patients appear to comprise a subgroup of 

patients with better premorbid adjustment and premorbid frontal cognitive functions (5). 

Thus, while cannabis use is traditionally associated with cognitive impairment, the relationship is more complex in the case of schizophrenia. 

Key words: Cannabis, cognitive functions 

References: 

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; 

37:117-25. 

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. 

3. Sofuoglu M, Sugarman DE, Carroll KM. Cognitive function as an emerging treatment target for marijuana addiction. Exp Clin Psychopharmacol 2010; 18:109-19. 

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 

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) 

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 

use and cognitive functioning in first-episode schizophrenia patients. Schizophr Res 2010;124:142-51. 


The differences between marijuana psychosis and other substance induced psychoses 

Mükerrem Güven 

Akdeniz University Research and Practice Center for Alcohol and Substance Addiction, Antalya,Turkey 

E-mail: mguven@akdeniz.edu.tr 

Psychosis may be observed in intoxication from cannabis, alcohol, opiates, inhalants, stimulants, amphetamines, hallucinogens, 

phencyclidine, anxiolytics, sedatives and hypnotics. The condition of psychosis may also occur due to abstinence from alcohol, anxiolytics, 

sedatives, and hypnotics (1). Although mostly alcohol-dependent psychotic disorders are reported, the cannabis-psychosis relationship 

arouses more interest among researchers. Hypomania and agitation are more frequently noted in cannabis users compared with users 

receiving other substances. The symptoms of cannabis-psychosis usually disappear with a decrease in cannabis use, but the true nature 

of perception (flashbacks) hallucinations may be re-lived. As distinct from psychosis depending on other substances, evidence regarding 

the relationship between cannabis usage and the first attack of schizophrenia is increasing (2). There are long-term clinical follow-up 

studies to distinguish the acute toxic psychosis revealed in cannabis users from psychoses similar to schizophrenia, and also some 

studies conducted on the assumption that “cannabis psychosis” is distinct from other psychoses caused by other substances. Auditory 

hallucinations and emotional blunting are reported less commonly in cannabis psychosis compared to non-substance dependent 

psychoses. In a study investigating cannabis-induced psychoses, no significant relationship was determined between usage and the onset 

age of receiving cannabis; however, it has been put forth that a relation exists between cannabis use, the length of addiction and the quality 

and amount of cannabis received (3). Capsi et al. have reported that the risk for cannabis-induced psychosis is high in people carrying 

the valine-158 allele of the catechol-O-methyltransferase (COMT) gene (2005). Abuse substances affect different neurotransmitters in the 

central nervous system (4). Positive psychotic symptoms such as paranoid delusions and hallucinations are observed in half of cocaine 

addicts. As the period of cocaine use increases, negative symptoms and paranoid psychosis can be recorded. Stimulants such as cocaine 

and amphetamine can reveal psychosis by increasing dopaminergic activity in the central nervous system (CNS). Cannabinoid-1 (CB-1) 

receptors are responsible for the effects of cannabis in the CNS. In the lateral putamen, pallidum and substantia nigra, CB-1 receptors 

are determined to be present in a high degree. Many neurotransmitter systems taking part in the etiology of schizophrenia, especially 

glutamatergic and dopaminergic systems, are affected by activation of the CB-1 receptor (5). Effects of substances on neurotransmission 

should be better investigated to understand how substance-induced psychotic disorder develops. 

Key words: Addiction, cannabis, psychosis, substance abuse 

S83


References: 

1. American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: APA. 

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. 

3. Makkos Z, Fejes L, Inczedy-Farkas G, Kassai-Farkas A, Faludi G, Lazary J. Clinical characteristics of cannabis-induced schizophrenia spectrum disorder. 

Neuropsychopharmacol Hung. 2011 Sep;13(3):127-38. 

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 

adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O methyltransferase gene: longitudinal evidence of a gene X 

environment interaction. Biol Psychiatry 2005; 15;57(10):1117-7. 

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. 


Selective serotonin reuptake inhibitors in the treatement of cannabis dependence 

Musa Tosun 

Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey 

E-mail: musatosun@hotmail.com 

Treatment of cannabis dependence should aim cannabis abstinence and psychosocial support as in general dependency treatment 

approach. 

The cannabis detoxification of the patient might be achieved by treatment interventions in hospital setting or following up the patient 

closely in outpatient setting. In outpatient setting, the regular urinalyses and close monitoring of the patient must be carried out. The 

metabolites of the cannabinoids could be detected in urinalysis from 3 days up to 4 weeks following the last use. 

Individual, family, and group psychotherapies might be beneficial while supporting the patient. Education is the most important element 

for both “abstinence” and “support programs,” as the motivation to quit and not to restart is primarily due to education on the effects and 

harmful consequences of cannabis abuse. Tranquilizer drugs might be efficient in short term withdrawal symptoms that might be seen 

in cannabis abusers or addicts. 

Selective serotonin reuptake inhibitors (SSRIs) as other antidepressant agents may be used in the treatment of depressive patients, who 

use cannabis as a self treatment for depression, and in co-morbid depression of cannabis use disorders or in depressive symptoms caused 

by cannabis abuse. In addition, SSRIs might also be used in the treatment of cannabis-induced anxiety disorders. 

There is growing interest in the use of antidepressants in cannabis abuse because of highly reported depression rates during the 

treatment of cannabis abuse or after the cessation. Nevertheless, there is a dearth of knowledge about the treatment of cannabis abuse 

with SSRIs. In a double blind placebo controlled study, fluoxetine has been reported to decrease the frequency of cannabis use in alcoholic 

patients with depression. 

References: 

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. 

1999 Jan-Feb;24(1):111-4. 

2. Hall W. & Degenhardt L. : Cannabis-Related Disorders. in Kaplan & Sadock’s Comprehensive Textbook of Psychiatry 8th ed. Lippincott Williams & Wilkins, 

Philadelphia, 2005. Vol. I: 1211-1220 

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. 



[PS-17] 

Symposium Title: Overcoming treatment resistance: An update 

Treatment strategies for treatment resistant depression 

Selçuk Aslan 

Gazi University, Medical School, Psychiatry Department, Ankara, Turkey 

E-mail: saslan@gazi.edu.tr 



Depression is a disorder with heterogenic etiology and variable clinical features. Response to the treatment is defined as a 50% reduction 

in admission symptoms. Recent studies with large numbers of patients have revealed that acute phase treatment should last for 6 weeks, 

including at least 4 weeks with effective dosages. Approximately 60% of patients have a response to the first antidepressant treatment. 

The remainder, 40% of patients, either has a partial response or they are non-responders (Fava 1996). 

At the end of 6 weeks with optimum treatment dosing, if symptoms have not reduced by 20-25%, patients are described as nonresponders 

and drug treatment should be switched to another type of antidepressant medication. Patients, who do not respond to 

trials of adequate dosages and periods of two or more different classes of antidepressant treatments, are considered as treatmentresistant 

depression (TRD). If there is a partial response to antidepressant treatment, waiting for couple of weeks is the rational approach. 

The patients who have high depression scores at the initial evaluation have relatively higher degrees of partial or non-response to 

antidepressant medications. These cases are more likely to have comorbid axis 1 and axis 3 physical disorders. An 8-12 week period of 

effective antidepressant treatment should be applied in these cases. Thase and Rush, proposed 5-stage-model for the description of TRD 

(1997). Later in the STAR D study, Rush et al. developed sequences of treatment alternatives for relieving depression (Rush et al. 2003). 

On the other hand, increasing drug dosages results in more side effects and adverse reactions. Some patients may be low metabolizers 

and higher doses may result in significant side effects. Also fast metabolizer patients may respond to higher doses of medications. Efficacy 

of atypical antipsychotics, stimulants, pindolol, lithium, and lamotrigine have been tested for augmentation in ongoing treatment for TRD 

in clinical trials (Caravalho et al 2009). In severe cases with no response or partial response to treatment, inpatient treatment should be 

considered. 

Non-responders or partial responders can be treated with electro convulsive therapy with anesthesia or non-responders can be treated 

with rTMS (Paul et al 2006). Selected non-responsive cases may be treated with more invasive techniques such as deep brain stimulation 

or vagus nerve stimulation. Biological predictors should be identified to irecognize patients who will not respond to two adequate trials 

of different antidepressant. 

In addition, psychotherapeutic interventions during the treatment period, such as observing and revealing automatic thoughts, 

assumptions, and basic beliefs and depressive schemas, should be evaluated and behavioral and cognitive interventions can be applied. 

Activity scheduling and participating in regular exercise might also be helpful to some degree. 

Key words: Depression, treatment resistant depression 


Treatment resistant psychiatric disorders and trauma history 

Mehmet Akif Ersoy 

Ege University School of Medicine, Department of Psychiatry, Izmir, Turkey 

E-mail: akifersoy@gmail.com 

Although many clinicians depending on their experience will agree that childhood trauma history will cause treatment resistance 

regardless of the diagnosis, studies investigating this issue directly are scarce. During our search of literature we have found publications 

on the relationship between childhood trauma and treatment resistance in a few disorders such as obsessive compulsive disorder (OCD), 

major depression, and bipolar affective disorder. One study reported that 82% of OCD cases had a history of childhood trauma. In this 

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 

PTSD criteria. It is noticeable that those who had major depression or borderline personality disorder, in addition to OCD, had a higher 

risk of having comorbid PTSD. Treatment resistant OCD cases should be screened for PTSD and having comorbid major depression and/ 

or borderline personality disorder helps to predict PTSD and may help to determine the severity of the illness. 

S85


An indirect approach is looking for comorbidity of trauma related disorders in treatment resistant cases. One study has pointed out that 

OCD cases with comorbid PTSD have worse treatment outcomes. A meta-analysis study has revealed that childhood trauma not only 

effects lifetime risk of major depression, it also negatively effects severity of clinical parameters and results of treatment. This particular 

study, which included 16 epidemiological studies (23544 cases), showed that childhood abuse is related to recurrent and persistent 

depressive episodes. Another meta-analysis of 10 clinical studies with a total of 3098 cases, found that childhood abuse is related to 

absence of remission and absence of treatment response in depression. 

In bipolar disorder, those who have had childhood trauma, had earlier onset of illness, more severe current symptoms of mania or 

depression and more frequent episodes of depression. Half of adult bipolar disorder patients were found to have severe childhood trauma. 

In patients with early childhood trauma such as early loss of parents and physical or sexual abuse or neglect, psychotherapy alone had 

favorable results compared to monotherapy of antidepressants, while interestingly combination of psychotherapy and pharmacotherapy 

was slightly more effective than psychotherapy alone. Researchers have stressed that psychotherapy must be included in the treatment 

of chronic depression patients with childhood trauma. 

Studies which directly investigate the relationship of treatment resistance and childhood trauma are scarce. Some comorbid conditions, 

such as personality disorders, that complicate treatment of depression are known to be related to childhood trauma. 

As a result, we can with great confidence state that childhood trauma is related to treatment resistance in most psychiatric conditions. 

Especially in cases of treatment resistance, childhood trauma should be investigated and appropriate treatment modalities should be 

added to the treatment regime. 

Key words: Treatment resistance, childhood trauma 


Pyshosocial approaches for treatment resistant symptoms in patients with schizophrenia 

Mustafa Yıldız 

Kocaeli University School of Medicine, Department of Psychiatry, Kocaeli, Turkey 

E-mail: myildiz60@yahoo.com 

One of the main goals in the treatment of schizophrenia is to increase psychosocial functioning and to provide a satisfying life for patients 

with schizophrenia who have persistent symptoms although all treatment efforts, including ECT, had been performed. Whatever the 

clinical conditions of the patients are, they have a right to live in dignity in their community like other people. The emphasis in psychiatric 

rehabilitation approaches is on enhancing psychosocial functioning and quality of life of patients. Increasing the functioning of patients 

depends on controlling symptoms as much as possible and preventing exacerbations. Patients should learn and practice coping skills 

(humming or singing, reading aloud, thinking “stop”, listening to the radio, watching TV, doing favorite hobbies, telling the voices to go 

away, doing physical exercise, going to movies etc.) for their persistent symptoms. Sometimes it may be necessary to use behavioral 

techniques; for example, a patient showing 20 aggressive behaviors due to command hallucinations a week, showed on aggressive 

behavior a month after applying a behavior modification program. Patients should be placed in a program, in which their healthy 

aspects can be developed and keep them in continuing daily activities, so that they become empowered. All these results can take place 

by collaboration and coordination of different services. Being provided a safe environment, getting positive feedback, participating in 

occupational activities and working in a less stimulating milieu are also important for patients. 

It could be possible for patients to live a more satisfying and more normal life by integrating treatment and rehabilitation services. The 

elements of integrated approaches are: patients’ participation in treatment and the maintenance of treatment, development of treatment 

alliances, teaching illness management, using cognitive behavioral treatment methods, modifying new resources to attain personal 

goals, accommodating community resources, establishing relationships with psychosocial clubs, involving families in the treatment, and 

providing personal support services (case management), supported employment, supported residence, and peer supports. 

Key words: Schizophrenia, persistent symptoms, functioning, rehabilitation 



[PS-18] 

Symposium Title: Chronobiotics and chronotherapeutics in psychiatry 

The use of sleep deprivation in the treatment of depressive disorders 

Adem Aydın 

Department of Psychiatry, Yuzuncu Yıl University, Van, Turkey 

E-mail: adem.dr@gmail.com 



Sleep deprivation has been used for exploring functions of sleep among healthy individuals and for treating patients suffering from 

depressive symptoms. Sleep deprivation is a rapid, effective and brief therapeutic alternative. Two types of sleep deprivation applications 

have been implemented; one is deprivation of sleep for whole night and the other is partial deprivation of sleep in the second part of 

the night. Although various hypotheses have been developed pertaining to the treatment potential of sleep deprivation in depression, 

the mechanisms underlying the process are still obscure (1). Early systematic research conducted by Pflug and Tolle proposed that 

patients characterized by endogenous depressive symptoms receptive to sleep deprivation have deficits in their circadian systems and 

sleep deprivation aids at ameliorating the dysregulation in the biological rhythm (2). Sleep deprivation and REM sleep deprivation act 

like antidepressants and some antidepressants have suppressing effects on REM sleep. Hence the role of REM sleep on the development 

of depression has received more attention. The reduction of REM latency and REM intensity are prominent features in patients with 

depression. Sleep deprivation reverses these two effects (3). 

The psychological response to sleep deprivation seems to occur regardless of diagnostic category such as endogenous-reactive, 

psychotic, nonpsychotic, unipolar, bipolar, schizoaffective, or seasonal (4). Merely diurnal variation (soothing of affect is typical in patients 

with depression in the later hours of daytime) and chronobiological differences are substantial in the psychological response to sleep 

deprivation (5). 

About 50-60 percent of patients with depression are prone to reflect antidepressant influences after one-night of sleep deprivation 

therapy. Deceleration in symptom severity as well as amelioration in suicidal thoughts occurs. The temporary antidepressant influence of 

the initial application does not predict inadequacy of further applications. If applications of sleep deprivation are continued one or two 

times per week, it has been claimed that it is likely to provide effective prophylaxis (6). 

Although sleep deprivation provides a rapid psychological response and a potent influence, its application is not prominent in major 

depression. Sleep deprivation can be qualified as an awkward method, because the application requires constant monitoring and to 

ensure wakefulness of patients as well as carrying a relapse risk in fiesta. The most prominent advantage of sleep deprivation compared 

to other medications and ECT is that it causes rapid and apparent improvement in affect. Therefore the pros and cons of sleep deprivation 

should be taken into account in treatment planning. 

Key words: Depression, sleep deprivation, treatment 

References: 

1. Rechtschaffen A. Current perspectives on the function of sleep. Perspect Biol Med 1998;41:359-390. 

2. Pflug B, Tolle R. Disturbance of the 24 hour rhythm in endogenous depression and treatment of endogenous depression by sleep deprivation. Int 

Pharmacopsychiatry 1971;6:187-196. 

3. Giedke H, Schwarzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev 2002;6:361–377. 

4. Wirz-Justice A. Biological rhythm disturbances in mood disorders. Int Clin Psychopharmacol 2006;21:11-5. 

5. Selvi Y, Gulec M, Agargun MY, Besiroglu L. Mood changes after sleep deprivation in morningness–eveningness chronotypes in healthy individuals. J Sleep Res 

2007;16:241–4. 

6. Hemmeter UM, Hemmeter-Spernal J, Krieg JC. Sleep deprivation in depression. Expert Rev Neurother 2010;10(7):1101-15. 


S87


Psychotropic drugs effecting biological rhythm (Chronobiotics) 

Elif Oral 

Department of Psychiatry, Faculty of Medicine, Atatürk University, Erzurum, Turkey 

E-mail: oralelif@yahoo.com 

Biological clocks such as circadian, ultradian, and infradian rhythms have their own organizations, independently from environmental 

conditions. Although there is biological sustainability, psychiatric disorders and also psychotropic medications have important effects 

on the synchronization of biological clocks. Various biological mediators such as glutamate, γ aminobutyric acid, histamine, dopamine, 

acetylcholine, serotonin and their receptor systems take on the mediation of inner clocks via psychotropic drugs. 

Histaminergic activity is highly increased during wakefulness. H1 antagonists, generally increase Slow-Wave Sleep and stage 2 sleep 

and reduce rapid eye movement sleep. Diphenhydramine can cause subjective sedation and decreased sleep latency with no effect 

on memory or learning processes. The long elimination half-lives of these drugs can result in next-day sedation and impairment of 

psychomotor and cognitive function the next morning. 

Benzodiazepines shorten sleep-onset latency, increase total sleep time and stage 2 sleep, and suppress rapid eye movement sleep and 

slow-wave sleep. The risk of rebound insomnia is greatest with rapid elimination of benzodiazepines. 

About 65% of major depressive disorder patients report sleep complaints. Based on polysomnography studies, sleep architecture is 

estimated to be disturbed in up to 90% of depressed patients. Except desipramine, all TCAs block H1 and α1 receptors to varying degrees. 

As a general rule, the noradrenergic TCAs (e.g. desipramine, protriptyline) are considered ‘activating’. These agents have a tendency to 

increase sleep-onset latency as well as to decrease total sleep time, associated with an increase in wake time after sleep onset. Paroxetine 

and fluoxetine clearly suppress REM sleep, both among healthy volunteers and depressed patients. Compared to other SSRIs, citalopram 

may be less activating and therefore less likely to disrupt sleep continuity. 

Lithium and valproate have many acute, subacute, and chronic effects on systems, at the cellular and molecular levels. Lithium treatment 

modifies circadian rhythms in humans and in most animals, primarily by lengthening the period of the cycle. 

Most of the sleep-promoting effects of antipsychotic drugs have been related to their potency to antagonize α adrenergic, histaminergic, 

or cholinergic neurotransmission. Among classical antipsychotics, drugs having these properties, such as phenothiazines and 

thioxanthenes, are clearly sedative and promote sleep. Among atypical antipsychotics, drugs having this pharmacodynamics profile are 

olanzapine, clozapine, and quetiapine. Clozapine and olanzapine increase total sleep time and sleep efficiency and have no clear-cut 

effect on REM sleep. 

Key words: Psychotropic drugs, biological rhythm 


A general overview of chronotherapeutics 

Yavuz Selvi 

Department of Psychiatry, Yuzuncu Yil University, Van, Turkey 

E-mail: dryavuzselvi@yahoo.com 

The sleep-wake cycle occurs because of the two independent but additive processes, homeostatic sleep and circadian processes. Circadian 

rhythms play a significant role in regulating daily behavioral rhythms, cortisol and melatonin secretions, body temperature, sleep/wake 

cycle, alertness and performance levels. Disrupted synchronization of circadian rhythms impairs cognition, behavior and mood with 

deterioration of sleep-wake cycle and social rhythms. Some clinical and neurobiological findings suggest circadian dysregulation in 

depressive patients. Diurnal variation of mood, early morning awakening, phase advance for body temperature, cortisol, latency of the 

first phase of REM sleep for several other hormones and monoamines or their metabolites and sleep disturbances are core features of 

depression that have linked depression with circadian rhythm function (1,2). 

Clinical and neurobiological findings have promoted the idea that the restoration of circadian rhythm could have an antidepressant effect. 

The term, chronotherapeutics, refers to biologically-based, non-pharmaceutical and clinical interventions that act on disrupted biological 

rhythms in order to achieve therapeutic effects in the treatment of psychiatric conditions (3). Delayed therapeutic effects, tolerability, 

side effects, and drug–drug interactions of pharmacotherapeutic agents, as well as pregnancy and the postpartum period, prevent 

antidepressant use and promote chronotherapeutic interventions. 




Chronotherapeutics are applied effectively in endogenous, reactive, unipolar, bipolar, schizoaffective depression, depression in the 

elderly, secondary depression, depression in pregnancy and postpartum depression. The target of chronotherapeutic interventions, as 

in antidepressant drug treatments, is to modulate the same neurotransmitter systems (5-HT, NA, DA), the same brain structures, and the 

same clinical symptoms and findings more rapidly and with fewer side effects. These interventions include wake therapy (the use of 

prolonged periods of wakefulness; partial or total sleep deprivation), shifting of sleep time (sleep phase advance therapy; stepwise shift 

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 

bipolar mania and rapid cycling patients. When the therapeutic effects are transient, different chronotherapeutic interventions can be 

combined to maximize antidepressant response and prevent relapse. Psychiatrists should consider chronotherapeutic interventions as 

strong and safe treatment approaches (3,4). 

Key words: Biological rhythm, chronotherapeutics, mood, sleep, sleep deprivation 

References: 

1. Lack LC, Wright HR. Chronobiology of sleep in humans. Cell Mol Life Sci. 2007; 64(10):1205-15. 

2. Selvi Y, Besiroglu L, Aydin A. Chronobiology and Mood Disorders. Current Approaches in Psychiatry 2011; 3(3):368-386. 

3. Benedetti F, Barbini B, Colombo C. Smeraldi E. Chronotherapeutics in a psychiatric ward. Sleep Med Rev. 2007;11(6):509-22. 

4. Hajak G, Landgrebe M. Time and depression: when the internal clock does not work. Medicographia. 2010;32:146-151. 


Bright light therapy in treatment of depressive disorders other than seasonal affective disorder 

Mustafa Güleç 

Department of Psychiatry, Ataturk University, Erzurum, Turkey 

E-mail: mustafagulec78@yahoo.com 

Studies of light therapy for non-seasonal depression have a history at least as long as studies of seasonal affective disorder (SAD), but 

on the whole the results have been less clear-cut (Tuunainen et al., 2005). The APA work group found, within its selection, positive 

evidence for efficacy except when light therapy and medication were combined (Golden et al., 2005). Studies completed by the time 

of the present congress clearly would have reversed that conclusion (Benedetti et al., 2003; Martiny, 2004; Terman, 2006). The strategy 

has been recommended by the Committee on Chronotherapeutics of the International Society for Affective Disorders (Wirz-Justice et 

al., 2005) and in an international response (Wirz-Justice et al., 2004) to a review of new antidepressants that overlooked light therapy, 

published in Science (Wirz-Justice et al., 2004). A difficulty with most non-seasonal studies has been their inability to confront the early 

hypothesis that light therapy is specifically tuned to patients with SAD as a countermeasure to long winter nights. Seasonality lies on a 

continuous dimension from noticeable (but not disturbing) to mildly, moderately and severely disturbing (Terman, 1988). SAD falls into 

the latter category, with major depressive episodes restricted to winter. In a far larger number of cases, recurrent or chronic depressions 

are exacerbated in winter but can occur at any time of year. Such patients provide moderate global seasonality scores (Rosenthal et al., 

1987) in comparison to higher scores for SAD. Thus, patients with non-seasonal depressions can still show seasonality, which might be 

the key to their response to light therapy. Subsequent to the aforementioned inconclusive meta-analysis of light therapy for non-seasonal 

depression (Tuunainen et al., 2005), some researchers conducted an investigation to clarify this issue with a patient sample in which 

depression was chronic and without any seasonal modulation (Goel et al., 2005). Under morning light therapy, the proportion of subjects 

with depression rating scale improvement of 50% or more was 0.60 vs. 0.10 for the low-output negative air ionizer placebo. Moreover, 

there are also very recent reports claiming that bright light therapy alone is effective in some patient groups with non-seasonal major 

depression (Kripke, 2011a; Kripke, 2011b; Martiny, 2011). Now, we can begin to surmise that light therapy for seasonal and non-seasonal 

depression is equally effective. Perhaps the patients with non-seasonal depression are light deprived at any time of year, and this situation 

results in exacerbation of circadian rhythm phase delay, given the absence of the critical early morning light signal that synchronizes the 

internal clock to local time. Such delay may be depressogenic regardless of the season. However, the growing concern about medication 

side effects would seem to fit well for our old-new alternative (Terman, 2007). 

Key words: Seasonal affective disorder, non-seasonal affective disorder, depression, treatment, bright light 


S89


[PS-19] 

Symposium Title: Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or 

neurodegenerative? Review of recent data 

Is the effect of psychotropic drugs neurodegenerative or neuroprotective? 

Ömer Aydemir 

Department of Psychiatry, Celal Bayar University, Manisa, Turkey 

E-mail: soaydemir@hotmail.com 

Various stress experiences affect gene expression of neurotrophic/growth factors in the hippocampus. Among the neurotrophic factors, 

brain-derived neurotrophic factor (BDNF) has the most prominent role. With the stress producing effects of early life traumas, the level 

of BDNF decreases and susceptibility to depression develops. Recurrent and insufficiently treated depressive episodes have further 

impact on decreased BDNF and increase neuronal atrophy. Decreased level of BDNF in patients with major depressive disorder has been 

demonstrated in many studies and BDNF levels increase after antidepressant treatment, along with symptom recovery, in comparison 

to those seen in healthy control subjects. This increase cannot be achieved in patients that do not respond to antidepressant treatment. 

The neuroprotective effect of antidepressants are mediated by mitogen activated protein kinases/extracellular regulated kinases (MAPK/ 

ERK) and wingless/glycogen synthase kinases (Wnt/GSK). In a meta-analysis, 23 studies were evaluated and data for 1504 patients were 

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, 

the change in the level of serum BDNF after antidepressant treatment was independent of the change in depressive symptomatology, 

duration of treatment, and history of antidepressant use. As clinical improvement obtained with antidepressant treatment persists, the 

level of serum BDNF remains unchanged. 

Beside antidepressants, mood stabilizers, especially lithium have been studied with respect to neuroplasticity. Neuroprotective effects of 

mood stabilizers are mediated by increasing transcriptional activity of (cAMP response element binding protein) CREB, inhibiting GSK-3B 

and increasing the expression of BDNF. In studies both with lithium and valproate, increased cerebral grey matter volume was reported. 

In lithium studies increases in left anterior cingulate volume, right anterior cingulate volume, hippocampal volume and amygdala volume, 

and in valproate studies an increase in left anterior cingulate volume were found. Both mood stabilizers are associated with increased 

hippocampal N-acetyl aspartate level. 

Antipsychotic drugs do not have a group effect. While haloperidol does not have any effect on phosphorilated ERK (pERK), olanzapine 

increases it. Haloperidol also decreases the level of BDNF and is suggested to have neurotoxic effects. Among the other antipsychotics, 

clozapine, quetiapine and risperidone prevent cell death. It has been demonstrated that clozapine and quetiapine increase the level of 

BDNF. Quetiapine is suggested to increase proliferation of mature neurons, although there is no evidence that clozapine and olanzapine 

have the same effect. 

Key words: Psychotropic drugs, neuroplasticity, neurodegeneration, neuroprotective effect 


Effect of psychotherapy on neurogenesis 

Mine Özmen 

Istanbul Universit Cerrahpasa Medical Faculty, Department of Psychiatry, İstanbul, Turkey 

E-mail: drmineozmen@yahoo.com 

Adverse life experiences in childhood are considered to be associated with emotional and cognitive development as well as brain 

structure and functions. It is suggested that they might reduce neurogenesis, which in turn may cause memory, learning, functional 

stress response disturbances. It is known that hippocampal neurogenesis is affected by stress, hormones, aging, environment and activity. 

Exposure to acute or chronic stress may result in suppression of one or more phases of neurogenesis. In animal studies, reduction of 

neurogenesis in the caudal part of the hippocampus was shown after maternal separation of 3-weeks old rats. Although it was reported 

that the suppression was reversible after appropriate time and treatment in some studies, some other writers suggest that early life stress 

in the first 2 weeks can cause irreversible reduction in neurogenesis. Besides, there is an argument that neurogenesis can not increase by 

learning in the animals which were exposed to prenatal stress. One suggested reason for this lifetime persistency of reduced neurogenesis 

is that stress occurring in early childhood coincides with the development of dentate gyrus. It has been shown that corticosteroids 




inhibit neurogenesis in the hippocampus, subventricular zone and olfactory epithelium and this inhibition can remit by pharmacological 

treatments. There are case reports and studies with limited cases, which suggest that effective psychotherapy can reduce symptoms and 

this reduction can change the in the hypothalamic-pituitary axis. It may be hypothesized that in an effective psychotherapy process, 

coping with stress, new relationship experiences and learning can increase neurogenesis and this may be one of the mechanisms of 

effectiveness of psychotherapy. This hypothesis should be tested with animal and human studies in which neurobiology; psychiatry and 

neuroscience disciplines can interact and work together. 

References: 

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 

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. 

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 

PTSD. Psychoneuroendocrinology (2007) 32, 619–626 


Are the effects of psychopharmacological and other therapeutic approaches neuroregenerative or 

neurodegenerative? Review of recent data and effects of physical exercise 

Hakan Balıbey 

Ankara Military Hospital, Psychiatry Clinic, Ankara, Turkey 

E-mail: hbalibey@gmail.com 

Research in humans and animals has shown that exercise improves mood and cognition. Physical activity has been consistently shown 

to be associated with improved physical health, life satisfaction, cognitive functioning, and psychological well-being. Conversely, physical 

inactivity appears to be associated with the development of psychological disorders. 

Physical activity also causes a robust increase in neurogenesis in the dentate gyrus of the hippocampus, an important brain area 

for learning and memory. The results of epidemiological studies (cross-sectional, prospective and retrospective) support a positive 

relationship between cognition and physical activities. They include supramolecular mechanisms (e.g. neurogenesis, synaptogenesis, 

and angiogenesis) which, are in turn controlled by molecular mechanisms, such as brain-derived neurotrophic factor (BDNF), insulin-like 

growth factor (IGF-1), hormones and second messengers. 

An active lifestyle might prevent or delay loss of cognitive function with aging or neurodegenerative disease. Exercise could involve 

common cellular pathways important for neurogenesis, cell survival, synaptic plasticity and vascular function. Optimal maintenance of 

brain health might depend on exercise. The beneficial effects of exercise are likely to be mediated in part by hippocampal neurogenesis. 

Further investigation into the functional significance of neurogenesis, by designing behavioral tasks that are specific for the dentate gyrus, 

will help to determine the relative contribution of the new cells. 

Exercise influences brain vasculature. In particular, physical activity increases the proliferation of brain endothelial cells and angiogenesis 

throughout the brain. Growth factors such as insulin-like growth factor (IGF) and vascular endothelial growth factor (VEGF) play an 

important role in the angiogenic and neurogenic effects of exercise on the brain. The neurotrophin BDNF is considered to be the most 

important factor upregulated by physical activity because it has an important role in synaptic plasticity and cell genesis, growth and 

survival. Interestingly, there is a positive interaction between BDNF expression and serotonin. Serotonin receptor activation enhances 

BDNF expression in hippocampal cells, BDNF is recognized to be a key protein modulating brain plasticity and it is distributed widely 

throughout the brain. In humans, serum BDNF concentrations rise after exercise. 

The involvement of such pathways, particularly in the hippocampus, may in turn lead to an improvement in cognitive function, 

enhancement of psychological well-being, and a decrease in the risks of Alzheimer’s disease (AD) and dementia as well as decreases in 

symptoms of depression and anxiety. While intense exercise (as observed in conditions such as “excessive exercise” and “overtraining 

syndrome”) leads to a lessening of anxiety, these mood variations are more related to the construct of depression than to the construct 

of anxiety. 

Physiological effects of exercise and the benefits of exercise on psychiatric disorders will be discussed in the light of current literature in 

this presentation. 

Key words: Physical activity, exercise, BDNF, hippocampal neurogenesis, neuroregeneration, neurodegeneration, synaptic plasticity, cognition, 

mood 

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References: 

1. Lista I, Sorrentino G. Biological mechanisms of physical activity in preventing cognitive decline. Cell Mol Neurobiol. 2010;30(4):493-503. 

2. van Praag H. Exercise and the brain: something to chew on. Trends Neurosci 2009;32(5 ):283–90. 

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 

T.R, Ahrendsen J.T at all. The Journal of Neuroscience, 2011; 31(32):11578 –86. 

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 

with dementia. Clinics (Sao Paulo). 2011; 66(4): 613–8. 

5. Ma Q. Beneficial effects of moderate voluntary physical exercise and its biological mechanisms on brain health. Neurosci Bull. 2008;24(4):265-70. 

6. van Praag H. Neurogenesis and exercise: past and future directions. Neuromolecular Med. 2008;10(2):128-40. 

7. Ang. ET, Tai YK, Lo SQ, Seet R, Soong TW.Neurodegenerative Diseases: Exercising Toward Neurogenesis and Neuroregeneration. Front Aging Neurosci. 2010; 2: 25. 

8. Tomporowski P. D., Lambourne K., Okumura M. S. Physical activity interventions and children’s mental function: an introduction and overview. Prev Med. 2011; 

52(Suppl 1): S3–S9. 

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 

Psychopharmacol 2000; 10(4):194-200. 


[PS-20] 

Symposium Title: Controversial topics in eating disorders 

Comorbidities in eating disorders 

Atila Erol 

Sakarya University, School of Medicine, Department of Psychiatry, Sakarya, Turkey 

E-mail: erolatila@gmail.com 

Patients with eating disorders exhibit high rates of psychiatric comorbidity and the number of comorbid psychiatric disorders is high. 

The treatment of co-occurring psychiatric problems in eating disordered patients is essential for good clinical management and the 

outcome of treatments. Higher rates of comorbidity often mean greater severity, treatment resistance and poor outcomes in eating 

disorders. The most prevalent Axis I disorders seem to be mood and anxiety disorders, alcohol and substance abuse, and bipolar disorder. 

Axis II disorders are also common. At least 80% of anorexia nervosa (AN) or bulimia nervosa (BN) patients have at least one additional 

psychiatric disorder over their lifetime. Mood disorders are very common among patients with AN. Major depressive disorder occurs in 

50-70% of AN patients. Bulimic patients have 52-75% affective disorder, with 63% having major depression. Lifetime prevalence rates of 

major depression in BN are 50-65%. 

Among study samples with restricting and binging /purging anorexia nervosa, prevalence rates of any anxiety disorder are found to be 

between 24% and 71%, respectively. Among patients with BN prevalence rates for any anxiety disorder, social phobia, generalised anxiety 

disoder (GAD) or panic disorder are reported to be 36%, 17%, 12% and 10% respectively. The approximate rates of any anxiety disorder in 

BN are reported to be between 57 and 75 %. 

Thirty-five percent of restricting AN patients have obsessive compulsive disorder (OCD) and binging/purging AN patients have 44% OCD. 

BN patients have comorbid OCD 40% of the time. Lifetime prevalence rates of substance abuse in AN ranged from 12% to 18% and in 

BN the rates ranged from 30% to 70%. The results of clinical studies indicate that patients with BPD have higher rates of eating disorders 

compared with the general population. Rates of lifetime BPD in eating disorders patients are variable but higher than rates of BPD in the 

general population. Among eating disorder patients post-traumatic stress disorder rates were found between 8% to 11%. 

Key words: Eating disorders, anorexia, bulimia, comorbidity 



Psychopharmacological treatments in eating disorders 

Alican Dalkilic 

St. Elizabeths Hospital, Washington, DC 20032, USA 

E-mail: drdalkilic@gmail.com 



Pharmacological treatment options have limited evidence of benefit in treatment of eating disorders, yet a comprehensive psychiatric 

evaluation besides a physical exam and basic screening tests (complete blood count (CBC), basic metabolic panel, Mg, P, thyroid 

stimulating hormone (TSH), lipid panel, pregnancy test, urine analysis (UA), urine drug screen (UDS), ECG, and Dexa scan) should be 

conducted. Establishing a therapeutic alliance with empathy, positive regard, reassurance, and support (1) sets up the foundation for a 

successful treatment process. The patient’s safety should be evaluated with particular attention paid to suicidal ideation, plans, intentions, 

history of attempts and impulsive or compulsive self-harm behaviors. After assessing eating disorder symptoms, signs, and behaviors and 

the general medical condition of the patient a decision about treatment site (specialized inpatient unit, residential treatment or partial 

hospital program, intensive outpatient, or outpatient care) can be made. In eating disorders in general, but especially in adolescences with 

eating disorders, inclusion of the family and primary support group in the treatment process is essential. 

The treatment options and goals in eating disorders include nutritional rehabilitation, psychosocial interventions, medications, and other 

somatic treatments. Nutritional rehabilitation aims to restore weight, normalize eating patterns, achieve normal perception of hunger 

and satiety cues, and correct biological and psychological problems caused by malnutrition (1). Psychosocial interventions include 

individual and group based cognitive behavioral and interpersonal therapies, acceptance and mindfulness therapies, and psychodynamic 

approaches, as well as nutritional counseling, dialectical behavioral therapy (DBT), and family therapies. There are more therapies with 

specific names such as mealtime support and multifamily group therapy, but they use similar approaches to the previously mentioned 

ones. 

Although there is clinical evidence about use of antidepressants in treatment of eating disorders (especially SSRIs, calcium, vitamin D, 

and zinc and limited data about benzodiazepines, mood stabilizers, and atypical antipsychotics), so far only fluoxetine is approved for the 

treatment of bulimia nervosa by the Federal Drug Administration (FDA) 1,2). Sertraline has been found to be effective in a randomized 

and controlled trial, as well. Medications have not been proven to be more effective than psychosocial interventions in treatment of eating 

disorders so far. Some studies have found the combination of CBT with medication to be more effective. Topiramate has been found to 

be effective in some small controlled trials especially in reducing binging behavior, but due to potential side effects is should be reserved 

as a secondary medication (1,3). Topiramate or zonisamide are prescribed to target binging behavior and also for weight reducing effects 

in patients who may benefit from weight loss. Bright light therapy is another intervention demonstrated to decrease binge frequency in 

several controlled trials (1). 

Although clinicians are advised to use caution when prescribing medications to eating disorder patients due to potentially dangerous 

medical co-morbidities, some medications should be avoided or used only as last resorts. Bupropion is contraindicated in bulimia due to 

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 

used, adverse events should be monitored closely. Sibutramine was taken off the market in USA in 2010 due to cardiac adverse events. In 

addition, medications with a narrow therapeutic range such as lithium should be avoided. Benzodiazepines, especially the ones with high 

addiction potential, should not be used in patients with addiction risk. In clinical practice many eating disorder patients end up being on 

multiple medications due to high rates of co-morbidity with anxiety and mood disorders, substance abuse and dependence conditions, 

trauma related disorders, and personality disorders. Beside reviewing pharmacological treatment options in eating disorders we will also 

discuss the management of cases with co-morbid conditions. 

Key words: Eating disorders, pharmacology, pharmacotherapy, treatment, pharmacological treatment 

References: 

1. American Psychiatric Association Practice Guidelines for the Treatment of Psychiatric Disorders Compendium. American Psychiatric Association 2006 1,612 

pages ISBN 978-0-89042-385-1. 

2. Pharmacotherapy of eating disorders. Jackson CW, Cates M, Lorenz R. Nutr Clin Pract. 2010 Apr;25(2):143-59. Review. 

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. 


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Obesity and impulsivity 

Bilge Burçak Annagür 

Department of Psychiatry, Selcuk University, Selcuklu Medical School, Konya, Turkey 

E-mail: bilgeannagur@yahoo.com 

Obesity is not inlcuded in eating disorders characterized by the DSM-IV classification of the American Psychiatry Association. Current 

clinical diagnosis depends on body mass index (BMI). Although it was not evaluated among eating disorders, it presents psychological 

characteristics seen commonly in eating disorders. Characteristics related with eating disorders such as low self-esteem, body 

dissatisfaction, perfectionistic attitudes, impulsivity and disinhibition have also been observed in obese patients (1,2). Obese patients are 

divided into two subgroups, with or without binge eating disorder (BED). Body weights of subjects with binge eating disorder are related 

to their overeating and psychopathologies, especially depression, are more frequent compared to the other group. 

Aggressiveness and anger are involved in significant psychopathological characteristics common in patients with eating disorders (3). 

Some researchers suggested that impaired eating behavior is related to low self-esteem and high self-directed hostility. Problems about 

revealing their anger were detected among these individuals. Besides, problems in controlling the expression of anger, accompanying 

impulsive explosive behaviors are also present (4). 

The current status of obesity treatment is not satisfactory. Some treated individuals regain the lost weight in a short time (5). Many 

researchers are investigating approaches to keep off the lost weight with treatment strategies to lose weight. In previous reports, it has 

been demonstrated that most obese individuals returned back to their basal BMIs or to higher values within 1-5 years (6). Nowadays, the 

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 

predictor of relapse in obesity treatment (5). Obese subjects are suggested to be more impulsive than lean ones. Impulsive characteristics 

are higher in obese patients with BED (7). Impulsive people appear to have no control over their behaviors on eating and they have more 

interest in food with higher calories. Impulsivity is also considered as a predicting factor among patients who quit treatment. In a survey 

among the children between the ages of 8-12 years in the Netherlands, impulsivity was measured by behavior and the results of treatment 

were evaluated. As a result, it was demonstrated that impulsive children lose less weight compared to the others. It was also concluded 

that impulsive children are more prone to eating delicious foods; therefore more attention should be given to their dietary control (5). 

Another issue supporting the relationship between obesity and impulsivity is the occurrence of obesity in children with attention deficiency 

and hyperactivity disorder (ADHD) (8). ADHD was detected in most of the children (58%) who were receiving obesity treatment. Also, the 

BMI of children with ADHD was higher than the control group (9). In addition, there is evidence for decreased levels of D2 receptors in 

the striatum of obese subjects (10-13). With regard to the therapeutic implications, recent studies indicate that methylphenidate (MPH), 

a drug widely used for ADHD, reduced overall energy intake with a selective reduction in dietary fat (14,15). Dopamine (DA) exerts 

neuromodulatory influences over behavior and cognition via the fronto-striato-cerebellar circuitry and pharmacotherapy is thought to 

target these systems to ameliorate problems with impulsivity, inattention and hyperactivity. To explain the comorbidity of ADHD and 

obesity, it has been hypothesized that a predisposition to glucose starving and obesity is due to inadequate dopaminergic activity in the 

reward center of the brain. Consumption of large quantities of carbohydrates (carbohydrate binging) stimulates production and usage of 

dopamine within the brain and it results in a kind of therapeutic effect (16,17). 

All this information should guide the planning of treatment. Specific cognitive behavioral approaches developed for the treatment of 

impulsive behavior could contribute much to the treatment of obesity(18). 

Key words: Eating disorders, impulsivity, obesity 


Efficacy of psychotherapy in bulimia nervosa 

Başak Yücel 

Department of Psychiatry, Istanbul University, Istanbul, Turkey 

E-mail: byucel@superonline.com, basakyucel@gmail.com 

The efficacy and importance of psychotherapy in bulimia nervosa have been examined in many studies recently. Most of the eating 

disorder experts acknowledge the notion that psychological interventions are the best available treatment for BN. Although different 

psychotherapeutic recommendations have been offered by NICE (National Institute for Health and Clinical Excellence) and APA (American 




Psychiatric Association), several treatment approaches received strong endorsement for BN. Cognitive behavioral therapy (CBT) is 

recommended as an effective treatment for bulimic patients and considered the ‘treatment choice’ for BN and binge eating disorder (BED), 

it is also supported by strong evidence-based literature. 

With regard to the efficacy of CBT specifically in BN, in various studies CBT was associated with more improvements in bulimic and 

depressive symptoms of patients than symtoms of control patients in waiting-list and any other psychotherapy cases. In terms of general 

psychiatric symptoms, studies have not shown any difference between CBT and any other psychotherapy. 

Other psychotherapy choices have included interpersonal psychotherapy (IPT), dialectical behavior therapy, supportive and psychodynamic 

psychotherapy, and certain self-help approaches. Thus, in clinical practice there have been a number of evidence-supported treatments 

for BN patients. 

IPT is a psychological treatment for BN that has demonstrated long-term outcomes that are comparable to those for CBT. Currently, 

all controlled studies of IPT for BN have been comparison studies with CBT. Although there have been only few controlled trials of 

psychodynamic treatment of eating disorders, these reports yielded important findings in this field. Standard dialectical behavior therapy 

(DBT) has been adapted to address a variety of problematic behaviors associated with emotion dysregulation in bulimia nervosa and 

also DBT may be used in BN patients with comorbid borderline personality disorder. Beside these, the knowledge in the field of self-help 

treatments continues to develope. 

Key words: Bulimia nervosa, psychotherapy 


[PS-21] 

Symposium Title: Treatment approaches to comorbidities of ADHD 

Treatment approaches to psychiatric comorbidities of ADHD in children 

Tümer Türkbay 

GATA, Department of Child and Adolescent Psychiatry, Ankara, Turkey 

E-mail: tumerturkbay@yahoo.com;tturkbay@gata.edu.tr 

Attention-deficit hyperactivity disorder (ADHD) is highly comorbid with other psychiatric disorders. Each of the comorbid disorders 

modifies the overall clinical presentation and treatment response. Sometimes there can be more complex situations. For example, 

depressed children demonstrate diminished concentration and irritability and it may be difficult to differentiate from the cardinal 

symptoms of ADHD. Children with ADHD and comorbid disorders have poorer prognoses than those with ADHD alone. 

Both stimulant medications and atomoxetine markedly reduce symptoms of comorbid oppositional defiant disorder, which often requires 

adjunctive parent training and behavior management. Severely explosive anger may require the use of atypical antipsychotics. In conduct 

disorder, stimulant medications and atomoxetine also reduce aggressive behavior and antisocial acts. Atypical psychotics or mood 

stabilizers may be used for highly aggressive-explosive cases. 

The majority of children with comorbid ADHD/depression can be managed with a psycho stimulant. However, initial treatment with 

antidepressant drugs should be saved for treating children with more severe depression. Stimulants can exacerbate symptoms of anxiety 

disorders. Atomoxetine, SSRIs and behavioral therapies reduce anxiety symptoms. 

If tic disorders are mild or episodic, they usually require no treatment. Most ADHD/tic disorder patients will not demonstrate an 

exacerbation of their tics with stimulants. Nevertheless, if tics worsen with stimulant use, an antipsychotic or alpha agonist should be 

added to the psychostimulant. 

Key words: Attention deficit hyperactivity disorder, comorbidity, management 


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Treatment approaches to psychiatric comorbidities of ADHD in adolescents 

Bengi Semerci 

Institute, Istanbul, Turkey 

E-mail: bengisemerci@bengisemerci.com, info@bengisemercienstitusu.com 

Adolescences with ADHD, who suffer from social problems, are under risk of depression, anxiety, destructive conduct disorder, and drug 

addiction. If there are co-morbid disorders associated with ADHD, it makes the treatment difficult and causes some other complications. 

The fundamental treatment principles of the psychiatric co-morbidities of ADHD are also effective for adolescence period. However, 

especially, we should be careful about the conditions that have high prevalence during adolescence period and the conditions which 

affect prognosis in a negative way. These situations need to be assessed in diagnosis and treatment plan. 

Anxiety Disorders: Some researches indicate that a stimulant treatment has small effects on anxiety disorder. The treatment of ADHD 

without anxiety disorder gets more successful results. However, according to recent research, treatment is also effective on anxiety 

disorder. 

In general, considering the effect of CBT on the anxiety disorder treatment, it is suggested that CBT beside medication treatment is 

effective on ADHD having co morbidity with anxiety disorder. If there is co morbidity, it is suggested that the priority needs to be given 

to ADHD and that if the anxiety symptoms continue, another medication treatment should be considered. 

Mood Disorders: Depression is an important problem in adolescence period. The important point in treatment is to identify that if ADHD 

causes to depressive findings or major depression. 

If ADHD cooccurs with major depression, both of them need to be treated. The treatment may be done either by stimulants or atomoxetine 

or only by SSRIs or tricyclic anti depressants. The last option is to use the two methods both. 

When there is co-morbid depression and ADHD, the efficacy of antidepressants is lower than when it is depression alone. In clinical 

observation, depression findings in adolescence period should be assessed attentively. If there is major depression, the treatment should 

be carried out together with ADHD. Selective serotonin reuptake inhibitors (SSRI) may be used with stimulants. 

Conduct Disorders: If ADHD is not treated, it may possibly turn to conduct disorder. In many studies, the use of stimulants for the 

treatment of co-morbid ADHD and conduct disorder is investigated. The results of these studies show that stimulants are effective when 

the morbidities are both separate or together. 

However, if there are co-morbid ADHD and conduct disorder, the effectiveness of stimulants on aggression is lower. If there are co-morbid 

ADHD and aggression and if the typical ADHD treatment does not work, it may be useful to add atypical antipsychotics to the treatment. If 

ADHD is co-morbid with conduct disorder, working with adolescents, using behavioural approaches, supporting families and to providing 

them education about the problem may be helpful. 

If ADHD co occurs with drug addiction, both disorders should be treated. Stimulants can be used in a controlled way. However, due 

to addiction, prescribing stimulants may be cause legal problems. Atomoxetine and bupropion could be other options. Eventhough, 

antidepressants are effective in ADHD, their effectiveness in addiction is limited. 

Key words: ADHD, adolescence, co-morbidity, treatment 


Treatment of neurological co-morbid disorders in children with ADHD 

Murat Yüce 

Department of Child and Adolescent Psychiatry, Ondokuz Mayıs University, Samsun, Turkey 

E-mail: muryuce@yahoo.com 

Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, and 

impulsive behaviors. ADHD is one of the most common childhood psychiatric disorders. 

Children with ADHD also have many comorbid disorders and psychiatric symptoms. ADHD may be accompanied with neurological 

disorders such as epilepsy, headache, and cerebral palsy. Neurological co-morbid conditions can lead to reduction in the level of function, 

adherence to treatment difficulty, increasing the price of healthcare and medical complications. Therefore, diagnosis and treatment of 

these neurological co-morbid problems with ADHD are important. 

ADHD is seen more commonly in children with epilepsy according to the normal population. Approximately 20% of children diagnosed 




with epilepsy have ADHD as well. Some antiepileptic drugs are known to cause lethargy and impairment of attention. Barbiturates and 

benzodiazepines may worsen the symptoms of ADHD. It has been reported that some drugs such as tiagabin, zonisamide, and topiramate 

can cause cognitive slowing and concentration problems. Psychostimulants are frequently used in the treatment of ADHD. It has been 

reported that these medications do not severely effect epileptic seizures and may improve cognitive functions. 

In this presentation treatment approaches for children and adolescents with ADHD and co-morbid neurological disorders will be 

discussed. 

Key words: ADHD, children, neurological co-morbidity, treatment 


Drug interactions of medications for comorbidities of ADHD 

Osman Abalı 

İstanbul Medical Faculty, Child and Adolescent Psychiatry, İstanbul, Turkey 

E-mail: osmanabal@hotmail.com 

ADHD is a very common psychiatric disorder in childhood. Children with ADHD have frequently another psychiatric disorder. Conduct 

disorder, learning disorder, addiction, and mood disorders are frequently seen in children with ADHD. It has been estimated that 23%- 

42% of youth receiving psychiatric drugs are receiving multiple drugs (1). Recently drug interactions have been emphasized in these 

patients. Stimulant drugs and atomoxetine, which is a non stimulant drug, are used in patients with ADHD. Interactions between these 

drugs and other psychotropic drugs are important for treatment quality. Drug interactions should be considered to prevent adverse 

effects and increase treatment quality. Possible drug interactions could impact on liver, intestine, or plasma. There are a lot of important 

risks due to drug interactions in patients with ADHD. Drug plasma levels can change due to CYP-P450 system interactions. It is estimated 

that approximately 7% of the population may be poor metabolizers, causing slow metabolism(2). Also inhibitors of the cytochrome P450 

can increase drug levels by several folds. Some drugs inhibit these systems very potently so that concentration of drug can reach very 

high levels. Important complications such as neuroleptic malignnant syndrome, serotonergic syndrome, and hallucinations can be seen 

during these interactions. Treatment strategies should be reviewed from this perspective. Possible drug interactions couldn’t be exactly 

predicted by the clinicians for every patient. But potential drug interactions should be considered for every patient. Drug interactions will 

be discussed at this presentation. The treatment strategies will be updated for long term good quality treatment based on the literature. 

Key words: ADHD, drug interactions, co-morbidity 

References: 

1. McIntyre RS, Jerrell JM. Polypharmacy in children and adolescents treated for major depressive disoerder: a claims database study. Journal of clinical 

psychiatry.2009;70(2):24-46. 

2. Barton J: Atomoxetin: a new pharmacotherapeutic approach in the managment of ADHD, Archives of disease in childhood 2005;1(90):26-29. 


[PS-22] 

Symposium Title: How to fight with bipolar disorder? From guidelines to clinical practice: Myths and realities 

Treatment of mixed episodes of bipolar disorders in manuals. What are the recommendations? 

Ahmet Ünal 

Gaziantep University, Faculty of Medicine, Department of Psychiatry, Gaziantep, Turkey 

E-mail: drahmetunal@hotmail.com 

There are still clinical states with uncertainties in psychiatry in terms of diagnosis and treatment. Mixed states in bipolar disorders is one 

of these states. The Diagnostic and Statistical Manual of Mental Disorders – IV (DSM – IV) defines mixed states as a period in which manic 

and depressive diagnosis criteria prevail together. However, observing all depressive and manic symptoms together during the mixed 

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episode is not a common occurrence. The Cincinnati criterion has a more flexible approach in terms of diagnosis; a complete manic states 

together with at least three depression symptoms is enough to diagnose the case as mixed mania. There are studies that identify mixed 

mania as “a severe form related to mania,” “a transition period between manic and depressive episodes,” or “a separate emotional state.” 

15-20% of all manic episodes have characteristics that belong to the mixed mania. In comparison to a classic manic episode, the mixed 

mania has a more severe psychopathology. Episodes of dysphoria are observed more frequently, and it is frequently reported that 

dysphoria is an important part of mixed states. In comparison to a classic manic episode, the duration of hospitalization is longer, the 

number of attacks is higher, and the good periods are shorter during mixed episode. In addition, the psychotic characteristics and 

catatonic symptoms are more, and the rate of suicide is higher. 

The most important element of treating the mixed episode is making the right diagnosis. The basis used to determine the treatment 

method is the same as those recommended for treating manic episodes. Unfortunately, there are no comprehensive studies that address 

treating mixed mania. There are limited data related to the efficacy of medications on mixed mania or which medication is better than 

the other. In general, combining drugs and clinical experiments are required for the short-term and long-term treatment of mixed mania 

patients. According to the Turkish Psychiatric Association (TPA), the treatment for mixed episodes of bipolar disorder is as follows: The 

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 

symptoms do not get better by 50% at the end of three weeks, an alternative is using an atypical antipsychotic and stopping the lithium- 

valproate combination by gradually reducing the amount given to the patient, or moving on to a lithium – carbamazepine combination, 

and if >50% progress is not reached at the end of Week 6, it is recommended that patients receive ECT. 

In comparison to classic manic episodes, the rate of response to mood stabilizers for mixed episodes is lower. Antidepressants should also 

not be used to treat symptoms of depression during this period. This situation proves the need for other treatment options. Olanzapine 

can be used effectively in acute and preventative treatment of mixed mania; however, its disadvantages are weight gain, diabetes, and 

metabolic syndrome risk. Ziprasidone has a high level of effectiveness that incorporated psychotic and mixed mania. There is evidence 

that risperidone is effective in treating manic episodes; however, the amount of information related to its efficacy in mixed episodes is 

limited. The number of studies about the efficacy of quetiapine on mixed episodes is also limited. The efficacy of aripiprazole on manic 

and mixed episodes is addressed by some studies. 

In conclusion, mixed states in bipolar disorder are common clinical reflections. Mood stabilizer treatment strategies are the form of 

treatment that gives the best results. Mood stabilizer and antipsychotics can be used in the form of monotherapy or combination. Among 

these mood stabilizers, valproate is the one that has been studied most and is the most recommended. Aripiprazole, ziprasidone, and 

olanzapine are the antipsychotics that should be utilized first and foremost. 

Key words: Bipolar disorder, mixed mania 


How are the guidelines prepared? Are they necessary? How to use them? 

Their benefits and limitations? 

Yasin Bez 

Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey 

E-mail: yasinbez@gmail.com 

Some important points when preparing guidelines are search strategies and methods to assess evidence and the criteria for rating the 

strenght of evidence and making a clinical recommendation. The development of treatment guidelines mostly aims to standardize 

treatment and to provide clinicians with algorithms, which would be able to carry research findings to everyday clinical practice, by 

organizing information from diverse sources into an easily accessible format (1). From this point of view, treatment guidelines may be useful 

to avoid non-evidence-based treatment decisions. Thus, their common use should be supported. On the other hand, they get quickly outof-date 

and may interfere with following the most recent treatment approaches. Besides, they may not fully apply to the everyday clinical 

setting. Besides the benefits and limitations of guidelines another important point is the adherence of the clinicians to these guidelines (1). 

Despite considerable efforts to develop them, adherence to the treatment guidelines for bipolar disorders are not enough yet. For 

example a study from United States demostrated adherence of 64.1% of the psychiatrists to the treatment guidelines (2). Another study 

conducted in France reported a 40% non-adherence rate to treatment guidelines of bipolar disorder among psychiatrists (3). 

Current and more detailed data about preparation, use, benefits, and limitations of treatment guidelines will be further discussed in this 

presentation. 

Key words: Bipolar disorders, guidelines 


References: 



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; 

86: 1-10. 

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. 

3. Samalin L, Guillaume S, Auclair C, Llorca PM. J Nerv Ment Dis 2011; 199: 239-243. 


Maintenance treatment in bipolar disorder: What do guidelines recommend? 

Ibrahim Eren 

Konya Research and Training Hospital, Psychiatry Department, Konya, Turkey 

E-mail: drieren@yahoo.com 

Bipolar disorder is a serious mental illness presenting with exacerbations and remissions. Relapses should be minimized and that is 

achieved by preventive treatments. Developing easily applicable and reachable algorithms by incorporating data coming from various 

sources, implementing research findings in daily practice, and providing standardized treatment choices are all important. Many 

guidelines have been published for bipolar disorders so far. 

American Psychiatric Association (APA) Guidelines: This guidelines recommend preventive treatment after one manic episode. The 

main goals of treatment are to prevent relapse, resolve subclinical residual symptoms, and to decrease suicide risk. Lithium and valproate 

are primary agents, as they have the most evidence of efficacy. Their alternatives lamotrigine, carbamezapine, and oxscarbamezapine are 

secondary agents. In general continuation of preventive medications used during acute management is first choice during maintenance 

treatment. ECT can be used as a maintenance treatment. Antipsychotics should be discontinued if there is no persistent psychotic symptoms. 

Cognitive behavioral, interpersonal, and psychodynamic therapies can be used in addition to medications. Psychoeducation is reported 

to be beneficial. Keeping lithium levels between 0.8-1.0 mEg/L during maintenance phase were mentioned to be more effective. In this 

guideline generally accepted treatments were mentioned as non-definite recommendations. 

Texas Medication Algorithm: Acute phase doses should be continued at least 3 months. All patients are recommended to receive 

antimanic medications during maintenance phase, if necessary some can receive low dose antidepressants. Lifelong maintenance 

treatment is recomended if patients had 2 manic episodes or one manic episode with positive family history, or the acute episode was 

very severe. This group of authors think antimanic medications are the core of the treatment and they emphasize depression less. In 

addition they recommend ECT and tricyclics, which were demonsterated to be effective, in final stages due to side effects and patient 

preferences. 

Expert Opinion Series on Medication Treatment in Bipolar Disorder: They recommend continuation of treatment, which was effective 

in acute phase except in divalproex monotherapy and predominantly depressive cases. They suggest adding lithium in those cases. 

They recommend that antipsychotics should be stopped during maintenance phase, but some patients may need to continue taking 

antipsychotics. In that case, one of olanzapine, risperidone, or quetiapine can be chosen. Against manic episode risk they suggest to 

increase the dose of mood stabilizer, add another mood stabilizer, and try additional treatments afterwards. This algorithm has many 

structural features and is very detailed. 

British Psychopharmacology Association Guidelines: According to this guideline lithium is the first choice and second choice 

medications include valproate, olanzapine, carbamazepine, oxcarbazepine, and lamotrigine. Treatment resistant cases can be treated with 

medication combinations, clozapine, or ECT. 

World Federation of Biological Psychiatry Associations Biological Treatments in Bipolar Disorders: It is recommended to use 

combination of antidepressant and mood stabilizers after depressive episodes. After manic episodes lithium, anticonvulsants, or 

antipsyhotics are suggested. When first line treatments fail, trying combinations of first line agents is recommended. It seems to be 

the most balanced guideline published so far. While they avoid newly discovered treatments , they support use of antipsychotics and 

antidepressants with caution. 

Canmat: Once the patient becomes asymptomatic, it is suggested to discontinue all medications other than mood stabilizers and to 

continue maintenance treatment for 6-12 months after a single episode of illness. This guideline has similarities with APA guideline and 

recommends lifelong maintenance treatment in patients with recurrent episodes or positive family history. 

Australia and New Zealand Bipolar Disorder Treatment Algorithm: It suggests to avoid antidepressant use during maintenance phase 

after depressive episodes due to precipitating mania and rapid cycling, but recommends mood stabilizer and antidepressant use in cases 

with recurrent depressive episodes. The duration of treatment after first manic episode is 6 months and lithium, valproate, carbamazepine, 

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or lamotrigine are listed as recommended medications to prevent recurrent episodes. 

NICE Treatment Guidelines: They recommend at least 2 year of maintenance treatment after 1 episode. Long term preventive treatment 

should be considered in the following cases: One manic episode with prominent risk factors and negative results and bipolar II cases 

with significant functional loss, suicide risk, and frequent recurrent episodes. Lithium, olanzapine, or valproate can be used in long term 

maintenance treatment, but valproate should not be used in women with pregnancy potential. 

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 

different agent. Possible combinations are lithium-valproate, lithium-olanzapine, or valproate-olanzapine. 

Turkish Psychiatry Association Guidelines: Maintenance treatment is suggested in general after second episode, but it can be started in cases 

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 

started. When a mood stabilizer will be chosen for maintenance phase, it should be lithium. After second episode, whatever the type of episode 

was, the same mood stabilizer should be continued if there was one. When there is not adequate response and recurrence occurs a second 

mood stabilizer should be added. In cases using lithium as first mood stabilizer, valproate should be given priority as the second mood stabilizer. 

In conclusion, even there are similarities in many areas among guidelines, there are also different recommendations regarding treatment options. 

Those differences stem from complex clinical presentations of bipolar disorder and different cultural and traditional treatment approaches. 

Key words: Bipolar disorder, maintenance phase, guidelines 

References: 

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; 

86: 1-10. 

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. 

3. Samalin L, Guillaume S, Auclair C, Llorca PM. J Nerv Ment Dis 2011; 199: 239-243. 


[PS-23] 

Symposium Title: Individualized medicine: Focus on pharmacogenetics 

Genetics and drugs: From research to clinical studies Turkish perspective 

Cem Şengül 

Pamukkale University, School of Medicine, Department of Psychiatry, Denizli, Turkey 

E-mail: acemsen@gmail.com 

Genetic studies in psychiatry are on the rise and they form an important portion of all psychiatric research in last years. The genetic studies 

in psychiatry vary from classical association and linkage studies to genome wide association, and copy number variant studies. Genetic 

studies were focusing on different dimensions of psychiatric conditions. First of all, associations of target genes with psychiatric disorders 

were investigated in majority of studies. Association of drugs and genetics were also studied in many research projects. Genetic drug 

association studies consist of studies with efficacy and frequency of side effects of drug on different genetic polymorphisms. Recently, 

μ-opiate receptor gene (OPRM1) Asn40Asp single-nucleotide polymorphism was found to be associated with naltrexone drug response in 

alcoholic patients. This finding was very important for revealing effect of genetics on drug response. Naltrexone was effective in aspartate 

(Asp) 40 allele carriers but drug was ineffective in homozygote asparagine (Asn) carriers. Different genetic polymorphisms of genes 

encoding enzymes and receptors that were related to dopaminergic, serotonergic and glutamatergic systems were also associated with 

antipsychotic and antidepressant drug response and side effects. For example 5-HT2C receptor 759C/T gene polymorphism was associated 

with antipsychotic induced weight gain and T102C polymorphism of 5HT2A receptor gene was associated with response to risperidone. 

Genome wide association and copy number variations are new genetic techniques revealing more detailed and reliable results. Studies 

using these techniques might be more useful for exploring interactions between drugs and genetics. Studies on association of genetics 

with psychiatric disorders were limited and there were only a few studies available on association of genetics with psychiatric drugs in 

Turkey. Financial problems and approval speed and requirements of ethics committees are important barriers for conducting studies on 

genetic drug interaction. Resolving these issues might increase interest of psychiatrists on this topic. 

Key words: Genetics, polymorphism, drug 





Pharmacogenetics and how individualized medicine can be applied to the practice of psychiatry 

Çiğdem Aydemir 

Ankara Numune Research and Education Hospital, First Psychiatry Clinic, Ankara, Turkey 

E-mail: aydemircigdem@yahoo.com 

Choice of psychotropic agents is a critical problem during the follow up of mentally ill patients. Some of the patients experience remission, 

however significant proportions of the patients continue to suffer from psychiatric symptoms and side or adverse effects. 

Psychotropic drug efficiency may not occur until a considerable time after the initiation of the therapy after which the clinician can 

determine, whether the regimen is effective or not. During this period treated patients may experience continuous psychiatric symptoms, 

employment loss, social dysfunction, and medical morbidity. 

Efforts to identify the best possible drug regimen for the patients focused on many points, such as clinical variables, predictors of possible 

side effects, plasma and CSF neurotransmitter levels, metabolite levels, and brain imaging, but they have only limited success. Up to date 

in practice, drug selection is made based on clinical symptom profile and possible side effects of treatments. 

The pharmacogenetics of the psychotropic drugs is a possible way to decide the suitable drug for the patient. Pharmacogenetics is the 

study of genetically determined interindividual differences in response to pharmalogical agents. In this field there are genetically coded 

pharmacokinetics (genetically based differences that influence the bioavailability of a drug), pharmacodynamics (genetically based 

differences in the proteins at which a drug acts) of the drugs, and dynamics of their side effects. 

The renal clearance of drugs appears to be similar in age- and weight-matched healthy subjects with no defined genetic polymorphisms. 

Studies regarding the inheritance mostly account for the ability to eliminate drugs. The genetic differences in pharmacokinetics have 

proved that they may be applied to the most of the drugs metabolism. Genetic polymorphisms have been identified and defined for 

some drug transporters, primarily P-gp, and several hepatic enzymes important for the cellular transport and metabolism of many drugs 

used in psychopharmacology. Genetic polymorphism in a drug-metabolizing enzyme can result in subpopulations of people who may 

deviate from the population mean in their ability to metabolize substrates of the affected enzyme. People who are poor metabolizers 

constitute at least 1% of the population, but the majority of people are normal or rapid metabolizers, and some are identified as ultra rapid 

metabolizers. The practical implications of metabolic phenotyping are most meaningful when the metabolic pathways of therapeutically 

administered drugs are known and when drug concentration has been correlated to either therapeutic or toxic effects. 

Genetic differences in the receptors, on which the drugs act, are another important factor in predicting the effects and side effects. Findings 

in this field are scarce in comparison to pharmacokinetics studies however some research projects are in progress. After the results of these 

studies are obtained; different variables other than plasma concentration of the drug would be available in pharmacotherapy practice. 

There is a dramatic increase in the amount of availability of the genetic information in public since samples can be easily collected by 

peripheral blood collection or mucosal smearing. Progress in genetic-molecular technology made possible to conduct genetic research 

on individual genes or entire genomes. In the future by the help of pharmacogenetic approach clinicians will be able to understand the 

predictors of drug efficacy and side effects, as a result individualized medicine will be applied in the practice of psychiatry. 

Key words: Pharmacogenetics, psychiatry, treatment, individualized medicine 


Pharmacogenomics biomarkers and personalized medicine in psychiatry 

Yeşim Aydın Son 

Middle East Technical University, Informatics Institute Department of Health Informatics, 06800, Ankara, Turkey 

E-mail: yesim@metu.edu.tr 

Transformation of clinical medicine was one of the long term goals of the Human Genome Project, expected to impact the practice 

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 

applications of technologies based on genomic research is indicating that Human Genome Project will be able keep its promise. 

Translational and clinical research to develop new personalized medicine approaches are going strongly; identification of predictive and 

diagnostic biomarkers is accelerating with the help of high-throughput technologies, and molecular diagnostics and pharmacogenomics 

is one of the growing markets worldwide with the goal of early detection, prevention, and intervention of diseases and to predict drug 

efficacy to guide dosing and avoid adverse reactions. 

S101


Single Nucleotide Polymorphisms (SNPs) are the most common form of genomic variations and the main genetic reason behind 

individual phenotypic differences. Also SNP variations are suggested to be the underlying reason of many complex diseases, they are 

considered as a good candidate for personalized medicine and pharmacogenomics applications. Genome-Wide Association Studies 

(GWAS) of SNPs are among the promising approaches for the identification of disease causing variants. The high-dimension of the SNP 

genotyping data presents a challenge for the understanding of the genotype and its possible implications for the etiology of the diseases 

and also for the identification of the representative SNPs to design the follow up studies for the validation of the associations. One of 

the bioinformatics tools developed to overcome this challenge is METU-SNP (http://metu.edu.tr/~yesim/metu-snp.htm), which aims to 

fasten the identification of associations described through GWAS. Today through genomic research and meta-analysis of genotyping 

experiments we are able to reveal SNP biomarkers associated with disease and drug reactions. Next, translational research has to be 

conducted in order to develop genomic diagnostics to apply this information into practice in medical clinics. Design of diagnostic assays 

for the diagnosis and prediction of drug response in psychiatric disorders can especially guide the initial selection of antipsychotics or 

antidepressants based on the individual genomic information of the patients. 

Development of personalized medicine approaches and utilizing genomic diagnostic assays like the examples will be presented in this 

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 

minimize emergency visits due to side effects of the drugs. Also prescription of right medicine and therapy plan at the initial diagnosis 

will increase trust between the healthcare professionals and the patients, which in return expected to provide higher cooperation and 

adherance rates of patients to their therapy. Application of pharmacogenomics and personalized medicine approaches in clinical decision 

making is expected to decrease the cost of healthcare in psychiatry as in other disciplines, while offering higher quality healthcare.. 

Key words: Personalized medicine, biomarkers, molecular diagnostics, pharmacogenomics, Single Nucleotide Polymorphisms (SNPs), METU-SNP, 

rational drug use 


[PS-24] 

Symposium Title: Effects of psychotropics and other drugs on quality of life, employee security, flight and traffic safety 

The effects of psychotropic and other drugs on flight and flight safety 

Muzaffer Çetingüç 

Aviation and Space Medicine Center, Anadolu University, Eskisehir, Turkey 

E-mail: mcetinguc@hotmail.com 

There are data that the side effects of many prescription drugs impair the psychomotor and cognitive performance of patients; with 

psychotropic drugs having even more of these negative side effects. Particularly drugs like benzodiazepines, antipsychotics, barbiturates, 

trycyclic antidepressants, stimulants, narcotic analgesics, and antihistamines that affect the central nervous system top the list for risks of 

accidents, injuries, and cognitive impairments. Along with these, anticoagulants, chemotherapeutic agents, antidiarrheals, antiemetics, 

and steroids should not be allowed for pilots. It is debatable that SSRIs have a mild side effect profile. SSRIs and bupropion are given 

to military pilots up to 6 months after resolution of anxiety and depressive symptoms in Canada and Australia. But the civil aviation 

authorities did not grant any privileges to these drugs. 

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 

any medication during flights. The regulations both international and national have clear rules that permanently or temporarily restrain 

pilots from flying activities in the case of any sickness or medication treatment. The rules stating that a sick person cannot function as 

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 

spread over a wide range, local health authorities can issue “waivers” for special situations. For example pilots with conditions like type-2 

diabetes, asthma, rheumatoid arthritis, sarcoidosis, or melanoma cannot fly; but in certain forms of these conditions that are stabilized 

with treatment, that have not caused serious limitations, and that do not affect performance, the pilot may be allowed to fly. Atopic 

dermatitis that recover with application of pomades, allergic rhinitis that is treated with nasal sprays, asthma that is treated with steroid 

inhalers, type-2 diabetes that is controlled with metformin are examples of allowed conditions. The drugs that are assumed not to have 

any side effects that might affect flight safety are: Aspirin, paracetamol, most antibiotics, depot penicillins, gout and thyroid medication, 

antiacids, nasal decongestants, oral contraceptives, topical analgesics and steroids, nonsteroidal anti-inflammatory drugs, vitamins, 

metformin, modafinil, caffeine, etc. Clearly, the patients need to be monitored for the first few days of use considering these drugs may 

have idiosyncrasies. 




It is a problem when pilots take drugs without consulting authorized doctors for fear of flight suspensions. Adding to that reasons like 

the cost of doctor’s visits, losing compensation for the duration of suspension, upsetting supervisors due to disrupted flight schedules 

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, 

and ads. There are several herbal supplements available in the market today that contain suspicious ingredients that claim to treat pain, 

help flu like symptoms, reduce stress, aid sleep, improve sexual performance, reduce blood fat levels, help lose weight, prevent aging, or 

provide vitamins and minerals. Therefore the attempts of the pilots to treat themselves create risks and the unknown side effects of those 

preparations pose serious problems to flight safety. 

Key words: Psychotropic drugs, SSRI, flight safety, pilots 


Sexual side effects of psychotropic and other drugs 

Adnan Özçetin 

Department of Psychiatry, Duzce University, Duzce, Turkey 

E-mail: adozcetin@gmail.com;adozcetin@yahoo.com 

Sexual dysfunctions are revealed by different organic and/or psychogenic factors and proceed with the addition of psychogenic reasons 

to almost all organic reasons. The organic/psychogenic discrimination of etiologies is crucial in sexual dysfunctions. The most important 

and practical way of discrimination is systematic and detailed history. The diffuse type sexual dysfunction established in elderly people 

should be considered primarily based on organic reasons. Furthermore alcohol/narcotics, drug abuse, the existence of somatic or systemic 

diseases also strengthen the possibility of organic based sexual dysfunction. The drugs and ingredients causing significant sexual side 

effects include: Alcohol and narcotics, antihistaminics, decongestants, diuretics, chemotherapeutics, antiulcer drugs, antihypertensives, 

anticonvulsants, asthmatic drugs, cardiac drugs, psychotropic drugs (antipsychotics, antidepressants, mood stabilizers, anxiolytics, 

sedative hypnotics), and others. 

It is mostly difficult even impossible to learn about the sexual side effects of drugs by physicians. Previous studies have revealed that 

patients usually didn’t mention the sexual side effects of drugs to their physicians. Therefore the physicians should specifically ask 

about the sexual side effects of drugs beside the dosage, preferred effects, and other side effects. Besides, relationship between sexual 

dysfunction and other diagnosis and drugs used by the patient should be considered. 

There are major unfavorable results of sexual side effects including: Loss of adaptation to drug use, abandonment of drug therapy, 

deterioration of psychiatric or other diseases, continuation of sexual dysfunctions, and disruption of quality of life. Significant side effects 

exist during the medical treatment of psychiatric disorders. The mechanism of emergence of sexual dysfunction due to medication use 

is complicated. Sexual dysfunctions due to medications occur by the effects of medications on peripheral and central neurotransmission. 

Serotonin mostly reveals negative effects on sexual behavior. However, its effects can also be positive according to receptor subtype 

and localization. Higher prolactin levels cause sexual dysfunction. The increase in dopaminergic activity has positive effects on sexual 

desire. Antipsychotics, antidepressants, anxiolytics, and other psychotropic drugs mostly have negative effects on sexual desire and 

behavior. Psychotropic drugs like bupropion, mirtazapine, moclobemid, reboxetine, and tianeptin have little or no sexual side effects. 

Even dopaminergic drugs like bupropion have positive effects on sexual desire. 

Key words: Drug, sexual dysfunction, side effect 


S103


COURSES 

[KC-01] 

Basic Biostatistics 

Selim Kılıç 

Gulhane Military Medical School, Department of Epidemiology, Ankara, Turkey 

E-mail: drselimkilic@gmail.com, skilic@gata.edu.tr, drselimkilic@yahoo.com 

The aims of this course are to teach the basic statistical approach and terminology, to teach the use of the SPSS for Windows package 

program and its basic characteristics and principals, to perform the basic descriptive and analytical statistics by using SPSS for Windows 

package program and to interpret the results. 

At the end of the course, the participants will be able to perform descriptive statistics, select the appropriate statistical tests to compare 

differences between or within groups and be able to draw some graphics by using the SPSS for Windows package program in a datasheet 

which is composed by the course director. 

The participants, upon completion of this course, will be able to generate and test hypotheses, compose a datasheet iusing the SPSS for Windows 

program, enter data in the datasheet, transform the data to other forms, select the appropriate statistical test for comparison of groups and computation 

of basic statistics, interpret and write the results, interpret the p value and confidence interval, and draw some graphs by using the SPSS program. 

The participants will learn to calculate mean, median, mode, standard deviation, quartiles, frequency and percents as descriptive statistics. 

They will learn and differentiate categorical, ordinal, and continuous variables by studying examples. To compare categorical variables, the 

use of the chi-square test and interpretation of the results will be discussed. For continuous variables, the appropriate test will be determined 

with respect to group numbers, whether groups are dependent or independent and whether the variables are parametric or nonparametric. 

According to the existing conditions, the participants will decide when they should use the independent samples t test, ANOVA, paired samples 

t test, or repeated measures of ANOVA as parametric tests and Mann Whitney U, Kruskal Wallis, Wilcoxon ranked signs test, or Friedman test 

as a nonparametric tests. They will also use correlation analysis to determine the linear association between continuous and ordinal variables. 

By using the SPSS program, participants will compose bar and pie graphs for nominal and box plot graphs for continuous variables to 

demonstrate the results. 

Key words: descriptive statistics, p value, confidence interval 


[KC-03] 


Axel Würz 

Department of Psychiatry, Marmara University, Istanbul, Turkey 

E-mail: messageaxel@googlemail.com, niz2hear@gmx.net 

Despite a high prevalence of somatic symptoms without demonstrable organic cause in nearly every branch of medicine, understanding, 

classification and treatment of these disorders have posed a considerable challenge. 

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 

non-organic physical symptoms. It is likely that somatization disorder, hypochondriasis, undifferentiated somatoform disorder and pain 

disorder will be combined into a new category entitled “Complex Somatic Symptom Disorder” (CSSD) which emphasizes the symptoms 

plus the patients’ abnormal cognitive processes. The term “complex” is intended to indicate that the symptoms must be persistent and 

must include both somatic symptoms (criterion A) as well as dysfunctional cognitive processes (criterion B) for the diagnosis to be made. 

Cognitive processes such as dysfunctional attention focusing, symptom catastrophizing, and symptom expectation that may be included 

in criterion B also show the influence cognitive models have exercised in the understanding of these disorders. 

These cognitive processes have to be evaluated against the background of possible psychiatric comorbidities, current life stressors, 

possible past traumatic events and learning experiences that shaped emotion regulation in an unhelpful way. Contributing to the 

maintenance of symptoms and resulting from dysfunctional cognitions are behaviours such as imbalanced level of activity, avoidance 

and safety-seeking and reassurance-seeking behaviors. 




In cognitive behavioural therapy (CBT) of these disorders all the factors maintaining and contributing to the disorder are possible targets 

for treatment. The first and possibly most important step is to develop, in cooperation with the patient, an alternative explanation of the 

patient’s symptoms other than the presence of an organic cause. During the course of treatment the patient can then collect evidence 

that supports the alternative explanation of symptoms. 

The techniques that can be employed within the framework of the cognitive-behavioral approach are aimed at addressing the underlying 

dysfunctional cognitive processes and behaviors. They may comprise cognitive restructuring, attention-training, behavioral experiments, 

exposure, activity planning, and emotional-regulation techniques. 

Conventionally, treatment can be conducted in individual and group sessions and usually comprises about 15 one-hour sessions. There is evidence 

showing that CBT is effective in decreasing symptom severity and overall distress. However, there are limited number of studies comparing 

different treatment modalities such as CBT and pharmacological interventions. Also it is not clear if combining CBT and pharmacological 

treatment increases effectiveness. In addition different forms of therapy such as computer-based treatment have been developed. 

The cognitive behavioral model has been influencing the current understanding of somatization and CBT has shown effectiveness in 

its treatment although further studies are welcomed. Even if a full course of CBT cannot be offered, e.g. in an outpatient setting, and 

pharmacological treatment is chosen, it appears promising to integrate at least certain parts of cognitive-behavioral treatment such 

as developing an alternative explanation for the patient’s symptoms and exploring the role of processes such as attention, avoidance, 

unbalanced activity levels and safety-seeking and reassurance-seeking behaviors. 

Key words: Somatization, CBT, somatoform, hypochondriasis, treatment 


[KC-04] 

Mindfulness and acceptance based therapies 

Kültegin Ögel 

Acibadem University, Medical Faculty, Istanbul, Turkey 

E-mail: ogelk@ogelk.net 

Mindfulness has reached far beyond the disciplines where it originated and has become an evidence-based psychotherapy method. In 

particule, the application of mindfulness based therapies in addition to traditional methods for psychiatric disorders prevents relapses. 

Mindfulness is concentrating with the aim of focusing at the moment in a nonjudgmental way. Mindfulness means being conscious of 

the current experience and accepting it. In other words, mindfulness is a unique and receptive form of consciousness in which stimulants 

are not evaluated, not classified and not analyzed. 

Mindfulness and acceptance based therapies deal with the thought itself instead of the content of the thought. It may be said that they 

help cognitive restructuring in this way. Mindfulness and acceptance based therapies differ from cognitive behavioral therapies in that 

way and are accepted as third wave therapies. 

Acceptance should not be confused with submission and giving up. Acceptance directs the person to turn to the current experience 

(opening up) instead of running away from the experience (closing up). By this means, the person learns to be with and accept 

experiences that are pleasant, unpleasant, or neutral. The person develops the skill of being fair to his or her own experiences. Being aware 

of what is happenibg causes a willingness to let things that are pleasant or unpleasant happen just as they are. 

Mindfulness acceptance therapies involves; Mindfulness Based Stress Reduction (MBSR), Mindfulnnes Based Cognitive Therapy (MBCT), 

Acceptance and Commitment Therapy (ACT), and Dialectical Behavior Therapy (DBT). 

The common basic strategies that all these therapies use are: 

- Acceptance 

- Focusing at the moment 

- Cognitive defusion and decentering 

- Being nonjudgmental 

- Observing 

Adaptation of the different viewpoints that are offered by mindfulness and acceptance based therapies by therapists, who have understood 

them, is useful. However, understanding of the basic rationale of the therapy by all psychiatrists and psychologists is also useful. 

Key words: Mindfulness, acceptance, psychotherapy 


S105


[KC-05] 

Eye movement desensitization and reprocessing method [EMDR] 

Specifically designed for Turkish patient population in the Netherlands 

Serdar Güner 

Praktijk Voor Psychiatrie, The Netherlands 

E-mail: serdarmineguner@gmail.com 

Dr. Serdar Guner reports that those behaviorally troubled Dutch patients with Turkish origin have not necessarily been benefitted by those 

10-15 sessions of EMDR during their psychiatric evaluations necessitated by different conditions. The clinicians have reportedly been applying 

traditional EMDR methods first to be objectifying relaxation through imagination and later on processing the completion of catharsis during 

as well as after the said eye movements. The patients, however, have been reporting no benefits and even at times, worsened clinical 

conditions after the given session. Dr. Guner has finally extracted the facts centered on this failure relevant to the given patient population. 

Those Turkish-Dutch clients have not been acknowledged about the rationale relevant to which-treats-what phenomenon through the 

catharsis. Lacking of explanation centralized around acknowledgement along with a possible language barrier has been hindering the 

therapeutic process. This finding has eventually led him to develop a sister method specifically designed for this patient population. He 

has slowly but steadily, started informing his patients about shock, repression of the feelings during it, and the effect of those repressed 

emotions on the people in short as well as long term trajectories. He, later on, used metaphors in picturing the process through which 

the said repressed emotions would be surfaced by means of EMDR. One of the interesting demographics has been the cultural difference 

of this given patient population. Those Dutch clients with Turkish origins have not been motivated in processing anything if they had not 

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 

more autonomous in directing themselves in comparison with the Western Europeans who have likely been more conformists with their 

clinicians even when they have not necessarily been understanding what and why they were doing in any recommended method. 

Dr. Guner reviews his methodology designed for this population during his presentation. Most of the work has been an “acknowledgement” 

in his following up with his patients. This variant method has been helping PTSD patients’ feeling relaxation even after first two sessions. 

Dr. Guner reports that about 150 of his patients have been very happy about the outcome of this EMDR variant. 

Key words: EMDR, PTSD, psychotherapy 


WORKSHOP 

[WS-01] 

Alternative CBT method of panic disorder treatment for Turkish patients 

Serdar Güner 

Praktijk Voor Psychiatrie, The Netherlands 

E-mail: serdarmineguner@gmail.com 

I have been working as a psychiatrist and psychotherapist in the Netherlands for more than 20 years during which I have diagnosed and 

treated many Turkish panic patients by the virtue of sharing the same language, culture, and other demographics of the native land, 

Turkish Republic. The most important factor that led me to develop a different approach than that of a classical cognitive behavioral 

therapy -- focusing on neuro-vegetative reactions, neutralizing them through psycho-education and home-work, generating an insight 

into catastophic thoughts while “living” and finally easing up the panic attacks -- was the given patients’ thinking of the methods as 

“ridicilous,” and not doing their homeworks or acting as if they completed them even they did not. 

The alternative method I devised was related to use a lot of metaphors corresponding to the patients’ lives, generating an insight into 

catastrophic thoughts while “understanding” their bodily dynamics, self-controlling neuro-vegetative reactions, and acknowledging 

“the mechanism of panic reaction.” Since it is relatively short, not necessitating homework, and easy to understand for the panic stricken 

patients, it promotes motivation leading to less relapses and even if relapses occur, achieving quicker and easier recovery. 

The method appears to be effective among the native Dutch patients, as well as immigrants. 

The presentation will be providing details of this newly applied successful panic treatment. 

Key words: CBT, panic disorder, psychotherapy 








November 23-27, 2011 



ABSTRACTS OF ORAL PRESENTATIONS


[SO-01] Ref. No: 93 

Bacopa monniera: Current trends and future directions 

Chris Neale 1 , Andrew Scholey 1 , Matthew Hughes 1 , Patrick Johnston 2 

1 Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University of Technology, Melbourne, Australia 

2 Department of Psychology, University of York, York, England 

E-mail: chrisneale@swin.edu.au 

Objectives: Bacopa monniera (BM) is an Indian herb used for centuries as a memory tonic in Ayurvedic medicine. Preclinical research has 

shown that BM acts as an antioxidant, improves memory, and reduces amyloid plaque deposition in animal models of Alzheimer’s disease. 

Human studies suggest that BM provides a fairly robust benefit to performance on certain attention, working memory, and learning tasks. 

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. 

Methods: Two studies will be discussed further to the review of BM: 

(1) An acute dose-ranging study of healthy young adults where participants were required to complete a multi-tasking framework (MTF) 

and mood scales at baseline, 1 hr and 3 hrs post dose. The dosage was 300 or 600mg of BM or a matched placebo. 

(2) The study utilized a double blind, placebo controlled crossover design where all participants completed a 90 day course of both 

Bacopa (300mg daily) and placebo during the study. The participants were aged between 40 and 65 years and in good health. The 

interventions were separated by a 120 day washout period. The scans were undertaken on a 3T Siemens TRIO magnet before and after 

each 90 day intervention where participants would complete two runs of the task per scan visit. 

Results: (1) There was a significant, dose-dependent effect of treatment on ratings of alertness favouring the 600 mg treatment at both 

post-dose assessment times. There was a trend for dose-related effects on performance of the MTF, in particular for the Stroop task where 

there was an advantage for the 300 mg dose. 

(2) The data collection is still ongoing. The baseline data show a bilateral increase in BOLD activation in the precentral gyrus and precuneus 

with activation extending to the left inferior frontal gyrus (n=7, p=.005) when compared with controls using a task greater than baseline mask. 

Conclusions: The conclusions are speculative at this point for both studies, one being still in the data collection stage, one being 

underpowered. However, the methodologies and the future directions of these studies will be discussed. 

Key words: Bacopa monniera, human cognition, fMRI, nutraceuticals 


[SO-02] Ref. No: 143 

Association of the DRD2 TaqIA, 5-HT1B A-161T, and CNR1 1359 G/A polymorphisms 

with alcohol dependence: A single center study in the Denizli Province of Turkey 

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 

1 Psychiatry Clinic, Denizli State Hospital, Denizli, Turkey 

2 Department of Psychiatry Pamukkale School of Medicine; Denizli,Turkey. 3 Department of Genetics Mersin School of Medicine, Mersin, Turkey 

E-mail: acemsen@gmail.com 

Background: Alcohol dependence is associated with genetic variants of alcohol-metabolizing enzymes and genes related to the 

dopaminergic, gamma-aminobutyric acidergic, glutamatergic, opioid, cholinergic, and serotonergic systems. Genetic variations in the 

endogenous cannabinoid system are also involved in alcohol dependence. 

Objective: The present study was aimed at evaluating the association between three polymorphisms, DRD2 TaqIA, 5-HT1B A-161T and 

CNR1 1359 G/A (rs1049353), and alcohol dependence. 

Methods: One hundred and twenty three patients, who were admitted to the Alcohol and Substance Abuse Center of Denizli State Hospital 

and diagnosed with alcohol dependence according to the DSM-IV criteria, and 125 healthy volunteers were included in the study. 

Results: Of the three polymorphisms investigated, 5-HT1B A-161T was the only one found to be associated with alcohol dependence. 

Conclusion: The 5-HT1B receptor A-161T polymorphism might be a promising marker for alcohol dependence; however, future studies 

are needed to clarify these findings. 

Key words: Alcohol dependence, DRD2 TaqIA, 5-HT1B A-161T, CNR1 1359 G/A, polymorphism 





[SO-03] Ref. No: 102 

Treating psychotic substance abuse patients with opioid agonist therapy and 

the atypical antipsychotic olanzapine 

Maria Chiara Pieri 1 

1 Department of Drug Addiction, Bologna Est, Italy 

E-mail: chiara.pieri@ausl.bologna.it 

Objectives: The aims of the study were: 1. To evaluate the efficacy of olanzapine in patients on methadone maintenance treatment; 2. To 

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 

the end of the study (30 months). 3. To compare the severity of the symptoms between patients on methadone and patients on buprenorphine. 

Methods: The patients were enrolled from the Outpatient Addiction Unit in Bologna, Italy. All patients gave written informed consent. We 

randomized 32 patients to treatment with methadone and 13 to treatment with buprenorphine. Based on inclusion and exclusion criteria, 

36 patients were included in the study and they were divided into three treatment groups. 

At the baseline and follow-up sessions the following rating scales were administered: The Minnesota Multiphasic Personality Inventory-2 

(MMPI-2), the SCID-II (to identify and determine DSM-IV Axis II disorders i.e. personality disorders), Bech-Rafaelsen Mania and Melancholia 

Scales (BRMAS, BRMES; Bech et al. 1988, to cover severity of manic and depressive symptoms, respectively), and a VAS (Visual Analogic 

Scale, to quantify craving for drugs). 

Also the body weight of the participants was registered and followed. 

Results: After six months, no significant difference was found among the three subgroups, even though the olanzapine+methadone 

group achieved better and quicker results and sustained them for longer periods. There was no significant difference at baseline and at 

the end of the study in all patients. 

Total and partial BRMES and BRMAS scores did not significantly change during the follow-up period (6 th -30 th month), eventhough the 

curve displayed a downward trend. The VAS total scores were significantly lower both at the 6th and 30th month (p


Materials & Methods: The experiments performed in this study were carried out according to the rules in the Guide for the Care and Use 

of Laboratory Animals adopted by the National Institutes of Health (U.S.A) and received Ege University Animal Ethics Committee’s consent. 

(Approval number: 2010-081) 

In this study, 9 Sprague-Dawley (450-500 g) adult male rats (16-20 weeks old) were used. The rats were maintained under controlled 

environmental conditions throughout the study: 21-25 °C ambient temperature, 12:12 light-dark cycle (light from 7:00-19:00h), and 

Standard laboratory food and tap water available ad libitum. Under anesthesia, a small hole was drilled. Then by using the bregma as a 

reference for the stereotaxic method (coordinates Anteroposterior: - 2.8 mm, Lateral: + 4.8 mm, Ventral: - 8.5 mm) (Paxinos Rat Brain), an 

exterior insulated bipolar EEG electrode was placed in the basolateral amygdala. 

The electrodes were fixed by using a dental acrylic (numerous alloys are used in the making of dental restorations). Rats were anesthetized 

by using ketamine (40 mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP). 

Three days after the electrode was fixed, spontaneous amygdala EEG records were taken from the rats by injecting saline, when they 

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, 

haloperidol 1 mg/kg, chlorpromazine 5 mg/kg or ziprasidone 1 mg/kg doses were IP administered. Before each drug injection amygdalar 

EEG records were taken to observe the baseline rhythm of the amygdala. These drug doses were chosen after consideration of the 

hypermetobolism of rats. 

EEG recording was started 30 minutes after drug injection and each rat was recorded for 20 minutes. Signals were amplified by 10,000 

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 

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 

12-20 Hz waves in the EEG are accepted as the ratio of percentage in PSA (Power Spectral Analyses) methods. We confirmed electrode 

locations histologically following euthanisation. 

Results: According to the data obtained, the perceptibly dominant frequency in amygdala spontaneous activity was founded to be 1-4 

Hz (Delta). 

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 

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 

Hz (Alpha) (Figure 4) bands, a significant (p < 0.005) increase was observed. 

When the EEG records of the group which was given atypical antipsychotics were compared to the typical antipsychotic administered 

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



[SO-05] Ref. No: 142 

The effect of cognitive-behavioral therapy in reducing the feeling of emotional 

pressure and blood sugar control in patients with type 2 diabetes 

Shahnam Abolghasemi 1 , Ghahraman Mahmodi 2 , Mandana Zafari 2 

1 Department of Medicine, Islamic Azad university,Tonekabon, Iran 

2 Department of Medicine, Islamic Azad university, Sari, Iran 

E-mail: ghahraman48@yahoo.com 

Objective: The results of some studies show that diabetes patients experience some psychological problems, such as depression, stress, selfnegative 

labeling, and lack of self confidence. In this study, we investigated the effect of cognitive-behavioral therapy (CBT) in reducing the 

feeling of emotional pressure and blood sugar control in type 2 diabetes patients, who were referred to the Tonekabon Society of Diabetes. 

Methods: This feeling was measured by using Marghan’s Measure for Feeling of Emotional Pressure. In addition, the blood sugar levels 

of all patients were tested and recorded. The 24 patients, who had the highest emotional pressure scores, were selected and randomly 

divided into two groups, each consisting of 12 patients. They were provided CBT. 

After the end of CBT, they were tested again. The collected data were tested by SPSS software, 10th edition and ANCOVA covariance 

statistical test. 

Results & Conclusions: There were some meaningful differences between the pre-and post-test levels of emotional pressure. The results 

of the blood sugar test also indicated a reduction in the level of blood sugar and normalization of blood sugar control in some patients 

with diabetes type 2. 

Key words: Stress, blood sugar, lack of self confidence, CBT 


[SO-06] Ref. No: 110 

Acute effects of nicotine on working and reference memory in rats using 

a 12-arm radial maze 

Mahsa Movahed Abtahi 1 , Hosein Molavi 1 , Jamal Moshtaghian 2 , Karim Askari 1 

1 University of Isfahan, Faculty of Education and Psychology, Department of Psychology 

2 University of Isfahan, Faculty of Science, Department of Biology 

E-mail: m.movahedabtahi@gmail.com 

Objectives: It has been shown that nicotine plays a significant role in improvement of memory. Based on this finding, nicotinic drugs are 

being developed for possible use as co-treatments for cognitive impairment in some kinds of mental disorders. However, past studies 

have mostly emphasized working memory function following acute administration of nicotine and the few studies concerned with 

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, 

provides a lower task difficulty, the present article aims to replicate previous studies with a specific emphasis on reference memory using 

a 12-Arm Radial Maze which provides a higher level of cognitive task demands. 

Methods: Three groups of male Wistar rats were used. The rats were subcutaneously injected with three doses of nicotine 20 min prior 

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 

injected with 0.4 mg/kg , and the third group was the control which received saline. 

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 

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 

maximum time of 6 minutes was over. There was at least 24 hours between drug injections during which time the rats were not tested. 

Results: The results of repeated analysis of variance showed a significant difference in working memory errors among the three groups, 

but there was no significant difference in reference memory errors between the groups. An inverted U-shaped dose-effect curve was seen 

for reference memory which showed that nicotine first results in increased reference memory errors and then, perhaps because of the 

effect of training, the number of errors decreased. 

Conclusions: The current study suggests a negative correlation between acute consumption of nicotine and long-term spatial 

performance on a 12-Arm Radial Maze, which contradicts the former assumption on an 8-Arm Radial Maze. This finding also emphasizes 

the different mechanisms underlying working and reference memory that should be considered in pharmacotherapeutic interventions 

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with nicotinic drugs and other drugs for memory impairments in various mental disorders. 

Key words: Nicotine, reference memory, learning, radial-arm maze 


[SO-07] Ref. No: 243 

The relationship between personality characteristics and internet addiction in adolescents 

Jalal Shafaie 1 , Sharooz Farjad 2 

1 Shafa jalal,Young Researchers Club, Islamic Azad University, Ardabil 

2 Farjad Sharooz, Department of Educational Managment, Islamshar Branch, Islamic Azad University, Tehran 

E-mail: jalal.shafa@gmail.com 

Introduction: Personality has been identified as a significant factor in internet addiction. The purpose of the present research was to 

investigate the role of personality factors in the prediction of internet addiction in adolescents. 

Materials-Methods: The research subjects consisted of 261 (146 females, 115 males) adolescents from the city of Ardabil. They were 

selected by using the random clustering method. The data of the Young Internet addiction (IAT) test and the NEO-FFI Personality 

Inventory were used together. The data were analyzed by Pearson’s correlation coefficient and multivariate regression analysis. 

Results: The result of the Pearson correlation coefficients showed that there were significant relationships in adolescent girls between 

neuroticism (r=0.42, P



[SO-09] Ref. No: 254 

Comparison of the effects of bupropion and fluoxetine on reaction time in adults 

with major depressive disorder in a 4-week, single-blind study 

Farshad Hashemian, Marjan Sadat Tabatabayi, Ali Sharifi, Marzieh Majd 

Department of Clinical Pharmacy, Islamic Azad University, Pharmaceutical Sciences Branch,Tehran, Iran 

E-mail: hashemian.f@iaups.ac.ir 

Objectives: Some studies have shown that adults diagnosed with major depression have longer reaction time compared to the 

healthy population. Longer reaction time may result in educational and occupational impairment and increased risk of fatal driving 

incidents. Consequently, any impact on reaction time induced by drug therapy may have either positive or negative effects on treatment 

outcome and quality of life of patients. Bupropion is an effective antidepressant, which clearly acts via different mechanisms than other 

antidepressants. Its mechanism of action is thought to be dopamine and/or norepinephrine reuptake inhibition with negligible effects 

on serotonin. 

While bupropion is considered an antidepressant with minimal effects on alertness and cognitive function, the present study was 

designed to evaluate the effects of bupropion on reaction time in comparison with fluoxetine, in adult patients with major depressive 

disorder. 

Methods: A total of 30 patients who met the DSM-IV criteria for major depression were recruited for this study. Patients were randomly 

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 

weeks of treatment using validated computer-generated tasks and keyboard tapping tests in which the data was collected and analyzed 

for auditory and visual stimuli. In addition, the participants were assessed using the Hamilton depression rating scale at baseline, 2 and 4 

weeks of treatment. The number of correct responses, omissions, and substitution errors for each stimulus were calculated. 

Results: No significant differences were observed between the groups regarding demographic characteristics and Hamilton depression 

score at baseline. 

In both groups, the number of correct responses to the visual stimuli increased significantly after 4 weeks of treatment (P


patients treated with methadone. 

Methods: A total of 36 male opioid-dependent patients, aged between 18 and 50 years who met the DSM-IV criteria for opioid dependence, 

were randomly assigned into two groups of 18 members, to receive either ginseng (two 250 mg capsules daily) or placebo for the first 15 

days of detoxification. All patients were treated with a Methadone Maintenance Treatment (MMT) protocol. Opioid withdrawal syndrome 

severity was measured by the Clinical Opioid Withdrawal Scale (COWS) on days 0, 1, 7, 10, and 15. In addition, the required daily methadone 

dosage was recorded and compared between the groups. This trial was registered in the Iranian Registry of Clinical trials (IRCT) under ID of 

IRCT201009063106N4 and was approved by the Ethics Committee of Azad University (approval number: 4115). 

Results: Patients in the two treatment groups did not differ significantly in socio-demographic and clinical variables at the baseline. 

As expected, a statistically significant decrease in the COWS total score and symptoms was observed from the first day to the end of the 

study in both treatment groups. 

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



Conclusions: The in vitro disintegration test is a proxy for the disintegration process in a patient’s mouth. Differences found in the 

formulation and manufacturing processes of ODO products may be associated with different disintegration times, which may potentially 

impact their use in clinical practice. 

Key words: In vitro analysis, orally disintegrating olanzapine 


[SO-12] Ref. No: 118 

Effect of duloxetine on functional outcomes in patients with major depressive disorder 

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 

1Eli Lilly Turkey, 

2University of South Florida College of Medicine, Tampa, USA 

3Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, USA 

4Lilly, Indianapolis, USA 

E-mail: alev_levent@lilly.com 

Objective: Patients with major depressive disorder (MDD) often have a reduced ability to function socially, maintain and enjoy 

relationships and work. The aim of this analysis was to investigate the efficacy of duloxetine vs. placebo on improvement in functioning 

after 8 weeks of treatment. 

Methods: This was a pooled analysis of data from two separate 9-month studies conducted under the same protocol in patients with 

MDD (DSM-IV-TR) to examine the efficacy of duloxetine 60 mg/day (n = 518) vs. placebo (n = 258) on impairment in functioning. Pooling 

the data from these studies was specified a priori in the protocol to allow for increased power to detect differences between duloxetine 

and placebo on secondary and exploratory objectives. The measures included in this analysis were: the Hamilton Depression Rating Scale 

(HAMD) Item 7 (Work / Activities), the Sheehan Disability Scale (SDS), the Social Adaptation Self-evaluation Scale (SASS) to assess social 

behavior, the Massachusetts General Hospital Cognitive and Physical Functioning Questionnaire (CPFQ) and the Profile of Mood States 

-brief form (BPOMS) subscales Vigor / Activity (VA) and Fatigue / Inertia (FI) used as surrogate measures of function. Mean changes from 

baseline were analyzed by using a mixed-effects model repeated measures approach (MMRM). An analysis of covariance (ANCOVA) using 

a last observation carried forward (LOCF) approach was conducted as a sensitivity analysis. The endpoint for this analysis was at week 8. 

Results: At baseline, patients had moderately severe levels of SDS global functional impairment scores (18.3±6.9). At the endpoint, 

there was significant improvement from baseline (MMRM) with duloxetine treatment on the HAMD Work / Activities (p


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), 

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 

recorded regularly during the experimental period. After three weeks, the animals were sacrificed and blood glucose, serum cholesterol, 

serum triglycerides, serum total protein, serum urea, serum zinc, liver zinc, kidney zinc, pancreatic zinc, femur zinc, liver glutathione 

concentrations, serum glutamic oxalic transaminase (GOT), serum glutamic pyruvic transaminase (GPT) and serum alkaline phosphatase 

activities were determined. 

Results: The body weight gain of the zinc deficient diabetic animals at the end of three weeks of dietary manipulation was significantly 

lower than that of the zinc adequate diabetic animals. The zinc deficient diet significantly increased the blood glucose, serum cholesterol, 

serum triglycerides, and serum urea of the zinc deficient diabetic rats as compared to their counterparts fed on an adequate zinc diet. 

Meanwhile serum zinc, femur zinc, pancreatic zinc, liver zinc, kidney zinc, serum total protein, and liver glutathione levels were diminished. 

The consumption of a zinc deficient diet led also to an increase in GOT and GPT and a decrease of serum alkaline phosphatase activities. 

However, vitamin D treatment ameliorated all of the previous physiological and biochemical parameters. 

Conclusion: In conclusion, this study demonstrated that vitamin D reduced the severity of diabetes development caused by zinc 

deficiency. In other words, vitamin D probably increased zinc absorption which led to insulin synthesis and secretion and improvement 

of insulin activity. 

Key words: Zinc deficiency, diabetic rats, alloxan, vitamin D, GOT, GPT, alkaline phosphatase 


[SO-14] Ref. No: 152 

Gabapentin in the treatment of opioid withdrawal 

Gholam Reza Kheirabadi, Mehrdad Salehi, Mohammad Reza Maracy, Mansor Ranjkesh 

Isfahan University of Medical Sciences, Iran 

E-mail: kheirabadi@bsrc.mui.ac.ir 

Objectives: To evaluate the efficacy of gabapentin (1600 mg/day) as an adjunct to methadone-assisted detoxification (MAD) in the 

treatment of opioid withdrawal symptoms. 

Methods: Design: A 3-week open label study (as the second phase) following a double blind placebo controlled study with 900mg/day of 

gabapentin (as the first phase of this study). Setting: A specialized outpatient clinic for the treatment of patients with addictive disorders. 

Participants: Twenty-seven opiate addicts, who met the DSM-IV-TR criteria for opioid dependency, randomly selected among outpatients 

referred to our clinic. Intervention: The subjects received adjunctive treatment with gabapentin (1600 mg/day) in addition to MAD for 

three weeks. Measurements: The Subjective Opiate Withdrawal Scale (SOWS) with a total score of 0 to 64 was administered at six timepoints 

during the study. 

Results: The total SOWS score was significantly decreased after the intervention. Compared with our previous trial, an almost significant 

difference was observed in total SOWS scores between groups treated with gabapentin 1600 mg/day and 900 mg/day at the end of the 

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 

severity of coldness, diarrhea, dysphoria, yawning, and muscle tension. 

Conclusion: Add-on gabapentin at a dose of 1600 mg/day may be effective in reducing some of the withdrawal symptoms in opiate 

addicts undergoing methadone-assisted detoxification. 

Key words: Opium dependence, opioid withdrawal, gabapentin 





[SO-15] Ref. No: 103 

The role of transcranial magnetic stimulation in cognitive processes and treatment 

of psychiatric disorders 

Serwa Mohamadzadeh Ashna 

Young Researchers Center, Islamic Azad University, Sanandaj Branch, Sanandaj, I.R. Iran 

E-mail: srwa.mohamadzade@gmail.com 

Background and Objectives: Transcranial magnetic stimulation (TMS) is a neurostimulation and neuromodulation technique, based on 

the principle of electromagnetic induction of an electric field in the brain. This field can be of sufficient magnitude and density to depolarize 

neurons. When TMS pulses are applied repetitively they can modulate cortical excitability, increasing or decreasing it depending on the 

parameters of stimulation, even beyond the duration of the train of stimulation. This effect has behavioral consequences and therapeutic 

potential. Due to its easy use and relatively minor side effects, transcranial magnetic stimulation is now widely used in neurosciences and 

medicine. The main areas of transcranial magnetic stimulation application are: 

1) the investigation of cortical and spinal excitability, 

2) the investigation of neuronal plasticity, 

3) the investigation of neuronal connectivity, 

4) functional mapping, and 

5) the treatment of some neurological and psychiatric disorders. 

Transcranial magnetic stimulation alone or in combination with other noninvasive neuroimaging (PET – positron emission topography, 

MRI – magnetic resonance imaging) and neurofunctional (EEG – electroencephalography, ERP – event-related potentials, FMRI – functional 

magnetic resonance imaging) methods allows the conduction of research on brain functions. Thus, transcranial magnetic stimulation is 

suitable as a diagnostic tool in neurological and neuropsychiatric brain investigations. 

Method: The method of research in this paper was a review of the literature regarding publications that applied TMS for treatment and 

investigation goals. A total of 104 relevant papers were identified and reviewed and the results are presented here. 

Results: TMS is, through inducement of an electrical field, a useful instrument to visualize regional activities in response to stimulation. 

The mechanism of effect of TMS is through inducing the depolarization of neurons that in turn activates other neurons and produces 

behavioral and cognitive outcomes, depending on the stimulated area and its function. For example some of the observable TMS-induced 

effects are: phosphene by stimulating the occipital cortex, interrupting working memory and speech processes by stimulating the 

frontal lobe, or improving verbal memory in major depressive disorder through modulating effects on the dopamine system. TMS, unlike 

electroconvulsive therapy (ECT), does not have any substantial cognitive side effects. TMS has effects on neurochemical and synaptic 

processes in neurons. There are reports in the literature that depression, mania, schizophrenia, pain disorder, hallucinations, catatonia, 

post traumatic stress disorder, obsessive compulsive disorder, Parkinson’s disease, epilepsy, neuronal plasticity studies, tick disorders, 

migraine and dystonia are improved by TMS procedures. 

Conclusions: Current published studies and meta-analyses have evaluated the efficacy of rTMS, given in treatment paradigms that were 

almost certainly suboptimal (e.g. duration of two weeks), and found that TMS is a safe and tolerable intervention. These findings raise the 

possibility of using TMS as a therapeutic device in psychiatric disorders and neuroscience research. 

This study summarizes the mechanisms of effect, advantages, and side effects of TMS and reviews studies of the efficacy of transcranial 

magnetic stimulation on psychiatric disorders. 

Key words: Transcranial magnetic stimulation (TMS), neuromodulation, electromagnetic induction 


[SO-16] Ref. No: 112 

Oxytocin inhibition of pentylenetetrazole-induced convulsions and its identification 

by behavioral measurement and thalamic EEG in the rats 

Oytun Erbas, Vedat Evren, Saylav Bora, Gonul O. Peker 

Department of Physiology, Ege University, School of Medicine, Izmir, Turkey 

E-mail: oytun.erbas@ege.edu.tr 

Objective: In this study, our aim was to reveal the possible anticonvulsant effects of oxytocin (OX) in high doses, as oxytocin has inhibitory 

S117


effects in brain. In addition, these effects were correlated with thalamic EEG recordings. To create the convulsions, pentilentetrazol (PTZ) 

was used. 

Materials-Methods: In this study sixty 8-12 weeks old Sprague-Dawley adult male rats, which were separated into 10 groups (n=6), were 

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 

(control), saline was injected. 

Five minutes after of each injection of OX, 70 mg/kg i.p. PTZ was injected into the all rats and seizures were induced. 

We evaluated the seizure behaviors with the Racine Convulsion Scale and we determined the threshold seizure dose of PTZ, around 35 

mg/kg, and the suppressive dose of OX, around 80 and 120 U/kg. 

The rats, which were placed in a Plexiglas cage, were evaluated according to the severity of convulsions from 0 to stage 5. 

The scale of convulsions was: (0):Normal,(1):Frozen,(2):Nodding,(3):Superficial clonic movements,(4): Bilateral clonus in front extremities 

(piano play)(5):generalized tonic clonic seizures and falling sideways. 

To show the anticonvulsant effects of oxytocin using the EEG, the seventh through the tenth groups were used. Under anesthesia a small 

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) 

(Paxinos Rat Brain), an exterior insulated bipolar EEG electrode was placed in the left thalamic nucleus. In the seventh group thalamic EEG 

records were taken after only saline injection. 

The rats in the eighth and ninth groups were injected intraperitoneally (ip) with 80 and 120 U/kg OX , respectively. In the tenth group 

(control), just saline was injected. Five minutes after each OX injection, 35 mg/kg i.p. PTZ was injected into the all rats. 

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 

were taken by a Biopac MP30 amplifier system and evaluated with the FFT (Fast 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 12-20 Hz waves in the EEG are accepted as the ratio of 

percentage in PSA methods. We affirmed the electrode location histologically following euthanisation. 

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 

3.0±0.57) doses moderately and which shows the maximum effect at 120 U/kg (Stage 1.57±0.53) doses (p



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 

calculate the QTc interval, Bazett’s formula was used. 

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 

and 1 mg/kg metoprolol and for the third group, 3 mg/kg ziprasidone and 2 mg/kg diltiazem were administered intraperitoneally. 

Two hours later, under anesthesia, the QTc interval was calculated by taking the ECG in derivation I. 

Results: In the first group of rats, given ziprasidone and saline the QTc interval (0.161±0.01 s) was significantly (p






November 23-27, 2011 



POSTER PRESENTATIONS


Poster Presentations 

[PP-001] Ref. No: 133 

Visual hallucinations induced by bupropion: A case report 

Sevda Korkmaz 1 , Murat Kuloglu 2 , Sadullah Saglam 3 , Murad Atmaca 2 

1 Department of Psychiatry, 3 Department of Neurology, Psychiatric Hospital 

2 Department of Psychiatry Firat University School of Medicine, Elazig-Turkey 

E-mail: skorkmaz23@hotmail.com 

Bupropion is an antidepressant, which inhibits reuptake of norepinephrine and dopamine. It is a relatively reliable antidepressant in terms 

of side effects and also is used in the treatment of nicotine deprivation (1, 2). Most frequent side effects are insomnia, dry mouth, and 

headache (3). Here we present a case who developed visual hallucinations during bupropion treatment. 

Case: F.Y: A 51 year old woman was admitted to the outpatient clinic with complaints of hump, horror, and seeing spider images. Visual 

hallucinations, anxiety, irritability, insomnia, and anhedonia were noted on psychiatric examination. Except for the visual hallucinations, 

there was no other perception abnormality nor other psychotic symptoms. History: she reported to a psychiatrist with complaints 

of joylessness, weakness, fatigue, and anhedonia. She was diagnosed with major depressive disorder and subsequently was put on 

bupropion 150mg/day. After a week, the dosage of bupropion was increased to 300mg/day. On the first day of the bupropion dose 

increase to 300 mg/day, spider images developed in both of her eyes and in the following days these images increasingly continued. The 

images lasted for days and scared the patient, ruined her sleep pattern, and increased her anxiety. The patient saw an ophthalmologist 

with these complaints and at the medical examination there was no evidence of an organic or pathological disorder. Her blood pressure 

was under control with treatment. The patient had been treated with escitalopram and duloxetine 6 years ago with a diagnosis of 

depressive disorder, but the patient specified that she had not had any visual complaints. There were not any relevant symptoms at 

that time and patient was not describing any clear stress factors. The family history was unremarkable. The patient did not have such 

complaints as dizziness, tinnitus, or paraesthesia and there was not any pathological finding at the neurological examination. Also there 

were no abnormal findings in the blood tests, urinalysis, and MR imaging. The Beck depression, Beck anxiety, and SCL-90 scales showed 

high levels of anxiety and moderate depression. After the assessment of all these data, suspicion was focused on the bupropion as the 

main cause of the spider images (visual hallucinations). The patient did not accept hospitalization, thus she was followed up periodically. 

First the dosage of bupropion was decreased to 150 mg and bupropion treatment was stopped completely in a few days. Alprazolam 0.5 

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 

weeks. Following the discontinuation of the bupropion, the visual hallucinations disappeared in a few days. The patient came for controls 

monthly and at the end of the 6th month the symptoms of depression and anxiety had decreased considerably. 

Comment: Bupropion has become a popular antidepressant in the treatment of depressive disorders in Turkey and is preferred frequently 

because of its relatively low incidence of side effects. Nevertheless every kind of side effects including psychotic symptoms that appear 

during treatment should be assessed carefully. 

Key words: Bupropion, hallucination, antidepressant 

References: 

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. 

2. Englisch S, Inta D, Eer A, Zink M (2010) Bupropion for depression in schizophrenia. Clin Neuropharmacol; 33(5): 257-259. 

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. 


[PP-002] Ref. No: 139 

Clinical features of patients with panic disorder in outpatient clinics of a psychiatric 

training and research hospital 

Ramazan Konkan 1 , Erkan Aydın 1 , Oya Güçlü 1 , Ömer Şenormancı 1 , Mehmet Z. Sungur 2 

1 MD, Psychiatrist in Deparment of Psychiatry in Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, Istanbul Turkey 

2 MD, Proffessor in Deparment of Psychiatry, Marmara University School of Medicine, Istanbul Turkey 

E-mail: ramazankonkan@gmail.com 

Objective: Panic disorder is a disorder characterized by recurrent unexpected panic attacks where the patient may exhibit avoidance 

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behavior by experiencing anticipatory anxiety for further attacks. According to the DSM-IV-TR, panic disorders are divided into two types: 

with and without agoraphobia. Agoraphobia is an anxiety disorder in which there are repeated attacks of intense fear and anxiety, and 

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 

feared places and situations. Panic attack is characterized by intense anxiety that occurs unexpectedly and spontaneously, accompanied 

by somatic and cognitive symptoms. A marked deterioration can be observed in patients’ functions, particularly due to the anticipatory 

anxiety and avoidance behaviors (1,2). The cognitive rationale of panic disorder is linked to a catastrophic interpretation of bodily 

sensations. Negative and anxiety-related processes of thought such as heart attack, cerebral hemorrhage, and loss of control are effective 

in the origin of panic attacks due to a catastrophic interpretation (3). The objective of our study was to identify clinical characteristics 

involved in the onset and maintenance of this disorder in patients who presented to a training and research hospital. 

Method: The study included 101 consecutive patients with panic disorder who presented to the clinics at the Bakirköy Hospital for 

Mental and Neurological Disorders, met the inclusion criteria, volunteered to participate in the study, and provided informed consent. 

The diagnosis was made by two psychiatrists, who were not involved in the study. The diagnosis was confirmed using the Structured 

Clinical Interview Form for the DSM-IV Axis I Disorders (SCID-I). The patients filled in a sociodemographic form, which examined clinical 

characteristics of the disease in detail, including the identifiable life events triggering the disease and the environmental conditions where 

the attacks developed, taking the SCID-I clinical interview guide into consideration. 

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, 

and the mean duration of disease was 6.73 ± 7.65 years. The sociodemographic characteristics of the participants are outlined in Table 1. 

Distribution of the complaints listed in accordance with the DSM-IV-TR panic disorder criteria by their incidence is provided in Table 2 (only 

the first 3 criteria among the DSM-IV-TR panic disorder criteria were included in the assessments). The clinical characteristics of patients 

specific to panic disorder are shown in Table 3. 

Discussion: Understanding the clinical characteristics specific to panic disorder, which have a significant impact on the functioning 

of a person due to escape, avoidance, and safety seeking behaviors as a result of a catastrophic interpretation of bodily sensations, is 

important in conceptualization and therapeutic interventions of the disorder. 

In the present study, the population was not well reflected in terms of gender as participants were consecutively enrolled from the clinics 

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 

studies eliminating such limitations would be beneficial. 

Key words: Panic disorder, panic symptoms, avoiding behavior 


[PP-003] Ref. No: 141 

Effect of calcium in treatment of premenstrual syndrome 

Mandana Zafari, Azar Aghamohammadi 

Department of Midwifery Group, Islamic Azad University, Sari Branch, Sari, Iran 

E-mail: mandanazafari@iausari.ac.ir 

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 

life. This natural phenomenon is often surrounded by vagary, delusions, and negative views, and for some women menses means disorder, 

wound or mental and physical impurity. This feeling is matched with premenstrual stress and its destructive complications overshadow 

the lives of these women. This syndrome as an unsolvable problem lasting during a significant portion of human life and causes family 

problems, misbehaviour with children, problems at work, or absences from work. All of these consequences have caused the public media 

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 

of premenstrual syndrome. 

Method: This study was done using a semi-experimental method, among all of medical students at the Medical School of Mazandaran, 

who filled in the questionnaire to diagnose this syndrome (Rosignol Bonlender Questionnaire) during a period of 3 months. This 

questionnaire included demographic information, entrance and omission criteria, check paper, and a symptom list of Rosignol Bolender. 

A total of 200 girls who suffered from the moderate or severe form of this syndrome were selected randomly and divided in two groups. 

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 

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 

symptoms was compared. Also the comparison after the intervention was done in two groups. 

Results: Based on the independent sample test, these two groups were homogeneous with respect to age (p = 0.233, based on 

independent sample test ), education level (p = 0.328, based on x2 tests , length of menstrual cycle (p = 0.245), based on independent 




sample test ), severity of physical symptoms before intervention (p = 0.141), severity of mental symptoms before the intervention (p = 

0.132), severity of physical and mental symptoms altogether before the intervention (p = 0.144). In the first group there was a meaningful 

difference between the severity of physical (p= 0.000), mental (p= 0.000) and physical & mental symptoms combined (p= 0.000 ) between 

before and after the intervention measurements. The reduction in severity of physical, mental, and physical and mental symptoms 

altogether after the intervention were meaningful between the two groups (p= 0.000). 

Conclusion: Based on our results calcium may improve the symptoms of premenstrual syndrome. 

Key words: Premenstrual syndrome, calcium, placebo, physical symptoms, mental symptoms 


[PP-004] Ref. No: 203 

Eye movement desensitization and reprocessing (EMDR) treatment in a patient 

with post-traumatic stress disorder: A case report 

Hakan Balibey 1 , Adem Balikci 2 

1 Department of Psychiatry Ankara Military Hospital, Ankara, Turkey 

2 Department of Psychiatry Samsun Military Hospital, Samsun, Turkey 


Post-traumatic stress disorder (PTSD) is a psychiatric disorder that is characterized by autonomic, dysphoric, and cognitive signs together 

with affective numbing and distressed re-experiencing and avoidance of previous traumatic events in a person who has encountered, 

lived, or heard an excessively traumatic event. 

EMDR is a psychological method, which has proven to be effective bringing together elements of well-established approaches such as 

psychodynamic, cognitive, behavioral, and client-centered approaches. 

In recent years, there has been an interest in using the EMDR (Eye Movement Desensitization and Reprocessing) therapy. One of the 

reasons for this interest may be its effectiveness shown by numerous studies, especially, conducted with individuals who suffer from Post 

-Traumatic Stress Disorder (PTSD). EMDR is known to be an innovative approach that accelerates information processing and facilitates 

the integration of fragmented traumatic memories. This process is stated to allow better integration of the information that a person 

has to handle in the future. Recent practice guidelines and meta-analyses have designated EMDR as a first-line treatment for trauma. 

Although the prevalence of trauma and trauma related disorders is high in Turkey, there have been a limited number of published studies 

highlighting treatment options (6-8). Given the effectiveness of EMDR regarding trauma and related disorders, the utilization of the 

technique by a broad number of mental health professionals may not only increase the professionals’ competency in treatment of these 

disorders, but also may provide patients suffering from the mentioned disorders a chance to recover in a relatively short period of time. 

In this paper, the treatment process with Eye Movement Desensitization and Reprocessing (EMDR) of a case, who showed signs of posttraumatic 

stress disorder after a car accident and the need to use this effective method by clinicians more frequently and broadly in posttraumatic 

stress disorder patients will be discussed. 

Key words: Eye movement desensitization and reprocessing, therapy, trauma, post-traumatic stress disorder (PTSD) 

References: 

1. Sadock BJ, Sadock VA. Kaplan & Sadocks’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry. Ninth ed., Philadelphia, Lippincott Williams & Wilkins,2003 

p.623-31. 

2. Amerikan Psikiyatri Birliği. Psikiyatride Hastalıkların Tanımlanması ve Sınıflandırılması El Kitabı. Yeniden gözden geçirilmiş dördüncü baskı (DSM-IV-TR),Washington 

DC, Amerikan Psikiyatri Birliği, 2000’den çeviren E Köroğlu, Ankara, Hekimler Yayın Birliği, 2001. 

3. Shapiro, F., Eye Movement Desensitization and Reprocessing: Basic Principles, Protocols and Procedures, 2nd Edition, Guilford Press,Newyork, 2001. 

4. Bisson J, Andrew M. Psychological treatment of post-traumatic stres disorder(PTSD). Cochrane Database Syst Rev 2007;18(3):CD003388. 

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 

Med 2006;36(11):1515-22. 

6. Kavakcı Ö, Doğan O, Kuğu N. EMDR (eye movement desensitization and reprocessing): a different option in psychotherapy. Düşünen Adam The Journal of 

Psiychiatry and Neurological Sciences 2010;23(3):195-205. 

7. Hocaoğlu Ç, Sağlam D. Post-traumatic Stress Disorder in the Elderly: A Case Report. Klinik Psikiyatri 2007;10:223-27. 

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. 


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[PP-005] Ref. No: 208 

Cabergoline induced manic episode: A case report 

Rabia Nazik Yuksel, Zeynep Elyas Kaya, Nesrin Dilbaz 

Department of Psychiatry, Ankara Numune Training and Research Hospital, Ankara, Turkey 

E-mail: rabia.nky@gmail.com 

Cabergoline is an orally administered synthetic dopamine agonist, which is used for the treatment of hyperprolactinemia, Parkinson 

Disease, and antipsychotic-induced prolactin elevation. 

One major characteristic of cabergoline is its long duration of effect. It is highly effective in suppressing prolactin levels up to 21 days after 

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 

of wash-out of adverse effects like psychosis. 

Cabergoline has been associated with adverse reactions consistent with other dopaminergic agonists including cardiovascular, 

gastrointestinal, and neuropsychiatric effects. It is known that dopaminergic treatment is a remarkable risk factor for psychosis. A number 

of reports implicate dopamine agonists in the development of psychosis. But there is no report in the literature on dopamine agonistinduced 

mania. In this case, we report the first manic episode occurring after cabergoline use for hyperprolactinemia treatment. In 

susceptible individuals, cabergoline can cause manic episodes and cabergoline should be used more carefully considering the risk-benefit 

ratio. 

Key words: Cabergoline, manic episode, bipolar disorder, dopamine agonists, hyperprolactinemia 


[PP-006] Ref. No: 218 

Substance use and eating patterns of female adolescent students 

Joung Sook Ahn, Jongho Shin, Ki Chang Park, Seongho Min, Min Hyuk Kim 

Department of Psychiatry, Wonju Medical Center, Yonsei University, Wonju, South Korea 

E-mail: jsahn@yonsei.ac.kr 

Introduction: The problems of smoking and/or drinking among female adolescents come to the front as a serious social problem, as 

the rate of occurrence of these behaviors among female adolescents is on the increase. Substance use disorders and eating disorders 

frequently co-occur in the presence of other psychiatric disorders. Although this co-occurrence suggests the possibility of shared factors 

in the etiology of these two problems, research to date has not established such links. Regardless of the meaning of the association, the 

reality that substance use disorders and eating disorders frequently co-occur has important implications for assessment, treatment, and 

future research, especially for female adolescents. 

Objectives: The first objective of this research was to estimate the rates of smoking and drinking problems among female adolescent 

students and the second was to examine their association with psychopathologies and eating behaviors. 

Methods: We surveyed 861 female adolescents, 405 students in the 8th grade of one middle school and 456 students in the 10th grade 

from two high schools in Wonju, South Korea. Each student completed a questionnaire that consisted of demographic data, parental 

monitoring, her attitude toward her parents (CATP), her own attitude toward alcohol, tobacco, and foods, BMI, and the difference between 

perceived and ideal body images (DoBI). The TFEQ (Three Factor Eating Questionnaire) for eating patterns and the self-report version of 

SDQ (Strengths and Difficulties Questionnaire-self report) for psychopathology were also administered. 

Results: 1) For the 8th graders, the prevalence of smoking and drinking were 8.6% and 18.4%, respectively. These prevalences were 

14% and 48.3% correspondingly in the 10th graders (Table 1). 2) Female adolescents with smoking and/or drinking habits, except for 

the 10th graders with smoking, showed inattention-hyperactivity and conduct problems more frequently than the students without 

substance use habits. 3) The 10th graders who reported drinking had eating patterns characterized by dietary restraints, and the 8th 

graders with drinking problems showed disinhibition of eating patterns (Table 2). 4) The female adolescents with a high score in the 

difference between perceived and ideal body image showed inattention-hyperactivity and emotional problems more frequently 

(Table 3). 

Conclusions: From these results, we suggest that middle-school girls may start smoking to reduce their weight. The lower the disinhibition 

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 

of drinking. In conclusion, smoking and drinking behaviors are closely related to externalizing problems such as inattention-hyperactivity 




and conduct problems and eating behavior is mainly related to drinking rather than smoking. The association of eating behavior and 

drinking is likely correlated through the medium of various psychopathologies. 

Key words: Substance use, eating pattern, psychopathology, female adolescents. 


[PP-007] Ref. No: 219 

Neuroleptic malignant syndrome: A case report 

Hale Yaci 1 , Esra Kaymak Koca 1 , Yasemin Uz 1 , Aysun Demir 1 , Aygun Akbay Ozşahin 2 , Fusun Mayda Domac 2 

1Department of Psychiatry, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey 

2Department of Neurology, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey 

E-mail: haleyaci@yahoo.com 

Summary: Neuroleptic Malignant Syndrome (NMS) is a state, which commonly presents with autonomic changes like fever exceeding 

40 degrees Celsius, muscle rigidity, changes in mental status, tachypnea, and fluctuations in blood pressure. It occurs mostly due to 

classical antipsychotic drugs with high potency. However, atypical antipsychotic drugs, such as fluoxetine, reserpine and phenothiazinelike 

antiemetics, can also cause NMS. We present a case of a 38 year-old patient with chronic schizophrenia, who developed NMS after 

ingestion of the intramuscular form of zuclopenthixol acetate 50 mg/ml twice, two days apart. 

Case: A 38 year-old, single, male patient with a diagnosis of chronic schizophrenia for 18 years. While being followed up with clozapine 

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 

apart, by his family for an acute psychotic flare, he presented to the emergency room with sweating, progressive dysphagia, refusal of 

food intake, hypersalivation, slowing of speech, dysuria, and muscle cramps. On examination, his body temperature was 39.3 degrees 

Celsius, heart rate was 110 bpm, blood pressure was 120/70 mm-Hg, and the patient was tachypneic (32/min). There were no pathological 

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, 

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 

with regards to his urinary output. All antipsychotic drugs were stopped. He was put on lorazepam 1 mg/dl because of agitation. On follow 

up, his leukocyte count went back to normal, CPK level was down from 3226 to 102 consecutively. Urea and creatinine levels were 20 mg/ 

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 

was still present but to a lesser extent and after 10 days the patient was discharged with clinical recovery. 

Conclusion: NMS is often seen within 10 days following antipsychotic use; however, regardless of dose and duration of usage, it can 

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 

antipsychotic drug. We believe that as the number of case reports on NMS increase, this issue will be better understood. 

Key words: Neuroleptic malignant syndrome, chronic schizophrenia, zuclopenthixol acetate. 


[PP-008] Ref. No: 223 

Treatment of clozapine induced obsessive compulsive behavior in a schizophrenic 

patient with valproic acid augmentation: A case report 

Fatih Canan 1 , Unsal Aydınoglu 2 , Gjergji Sinani 3 

1 Bolu İzzet Baysal Ruh Sağlığı ve Hastalıkları Hastanesi, Bolu, Turkey 

2 Atatürk Üniversitesi, Psikiyatri Anabilim Dalı, Erzurum, Turkey 

3 Marmara Üniversitesi, Psikiyatri Anabilim Dalı, İstanbul, Turkey 

E-mail: fatihcanan@gmail.com 

Introduction: The comorbidity of obsessive-compulsive disorders (OCD) and schizophrenia has been documented by epidemiological 

investigations. Within the multiple pathogenetic factors leading to OCD in schizophrenic patients, treatment with atypical antipsychotics 

has been proposed for a significant subgroup of these patients. Herein, we report the case of a schizophrenic patient who developed 

clozapine-induced obsessive compulsive symptoms that responded to valproic acid augmentation. 

Case Report: A 51-year-old male patient first developed paranoid delusions and auditory and visual hallucinations at the age of 23, 

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fulfilling the diagnostic criteria of the DSM-IV for schizophrenia. He had been hospitalized several times and underwent various treatment 

regimens (including electroconvulsive therapy) in the past for acute schizophrenic episodes. He had been in remission with clozapine 500 

mg/day for approximately one year before relapse occurred as a result of treatment noncompliance. He was admitted to hospital with 

exacerbation of positive symptoms. He was started on clozapine 50 mg/day and titrated up to 500 mg/day. A significant improvement 

was observed in positive symptoms. However, he developed compulsive hand washing behavior in the 3rd week of the treatment. He had 

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 

disorder. We assumed clozapine-induced obsessive compulsive symptoms and gradually decreased the dosage of clozapine 

which resulted in aggravation of positive symptoms and elevated mood. Therefore, valproic acid 1000 mg/day was added to the regimen 

of clozapine 500 mg/day. Two weeks after starting valproic acid, the patient`s positive symptoms and elevated mood were significantly 

reduced and his compulsive hand-washing disappeared. He was discharged and in a 3 month-follow-up, he was maintained well under a 

combined treatment with clozapine and valproic acid. 

Discussion: Our patient developed hand-washing compulsion during treatment with clozapine,an atypical antipsychotic, which 

disappeared after augmentation of valproic acid. Although a few case reports have mentioned the efficacy of valproic acid in the treatment 

of OCD, there is only one case report showing alleviation of clozapine-induced OCD symptoms with valproic acid augmentation in a 

patient with schizophrenia. In light of our case report, we suggest that valproic acid may be a choice when treating OCD symptoms which 

may appear as an adverse effect of atypical antipsychotics in patients with schizophrenia. Case-controlled studies are required to establish 

the efficacy of valproic acid in the treatment of antipsychotic-induced OCD symptoms before definitive conclusions can be reached. 

Key words: Clozapine, obsessive compulsive behavior, schizophrenia, valproic acid, augmentation 


[PP-009] Ref. No: 227 

Treatment of bipolar disorder in adolescents: A case report 

Çagdas Hunkar Yeloglu 1 , Hulya Guveli 1 , Kadir Sarp 3 , Bulent Bahceci 2 , Cicecek Hocaoglu 2 

1Psychiatry Clinic, Rize Training and Research Hospital, Rize-Turkey 

2Department of Psychiatry, Rize University, Faculty of Medicine, Rize-Turkey 

3Gynecology and Pediatrics Hospital, Trabzon-Turkey 

E-mail: chocaoglu@superonline.com 

Bipolar disorder in adolescents is a chronic and recurrent psychiatric disorder with significant short-term and long-term morbidity. Bipolar 

disorder can occur with different clinical manifestations in the adolescent stage compared to the adult form and usually results in a wrong 

diagnosis. Mixed and rapid cycling type mania can be seen more frequently in adolescents than adults. This disorder often results in poor 

academic and social-family performance, legal problems, and increased risk of suicide. For these reasons, it should be treated in a timely 

and effective manner. However, information on the treatment of bipolar disorder in children and adolescents is limited. We discussed 

prospective studies with more reliable methods that have been published in the last 10 years. With the recent indication of risperidone, 

aripiprazole, quetiapine and olanzapine for treatment of bipolar disorders in children and adolescents, the atypical antipsychotics are 

rapidly becoming a first-line treatment option. The effectiveness of lithium and other mood-stabilizing drug are also supported in 

monotherapy and combination treatment. Studies concerning the pharmacological treatment of bipolar disorders in adolescents have 

commonly focused on the treatment of manic episodes, and very few data are available regarding the treatment of bipolar depression, 

maintenance treatments, and comorbid diseases. Also, further studies examining the safety, efficacy, tolerability and neurobiological 

effects of psychotropic medications in children and adolescents with or at familial risk for developing bipolar disorder are needed. In this 

case report, we will review clinical manifestations, differential diagnosis, and current treatment approaches of bipolar mood disorder. To 

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 

our clinic, has had a bipolar mood disorder diagnosis for 2 years and has been taking an atypical antipsychotic medication with lithium. 

Key words: Bipolar disorder, treatment, adolescents 

References: 

1. Kılınçaslan A, Savaş HA. Çocuk ve Ergenlerde İki Uçlu Bozukluğun İlaçla Tedavisinde Yeni Gelişmeler Güncel Psikiyatri ve Psikonörofarmakoloji 2011;1(1):24-36. 

2. Taylor E. Managing bipolar disorders in children and adolescents. Nat Rev Neurol 2009;5(9):484-91. 

3. Sayar K, Öztürk M, Özer AÖ. Üç Olgu Nedeniyle Ergenlik Döneminde Bipolar Bozukluk Van Tıp Dergisi, 2000; 7(2):66-77. 





[PP-010] Ref. No: 273 

Leukopenia and neutropenia due to venlafaxine use: A case report 

Erdem Onder Sonmez, Nazmiye Kaya 

Department of Psychiatry, Selçuk University, Meram School of Medicine, Konya-Turkey 

E-mail: dr_eondersonmez@hotmail.com 

Background: Neutropenia is a serious side effect of psychopharmacological treatment. Neutropenia is defined as less than 0.5 x 109/L 

mature neutrophil cells. Patients with such severe acute neutropenia are likely to experience life-threatening and sometimes fatal infections. 

This report includes a case, who developed leukopenia and neutropenia due to venlafaxine use and a review of the relevant literature. 

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 

ago. The patient reported a significant decrease in psychiatric symptoms and no side effects due to the treatment in this period. The 

patient reported that the symptom remission had been sustained for 4 years. She reported that complaints including anxiety, palpitation, 

dyspnea, paresthesia, and fear of death started recently following a psychosocial stress. A psychiatrist prescribed venlafaxine 75mg/day 

with a diagnosis of panic disorder. After one month a complete blood count test was performed because the patient complained of 

fatigue. It indicated neutropenia and leukopenia (neutrophil count, 1.2K/uL; leukocyte count, 3.26K/uL). The same test was repeated after 

2 weeks and it indicated a progression in severity of neutropenia and leukopenia (neutrophil count, 0.37K/uL; leucocyte count,2.38K/ 

uL). She had no other concerning pharmacological agent. Because medical evaluations found no other medical problem associated with 

neutropenia, venlafaxine was stopped. Two weeks later, the neutrophil count was 2.54K/uL and the leukocyte count was 4.77K/uL. The 

patient’s hematological table recovered within one month. 

Conclusion: Neutropenia and leukopenia have never been reported during treatment with venlafaxine. A case presentation of 

neutropenia is reported with combined treatment of mianserin and venlafaxine. When neutropenia and/or leukopenia develop during 

a drug treatment the drug should be stopped immediately. Blood cell counts can return to normal after stopping the drug. In our 

case blood cell counts were completely normal in 2 weeks after stopping venlafaxine. It is important to consider routine blood tests in 

psychopharmacological treatments. 

Key words: Leukopenia, neutropenia, side effect, venlafaxine 

References: 

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. 

2. Andrès E, Maloisel F. Idiosyncratic drug-induced agranulocytosis or acute neutropenia. Curr Opin Hematol 2008; 15(1):15-21. 

3. Lucht MJ, Kleinschmidt R, Maier W, Rietschel M. Agranulocytosis during treatment with mianserin and venlafaxine. J Clin Psychopharmacol 2000; 20(4):490-1. 


[PP-011] Ref. No: 138 

EMDR treatment for a sexual rape victim: A case report 

Mehmet Ak, Ebru Sinici, Ozgur Maden, Ali Bozkurt, Aytekin Ozsahin 

Department of Psychiatry, Gulhane School of Medicine, Ankara, Turkey 

E-mail: esinici@gmail.com 

Almost anyone who has had a traumatic experience might show intense stress symptoms. It is possible to see post-traumatic stress symptoms 

especially among people who have been raped. Recently, efforts to provide counseling for rape victims have become common. The EMDR 

treatment focuses on the sensorial units of the memory (emotional, cognitive, and physical) to reach the disturbing events, accelerate 

functions, and improve the learning process. It is thought that EMDR treatment relieves post-traumatic stress symptoms for rape victims. In 

this case 90 minute EMDR sessions were applied. The Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), State and Trait Anxiety 

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 

session. It was observed that the stress symptoms of the patient decreased shortly after the EMDR treatment and 1 month later in the follow 

up session. Although the study was conducted with one individual, in patients with sexual trauma, the EMDR application might be beneficial. 

Key words: Trauma, rape, EMDR 


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[PP-012] Ref. No: 124 

Influence of family and education factors on the inclination to commit crimes in 

Soviet times and today 

Elena Valzdorf 

Irkutsk Regional Psychoneurologic Dispensary, Irkutsk, Russia. 

E-mail: elenavalzdorf@yandex.ru 

Objective: The objectives of the research were to study the influence of education level and some family factors (alcohol addiction of 

parents, upbringing in a one-parent family) on the inclination to commit criminal offences in the examined individuals in Soviet times in 

comparison to the current situation. Material and methods: 35 reports of the Commission of forensic psychiatric experts over the period 

of January - March 2010 (the examined individuals of group 1) and 35 archive acts of outpatient forensic psychiatric examination that 

covered the period of January-March 1991 (the examined individuals of group 2) were analyzed. In total 70 men aged between 15 and 75 

were considered. The statistic method, comparative analysis, in combination with the data on the somatoneurological state and the data 

of an experimental psychological study were applied. 

Results: The study found out that 20 patients of group 1 were held criminally responsible under article 131 of the RF Criminal Code (CC), 

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, 

14 had received incomplete secondary education, 7 did not receive any education at all, 6 individuals received full secondary education, 

4 incomplete secondary vocational education, 4 higher vocational education, and 1 patient received education in the form of 8 years of 

special school. The family history data showed that 10 patients were brought up in the family in which either 1 or both parents abused 

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 

35 patients of group 1 were brought up in secure families. The 35 patients of group 2 included 9 individuals that were held criminally 

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 

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 

2 there were 15 individuals with incomplete secondary education, 13 with incomplete secondary vocational education, 5 with full 

secondary education and 2 with full secondary vocational education. The family history data showed that 18 patients from group 2 were 

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 

were raised in a one-parent family. 

Conclusion: The study demonstrated a clear relationship between the education level and some family factors affecting the inclination 

to commit criminal offences. Now the number of criminal offenses against the person that are committed by uneducated individuals 

has increased, as well as crimes committed by those who have higher vocational education, while the number of secure families has 

decreased, which in turn has exacerbated the criminal situation in the country. 

Key words: Education factors, Soviet times, forensic psychiatric examination 


[PP-013] Ref. No: 108 

Survey of referral pathways to a crisis team 

Mahesh Nachnani, Stuart Beatson 

Department of psychiatry, Pilgrim Hospital, NHS, Boston, United Kingdom 

E-mail: mahesh.nachnani@nhs.net 

Introduction: Crisis Teams are well established in many trusts in the departments of psychiatry around the UK. The crisis team based 

at Pilgrim Hospital, Boston receives 1300 referrals per year approximately. Not only is it important to know what the sources of referrals 

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. 

This information will have implications in terms of service provision, as well as targeting potential sources of referrals in terms of psychoeducation 

of not only service users, but also of referring agencies at different tiers of mental health services, from a general practitioner 

to a care provider in the community. 

Objectives and Methods: To ascertain sources of referrals to a crisis team and the destination to which service users were discharged at 

the time of closure of a case by the crisis team. 

Results and Conclusion: N = 92 records of service users were randomly selected. They all completed their journey through the crisis team 


from triage to discharge. 

Key words: Crisis team, referral pathways, community care 




[PP-014 Ref. No: 122 

Fluanxol and haloperidol efficacy evaluation in treatment of schizophrenic patients 


Irkutsk Regional Psychoneurologic Dispensary, Irkutsk, Russia. 


Objective: The purpose of the research was to study the efficacy of Fluanxol in the treatment of schizophrenic patients compared with haloperidol. 

Method: Research subjects were 23 paroxysmal progredient schizophrenia patients, who were stationary examined. There were 18 men 

and 5 women among them, 6 patients of 16 to 20 years of age and 17 patients aged between 20 to 40 years. 

A clinical-psychopathological research method with a psychopharmacological approach was used. 

Results: Three groups of patients were picked out. The first group of 9 patients included patients with an acute and subacute exacerbation, 

Kandinski-Klerambo syndrome, acute sensitive delusions of grandeur, of influence, of persecution with imperative pseudo hallucinations, 

and open thought symptoms. 

The second group of 4 cases included patients with paraphrenia acute exacerbations, expansive delusions, and auditory pseudo 

hallucinations with oneric inclusions. 

In both groups the therapy began with traditional neuroleptics. Haloperidol depot 5 mg was prescribed intramuscularly once every 2 

weeks, but haloperidol intravenously from 5 to 10 mg a day. During 7-10 days of treatment, productive psychotic symptoms were reduced 

only through intensity in order to change preparation closed to atypical antipsychotic drug. So Fluanxol depot from 10-20 mg was 

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 

therapy, psychotic symptoms were reduced after 5-7 days of treatment. 

The third group of 10 people included less progredient schizophrenia patients with neurosis-like negative symptomatology. Haloperidol 

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 

twice a day inside for 7-12 days of treatment, caused a decrease in intensity or a complete reduction in negative symptomatology, so as 

mimics, mood, emotions were improved. This Fluanxol effect was shown by the two first groups having negative symptoms. Most patients 

took it without any corrector-preparation. 

Conclusion: Fluanxol is more effective in the treatment of schizophrenic patients. 

In comparison with haloperidol it decreased positive symptomatology more quickly, decreased or completely reduced negative 

symptoms and only in some cases caused drug side effects. 

Key words: Fluanxol, haloperidol, schizophrenia 


[PP-015] Ref. No: 241 

Anorexia nervosa and cannabis abuse: A case report 

Semra Karayılan, Atila Erol 

Department of Psychiatry, Sakarya University School of Medicine, Sakarya, Turkey 

E-mail: skryln@gmail.com 

Rates of comorbidity are higher in patients with eating disorders and also the number of comorbid disorders is numerous. Most 

comorbidities associated with eating disorders are mood disorders, anxiety disorders, personality disorders, and substance use disorders. 

According to past research, there is a high rate of comorbidity of alcohol-substance abuse and eating disorders. Although the majority of 

studies in this area are focused on the use of alcohol, studies that have identified an association between illegal substance use and eating 

disorders are also available. In a study in the USA, the use of cannabis with anorexia nervosa (AN) and bulimia nervosa (BN) disorders is 

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 

cannabis was reported in cases of BN, but the use of psychoactive substances and cannabis was not established in cases of AN. Among 

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eating disorders, alcohol or drug abuse are most often found in individuals with bulimia nervosa and bulimic behaviors. Also, binge eating/ 

purging anorexics appear to be more likely than restricting anorexics to indulge in substance use. Patients with bulimia nervosa have 

significantly higher rates of use of amphetamines, barbiturates, marijuana, tranquilizers, and cocaine than patients with anorexia nervosa. 

Compounds of cannabis like tetrahydrocannabinol activate endogenous cannabinoid receptors (CB1 and CB2) in brain. Stimulating the CB1 

receptor is known to cause increased appetite and an antiemetic effect and because of these effects cannabinoids are included in clinical 

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, 

high school student, lived with her family, had complaints of weight loss and had used cannabis for three years. Before beginning to 

use cannabis her BMI was approximately 22, when referred to our clinic it was 15.6. She indicated that at first cannabis caused increased 

appetite, but excessive vomiting occurred in the first few months and then she started to exercise excessively. Although she noticed losing 

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 

anorexia nervosa comorbidity hasn’t previously been reported. In this respect, discussion of the case in detail is important. 

Key words: Anorexia nervosa, cannabis, substance abuse, eating disorders 


[PP-016] Ref. No: 249 

Fluoxetine-induced thrombocytopenia: A case report 

Atakan Yucel 1 , Mustafa Gulec 1 , Adem Aydin 2 

1Department of Psychiatry, Atatürk University, School of Medicine, Erzurum-Turkey 

2Department of Psychiatry, Yuzuncu Yil University, School of Medicine, Van-Turkey 


Case: A 44 year old, university graduate, married male with 2 children was diagnosed with a first episode major depressive disorder 

and no abnormalities were observed in the routine tests, including the total blood count test carried out prior to commencing drug 

therapy. Afterwards the patient was prescribed fluoxetine and the daily total drug dose was set at 10 mg for the first week of treatment 

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 

total remission and no change was made in the pharmacotherapy. However, it was learned that thrombocytopenia was detected in the 

total blood count test requested by the family doctor because of a suspicion of a urinary tract infection. Since no pathology that could 

account for the thrombocytopenia that was detected by a hematology expert following standard consultation and further tests, the 

patient was transferred back to us with a suspicion of fluoxetine induced thrombocytopenia. Fluoxetine was immediately discontinued 

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. 

The thrombocytopenia of the patient went into total remission within 7 days and no problem was observed during the total blood count 

tests for the next 6 months. 

Even though the most common side effects of fluoxetine are nausea, nervousness, and insomnia, side effects of the hematological 

system have also been noted. To this end, there are publications which suggest possible negative effects on the number and function of 

thrombocytes. It is thought that the mechanism behind these hemostasis related side effects of fluoxetine is the depletion of serotonin 

stores by preventing the reuptake of serotonin into thrombocytes. Starting from this hypothesis, the presumption is that reboxetine, 

which is a pure noradrenaline reuptake inhibitor, will have no effect on these processes. In fact, there have been no reports that relate 

reboxetine with thrombocytopenia and/or thrombocyte functional disorders. However it should be clarified with further studies whether 

this is purely coincidental or if reboxetine has no effect on serotonergic systems. 

Conclusion: Reboxetine may be a good alternative for patients with thrombocytopenia and/or with functional thrombocyte disorders in 

the treatment of major depressive disorders. However, more research is required in order to reach more certain conclusions. 

Key words: Depression, hematological, side effect, switching, reboxetine, fluoxetine, thrombocytopenia 

References: 

1. Pai VB, Kelly MW. Bruising associated with the use of fluoxetine. Ann Pharmacother 1996; 30(7-8):786-788 

2. Mirsal H, Kalyoncu A, Pektaş O. Ecchymosis associated with the use of fluoxetine: case report. Turk Psikiyatri Derg 2002; 13(4):320-324 

3. Halperin D, Reber G. Influence of antidepressants on hemostasis. Dialogues Clin Neurosci 2007; 9(1):47-59 

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 

trial. Br J Psychiatry 2011; 198(6):464-471 





[PP-017] Ref. No: 312 

Interethnic differences in UGT1A4 genetic polymorphisms in Mexican and 

Spanish populations 

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 

1 Department of Biological Systems, Universidad Autónoma Metropolitana-Xochimilco, Mexico City, Mexico 

2 CICAB Clinical Research Centre. Extremadura University Hospital and Medical School. Servicio Extremeño de Salud, Badajoz, Spain 

3 Department of Neurogenetics and Molecular Biology, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico 


Clinical treatment with antiepileptics exhibits large interpatient variability. The UDP-glucuronosyltransferase (UGT) 1A4 is an enzyme 

responsible for the conjugation of glucuronic acid in diverse functional groups included in various antiepileptic drugs, such as lamotrigine 

and phenytoin. Several genetic polymorphisms of UGT1A4 have been described in different populations; among them, two nonsynonymous 

single nucleotide polymorphisms (SNPs) 70A>C (P24T; UGT1A4*2) and 142T>G (L48V; UGT1A4*3b), as well as a synonymous 

variant SNP 471T>C (C157C; UGT1A4*1b). P24T and L48V polymorphisms reduce the glucuronidation activity on various substrates. 

Recently, it has been shown that L48V polymorphism decreases the serum concentration of lamotrigine in patients on monotherapy or 

polytherapy, resulting in clinical outcome variability. 

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 

Mestizo (MM) and Spaniard (SP) healthy volunteers. UGT1A4 genotyping is clinically important in order to identify patients who may be 

at an increased risk for failure of therapy and/or adverse effects to anticonvulsants such as phenytoin and lamotrigine. 

In this study, the allelic frequencies of these three UGT1A4 variants were determined by combined methodology of RFLPs and RT-PCR in 

MM and SP populations. The allelic frequencies of the three UGT1A4 polymorphisms analyzed showed interethnic differences between 

MM and SP, that was statistically significant for UGT1A4*1b (0.17 and 0.08, respectively; p=0.002). 

These data could help clinicians to improve clinical response during treatment with UGT1A4 antiepileptic drug substrates in these 

populations. 

Key words: Interethnic differences, UGT1A4, genetic polymorphism. 


[PP-018] Ref. No: 315 

Influence of CYP2C9 genetic polymorphism on losartan oxidation in an 

Ecuadorian population 

Pedro Dorado, Eva Peñas Lledó, Esther Machín, Adrián Llerena, Enrique Terán, Leonardo Beltrán 

CICAB Clinical Research Centre. Extremadura University Hospital and Medical School. Servicio Extremeño de Salud, Badajoz, Spain. Biomedical Centre, Central University 

of Ecuador and Health Science College, Universidad San Francisco de Quito, Quito, Ecuador 


Background: Cytochrome P450 2C9 (CYP2C9) is a polymorphic enzyme catalyzing the metabolism of several important drugs. CYP2C9 

metabolizes a number of therapeutically important drugs, including most nonsteroidal anti-inflammatory drugs, S-warfarin, phenytoin, 

and losartan. CYP2C9 is also involved in the metabolism of several important psychoactive substances (tetrahydrocannabinol, fluoxetine, 

amitriptyline, phenytoin, etc.). It has been reported that CYP2C9 activity is modulated by endogenous substrates such as adrenaline and 

serotonin. The involvement of CYP2C9 in the metabolism of melatonin has also been suggested. 

Losartan has recently been suggested as a selective probe for CYP2C9 metabolic activity. 

Objective: The aim of the study was to determine the activity of CYP2C9, using losartan as a probe drug, in relation to CYP2C9 genotype 

in healthy Ecuadorian subjects. 

Methods: A single oral dose of 50 mg losartan was given to 194 Ecuadorian unrelated subjects. Concentrations of losartan and its 

carboxylic acid metabolite, E3174, were analyzed by means of high-performance liquid chromatography in urine collected for 8 h. The 

CYP2C9 genotypes were determined in 194 subjects using specific methods for CYP2C9*2 and CYP2C9*3. 

Results: The frequencies of the allelic variants CYP2C9*2 and CYP2C9*3 were 0.054 and 0.015, respectively. The urinary losartan/E3174 

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 

CYP2C9*1/*1 (4.9±7.0; n=167). 

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Conclusion: This is the first most extensive population where losartan has been used as a probe drug to evaluate the CYP2C9 activity in 

vivo. The urinary losartan to E3174 metabolic ratio after a 50mg losartan dose was found to be a safe and useful phenotyping assay for 

CYP2C9 activity in vivo. The CYP2C9*3 variant allele is a major determinant of the enzyme activity, and it decreases losartan metabolism 

significantly, while the CYP2C9*2 allele has less impact on enzyme function. 

Key words: Cytochrome P450 2C9, genetic polymorphism, losartan, ecuadorian population 


[PP-019] Ref. No: 194 

Efficacy of progressive muscle relaxation training on anxiety, depression and 

quality of life in cancer patients under chemotherapy 

Sepideh Ershadmanesh Herizchi 1 , Isa Tt Piri 2 , Iraj Tt Asvadi 3 , Zohreh Tt Sanaat 4 , Mrs Tt Golchin 5 , Reza Tt Shabanloui 5 

1 Assistant Professor of Psychiatry, 2 Psychologist, 3 Professor of Oncology, 

4 Z.Sanaat, Assistant Professor of Oncology, 5 MS of Nursing, Hematology & Oncology Research Center-2010, Tabriz, Iran 

E-mail: sherizchi@gmail.com 

Introduction: Chemotherapy is one of the common treatment methods for cancer. However, many side effects can be seen among 

patients and some of them are very serious and painful. Alopecia, anorexia, vomiting, pain in the limbs, headache, and backache are some 

unwanted effects. On the other hand many patients suffer from psychiatric disorders especially anxiety and depression probably due to 

the drugs or coping with the disease state. These disorders can cause some problems in the treatment process and the Quality of life. 

Patients with anxiety and depression can be treated with drugs or psychotherapy. 

Progressive Muscle Relaxation [PMR] training is a cost effective self-help method promoting mental health in healthy participants. 

The aim of this study was to determine anxiety, depression, and quality of life dimensions of cancer patients undergoing chemotherapy 

and the effect of progressive muscle relaxation training in improving their mental health and quality of life. 

Materials and Methods: This research was designed as a randomized clinical trial. Sixty cancer inpatients undergoing chemotherapy 

in the Tabriz Hematology & Oncology ward in 2009 were randomly selected and divided into two groups, intervention or control. All 

participants provided a written formal consent. 

Anxiety, depression, and quality of life dimensions were determined with HADS and EORTC QLQ-C30 questionnaires. SPSS 16 software 

was employed for the data analysis. 

After completion of the 1st questionnaires by all participants, the case group was trained in progressive muscle relaxation in 3-6 person 

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 

after the intervention, questionnaires were completed again by both groups, and the results were compared. 

Results: After initial data analysis almost all of the participants were satisfied with the learning and the experience of this technique. 

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). 

However, after 3 months, anxiety, depression and quality of life dimensions were significantly improved (p



[PP-020] Ref. No: 127 

Anxiety reducing effects of oxytocin on the basolateral amygdala by using 

an electrophysiological method 

Oytun Erbas, Saylav Bora, Serdar Demirgoren, Gonul Peker 

Physiology Department, Ege University, School of Medicine, Izmir, Turkey 

E-mail: oytun.erbas@ege.edu.tr 

Objective: It has been shown by behavioral studies that oxytocin has anxiolytic effects and that oxytocin in nasal spray form suppresses 

amygdala activity, which is powered by anxiety as demonstrated in functional MRI studies in humans. The amygdala is a part of the 

limbic system and is activated in case of fear and anxiety. This study evaluated the effects of oxytocin on the basolateral amygdala using 

a spontaneous EEG. 

Material and Methods: The experiments performed in this study have been carried out according to the rules in the Guide for the Care 

and Use of Laboratory Animals adopted by National Institutes of Health (U.S.A) and have received consent from Ege University Animal 

Ethics Committee. 

The rats were maintained under controlled environmental conditions throughout the study: 22-24 °C ambient temperature, 12:12 lightdark 

cycle (light from 7:00-19:00), and standard laboratory food and tap water available ad libitum. 

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 

taking the bregma as a reference using the stereotaxic method (coordinates Anteroposterior: - 2.8 mm, Lateral: + 4.8 mm, Ventral: - 8.5 

mm) (Paxinos Rat Brain), an exterior insulated bipolar EEG electrode was placed in the basolateral amygdala. 

Electrodes were fixed by using a dental acrylic (numerous alloys are used in the making of dental restorations). The rats were anesthetized 

using ketamine (40 mg/kg) and xylazine (4 mg/kg) intraperitoneally (IP). 

Electrodes were placed and 3 days later, while the animals were awake in their cages, spontaneous EEG recordings were taken from 

the amygdala. Then, 0.9% isotonic NaCl solution was injected intraperitoneally into the rats (n = 7), and the EEG was recorded from the 

amygdala while they were in their cages. 

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 

taken in their own cage. 

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 

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 

of percentage in PSA (Power Spectral Analyses) methods. We affirmed electrode location histologically following euthanisation. 

Results: There was significant (p


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. 

Autism, flattening of affect, incoherent speech and bizarre, somatic, nihilistic delusions were found in the psychiatric examination. 

Flupentixol decanoate 20 mg every 15 days IM, haloperidol 20 mg/day and biperiden 10mg/day were administered first IM then orally. 

There was no remission even after adding ECT for ten sessions. Then clozapine was begun at 25mg/day and titrated to 500mg/day. He 

was discharged with symptoms which were much improved by using clozapine 500 mg/day, haloperidol 10 mg/day, biperiden 4mg/day, 

quetiapine 300 mg/day. 

In this paper a schizophrenic patient with testicular mutilation was presented and genital amputation was discussed along with reports 

in the literature. 

Key words: Schizophrenia, testicular mutilation 


[PP-022] Ref. No: 135 

Hoarding and mood disorder: A case report 

Özlem Çetinkaya Girit 1 , Fulya Maner 1 , Emine Kılınç 2 , Derya İpekçioğlu 1 , Mehmet Emin Ceylan 1 

1 Psychiatry Unit, Bakırköy Nueropsychiatry Research & Training Hospital, Istanbul-Turkey 

2NPİ Nueropsychiatric Hospital , İstanbul 

E-mail: fmaner@ttmail.com 

Hoarding is the excessive acquisition of possessions and failure to use or discard them even if the items are worthless or hazardous. The 

hoarder may believe that the hoarded items are very valuable, know that the accumulated items are useless, or attach a strong personal 

value to items. It is not clear whether hoarding is an isolated disorder or rather a symptom of another condition such as obsessive 

compulsive disorder. Hoarding seems to involve some neurological mechanisms which are detected by brain imaging studies. In this case 

report a patient with mood disorder whose predominant symptom was hoarding is presented and the status of literature about hoarding 

is reviewed. 

Key words: Hoarding, obsessive compulsive disorder, mood disorder, dementia 


[PP-023] Ref. No: 140 

Effect of fish oil on treatment of premenstrual syndrome 

Mandana Zafari, Azar Aghamohammadi 

Department of Midwifery Group, Islamic Azad University, Sari Branch, Sari, Iran 

E-mail: mandanazafari@iausari.ac.ir 

Objective: Women go through many hormonal changes throughout their lives from birth to death and this causes many physical and 

mental challenges that are directly related to their unique reproduction delicacy. Premenstrual syndrome refers to a cyclic appearance of 

somatic and psychiatric symptoms in some women. Different theories and hypotheses have been proposed and discussed on this issue. 

Finding an effective and safe solution for the treatment of PMS has always been under consideration. The purpose of our study was to 

determine the effect of fish oil on treatment of premenstrual syndrome. 

Methods: This study was a double blind randomized placebo controlled trial. All of the medical students at the Medicine School of 

Mazandaran filled in the Rosignol Bonlender Questionnaire for 3 months. This questionnaire included demographic information, inclusion 

and exclusion criteria, check paper and the symptom list of Rosignol Bolender. A total of 200 girls suffering from the moderate and severe 

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 

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 

months. After treatment, the severity of physical, mental, and combined physical-mental symptoms were compared before and after the 

intervention. Also the comparison after intervention was done in two groups. 

Results: Based on this and based on the independent sample test, these two groups were homogeneous from the point of view of age 

(p = 0.287, based on independent sample test ), education level (p = 0.954, based on x2 tests), length of menstrual cycle (p = 0.305), 

based on independent sample test ), severity of physical symptoms before intervention ( p = 0.039 ), severity of mental symptoms before 




intervention (p = 0.144), severity of combined physical-mental symptoms before intervention (p = 0.242) in the first group. There was a 

significant difference among the severity of physical (p= 0.000), mental (p= 0.000), combined physical-mental symptoms (p= 0.000) before 

and after intervention. The reduction in severity of physical, mental, and combined physical-mental symptoms after intervention was 

significant between the two groups (p= 0.000). 

Conclusion: Based on our results 1000mg/day fish oil may reduce the severity of physical, mental, and combined physical-mental 

symptoms of PMS. 

Key words: Premenstrual syndrome, fish oil, placebo, physical symptom, mental symptom 


[PP-024] Ref. No: 145 

Improvement of risperidone-induced hyperprolactinemia with the addition 

of aripiprazole: Case report 

Medine Gıynaş Ayhan, Faruk Uguz, Nazmiye Kaya 

Department of Psychiatry, Selcuk University,Meram School of Medicine, Konya, Turkey. 

E-mail: drmedineayhan@gmail.com 

Objective: Hyperprolactinemia is an important side effect of antipsychotic treatment. All typical antipsychotics and some atypical 

antipsychotics such as risperidone and amisulpiride have been shown to cause marked elevation in serum prolactin levels, whereas most 

other atypical antipsychotics such as quetiapine, olanzapine, clozapine, ziprasidone, and aripiprazole appear to have little or no effect on 

serum prolactin levels. Hyperprolactinemia can lead to gynecomastia, galactorrhea, sexual dysfunction, infertility, oligomenorrhea, and 

amenorrhea. It also reduces the bone mineral density and contributes to osteoporosis in the long term. These important side effects cause 

patients in remission not to continue treatment. 

Case: We report two clinical cases of risperidone-induced hyperprolactinemia and amenorrhea, who with treatment by the partial 

dopamine agonist aripiprazole, showed prolactin normalization. 

Conclusion: Addition of aripiprazole to treatment may be considered as a first option in hyperprolactinemia cases with significant 

improvement in psychotic symptoms. 

Key words: Hyperprolactinemia, amenorrhea, antipsychotic, risperidone, aripiprazole 


[PP-025] Ref. No: 146 

Atomoxetine for the treatment of ADHD in young adults with an assessment 

of associated functional outcomes 

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 , 

Paul E. Glaser 5 , Richard L. Rubin 6 , Elias S. Sarkis 7 , Teresa A. Pigott 8 , Bethany K. Boardman 2 

1 Eli Lilly and Company, Istanbul,Turkey 

2 Eli Lilly and Company and/or one of its subsidiaries, Indianapolis, IN, USA 

3 Department of Psychiatry, NYU School of Medicine; and Psychiatry Service, New York VA Harbor Healthcare System, New York, NY, USA 

4 UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA 

5 University of Kentucky, Department of Psychiatry, Lexington, KY, USA, 

6 Vermont Clinical Study Center, Burlington, VT, USA 

7 Division of Child and Adolescent Psychiatry, University of Florida, Gainesville, FL, USA 

8 Department of Psychiatry, University of Florida, Gainesville, FL, USA 

E-mail: altin_murat@lilly.com 

Objectives: ADHD in young adults is associated with significant impairment in multiple functional domains. This trial examined the 

efficacy of atomoxetine (ATX) in young adults and evaluated improvements in core ADHD symptoms and associated functional outcomes. 

Method: Patients aged 18-30 years were randomized to 12 weeks of double-blind treatment with ATX (n=220) or placebo (PBO, n=225). 

Patients in the atomoxetine treatment arm began treatment with 40 mg/day (dosed 20 mg BID) for a minimum of 7 days followed by 

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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 

100 mg/day (dosed 50 mg BID) depending upon continued ADHD symptoms. One unscheduled dose change was allowed if needed for 

tolerability or safety. The Conners’ Adult ADHD Rating Scale- Investigator Rated, Screening Version Total ADHD Symptoms score (CAARS 

– Inv:SV) with adult ADHD prompts, assessed core ADHD symptoms and was the primary efficacy measure. The adult ADHD Quality of 

Life-29 (AAQOL-29) scale evaluated functional outcomes in various life domains. Other assessments included Clinical Global Impression- 

ADHD-Severity (CGI-ADHD-S), CAARS Self Report (CAARS-S:SV), Patient Global Impression-Improvement (PGI-I), Behavior Rating Inventory 

of Executive Function-Adult Version Self Report (BRIEF-A), and measures for depression, anxiety, sleepiness, driving behaviors, social 

adaptation, and substance use. Reported means are least-squares means from last-observation-carried-forward ANCOVA models. A 

mixed-model repeated measures visit-wise analysis was also conducted. 

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], 

p



domains, considered to be important in OCD patients, are also valid for Panic Disorder. 

Method: Our sample group included 101 Panic Disorder group, and 155 healthy volunteers with similar sociodemographic characteristics. 

The instruments used included the Beck Depression Inventory (BDI), State-Trait Anxiety Inventory (STAI), Panic Agoraphobia Scale (PAS), and 

Obsessive Beliefs Questionnaire (OBQ-44). Total and sub-scale scores of obsessive beliefs as assessed by the Obsessive Beliefs Questionnaire-44 

(OBQ-44) were compared between the groups. Total and sub-scale scores in the panic disorder group were re-evaluated against the state, 

trait, and depression factors of the State-Trait Anxiety Inventory (STAI). SPSS 18.0 for Windows was used for statistical analysis. 

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 

total score, Trait Anxiety Scale total score, Beck Depression Inventory total score, OBQ-44 total, and subscale scores in patients with a PAS 

score of 12 or more were statistically significantly higher compared to the control group (p


[PP-029] Ref. No: 154 

Cerebellar contusion presenting with pure psychiatric symptoms and cerebellar 

cognitive affective syndrome: A case report 

Baise Tıkır, Erol Göka, Makbule Çiğdem Aydemir, Sinem Duran 

Ankara Numune Education and Research Hospital, Department of Psychiatry, Ankara, Turkey 

E-mail: baisetikir@yahoo.com 

The cerebellum is known to be responsible for posture and motor coordination of the body. Recent studies indicate that the cerebellum 

has a role in conduction of higher brain functions, such as perception, affect, capacity to analyze, and memory, via neuronal connections 

between the cerebellum and the other regions of the brain. Schmahmann and Shermann described a new syndrome called “the Cerebellar 

Cognitive Affective Syndrome” (SCAS) and drew attention on cognitive functions of cerebellum. The syndrome was described in a group 

of patients who had impairment of executive functions, difficulties with spatial cognition, personality changes, blunt affect and language 

deficits in addition to primary neurological symptoms. In this case report we present a rare case of cerebellar cognitive affective syndrome 

presenting with pure psychiatric symptoms,who had a posterior cerebellar lobe lesion due to a contusion at the back of the skull. 

Key words: Cerebellar cognitive affective syndrome, cerebellum, cognitive functions 


[PP-030] Ref. No: 226 

Self-perception and anger with chest pain without cardiac etiology 

Esra Aydın Sünbül 1 , Murat Sünbül 2 , Fatma Feriha Cengiz 1 

1Erenkoy Ruh ve Sinir Hastalıkları Eğitim ve Araştırma Hastanesi, Istanbul, Turkey 

2Department of Cardiology, Marmara Universitesi, Istanbul, Turkey 

E-mail: mrm_esra@yahoo.com 

Objective: Physical symptoms are the most common expressions of social problems and emotional inconvenience. This problem is 

usually medically unexplained in patients with chest pain. ‘Chest Pain without Cardiac Etiology’ is diagnosed in more than fifty percent 

of patients with chest pain. Anger and suppressed hostility are important factors the development of somatic symptoms. It is important 

to point out that somatization in depressive disorders is due to expression of anger while somatization in anxiety is due to anger 

suppression. It is known that, while patients with chronic pain experience anger, they do not care enough to express it because they are 

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 

the subjects to be emphasized. Suppression of intense anger leads to the development of chronic pain and suppressed anger scores are 

higher than healthy controls. In this study, we compared patients with chest pain without detected cardiac etiology and healthy controls 

in terms of anger and self perception. 

Methods: Twenty five patients were included in the study. They all presented to the cardiology clinic with complaints of chest pain, but 

did not have any detected cardiac etiology. The healthy control group of 80 persons was organized by matching them with the patients 

according to their age, gender, and education. The Socio-demographical data collection form, Multidimensional Anger Scale, and Social 

Comparison Scale were given to both of the groups. 

Results: There was no significant difference between the socio-demographic features of the two groups. The non-cardiac chest pain 

group scored higher on the Social Comparison Scale. The healthy control group scored higher on calm behaviour and nonchalant 

response. Revenge for the reaction and inward looking responses were significantly higher in the non-cardiac chest pain group. 

Conclusions: The non-cardiac chest pain group had more negative perception of self as compared to healthy individuals, further they 

were found to be more negative in their forms of expressing anger. Repressed anger and hostility are important factors in the development 

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 

perceives himself, but also how other people perceive and relate to him, probably effects the physiological system of that individual. 

Key words: Chest pain without cardiac etiology, self-perception, anger 

References: 

1. Kirmayer lj, Young A. Culture and somatization: clinical, epidemiological and ethnographic perspectives. Psychosom Med 1998; 60: 420-430. 

2. Mayou R. Invited review: atypical chest pain. J Psychosom Res 1989; 33: 393-406. 


3. Koh KB. Anger and somatization. J Psychosom Res 2003; 55:113. 

4. Sayar K, Bilen A, Arıkan M. Kronik ağrı hastalrında öfke, benlik saygısı ve aleksitimi. Türkiye Klinikleri Psikiyatri 2001; 2: 36-42. 

5. Güleç MY, Hocaoğlu Ç, Gökçe M, Sayar K. Anadolu Psikiyatri Derg 2007; 8:14-21. 




[PP-031] Ref. No: 155 

Mirtazapine treatment for weight loss and insomnia associated with methylphenidate: 

A chart review 

Sabri Hergüner, Arzu Hergüner 

Meram Faculty of Medicine, Department of Child and Adolescent Psychiatry 

E-mail: cocukergen@yahoo.com 

Introduction: Stimulants are used as first-line treatment for children with attention deficit hyperactivity disorder (ADHD), and their safety 

and efficacy are well established. Their most frequent adverse effects are sleep disturbance and decreased appetite which may limit 

optimal dosing and compliance. The aim of this study was to investigate the efficacy of mirtazapine on OROS methylphenidate (MPH) - 

induced weight loss and insomnia in children and adolescents with ADHD. 

Methods: We reviewed the charts of children and adolescents diagnosed with ADHD and identified 18 individuals prescribed mirtazapine for weight 

loss and/or insomnia while on OROS – MPH treatment. Of these, 2 discontinued mirtazapine within the first week due to excessive daytime sedation. 

Results: Mirtazapine was well tolerated by the remaining 16 subjects and no other side effects were reported. All subjects gained weight 

during concomitant mirtazapine treatment, with a mean gain of 2.1 kg. Fourteen of 16 children who had reported insomnia on MPH alone 

noted significant improvements in sleep after initiation of mirtazapine. 

Conclusion: In this chart review, mirtazapine was found to be beneficial for weight loss and insomnia associated with MPH treatment in 

children and adolescents with ADHD. 

Key words: Attention-deficit/hyperactivity disorder, children, methylphenidate, mirtazapine, insomnia, weight loss 


[PP-032] Ref. No: 157 

Rapid-onset hyponatremia induced by duloxetine in a middle-aged male with 

depression and somatic symptoms 

Jung Seok Choi, Hae Woo Lee, Jun Young Lee, Hee Yeon Jung 

Department of psychiatry, Smg-Snu Boramae Medical Center, Seoul, Korea 

E-mail: choijs@neuroimage.snu.ac.kr 

Duloxetine is a relatively balanced selective serotonin and noradrenaline reuptake inhibitor. We report a case of hyponatremia induced by 

duloxetine that developed rapidly after starting the medication in a middle-aged male with multiple somatic symptoms and depression. 

Two days after discontinuation of duloxetine and management with hypertonic saline as well as fluid restriction, the serum sodium level 

normalized. The patient had two risk factors for developing hyponatremia, namely severe weight loss and pneumonia. Therefore, when 

treating patients with depression and somatic symptoms, especially with risk factors for developing hyponatremia, close monitoring for 

clinical and laboratory evidence of hyponatremia may be essential. 

Key words: Duloxetine, hyponatremia, middle-aged male, somatic symptoms, depression 


S139


[PP-033] Ref. No: 192 

Gender specific metabolic adverse effects in bipolar patients: A comparison 

between lithium, quetiapine and olanzapine 

Sermin Kesebir, Burak Baykaran, Burak Toprak, Ahmet Ertan Tezcan 

Erenkoy TEHMND, Istanbul, Turkey 

E-mail: serminkesebir@hotmail.com 

Objective: There is some evidence showing gender based differences in the side effects of atypical antipsychotic drugs. The aim of this 

study was to determine the differences between lithium, quetiapine and olanzapine with regard to their effects on metabolic variables in 

bipolar disorder and to assess the findings in terms of gender differences. 

Method: Twenty-eight female and 29 male cases diagnosed with bipolar disorder type I according to the DSM-IV, taking lithium or 

quetiapine or quetiapine+lithium or olanzapine or olanzapine+lithium, were evaluated consecutively. For evaluation, being in a remission 

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 

the patients in order to determine PRL, blood lipids and HbA1c levels. 

Results: Mean age, mean age of onset, number of manic, depressive, and total episodes, functionality, and PRL levels were similar between 

female and male patients. BMI, HbA1c, cholesterol, triglycerides, LDL and HDL levels are found to be similar between the two groups. Both 

in female and male patients, no difference was found between the lithium, quetiapine and quetiapine+lithium and the olanzapine and 

olanzapine+lithium groups in terms of BMI, HbA1c, cholesterol, triglyceride, LDL and HDL levels. The only difference (although not significant) 

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. 

Conclusions: This insignificant difference was found while the clinical properties and PRL levels were similar among the lithium, 

quetiapine and quetiapine+lithium and the olanzapine and olanzapine+lithium groups. Future studies with a specific focus on this topic 

are needed in order to have a better understanding of the basic mechanisms of gender differences. 

Key words: Gender, metabolic side effect, psychotropics, bipolar disorder 


[PP-034] Ref. No: 161 

New model of psychogenic stress-induced depression and antioxidant system of rat brain 

Konstantin Chichinadze 1 , Tamar Domianidze 1 , Tamar Matitaishvili 1 , Ia Labadze 1 , Ann Lazarashvili 2 , Mikhail Khananashvili 1 

1Laboratory of Behavior and Cognitive Functions, Life Sciences Research Center, Tbilisi, Georgia 

2Department of Pathology, Tbilisi State University, Tbilisi, Georgia 

E-mail: k.chichinadze@lifescience.org.ge 

The present article describes results of investigation of lipid peroxidation and antioxidant enzyme activity in the brain cells of laboratory 

rats, that were subjected to a depression-like state. The above-mentioned state was achieved by means of a new model of depression 

elaborated by us. The model is based on the application of stressors of psychogenic nature. 

Our investigations demonstrated that in the depression-like state activity of lipid peroxidation processes increase, which was confirmed 

by increase of concentration of its end product – malondialdehyde, both in mitochondrial and cytosolic fractions of brain cells. In 

response to oxidative stress in mitochondria, activity of antioxidant system –namely the leading intracellular antioxidant superoxide 

dismutase (SOD) – increased. On the other hand, concentration of another important antioxidant –catalase– decreased. Most probably, 

the depletion of antioxidative potential of the cell, related to depression, proceeds at various speeds in various enzymatic systems. 

Administration of the antidepressant drug –fluoxetine– led to the normalization of intensity of lipid peroxidation and overall activity of 

antioxidative systems. Thus, if activity of these processes increases, antidepressants cause their down-regulation and in they decrease 

–antidepressants lead to their up-regulation. As a final result, this leads to normalization of cell functioning. 

Key words: Animal model of depression, lipid peroxidation, antidepressants 





[PP-035] Ref. No: 216 

Effects of strawberry leaf and celery seed extracts in terlipressin-induced chronic 

hyponatremia in rats 

Rehab R. Hegazy 1 , Hala F. Zaki 2 , Ola A. Sharaf 1 , Ismail E. Ismail 1 , Sanaa A. Kenawy 2 

1 Departement of Pharmacology, Medical Division, National Research Center, Giza, Egypt 

2 Departement of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt 

E-mail: rehab_hegazy@hotmail.com 

Hyponatremia (HN) is associated with mortality and morbidity risks due to development of encephalopathy and neurogenic pulmonary 

edema. Moreover, its rapid correction carries a high risk of development of the serious cerebral disorder known as osmotic demyelination 

syndrome (ODS). 

In the present study, chronic HN was induced in rats using a single daily administration of terlipressin (TP), a synthetic, long-acting analogue 

of vasopressin, for 3 days. TP-induced HN was then used to study the possible therapeutic effects of strawberry leaf extract (StrwLE) and 

celery seed extract (CelrSE), and to compare their effects with that resulting from rapid correction using hypertonic saline (HtNaCl). Serum 

sodium level, as a marker of HN, was measured following induction and treatment, respectively. The study was extended to investigate 

changes in locomotor activity, pain reflex and lung function using an activity cage, hot-plate test, and spirometer, respectively. Furthermore, 

assessment of brain nitric oxide (NO) content, that has been shown to play a role in the pathogenesis of ODS, was carried out. 

It was found that TP induced a profound (48 h) HN that was coupled by decreased locomotor activity, delayed pain 

reflex and impaired lung function. Administration of StrwLE resulted in a correction of HN with its subsequent neurological dysfunction 

without elevation of the brain content of NO; however, it resulted in deterioration of the lung function parameters of hyponatremic rats. These 

findings suggested that StrwLE is useful for treatment of chronic HN, yet, further investigations are required to study its effect on the lungs. 

Key words: Hyponatremia, terlipressin, rats, locomotor activity, pain reflex, lung functions 


[PP-036] Ref. No: 165 

Post traumatic stress disorder in patients with spinal cord injury and relevant factors 

Murat İlhan Atagün 1 , Ünal Altınok 1 , Özlem Devrim Balaban 1 , Zeliha Atagün 2 , Latif Ruhşat Alpkan 1 , Kadriye Öneş 2 

1Bakirkoy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

2İstanbul Physical Therapy and Rehabilitation Research and Training Hospital, İstanbul, Turkey 

E-mail: muratilhanatagun@gmail.com 

Objective: Although spinal cord injury (SCI) was thought to be a fatal case, development of rehabilitation approaches in the early 20th 

century prolonged survival rates and longevity. Physical and psychological trauma and permanent results of the injury are difficult to cope 

with. Post traumatic stress disorder rates following SCI range from 10 to 44%. In this study we aimed to assess PTSD frequencies in patients 

with SPI in Turkey and the association of PTSD to factors like depression, anxiety and caregiver burden. 

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 

female, 16 male) were enrolled. Patients with mental retardation, premorbid psychiatric disorder, comorbid central nerve system disease 

and patients with professional caregivers were excluded. Clinican administered post traumatic stress disorder rating scale (CAPS), the Beck 

depression and anxiety, and Zarit caregiver burden scales were assessment tools. 

Results: Although they had experienced traumatic events, 32.1% (n=27) of the patients did not have PTSD, while 40.5% (n=34) had 

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 

statistically significant higher scores of depression, anxiety and caregiver burden. 

Discussion: Perception of stress may be influenced by several factors including personality and economical factors. Expression of feelings 

may increase stress tolerance. The differing results may be due to the factors above as well as methodologies, different stages of assessed 

samples, social and cultural differences, and tolerance to stress. On the other hand, some negative effects of PTSD are screened in this 

study. These negative factors may influence adjustment of the disabled person and thus may cause a vicious circle. 

Key words: Spinal Cord Injury, post traumatic stress disorder, depression, anxiety, caregiver burden 


S141


[PP-037] Ref. No: 230 

A comparison before and after using lamotrigine in long term continued treatment: 

the effect of blood levels 

Sermin Kesebir 1 , Fisun Akdeniz 2 , Aysun Demir 1 , Mustafa Bilici 1 

1 Erenkoy TEHMND, Istanbul, Turkey 

2 Ege University, Psychiatry, Izmir, Turkey 

E-mail: serminkesebir@hotmail.com 

Objective: The purpose of this study is that determine whether or not the efficacy of lamotrigine, which is an anticonvulsant with a 

stabilizer quality in neuronal membranes and has inhibitor activity in sodium and calcium channels and presynaptic neurons, is related 

to blood levels in bipolar disorder. We compared the period before and after lamotrigine use in bipolar cases and studied if there was any 

relationship between lamotrigine blood levels and clinical progress. 

Method: Forty cases, diagnosed with bipolar disorder type I according to the DSM-IV, and taking lamotrigine for at least two years 

together with any mood stabilizer (lithium, anticonvulsants or atypical antipsychotics), were evaluated consecutively. For evaluation, 

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 

or after protective treatment, the SCIP-TURK Mood Disorders Diagnosis and Patient Registration Form were filled in by the patients and 

their relatives. Later blood samples were taken from the bipolar cases in order to analyze lamotrigine blood levels. 

Results: In the bipolar cases, when comparing before and after long term maintenance of lamotrigine, it was determined that after using 

lamotrigine, total episode and depressive episode frequency decreased, episode severity was less (p< 0.001, 0.039, and 0.04, respectively) 

and the fast onset and termination ratio decreased (p= 0.027). When evaluated according to these variables, in long term maintenance, 

the ratio of good treatment response to lamotrigine among bipolar cases was 77.5%. In cases with good treatment response to 

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 

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 

levels (r= 0.185, p= 0.254). 

Conclusion: As a result, lamotrigine is an efficient choice in long term maintenance treatment of bipolar disorder. The relationship of this 

efficacy to lamotrigine blood levels must be explored in future studies. 

Key words: Lamotrigine, bipolar disorder, blood level 


[PP-038] Ref. No: 172 

ICAM, VCAM and E-selectin levels in first episode schizophrenic patients 

Semine Özdoğan Kavzoğlu, Aytül Gürsu Hariri 

Erenköy Research and Training Hospital for Neuropsychiatry, Istanbul, Turkey 

E-mail: sokavzoglu@hotmail.com 

Objective: It is known that mortality rates in schizophrenic patients with cardiovascular diseases are twice as high as other diseases. 

Some of the research has revealed that the risks of cardiovascular disease were dependent on adhesion molecules. The main adhesion 

molecules are intracellular adhesive molecule (ICAM-1), vascular cell adhesive molecule (VCAM-1) and E-selectin. The aim of this study 

was to determine whether or not ICAM-1, V-CAM-1 and E-selectin levels, which are considered as possible biological determinants in the 

prognosis and progression of atherosclerosis, change with treatment in schizophrenic patients with respect to controls. 

Method: In the Erenköy Research and Training Hospital for Neuropsychiatry, 50 patients who were diagnosed with first episode 

schizophrenia according to the DSM-IV-TR diagnostic criteria and had never received antipsychotic treatment and a control group 

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, 

VCAM, E-selectin, Fasting Blood Glucose, Total Cholesterol, LDL Cholesterol, HDL Cholesterol and Triglyceride levels were checked in the 

plasma of each patient and compared with each other. For the control group, the same biochemical parameters were investigated only at 

the beginning of the study. In order to assess the termination of the acute episode, the patient group was given the Positive Symptoms 

Assessment Scale (SAPS) and Negative Symptoms Assessment Scale (SANS) in the beginning and at the end of the third month. 

Results: In the first episode schizophrenic patients, the average age was 30.14±7.50 years. In the patients, the beginning ICAM-1 levels 

were lower than the control group (t= 3.41, p=0.001) and increased during treatment (t=-6.73 p



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 

determined to be lower than the pretreatment level (t=7.17, p


[PP-040] Ref. No: 176 

Tardive akathisia with aripiprazole: A case report 

Ömer Şenormancı, Oya Gönüllü Güçlü, Ramazan Konkan, Yavuz Altunkaynak, Güliz Şenormancı 

Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

E-mail: senorman_7@hotmail.com 

Tardive akathisia is characterized by feelings of restlessness, discomfort, and tension causing the patient to be unable to settle down and 

sit still. The patient should also be taking a long term antipsychotic medication without any recent changes in dosage or type, and no 

withdrawal of antiakathisic drugs. Aripiprazole is a potent partial agonist that shows high affinity binding to dopamine (D2) and serotonin 

(5HT1a) receptors and is an antagonist at 5HT2a, 5HT2b receptors. Although there are a number of case reports about arippiprazole 

causing acute akathisia, only one tardive akathisia case, who was a nonpsychotic female patient, has been reported so far. In this case 

tardive akathisia with aripiprazole developed in a patient who had diagnoses of mental retardation and psychotic disorder not otherwise 

specified and who was treated by supplementary drugs without stopping aripiprazole. 

Key words: Antipsychiotics, aripiprazole, extrapyramidal side effects, atypical antipsychotics, tardive akathisia, tardive syndromes 


[PP-041] Ref. No: 178 

Comparing mental disorders between divorced couples and normal 

couples in a city of Iran 

Majid Kazemi 1 , Sima Karimi 2 , Hadi Hasankhani 3 , Somayeh Kazemi 4 

1 Rafsanjan University of Medical Science, Iran 

2 Islamic Azad University- Sirjan Branch, Iran 

3 Tabriz University of Medical sciences, Iran 

4 Islamic Azad University- Mashhad Branch, Iran 

E-mail: maj_kaz@yahoo.com 

Background: The family is the first and the most important source for fulfilling needs of human beings including love, satisfaction and 

peace. One serious difficulty in couple’s lives is the phenomenon of divorce, which recently has been increasing in Iran. Divorce has a lot 

of negative effects, both physical and psychological, on couples. 

Objective: The aim of this study was to compare mental disorders between the couples who were divorced and normal couples in a town 

in Iran. 

Method: This research was causal –comparative on couples in Sirjan in 2010. Seventy couples were chosen voluntarily and randomly 

based on the duration of their marriage from couples applying for divorce and refereeing to the administration of justice and normal 

couples. The questionnaire symptom checklist-90-revised (SCL-90-R) was used. The data were collected and analyzed. 

Results: The averages of mental disorder scores between two groups in nine dimensions were compared and showed different 

significances. People who had gotten divorced had more high scores comparing the total coefficient of global severity index (GSI). 

The findings revealed that the divorced couples had higher GSIs and a significant correlation was observed (p



[PP-042] Ref. No: 238 

Suicide rate in Oman in the period between January 2000 and December 2010 

Saif Salam Al Hashmi, Ahmed Ali Al Sabri, Nasser Mubarak Al Felati 

Armed forces hospital, Muscat, Oman 

E-mail: nouralmanar@gmail.com 

Background: Suicide rates have been explored in different parts of the world, including many Arab /Islamic countries. To our knowledge, 

no study has been conducted in Oman so far. 

Objective: To examine the rate of suicide in the Sultanate of Oman in a ten year period (2000-2010). 

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 

10 year period (2000-2010) 

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 

year. 

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 

rate countries in the world. 

Key words: Suicide rate, Oman, ten year period 


[PP-043] Ref. No: 179 

The effect of the recitation of the Quran on depressed patients in the psychiatry 

department of Moradi hospital in Rafsanjan (IRAN) 

Ali Ansari, Tayebeh Negahban, Ahmad Reza Sayyadi 

Rafsanjan University of Medical Sciences 

E-mail: shibonraf@yahoo.com 

Background and Objective:: Depression is a common psychiatric disorder and has a huge impact on human life. Data published in 

scientific sources suggest that about one hundred million cases are diagnosed annually. Depression comprises about 35 to 45% of 

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 

treatment and prevention of this psychiatric disorder. One of the non- medicinal methods of treatment is music therapy, which seems to 

be a safe and effective therapeutic method. Reading the Koran with a pleasant voice can be regarded as a kind of agreeable Gnostic music. 

The main purpose of this research was to determine the effect of the recitation of the Koran on depression. 

Methods: This study was a semi-experimental one and included all the depressed patients who had been hospitalized in the psychiatry 

department of the Rafsanjan Moradi Center. The sampling time period was one year. The patients were divided into two groups randomly, 

(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 

depression scale and the condition of the patients. The questionnaires were filled out for the case group. Recitation of Yousof Verse of 

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 

weeks of hospitalization, both of the groups were retested by another questionnaire and the results were analyzed by paired t- test and 

Student’s t test by EPI6. 

Results: The result of this research showed that the Koran reciting had a beneficial effect on the depressed patients (p


[PP-044] Ref. No: 239 

Dissociative symptoms associated with piracetam use: a case report 

Adem Aydın 1 , Pınar Güzel Özdemir 1 , Yavuz Selvi 1 , Faruk Uğuz 2 

1 Department of Psychiatry, Yuzuncu Yıl University, Van, Turkey 

2 Department of Psychiatry, Selcuk University, Konya, Turkey 

E-mail: adem.dr@gmail.com 

Piracetam is a cyclic derivative of a gamma-aminobutyric acid drug that is often used in neurology practice (1). It has antithrombotic and 

neuroprotective properties and improves cognitive performance (2). 

In this article, a case report, piracetam is used for combined therapy, but after piracetam use, dissociative symptoms like depersonalization 

and derealization were detected. 

Case: A 29-year-old female patient applied to the psychiatric clinic with the following complaints: Intense discomfort, alienation from herself, 

perceiving herself odd , that perception that her hands and feet were bigger, feeling like not living in the society, the feeling that colors and 

sizes of objects seemed abnormal, and feelings of alienation from objects and people in her surroundings. These complaints continued for 

10 days and she had never had any psychological complaints before. She also expressed that these complaints bothered her greatly. Except 

for these complaints, she did not describe any other abnormality in perception and thought content. She did not have prominent depressive 

symptoms and psychosocial stress in her history. One month ago, she had seen a neurologist for vertigo. She was diagnosed with peripheral 

vertigo and prescribed betahistine 16mg/day. After this medication, she described a marked reduction in the vertigo, however since she did 

not get rid of her complaints completely, after 12 days she was prescribed piracetam 2400mg/day as combination treatment. 

On psychiatric examination, she was conscious, oriented normally, anxious,appeared ready to cry, thought contents were normal, positive 

depersonalization and derealization in the perception, psychomotor activation was normal. Nothing abnormal was detected in her 

hemogram, biochemistry, serum B12, thyroid function tests, EEG, and brain MRI. 

In clinical follow-up, since there was a connection between the patient’s administration of piracetam and the dissociative indications, 

piracetam was stopped. Betahistine was continued in the same dosage. It was observed in daily observation that after a day, a decrease 

in her dissociative symptoms began and in 5 days they had totally disappeared. In further follow up visits dissociative symptoms were 

not observed in a month. 

The dissociative symptoms like derealization and depersonalization were started with addition of piracetam to the treatment, and 

diminished quickly after piracetam was stopped. This directed us to think that those dissociative symptoms were related to the piracetam 

administration. This relation is not established in literature (3). 

Trauma is usually reported as the origin of dissociative symptoms. There generally is childhood period trauma and dissociative symptoms 

come up in later life. There is still no etiopathogenesis described related to development of dissociative symptoms. Traumatic stress and 

neurobiological theories are basic models suggested in etiology (3). In the medication studies, depersonalization is the basic dissociative 

symptom in dissociation’s neurobiological theories. In those studies, it is also shown that serotonergic and glutamate receptors have a 

role in depersonalization (3). 

We think that this case report which shows the administration of piracetam and development of dissociative indications may contribute 

to the neurobiological theories on dissociative disorder’s etiology. 

Key words: Dissociative symptoms, piracetam 

References: 

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 

Psikofarmakoloji 2006;16:93-7 

2. Winbland B. Piracetam: a review of pharmacological properties and clinical uses. CNS Drug Rev 2005;11:169-82 

3. Wınnica K, Tomasiak M, Bielawska A. Piracetam-an old drug with novel properties? Acta Poloniae Pharmaceutica- Drug Research 2005;62:405-409 





[PP-045] Ref. No: 181 

Reversible normoprolactinemic galactorrhea induced by fluoxetine 

Fatih Canan 1 , Ünsal Aydınoğlu 2 , Gjiergji Sinani 3 

1 Bolu Izzet Baysal Mental Health Hospital, Bolu, Turkey 

2 Department of Psychiatry, Ataturk University, Erzurum, Turkey 

3 Department of Psychiatry, Marmara University, Istanbul, Turkey 

E-mail: fatihcanan@gmail.com 

Introduction: Several drugs can cause galactorrhea and it’s etiology needs to be differentiated from other local or neuroendocrinological 

causes. All conventional antipsychotic drugs block D2 receptors on lactotroph cells and thus remove the main inhibitory influence on 

prolactin secretion. Tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors are less frequent 

causes. There is evidence that serotonin may stimulate prolactin release directly via postsynaptic 5-HT receptors in the hypothalamus or 

indirectly via 5-HT mediated inhibition of tubuloinfundibular dopaminergic neurons. However, galactorrhea due to antidepressants is 

not consistently associated with elevated prolactin levels, which may suggest still unexplained mechanisms of antidepressant-induced 

galactorrhea. 

We report a case of euprolactinemic galactorrhea in a woman with generalized anxiety disorder while on treatment with fluoxetine. 

Case Report: A 29-year-old woman visited a psychiatric outpatient clinic with complaints of excessive and uncontrollable worry about 

minor life events, feeling restlessness, irritability, muscle tension, tiring easily, and poor sleep that started 8 months prior to admission. She 

had no history of endocrine or reproductive pathology or psychiatric problems. She was diagnosed as having generalized anxiety disorder 

according to the DSM-IV criteria and was started on fluoxetine 20 mg per day. After 4 weeks of medication, her symptoms diminished. 

However, she developed unilateral galactorrhea (the nonpuerperal discharge of milk-containing fluid from the breast). She had no history 

of galactorrhea. She first noticed the discharge on treatment day 21 and described it as white-creamy and from the right nipple. She did 

not notice any bloody, greenish, or foul-smelling discharge, nor did she report any sexual dysfunction. She consulted her gynecologist, 

who recommended a mammogram and breast ultrasonography. The pregnancy test was negative. The results of these tests and breast 

examination were normal. Serum prolactin level on treatment day 28 was 18.18 ng/mL (reference range: 2.5-29 ng/mL). Because her 

galactorrhea developed after the initiation of fluoxetine, her medication was discontinued. Buspirone 5 mg/day was started and gradually 

raised to 20 mg/day. Eight days after stopping fluoxetine, the patient reported reduction and cessation of galactorrhea. At the 3 month 

follow-up visit, the patient was well maintained on buspirone and there was no re-emergence of galactorrhea. 

Discussion: Although galactorrhea caused by the use of fluoxetine has been reported earlier, the commonly perceived cause is 

hyperprolactinemia. Fluoxetine has been shown to potentiate elevation of prolactin levels from other stimuli, including insulin, 

fenfluramine, and 5-HT. However, hyperprolactinemia is not the only mechanism responsible for the development of SSRI-induced 

galactorrhea. The exact mechanism of galactorrhea remains unknown in many cases. 

Our patient developed galactorrhea without hyperprolactinemia after beginning fluoxetine therapy. The strict temporal relationship 

between the use of the drug and the onset of galactorrhea, as well as the resolution once treatment was discontinued, suggests a causal 

link between the two phenomena. 

To the best of our knowledge, we are the first to report an association with fluoxetine use and galactorrhea without elevated prolactin 

levels. Clinicians should consider fluoxetine as a possible cause of galactorrhea even with normal prolactin levels. Future research should 

investigate the precise mechanisms of antidepressant-induced normoprolactinemic galactorrhea. 

Key words: Fluoxetine, galactorrhea 


S147


[PP-046] Ref. No: 240 

Influence of polymorphism of the norepinephrine transporter gene (SLC6A2) and 

alpha-2 adrenergic receptor gene (ADRA2A) on regional cerebral blood flow 

in a Korean ADHD sample: a preliminary study 

Younghui Yang 1 , Jaewon Kim 2 , Boongnyun Kim 2 , Minsup Shin 2 , Soochurl Cho 2 

1 Department of Psychiatry, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea 

2 Division of Child and Adolescent Psychiatry, Seoul National University Hospital, Seoul, Republic of Korea 

E-mail: nauyoung@gmail.com 

Some genes related to the noradrenergic system have been investigated as candidate genes in Attention Deficit Hyperactivity Disorder 

(ADHD). Through functional brain imaging studies, it has been reported that brain areas such as the prefrontal cortex (PFC), dorsal 

anterior cingulate cortex, and striatum show abnormal findings in ADHD patients. We have investigated whether there was an association 

between polymorphism of the noradrenergic system related genes (SLC6A2 and ADRA2A) and regional cerebral blood flow (rCBF) in a 

Korean ADHD sample. 

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 

from the outpatient’s clinic of child and adolescent psychiatry in the Seoul National University Hospital. The diagnosis of ADHD was made 

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 

ADRA2A (Dral, Mspl) was done. SPM8 (Statistical parametric mapping 8) was used to compare images between the two groups divided 

by each genotype. 

Results: Children with the G/A and A/A genotypes at the SLC6A2 G1287A polymorphism showed decreased rCBF in the right inferior 

temporal gyrus and the left middle temporal gyrus compared to children with G/G genotype (uncorrected p-value< 0.001). In ADRA2A 

Mspl polymorphism, children with the C/G and C/C genotypes showed increased rCBF in the left striatum and the left cingulate gyrus and 

decreased rCBF in the left cerebellar vermis compared to children with G/G genotype. 

There were no significant rCBF alterations across genotypes in the SLC6A2 -3081(A/T) and ADRA2A Mspl genes. 

Conclusion: This study showed that the noradrenergic system related genes might be associated with functional brain abnormalities in 

children with ADHD. 

Key words: ADHD, neuroimaging, SLC6A2, ADRA2A 


[PP-047] Ref. No: 129 

Do we need specialist clinics to monitor metabolic side effects on chronic 

bipolar patients in Treatment? – Audit of management of bipolar disorder against 

NICE guidelines in South Staffordshire NHS Trust, UK 

Fiesal Jan, Vanathi Kennedy 

Foundation House, St. Georges’ Hospital, Corporation Street, ST16 3AG, Stafford 

E-mail: khalidnoma@hotmail.com 

Objective: To highlight the pharmacological management of patients with Bipolar Affective Disorder and to evaluate whether the 

management meets the current standards as set up by recognised guidelines, especially those underlined by NICE guidelines. 

Method: The audit data were collected from a patient population from the West patch of South Staffordshire and focussed on inpatients 

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 

community teams. The selection was random and not based on severity or duration of the disorder, co-morbidity or other accompanying 

diagnoses, for e.g, Personality disorder. 

The audit tool was devised by the clinical audit coordinator in conjunction with clinicians. 

Results: Twenty of twenty-eight 28 patients (72%) were on mood stabilizers, either lithium or sodium valproate, with sodium valproate 

the more preferred drug. 

Twelve of twenty-eight (43%) were on antipsychotics. Three of seven (43%) patients, who did not respond to combination treatment, 

were started on lamotrigine. 

In 21/22 (95%) of the patients, antidepressants were stopped. 




Nine of the twenty-eight (32%) patients continued to be on antidepressants even after resolution of the depressive episode. 

The compliance of monitoring for physical side effects during the initial period of starting medications was not satisfactory with only: 

19/24 (79%) monitored for renal disease, 

18/24 (75%) monitored for diabetes, 

15/24 (63%) monitored and advised about obesity and 

15/24 (63%) drug levels checked regularly. 

In 4/28 (15%), there was no documentation about any physical health monitoring. 

Only in 50-60% of patients had the monitoring been done annually, but it was regardless of any recognised guidelines. 

In 19/26 (73%) the patient’s preference of drug choices was recorded. 

In 21/28 (75%) patients, there was documentation about discussion of potential benefits and side effects of the medications. 

Five of twenty-eight (18%) patients who were prescribed valproate were of child bearing age; 4 were advised to use contraception and 

one had been sterilized. 

Clinical implications: Monitoring cognitive function tests is often dependent on patient mental health, illness, age, and lack of side 

effects. 

Patient preference for drugs should be taken into consideration. 

Evidence should be documented regarding clinical need or history of risk on antidepressant medication. 

Evidence of long term treatment with antidepressants after resolution of a depressive episode should be documented in the patient 

notes. 

Annual check-ups of parameters should be documented by either the GP or Mental Health Team. However, weight and BP machines may 

not be available at clinic appointments. There is a need for closer understanding among clinicians about the responsibility for initiation 

and maintenance of close physical monitoring. 

Discussions should be held with women of child bearing age regarding contraception. 

Teams to monitor the need for referral to specialist Bipolar Units should be available, regardless of any cost implications. 

Key words: Bipolar, mood disorder, mood stabiliser, antipsychotics, physical health monitoring, serum drug levels, cognitive side effects, relapse, 

pregnant women 


[PP-048] Ref. No: 186 

Assessment of risk of absenteeism in elemantary school students 

Kültegin Ögel 1 , Gülşah Karadayı 2 , Zeynep Karaman 3 , Hediye Atıcı Arıcan 3 , Niyazi Kaya 3 , Uğur Karaman 3 , Ahmet Murat Altuğ 3 

1Acibadem University Medical Faculty 

2Yeniden Society 

3Ministry of National Education Primary School Department 


Finding a resolution to the absenteeism problem is important in terms of children’s development. It is necessary that the risk of 

absenteeism is determined in an early stage and an early warning system is established to prevent absenteeism. For this reason, 

development of an assessment tool was targeted. 

Methods: A qualitative research design was carried out at the first stage of the study. During this research procedure, 97 teachers, 53 

administrators, 73 elementary school students who hadleft school, and 76 of their parents who were selected to represent the overall 

structure of the population in Turkey were included in the study. With the information retrieved from this research, a scale named the Risk 

Assessment Form (RIDEF) was developed. RIDEF consists of 111 questions within 9 risk categories. 

The second stage of the study was carried out with 3871 students studying in 21 schools from 5 different cities, which were selected at 

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 

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 

academic year, during which time this research was implemented, was 6.62±8.93 days and the mean of days of their unexcused absences 

the year before was 6.08±7.21 days. 

At the second stage, the RIDEF was applied to the same students 15 days after the first application and also a different interviewer filled 

the form for half of the students. The School Atmosphere Scale was applied during the study, as well. 

Results: When the total score derived from the scale was compared with the Pearson correlation analysis the interrater reliability was 

found as r= 0.96 (p


Based on the risk indicators obtained from RIDEF, the Cronbach alpha validity of the scale was calculated as 0.79. When any item is 

removed from the scale, the value of the internal consistency coefficient varies between 0.77 and 0.79. 

It has been observed that there is a statistically significant level of correlation between the School Atmosphere Scale and RIDEF sub-scales 

(r=0.51, p=0.001). 

As a result of the analysis, categorized risk indicators were grouped under two factors, which accounted for 44.73% of the total variance 

with eigen values over one. The first factor, consisting of 4 items grouped under the title of individual problems related to childhood, 

explains 30.98% of the variance and the second factor, consisting of 5 items with the title social and economic problems related to the 

family, accounts for 13.75% of the variance. 

The mean scores of the risk points derived from all of the categories showed a statistically significant difference between students with 

high and low levels of absenteeism. 

Discussion: This research study showed that the RIDEF is a reliable and valid scale in determining the risk of absenteeism. 

Key words: Absenteeism, assessment 


[PP-049] Ref. No: 185 

Effectiveness of an addiction treatment program called SAMBA: A pilot study 

Kültegin Ögel 1 , Ceren Koç 2 , Bircan Karalar 2 , Aslı Başabak 2 , Alper Aksoy 2 , Mebrure İşmen 3 , Romina Yeroham 2 



3Umraniye Prison 


Description of SAMBA program: SAMBA (Sigara, Alkol ve Madde Bağımlılığı Tedavi Programı / Tobacco, Alcohol, and Drug Addiction 

Treatment Program) is a treatment program which is designed to treat tobacco, alcohol, and drug addiction problems. 

Development of SAMBA: Before developing this program, a comprehensive literature review was done. Addiction treatment programs 

that are still applied in addiction centers in Turkey were reviewed. Necessary meetings with the specialists working in the addiction field 

were conducted. The weaknesses and strengths of the programs were discussed with the specialists and expectations from an addiction 

program were reviewed. SAMBA was developed according to the findings of the literature review and suggestions made in the meetings 

with professionals. 

The Content of SAMBA: SAMBA is a program that is based on Cognitive Behavioral Theory. In some sessions, some interventions that are 

based on Mindfulness and Acceptance Therapy are used. In addition, in some sessions, some techniques of Dialectical Behavior Therapy 

and Emotion Regulation are applied. 

The Structure of SAMBA: SAMBA is composed of 7 modules and 13 sessions. The modules of SAMBA are: 

1. The Effects of Drugs, Alcohol, and Tobacco 

2. Motivation 

3. Mindfulness 

4. Anger and Stress Management 

5. Relapse Prevention 

6. Communication Skills 

7. Thinking Errors 

Each session lasts around one and half to two hours. All sessions are designed in an interactive mode. It contains activities and didactic 

lectures. 

SAMBA should be applied in group format and by professionals such as psychologists, social workers and psychiatrists. 

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 

consisted of members who are alcohol and drug addicts. After all the modules were applied, feedback from the group members was 

collected. According to the feedback, necessary changes were made. Afterwards, the second pilot scheme was done with other members 

who were again alcohol and drug addicts from the same prison. Based on the feedbacks, SAMBA was reviewed and reached its final form. 

The results showed that there was a significant difference between the pre-test and post-test of the dimensions of Anger and Stress 

Management (Z= -1.919, p



There was not a significant difference between the results pre-test and post-test of the dimension of Motivation. The results showed that 

the participants were not well-informed about relapse prevention. Therefore, it is suggested that the focus of the program should be on 

relapse prevention. 

According to the results of the feedback form, 66.6% of the participants claimed that they have learned moderate or very much information 

from the SAMBA program. 91.6% of the participants claimed that the trainers were moderately or very much successful. Lastly, 75% of the 

participants reported that they had the opportunity to participate and share ideas during the sessions again moderately or very much. 

Key words: Addiction, psychotherapy, treatment, effectiveness 


[PP-050] Ref. No: 187 

Psychometric properties of different forms of the Addiction Profile Index (BAPI) 

Kültegin Ögel 1 , Aslı Başabak 2 , Ceren Koç 2 , Alper Aksoy 2 , Gülşah Karadayı 2 




The Addiction Profile Index (BAPI) is composed of 37 items and 5 subscales assessing the characteristics of substance use, dependency 

diagnosis, the effect of substance use on the person’s life, craving, and the motivation to quit using substances. The reliability and validity 

of the scale were reported in a very recent study. 

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). 

Study 1: Psychometric properties of clinician-administered form of BAPI 

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 

used 3-point likert ratings. 

A total of 150 male inmates were recruited from the Umraniye, Istanbul T-type prison. Cinical Psychologists and guardians of the prison 

conducted face-to-face interviews with inmates to complete the BAPI. 

The BAPI-U items were found to be significantly correlated with the self-reported form (0.89). High correlations between interviewer 

ratings in all subscales were found. Factor analyses yielded four factors for the BAPI-U, which were similar to the BAPI. 

It was concluded that the BAPI-U has similarities with the BAPI and therefore it may be applied by non-clinical professionals (such as 

nurses, guardians etc) after a short training period. 

Study 2: Development and psychometric properties of the clinical form of the BAPI 

It is important to know the factors causing alcohol or substance dependence disorders in order to choose the treatment modality and to 

prevent relapses. 

In order to assess depression, anxiety, anger, and assertiveness, new items were added to the original BAPI items. This new instrument 

was named the BAPI-II. 

The research sample was similar to study 1. The Beck Depression Inventory, Rathus Assertiveness Inventory, Multi-dimensional Anger 

Scale and STAI-1 were used in this study. 

The Cronbach Alpha value of the whole scale was found to be 0.79. The self and clinican administered rating correlations were statistically significant. 

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. 

High correlations were found between the ratings of psychologists and prison guardians in all subscales. This shows that the BAPI may be 

administered by non clinical professionals efficiently. 

Study 3: Development and psychometric properties of the short form of the BAPI 

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 

people in 7 different prisons. Based on the results of the statistical analyses, some questions were removed. The short version of the BAPI 

is composed of 23 questions and is named as BAPI-K. 

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 

scales were found to be correlated. The scores of the correlations of the BAPI with CAGE and AUDIT were also found to be statistically 

significant. The internal consistency of the new scale was found to be satisfactory (0.89). 

The results have shown that the BAPI-K is a valid and reliable instrument, and can be used as a screening tool. 

Key words: Addiction, assesment, questionnaire 


S151


[PP-051] Ref. No: 199 

Aripiprazole treatment for the choreoathetoid movements and psychotic 

symptoms of Huntington’s disease: A case report 

Sevinç Ulusoy, İzgi Alnıak, Kasım Fatih Yavuz, Tuğba Kara 

Bakirkoy Research and Training Hospital for Psychiatry and Neurology, Istanbul, Turkey 

E-mail: tugbakara111@yahoo.com 

Introduction: Huntington’s Disease, that is caused by CAG trinucleotide repeat expansion in the IT15 gene located on the short 

arm of chromosome 4, is an autosomal dominant, progressive neurodegenerative disorder characterized by motor, cognitive, and 

psychopathological symptoms (1). The disease is accompanied by a variety of psychiatric disorders and its incidence rates range from 33 

to 76%. Although depression is the most common accompanying psychiatric disorder, anxiety, obsessive-compulsive disorder, irritability 

and manic and psychotic symptoms may be associated with Huntington’s Disease (2). 

In this case report, we discuss the effectiveness of aripiprazole on the motor and psychiatric symptoms of a patient with Huntington’s 

disease, who had psychotic symptoms. 

Case: Two years ago, psychotic symptoms developed in addition to existing neurological symptoms in a fifty-year-old patient who was 

known to have had Huntington’s disease for twenty years. 

After one month of 30 mg/day aripiprazole treatment for a diagnosis of ‘Psychotic Disorder Due to a General Medical Condition’, a 

significant decline was observed in the motor and psychotic symptoms that had been present at the beginning of the disease. 

Discussion: Although the pathogenesis of the Huntington’s disease has not been exactly solved, the glutamatergic and dopaminergic 

systems with striatal neurodegeneration are thought to be responsible for the clinical signs of the disease (3). 

By the consideration of this process it is conceivable that aripiprazole, which is used in the treatment of psychosis and chorea, may be a 

well-tolerated agent for its effects on the negative and positive symptoms with low metabolic and extrapyramidal side effects. 

Key words: Aripiprazole, choreoathetoid movement, Huntington’s disease 

References: 

1. Walker FO: Huntington’s disease. Lancet 2007; 369:218–228 

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. 

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 

kinase 5. J Neurosci 2008; 28:1090–1101 


[PP-052] Ref. No: 189 

Acute effects of Bacopa monnieri on mood in healthy young adults 

Chris Neale, Sarah Benson, Con Stough, Andrew Scholey 

Centre for Human Psychopharmacology, Swinburne University, Melbourne, Australia 

E-mail: chrisneale02@gmail.com 

Objectives: Previous research has identified that Bacopa monnieri (BM) improves aspects of cognitive functioning such as attention, 

speed of information processing and verbal learning with chronic dosing (300mg daily). To date there have been no reports of acute 

neurocognitive benefits of BM where acute testing has been evaluated; only one known study has reported on acute Bacopa measures[1]. 

It is possible that in this previous study the cognitive instruments were not demanding enough to detect acute effects. This study is the 

first acute dose ranging study of BM using multi-tasking cognitive assessment and measurement of mood. 

Methods: Seventeen healthy young adults took part in this double-blind, placebo-controlled three-period crossover study. They were 

administered 300 mg BM, 600 mg BM, or a matching placebo on different days with a seven-day washout period between visits. The 

treatment order was determined using a Latin Squares design. Following baseline assessment, participants were administered the day’s 

treatment and further assessment took place 1 h and 4 h later. The assessments included the Purple multi-tasking framework (MTF) and 

the Bond-Lader mood visual analogue scales (administered before and after each 20 min MTF session). The MTF is a 20 minute framework 

where participants are required to complete four tasks simultaneously. Tasks include Stroop, maths, tracking and working memory. 

Results: There was a significant, dose-dependent effect of treatment on ratings of alertness favouring the 600 mg treatment at both 




post-dose assessment times. There was a trend for dose-related effects on performance of the MTF, in particular for the Stroop task, where 

there was an advantage for the 300 mg dose. 

Conclusions: This is the first demonstration of acute neurocognitive effects of BM. The combination of increased alertness for 600 mg and 

better selective attentional performance for 300 mg suggests that mood and cognitive processes can be dissociated and that different 

doses of Bacopa may benefit different neural mechanisms. 

Further participants are needed for this cohort to increase the statistical power of these findings. 

Key words: Bacopa monnieri, nutraceuticals, mood, cognition 

References: 

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: 

Clinical & Experimental. 2001, John Wiley & Sons Ltd. 1996. p. 345-351. 


[PP-053] Ref. No: 201 

Anxiety and depressive symptom levels among adolescents with risk taking behaviour 

Nuray Sarp 1 , Aylin Aksoy Çoban 2 , Kültegin Ögel 3 

1Acıbadem Fulya Hospital, Psychiatry service, Psychology Department, İstanbul, Turkey 

2Acıbadem Fulya Hospital, Psychiatry service, Istanbul, Turkey 

3Acıbadem University School of medicine, Department of Mental Heath Disease, Istanbul, Turkey 


Background: In our country, risk taking behavior has increased among adolescents in recent years. Risky behaviours are defined as 

behaviors that affect an adolescent’s health and wellness and daily life directly or indirectly. These behaviours can cause potential 

negative results. Bullying, smoking, using alcohol or drugs, early or unprotected sexual activity, skipping school, elopement, damaging 

friends and self destruction are the most frequent risky behaviors among adolescents. Through previous research, it has been shown that 

the moods of adolescents with risky behaviors differ from other adolescents. Thus it is thought that there may be an association between 

risky behavior and depression and anxiety. 

Objective: This study investigated the differences between adolescents with risky behaviour and the ones with non-risky behaviour in 

terms of depressive and anxiety symptom levels. 

Methods: The participants were from different regions and different socio-economic statuses. A total of 3483 students from forty-three 

schools (12 vocational high schools, 23 state schools and 6 private high schools ) and104 classes were included in this study. The multistage 

cluster sampling method was used for the selection of the sample. In the study, YSR 11-18 (Youth Self Report) and a questionnaire, 

which was developed by the researchers, were used. The research survey consisted of 238 items; The questions covered demographical 

information, parent and region features, problems about school life, risky behaviours, neglect and abuse, disease, trauma, and health. 

Results: In this study, 45.5% of participants were female, 54.5% were male. According to the analysis of each risky behaviour, significant 

differences were found for depressive and anxiety symptom levels between groups. 

Adolescents who exhibit bullying, elopement, self destruction, commit crimes, and have damaging friends are more likely to show 

anxiety and depressive symptoms compared to non-risky behavior adolescents.(p=0.000). In addition, the level of depressive and anxiety 

symptoms of drug users were higher than the level of depressive and anxiety symptoms of non-users (depressive; p=0.000, anxiety; 

p=0.019). 

Adolescents who are carrying a weapon, using alcohol, working in a job and skipping school had a higher level of only depressive 

symptoms (p=0.0000). On the other hand, only the high level anxiety group had unprotected sexual activity (p=0.092). 

Conclusions: A comparison of non-risky behavior adolescents to risky behavior adolescents showed significant differences in terms of 

anxiety and depressive symptom levels and these symptom levels changed according to the risky behaviour type. 

Key words: Adolescents, anxiety symptom levels, depressive symmptom levels, risky behavior 


S153


[PP-054] Ref. No: 153 

The relationship between mental health and academic achievement among 

Kordestan high school students 

Fayegh Yousefi, Srwa Mohamadzadeh 

Department of Psychiatry at Kordestan University of Medical Sciences, Sanandaj, Kordestan, Iran 

E-mail: fyousefi_kms@yahoo.com 

Objective: Academic achievement is one of the important factors to which parents, teachers and society pay attention and also, it is 

related to students’ mental health. The main objective in the present study was to determine the relationship between students’ mental 

health and their academic achievement. 

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 

sampling method of this study satisfied random sampling. Also, data were gathered by using the GHQ-28. The GHQ-28 is an instrument 

to determine mental health and it includes four scales measuring depression, anxiety, somatization and social function. The reliability of 

this scale is 0.91 by Cronbach’s alpha. 

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 

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 

were among Pre-University students. 

In addition, the results from the present study indicated that there is significant relationship between the education of the respondents’ 

father and students’ mental health (p



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 

for alcohol abusers was 0.81 and for substance abusers was 0.93 (Graph 1 and 2). 

The BAPI craving subscale was found to be consistent with the PACS and the motivation subscale was found to be consistent with the 

SOCRATES. The BAPI total score showed a significant correlation with the MATT average score and the composite score of the Medical 

Condition, Substance Use, and Legal Status and Family Social Relations subscales of the ASI questionnaire. 

Discussion: The results have shown that psychometric properties of the BAPI are satisfactory for alcohol and substance abusers. The 

psychometric properties of the total scale and the data of alcohol and substance abuse are similar. Finally, we can say that the BAPI can 

assess both alcohol and substance abuse rather than just alcohol use. 

Key words: Addiction, alcohol, assessment 


[PP-056] Ref. No: 160 

Death anxiety among terminally ill inpatients 

Marjan Anvar Abnavi, Ali Javadpour, Sahand Mohamadzadeh 

Department of Psychiatry, Shiraz University of Medical Sciences, Shiraz, Iran 

E-mail: anvarm@sums.ac.ir 

Objective: In spite of the certainty of death, people seem unable to escape anxiety at the prospect of it. Death anxiety contributes 

to important emotional and behavioral consequences. The aim of this study was to investigate the relationship of death anxiety with 

variables such as severity of illness, depression, and religious beliefs. 

Methods: The study is a cross-sectional descriptive study. The data were collected by using a demographic questionnaire, the Templar 

Death Anxiety Scale, the Beck Depression Questionnaire, the Cumulative Illness Rating Scale and the Religious Attitude Questionnaire. 

Stepwise multiple regression analysis was conducted to identify the factors that influenced the degree of death anxiety. 

Results: A group of one hundred and fifty persons, (50 severely ill patients, 50 relatives, and 50 normal controls) completed the 

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 

had a positive correlation with death anxiety (p


study, the Cronbach alpha coefficient of the questionnaire was calculated to be 0.88 for patients and 0.80 for experts, which was very 

satisfactory. The data were analyzed by the SPSS software and Lisrel through the factor analysis method. 

Results: Based on the responses of 401 patients and 406 experts, the current situation of access to medical care in the public hospitals 

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 

in the current situation. In addition, the findings showed that the structure of access to medical care in Iranian public hospitals has a 

5-dimensional structure containing individual characteristics, service providing system, social-geographic features, health policy making 

and management strategies. The relationship among the 5 dimensions was meaningful from 0.13 for the correlation of health policy 

making with the individual characteristics to 0.40 for the correlation of health policy making with the management strategies. 

Conclusions: The findings show that the service providing system had the highest quality and was the most effective factor on having 

access to medical care structure. It seems that it can be helpful to pay attention to the above factors especially in programming and policy 

making to improve access to medical care by distributing the standardized number of beds and specialists based on the population of 

each region, training, organizing, and managing the human resources, and improving the service providing system process. 

Key words: Feature, access, access to health care, medical care 


[PP-058] Ref. No: 174 

Smoking behaviour during the course of paroxetine treatment: A case report 

Neslihan Akkişi Kumsar, Atila Erol 

Sakarya Training and Research Hospital, Sakarya, Turkey 

E-mail: drneslihanakkisi@yahoo.com 

Selective serotonin reuptake inhibitors are used for the treatment of a wide range of psychiatric disorders, although nicotine craving 

attributed to the use of serotonin reuptake inhibitors especially paroxetine has not yet been reported in the literature. Here we present 

a case, who developed nicotine craving and started to smoke cigarettes after initiation of 20mg/day paroxetine, and discuss possible 

mechanisms of this side effect while reviewing current status of the literature. A 25 year-old female patient was evaluated at our outpatient 

clinic and diagnosed with generalized anxiety disorder. She was given paroxetine 20mg/day for four weeks. While her symptomatology 

improved by the second week of the treatment, she complained of nicotine craving at the fourth week. During psychiatric assessment 

there was not any history of smoking, alcohol or any other substance use disorder. She mentioned that she started smoking one package/ 

day after starting the paroxetine treatment. The craving for nicotine decreased after the drug was discontinued and she quit smoking 

within two weeks. We did not find any report of smoking behaviour attributed to SSRIs in the literature, although there is a study about 

decreased smoking behaviour during paroxetine treatment. To the best of our knowledge this case is the first one in the literature. More 

research is needed to exlore nicotine craving and SSRIs. 

Key words: Craving, cigarette, paroxetine 


[PP-059] Ref. No: 190 

Development of a SNP genotyping panel and a medical decision support algorithm 

to predict drug response in schizophrenia 

Hüseyin Alper Döm 1 , Mehmet Ali Döke 2 , Yemliha Yener Tuncel 1 , Gürkan Üstünkar 3 , Yeşim Aydın Son 4 

1 Middle East Technical University, Bioinformatics Graduate Program Ankara, Turkey 

2 Middle East Technical University, Department of Biological Sciences, Ankara, Turkey 

3 Middle East Technical University, Informatics Institute, Department of Information Science, Ankara, Turkey 

4 Middle East Technical University, Informatics Institute, Department of Health Informatics, Ankara, Turkey 

E-mail: h.alper.dom@gmail.com 

Genome Wide Association Studies (GWAS) of Single Nucleotide Polymorphisms (SNPs) is leading the development of personalized 

medicine approaches to predict and diagnose diseases or to determine drug response in individual patients. As the basic research 

provides all the genomic information and interpretation of these data, translational research has to be conducted in order to develop 




genomic diagnostics to apply this information into practice in medical clinics. In this perspective, our goal is to design a diagnostic assay 

for the Prediction of Drug Response for Schizophrenia to especially guide the initial selection of antipsychotics based on the individual 

genomic information of the patients. 

Initially a literature search has been done to identify previously described SNPs associated with schizophrenia that are known to effect 

the response to antipsychotics or predict the side effects of antipsychotic drugs. Twenty-two SNPs are identified, that map to 8 genes. 

Next, we have applied the novel AHP based SNP prioritization approach implemented in the METU-SNP software for GWAS to the SNP 

Genotyping data for the European American population (from dbGAP database), with 1351 patients and 1378 controls genotyped for 

over 729454 SNPs. The 22 SNPs selected based on the literature were cross-checked with the results of GWAS and prioritized in order to 

finalize the pharmacogenomics of the SNP (p-SNP) panel for schizophrenia and to determine the order of SNPs to be targeted in the assay 

development process. The pyro-sequencing approach was used during the development of the assay to determine the genotypes of the 

patients for the SNPs selected for the panel. After the next phase of our project, which is the development and optimization of primer 

sets, is completed a validation study will be designed in collaboration with psychiatric clinics for the described p-SNP kit panel and the 

supporting software that is in-line, for development of easy translation of the genotyping results to support the clinical decision of the 

choice of therapy. 

Application of personalized medicine approaches and utilizing genomic diagnostic assays as presented here will eliminate or decrease 

the number of trials-and-errors in selecting sthe right treatment and dosage for particuler patient, and will also minimize emergency 

visits due to side effects of the drugs. In addition, the prescription of the right medicine and treatment plan at the initial diagnosis 

of schizophrenia will increase trust between healthcare professionals and patients, which in return is expected to provide higher 

cooperation and adherance rates of patients to their treatment. Overall the personalized medicine approach is expected to decrease the 

cost of healthcare in psychiatry and other disciplines, while offering higher quality healthcare. 

Key words: Pharmacogenomics, personalized medicine, translational medicine, genomic diagnostics, medical decision support systems, GWAS, 

SNP genotyping, METU-SNP, schizophrenia 


[PP-060] Ref. No: 200 

Basal ganglial hemorrhage induced mania 

Barış Yılbaş 1 , Murat Gönen 2 

1Department of Psychiatry, Elbistan State Hospital, Elbistan-K.Maraş, Turkey 

2Department of Neurology, Elbistan State Hospital, Elbistan-K.Maraş, Turkey 

E-mail: barisyilbas@mynet.com 

Neuroimaging studies on mood disorders concentrate on the limbic system, especially on the hippocampus and amygdala. Accumulating 

evidence suggests an association between abnormalities of the basal ganglia and mood disorders. We present a case of mania following 

basal ganglial hemorrhage. 

A 30-year old male, with no history of bipolar disorder, was admitted to the emergency room with complaints of euphoria and decreased 

need for sleep. During psychiatric assessment, he exhibited grandiosity, psychomotor activation, irritability, and flight of ideas. The 

patient,whose cranial MRI showed hemorrhage in the basal ganglia, was hospitalized with a diagnosis of mood disorder due to a general 

medical condition. Lorazepam 5mg/day and olanzapine 10mg/day was started. On the tenth day of treatment his episode ended. 

The basal ganglia are interconnected with the limbic system and prefrontal cortex and therefore are implicated in bipolar disorder. 

Key words: Basal ganglia hemorrhage, mania 


S157


[PP-061] Ref. No: 233 

Evaluation of cognitive functions in euthymic bipolar patients using 

mono- and multi- drug treatments 

Birgül Elbozan Cumurcu 1 , Rıfat Karlıdağ 1 , Şükrü Kartalcı 1 , Işıl Göğcegöz Gül 1 , Süleyman Demir 2 , Bahar Yeşil 1 

1 Inonu University Medical Faculty, Turgut Ozal Medical Center, Department of Psychiatry, Malatya, Turkey 

2 Gaziosmanpasa University School of Medicine, Department of Psychiartry, Tokat, Turkey 

E-mail: baharyesilege@hotmail.com 

Objective: Some studies on patients suffering from bipolar disorder show that in active and remission periods of the disorder there are 

cognitive insufficiencies (1,2,3). The causes of cognitive insuffuciencies in bipolar disorder is not understood yet. We anticipate that multidrug 

usage has more adverse effects on cognitive functions than mono- drug usage and our aim in this study was to investigate effects of 

drugs used in treatment of bipolar disorder on cognitive functions. In this study we evaluated the cognitive functions of bipolar patients 

who were in their euthymic period taking mono- and multi-drug regimens and compared them with a healthy control group. 

Methods: Eighty bipolar I and II patients diagnosed based on the DSM-IV criteria and 80 healthy controls were included in the study and 

two groups matched according to age, sex, and education aspects. The patients and controls gave written informed consent to participate 

in the study. The necessary approval and ethic committee reviews and permits were obtained prior to the study. The patients were 

evaluated using a psychiatric interview, the Young Mania Scale and the Hamilton Depression Rating Scale. A large neurocognitive battery 

(Wechsler Memory Scale-Revised, Stroop,Verbal Memory Processes Scale) was used for neurocognitive assessment. 

Results: In most cognitive tests the results of the patient group were worse than the control group. The Verbal Memory Processes 

Scale-learning scores and long term memory scores were higher in the patients on a mono-drug regimen. All other tests did not show 

significant differences. 

Conclusions: Our study showed that the cognitive function of bipolar patients had deficiencies not only in active periods of bipolar 

disorder but also in remission periods, like previous studies (4,5,6). 

The Verbal Memory Processes Scale learning scores and long term memory scores showed better results in patients using a mono-drug 

compared to the ones on a multi-drug regimen. Other tests did not show significant differences. Future studies with larger number of 

patients may show different results. Also other studies to investigate the effects of each drug group on cognitive functions in bipolar 

patients are needed. 

Key words: Bipolar disorder, cognitive functions, euthymia 


[PP-062] Ref. No: 247 

Adult ADHD symptoms in cannabis dependence and the importance of 

comorbidity in Adult ADHD 

Umut Mert Aksoy, Şennur Günay Aksoy, Fulya Maner 

Bakirkoy Research And Teaching Hospital For Neuropsychiatry, İstanbul, Turkey 

E-mail: drumutmertaksoy@gmail.com 

Background: Adult Attention Deficit Hyperactivity Disoeder (A-ADHD) is one of the most important neuropsychiatric disorders originating 

in childhood. According to the last epidemiological studies, ADHD can be persistent into adulthood. Sixty percent of childhood ADHD 

cases present with at one or more symptoms in adulthood (Biedermann 2000, Wilens 2006). A prevalance rate of 4.4% of adults has been 

reported for ADHD (Fayyad 2007, Kessler 2006). 

Comorbidity with alcohol and substance use disorders in A-ADHD is also common and reported as 50%, which is 2-3 times more common 

than in the normal population (15%) (Katusic 2005). A-ADHD is reported to be an independent risk factor for substance abuse. Comorbid 

substance use disorders have been observed at rates of 9-30& (Wilens 2006). 

Individuals with substance use dişorders comorbid with A-ADHD do not differ in substance preference from individuals without A-ADHD 

comorbidity. Cannabis is the most abused substance. 

Objective: We aimed to demonstrate the existence and intensity of Adult ADHD symptoms in cannabis dependent individiuals and 

discuss the importance of comorbid A-ADHD. 

Methods: Seventy patients participated and gave informed consent. The participants were selected from patients who underwent 




inpatient treatment in the Department for Addiction at Samsun Neuropsychiatry Hospital. Diagnostic interviews were conducted for 

cannabis dependence syndrome (ICD 10; DSM-IV); the earliest interview was after 21 days of detoxification therapy. For assesment, the 

Adult ADD/ADHD DSM IV based Diagnostic Screening and Rating Scale was used. The reliability, validity, and transliteral equivalance study 

had been performed by Günay et.al in 2005 (Günay 2006). The scale was developed by Prof. Dr.Turgay, former Director of the Toronto 

ADHD Clinic, Ontario,Canada. It is a self assessment scale. 

General total and subscale mean scores and standard deviation of the ADHD scale according to group factors were calculated. Mean 

ADHD total and subscale scores were compared by using the group variable independent t test. The analyses were conducted using SPSS 

for Windows 16.00. 

Results: The ADHD general total mean scores and subscale mean scores were compared between the groups. Considerably higher scores 

were observed in cannabis dependent individuals. 

Twenty-two patients met the criterion of inattention whereas 24 patients met both the criteria of hyperactivity and inattention. Twentyfour 

patients were re-evaluated and interviewed and Adult ADHD was diagnosed. 

Five individuals in the control group met the criterion of inattention, and there were no individuals who met the criteria for both 

hyperactivity and inattention. 

All three subdimensions of the Turgay Adult ADHD Scale were found to be statistically higher in the cannabis dependent patients. 

Conclusions: As this study shows, Adult ADHD is highly represented in cannabis dependent patients.(in our sample 35% of patients were 

diagnosed with Adult ADHD). 

The awareness of the ADHD diagnosis in Turkey has rapidly increased over time. However it is not commonly researched, diagnosed, or 

treated in adult psychiatric units. A major difficulty may be that ADHD has been misdiagnosed because comorbidity is common and 90% 

of A-ADHD patients present with another psychiatric disorder in clinical practice. Recent studies clearly show a strong relation between 

ADHD and addiction, which supports the idea that a high percentage of drug dependent individuals are also suffering from undiagnosed 

A-ADHD. Individuals who are diagnosed and treated are less vulnerable to addiction (Biedermann 1999) 

Key words: Adult ADHD, cannabis dependency, substance use 

References: 

1. Biederman J, Mick E, Faraone SV (2000) Age-de¬pendent decline of symptoms of attention deficit hyperactivity disorder: impact of remission definition and 

symptom type. Am J Psychiatry 157:816–818 

2. Wilens TE (2006) Attention-deficit/hyperactivity disorder and the substance use disorders: the nature of the relationship, subtypes at risk, and treatment issues. 

Psychiatr Clin North Am 27:283–30. 

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 


[PP-063] Ref. No: 270 

Ganser syndrome as a dissociative disorder: A case report 

Beliz Soyer, Jülide Kenar, Kader Semra Karataş 

Erenkoy Mental and Nervous Diseases Training and Research Hospital, Istanbul, Turkey 

E-mail: blz_syr@hotmail.com 

Ganser syndrome was first described in 1898 by Sigbert Ganser in 4 prisoners. Initially, it was believed to be rare, occurring mainly in 

forensic settings. Hence, it was referred to as prison psychosis. Later, such cases were reported more frequently in non-forensic settings. 

The syndrome has found a place in both the ICD-10 and DSM-IV, despite controversy about its existence and distinctiveness. This disorder 

was previously classified as a fictitious disorder; currently, it is classified under ‘dissociative disorder not otherwise specified.’ We report a 

case of a 38 year old woman with Ganser syndrome. The symptoms started 9 months after the death of her brother’s children. 

Key words: Ganser Syndrome, vorbeireden, dissociative disorder 


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[PP-064] Ref. No: 272 

Escitalopram induced galacthorrea: Phenomenon presentation 

Aslı Aktümen Bilgin 1 , Birmay Çam 2 

1 Zonguldak Atatürk Devlet Hastanesi Psikiyatri Kliniği, Zonguldak, Turkey 

2 Gönen Devlet Hastanesi Psikiyatri Kliniği Balıkesir, Turkey 

E-mail: draslibilgin@gmail.com 

Hyperprolactinemia can present with many physical symptoms such as galactorrhea, amenorrhea, infertility and osteoporosis and 

can also cause psychological problems like depression and anxiety. Hyperprolactinemia is mostly seen as a side effect of antipsychotic 

medications and rarely can also occur as a side effect of an SSRI. Hyperprolactinemia and galactorrhea as adverse effects of escitalopram 

are rarely encountered. In this text we present a case, who developed hyperprolactinemia and galactorrhea on the sixth day of treatment. 

The prolactin level decreased to normal after stopping the medication. 

Key words: Escitalopram, galactorrhea, hyperprolactinemia 


[PP-065] Ref. No: 276 

Amisulpride use in treatment of Tourette’s disorder 

Yasemen Taner, Hande Ayraler Taner 

Departmant of Child and Adolescent Psychiatry, Gazi University, Ankara, Turkey 

E-mail: taneryasemen@yahoo.com 

Tourette’s disorder is a neuropsychiatric disease characterised by chronic vocal and motor tics that leads to severe psychosocial disability. 

Many old and new generation antipsyshotics had been used in the treatment of Tourette’s Disorder, especially antipsychotics which have 

strong effects on D2 receptors. Amisulpride is an antipsychotic which has strong effects on D2 and D3 receptors. Parkinsonism, endocrine 

system side effects, and weight gain are less frequent than with the other antipsychotics. Amisulpride is safely used in the treatment of 

schizophrenia and the other psychoses in adults. In this case report we discuss amisulpride use in 3 cases with Tourette’s disorder. These 

cases previously used other antipsychotics for Tourette’s disorder treatment. Amisulpride was used at a dose of 75-200 mg/day. After 

treatment in all three of these cases, the Yale Global Tic Severity Scale score decreased. 

Key words: Tourette’s disorder, amisulpride 


[PP-066] Ref. No: 299 

Lithium associated glossodynia syndrome: A case report 

Hasan Toğul 

Gata Haydarpasa Training Hospital, İstanbul, Turkey 

E-mail: hasan_togul@hotmail.com 

Lithium revolutionized the treatment of bipolar disorder and continues to be the most widely used treatment for this disorder. There 

are several side effects that result from lithium carbonate therapy and among the most commonly reported are polydipsia, polyuria, 

tremor and weight gain. There have also been reports of various skin lesions with lithium treatment. The following case report suggests 

that mucosal lesions may possibly result from lithium therapy. Glossodynia is commonly seen in old female patients. In our case, a 45 

year old male had glossodynia after lithium carbonate therapy. The patient’s symptoms were under control with a lithium regimen for a 

year. He stopped using lithium in January 2011 and one and a half months later he was hospitilazed because of dysphoric mania. After 

his hospitalization, lithium therapy was started again. Three weeks later he reported mucosal ulcerations in the mouth, with associated 

soreness of the tongue. The tongue appeared inflamed, with cracks or irregular reddish areas. He was evaluated by a dermatologist, who 

diagnosed him with glossodynia. No other medical causes for the lesions were found; the lesions were presumed to be secondary to 




lithium treatment. His lithium treatment was stopped and glossodynia treatment begun. Shortly thereafter, his glossodynia symptoms 

disappeared. Psychotropic medications can cause mucosal ulcerations and it is important to consider these side effects in the differential 

diagnosis and and begin treatment as soon as possible. 

Key words: Lithium carbonate, glossodynia, side effects 


[PP-067] Ref. No: 300 

Two cases of affective disorder due to immunosuppresive treatment 

that followed renal transplantation 

Hüseyin Ünübol, Başak Ünübol, Jülide Güler, Alper Ünal 

Erenkoy Mental Health Education and Research Hospital, İstanbul, Turkey 

E-mail: hunubol@hotmail.com 

The advent of effective immunosuppressive medicines in the mid-1980s, most notably cyclosporine, revolutionized solid-organ transplant 

surgery. For the first time, survival rates reached acceptable levels and rendered organ transplantation a reasonable, non-experimental 

standard of medical practice. From the beginning, the immunosuppressive medications were noted to have significant neurological and 

psychiatric side effects. From that time to this, the neuropsychiatric side effects such as subjective anxiety or jitteriness, along with tremor, 

have served as endpoints in the clinical titration of the the most frequently used immunosuppressive medications, cyclosporine and 

tacrolimus. Experience over the past 15 years, however, has established the fact that there are other neuropsychiatric side effects, varying 

from seizures, stroke, and profound cognitive impairment to very subtle forms of neuropsychiatric difficulty. Here we present two cases 

that underwent uncomplicated renal transplantation and after the immunosuppressive therapy, developed psychiatric symptoms. The 

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 

hypomanic episode (1-3). 

Case No 1: A 29 year-old female patient, with a history of kidney transplantation 9 months ago, developed 

insomnia, nervousness, mobility, speaking too much, aggressive behavior towards her mother at home, destruction of items, thinking 

people were trying to poison her, self-talk in the office, increased skepticism, left her workplace without permission, angry and rowdy 

behavior. 

History: No previous psychiatric treatment. No family history of substance abuse and psychiatric illness. Surgery for kidney transplantation 

9 months ago. Twenty mg/day oral olanzapine treatment was started. 

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 

100 mg tb 1*1 21:30 therapy was continued. 

Blood samples for monitoring of cyclosporine levels were sent outside the center. MPPI, Rorschach, and psychometric examinations were 

performed and she was evaluated in the direction of psychotic process. PMA is returning to normal; irritability and the patient’s insight 

improved on olanzapine 20 mg/day treatment and she was discharged. 

Case No 2: A 25 year-old, male patient, with a history of kidney transplantation 4 years ago. The symptoms included unhappiness, 

reluctance, discomfort, passive thoughts of death, and insomnia. 

Hisstory Kidney transplant in 2007. Approximately 1.5 years ago he had increased speech and movement and affective elation observed 

indicated a hypomanic episode in the hospital outpatient clinic as the patient was evaluated. Risperidone 2 mg/day treatment was 

started. Two months ago the patient presented with depressive symptoms and started sertraline 50 mg/day, quetiapine 25 mg/day, 500 

mg 2 * 2, Mycophenolate mofetil, prednisolone 5 mg, 1 * 1, tacrolimus 1 mg tb 2 * 2, a month after inpatient treatment, the patient became 

euthymic, anxiety resolved, and after the disappearance of suicidal ideation the patient was discharged. 

Key words: Renal transplantation, immunosuppresive treatment, depression, affective disorder 

References: 

1. Trzepacz PT, Brenner R, Van Thiel DH. A psychiatric study of 247 liver transplantation candidates. Psychosomatics 1989;30: 147-153. 


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[PP-068] Ref. No: 303 

Varenicline induced psychotic disorders: A case report 

İkbal İnanlı, İbrahim Eren, Tahsin Etli 

Konya Eğitim ve Araştırma Hastanesi Beyhekim Psikiyatri Kliniği, Konya, Turkey 

E-mail: ikbalcivi@yahoo.com 

Varenicline is a new agent, commonly used to assist individuals with smoking cessation. There is an increase in case reports of psychiatric 

disorders induced or activated by using the agent. Due to the agent’s mechanism of actions, it is possible to make this correlation. Patients 

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 

induced by varenicline is presented. 

Key words: Psychotic disorder, smoking cessation, varenicline 


[PP-069] Ref. No: 309 

Affective disorders and catatonia: Report of two cases 

Feride Büyükşahin, Jülide Güler, Başak Ünübol, Hüseyin Ünübol, Alper Ünal 

Erenkoy Mental Health Education and Research Hospital, İstanbul, Turkey 

E-mail: basakctf@hotmail.com 

Catatonia refers to a broad group of movement abnormalities usually associated with schizophrenia, but also found in other disorders 

such as mania, depression, many neurological disorders (especially those involving the basal ganglia, limbic system, diencephalon, and 

frontal lobes), systemic metabolic disorders, and toxic drug states. Catatonia is often neglected when screening and examining psychiatric 

patients. Undiagnosed catatonia can increase morbidity and mortality, illustrating the need to effectively screen patients for presence 

of catatonia, as well as their response to treatment. We describe the clinical presentation of catatonia in a 32 year-old woman with 

schizoaffective disorder and in a 25 year-old woman with severe psychotic depression. 

Key words: Catatonia, mood disorders, depression 


[PP-070] Ref. No: 224 

The relationship of incarceration, past suicide attempts, depression, anxiety and 

attention deficit hyperactivity disorder in cases of anti-social personality disorder 

Hakan Balıbey 1 , Türker Türker2, Zülküf Perdeci 1 , Nalan Bayar 1 , Mehmet Boran Evren 1 

1 Department of Psychiatry Ankara Military Hospital, Ankara, Turkey 

2 Department of Public Health Division of Epidemiology Gulhane Military Medical Faculty, Ankara, Turkey 


Bacgrounds and Objective: Even though attention deficit/hyperactivity disorder (ADHD) has been considered as a childhood disorder 

for a long time, currently it is widely accepted that this is a disorder that continues well into adulthood. Attention deficit hyperactivity 

disorder (ADHD) is a chronic developmental psychiatric disorder, which starts in early childhood, although its primary symptoms can 

still be observed in adulthood. The main symptoms are attention loss, impulsiveness, and hyperactivity which result in mental, social, 

and educational/occupational problems in adulthood (1). The current study aimed to study the relationship of incarceration, suicide 

attempts, depression, anxiety, and attention deficit hyperactivity disorder in men, who had been diagnosed with antisocial personality 

disorder (APD). There are previous studies in the literature for equivalent diagnoses (2,3). METHODS: A total of 80 subjects, 44 of whom 

were diagnosed with antisocial personality disorder according to the DSM-IV-TR diagnostic criteria in Ankara Military Hospital psychiatry 

clinic and 36 controls, who did not have a psychiatric diagnosis were included in the study. The subjects had been administered a semistructured 

interview form for identifying their demographic properties, criminal history, and past suicide attempts. The subjects had also 




been given the Wender-Utah rating scale, Hamilton anxiety scale, and Hamilton depression scales. The diagnosis of anti-social personality 

disorder has been corroborated by a second mental health professional for all such cases. 

Results: There was a statistically significant difference between the Wender-Utah test scores of the APD group and the control group 

(p


motivations for the use of antipsychotic prescription by psychiatrists. 

Five hundred and sixty patients, who applied to the psychiatry clinic of the SSK Ankara Education and Research Hospital in 2004 and 

were diagnosed with schizophrenia and 423 patients who presented to the same clinic (name changed to the Psychiatry Clinic of Dışkapı 

Yıldırım Beyazıd Education and Research Hospital) in 2009 and were diagnosed with schizophrenia were included in the study. The data 

were recorded on the data gathering form that we prepared and included socio-demographic information and details of medication use. 

We determined that 77.5 percent of the schizophrenic patients were prescribed atypical antipsychotics in single or combined (typicalatypical 

or atypical-atypical) form in 2004. Forty-five percent of patients were using typical antipschotics as monotheraphy or in 

combination. In 2009, 91.7 percent of patients were using atypical antipschotics in single or combined form. Only 19.9 percent of patients 

were taking typical antipschotics in single or combined form. Using atypical antipsychotics reduced the use of typical antipsychotics 

by a significant amount ( χ2=246.26 and p

References: 



1. Segura-Bruna N, Rodriguez-Campello A, Puente V, Roquer J. Valproate-induced hyperammonemic encephalopathy. Acta Neurol Scand 2006; 114(1):1-7. 

2. Chen WT, Yen DJ, Yu HY, Liao KK. Valproate-induced encephalopathy. Zhonghua Yi Xue Za Zhi (Taipei) 2001; 64(8):474-8. 

3. Wadzinski J, Franks R, Roane D, Bayard M. Valproate-associated hyperammonemic encephalopathy. J Am Board Fam Med 2007; 20(5):499-502. 

4. Gurjar M, Singhal S, Baronia AK, Azim A, Poddar B. Valproate-induced hyperammonemic encephalopathy: A reminder of rare complication of valproate. J Emerg 

Trauma Shock 2011; 4(2):321-2. 


[PP-074] Ref. No: 274 

Two cases of tardive dyskinesia associated with the use of paliperidone ER and 

their management 

Ömer Yanartaş, Yücel Yılmaz, İshak Saygılı, Selma Bozkurt Zincir, Ümit Başar Semiz 

Erenkoy Mental Health and Disorders Training and Research Hospital, Istanbul, Turkey 

E-mail: yanartas2005@yahoo.com 

Paliperidone is an extended-release (ER) medication used in the treatment of schizophrenia and the recommended dose range is 3-12 

mg/day (1). Tardive dyskinesia (TD) associated with the use of antipsychotics is characterized by involuntary choreic-athetoid movements 

occurring in the late stages of the treatment. Choreathetoid movements mostly occur around the mouth and face and athetoid 

movements alone mostly occur on the head-neck and pelvis (2, 3). We hereby present two cases of perioral dyskinesia who were using 

paliperidone, and discuss their response to the treatment. 

Both patients were females in their 20s and had been diagnosed with paranoid schizophrenia according to the DSM-IV-TR diagnostic 

criteria. Both patients had been using olanzapine before being switched to paliperidone ER. Olanzapine treatment had been discontinued 

due to side effects and treatment failure. The durations of paliperidone ER use were 9 months and 1 year, respectively; the doses of 

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 

occurrence of side effects in combination with a psychotic exacerbation led to a change in antipsychotic drug therapy. In the other case, 

the drug was not discontinued due to the remission of initial psychotic symptoms and satisfaction of the patient with the treatment; 

however, the drug dose was reduced. In the treatment of TD associated with the use of paliperidone ER, one case responded to vitamin 

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 

month, the scores of both patients on the extrapyramidal symptoms assessment scale were markedly reduced. The patient who had the 

psychotic exacerbation also had a history of childhood trauma, which we feel had negatively influenced the course of the treatment. 

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 

vitamin E, omega 3 fatty acids, propranolol, and clonazepam may lead to a significant improvement in symptoms. 

Key words: Extrapyramidal side effects, paliperidone, tardive dyskinesia 

References: 

1. Janicak PG, Winans EA. Paliperidone ER: a review of the clinical trial data Neuropsychiatric Disease and Treatment 2007:3(6) 869–883. 

2. Kaplan HI, Sadock BJ Synopsis of Psychiatry: Eighth ed. Baltimore: Williams & Wilkins, 1998 

3. Bernstein JG. Drug Therapy in Psychiatry. Third ed. St.Louis: Mosby-Year Book, 1995 

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 

of acute schizophrenia: pooled data from three 6-week, placebo-controlled studies. J Clin Psychiatry 2008 May;69(5):817-29. 


S165


[PP-075] Ref. No: 301 

Effects of agmatine in rats with chronic unpredictable mild stress 

Feyza Arıcıoğlu 1 , Tijen Utkan 2 

1 Department of Pharmacology and Psychopharmacology Research Unit, Marmara University, Faculty of Pharmacy, Istanbul, Turkey 

2 Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey 

E-mail: feyza.aricioglu@gmail.com 

Depression is one of the most common psychiatric disorders which is a leading cause of total disability and economic burden. 

Although there are medications that alleviate depressive symptoms, they have serious limitations. Therefore better understanding of 

the neurobiology of the disease is required. Agmatine (l-amino-4-guanidinobutane) is an endogenous amine synthesized from the 

decarboxylation of arginine. Agmatine has been quantified in nearly all of the organs of the rat including brain and plasma. Agmatine 

exerts a wide range of biological activities on several organ systems, including the central nervous system, where it has been proposed 

to act as a neurotransmitter. Agmatine interacts with the imidazoline receptors, alpha-2-adrenoceptors, nicotinic cholinergic receptors, 

and serotonergic 5-HT3 receptors. It selectively modulates the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors in rat 

hippocampal neurons via an interaction between the guanidino group of agmatine and the NMDA channel pore and is an endogenous 

inhibitor of all isoforms of nitric oxide synthase. Agmatine is released from neurons and has neuroprotective properties. The present study 

was designed to evaluate the effect of agmatine in a chronic unpredictable mild stress (CUMS)-induced depression model. 

Animals were allocated to the following study groups: animals not exposed to CUMS (Control group, n=12), animals exposed to CUMS for 

5 weeks (CUMS group, n=12), and animals exposed to CUMS and treated with agmatine (CUMS+Agmatine group, n=12). The control and 

CUMS groups were injected with saline and the CUMS+Agmatine group was injected with agmatine 40 mg/kg, i.p. daily throughout the 

experiment. CUMS was applied as previously described with a minor modification. Briefly, the CUMS and CUMS+Agmatine groups were 

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 

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 

inversion of the light/dark cycle for 24 h. These nine stressors were randomly applied for 5 weeks, during which each stressor was applied 

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 

animals could not predict the occurence of stimulation. The control group not receiving stress treatment had free access to food and water 

but all groups were food and water deprived 24 h before the sucrose consumption test only. After 5 weeks, the sucrose consumption, 

sucrose preference and forced swimming tests were performed. 

The results of this study showed that agmatine administration during CUMS suppressed CUMS-induced depression-like behavioral 

changes, including a reduction in sucrose preference, body weight, locomotor activity, and a decrease in immobility time in the forced 

swimming test. Our findings suggest that agmatine may have a protective effect either by inhibiting oxidative damage and/or by 

modulating neuronal activity in CUMS. Based on these findings, agmatine, as an endogenous molecule, has a promising effect and further 

studies are required to understand the underlying mechanism. 

Key words: Agmatine, sucrose preference, forced swimming test, chronic unpredictable mild stress 


[PP-076] Ref. No: 302 

A case of obsessive compulsive disorder with psychotic features that suffered 

from sexual trauma 

Fatma Fariha Cengiz, Esra Aydın Sünbül 

Erenköy Psychiatric Training and Research Hospital, İstanbul, Turkey 

E-mail: dr_ffatmacengiz@yahoo.com.tr 

Introduction: Although the relationship between obsessive compulsive disorder (OCD) and psychosis is a noteworthy phenomenon, the 

limits of the two disorders have not been defined. Eisen and Rasmussen (1993) evaluated a total of 475 patients with OCD and 14% were 

identified as having psychotic symptoms in addition to OCD. They classified the patients into 4 groups: 6% OCD without insight, OCD 

and schizophrenia (4%), OCD and delusional disorder (2%), OCD and schizotypal personality disorder (3%) (1). In clinical observation it is 

seen that, the shift from an obsession to a delusion is described when insight into obsessive signs is lost and resistance abandoned. These 

delusions do not signify a schizophrenic diagnosis but represent reactive affective or paranoid psychoses (3). 




Case: A 32 year old single man, who has not been a soldier, presented with aggressive, contamination, sexual, need for symmetry, somatic 

obsessions; checking, washing, counting, need for confession compulsions; thinking he was followed by the secret service, sense of anal 

burning, and inability to sleep. His mood and affect were anxious, speech increased, and associations were dispersed. He had a history 

of sexual abuse by his brother. Obsessive symptoms started at the age of 12, feeling some problems about his gender, anxiety about 

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 

because of a myocardial infarction and he started to blame himself. He lost 15 kg in 6 months and started to experience auditory and 

visual hallucinations. He was treated with many antipsychotics, SRIs, TCAs, and benzodiazapines. He had a hypomanic attack under the 

treatment of aripiprazole. In the Rorschach test he showed schizoid reactions and dissociation in 2003. He was hospitalized 2 times. At his 

last visit his treatment was sertraline 200 mg/day and olanzapine 5 mg/day. The appearance of the psychotic symptoms occurred, when 

the depressive symptoms started. Olanzapine was increased to 10 mg/day after sleeplessness and psychotic symptoms flared up. The last 

Rorschach test assessed the patient as being in pregenital organization and requiring close control of affective and psychotic symptoms. 

Discussion: The clinical observations emphasize the interest in OCD patients with psychosis, who are neglected often. The shift from 

an obsession to delusion is triggered by stress and is generally transient (2). The strong association between psychotic features and 

depressive features in OCD may also have important implications in the treatment strategies (3). OCD represents a psychopathological 

spectrum varying along a continuum of insight and requires careful clinical observation and treatment. 

Key words: Obsesive compulsive disorder, psychosis, sexual trauma 

References: 

1. Eisen JL, Rasmussen SA. Obsessive-compulsive disorder with psychotic features. J Clin Psychiatry1993; 54(10):373-379. 

2. Özerdem A. Obsesif-Kompulsif Bozukluk ve Psikoz Üzerine Bir Gözden Geçirme. Klinik Psikiyatri 1998;2:98-102 

3. Khess CDJ, Das J, Parial A et. al. Obsesive Compulsive Disorder with psychotic features.Hong Kong J Psychiatry1999;9(1): 21-25 


[PP-077] Ref. No: 304 

Priapism associated with zuclopenthixol treatment: A case report 

Alparslan Asil Budaklı, Mehmet Alpay Ateş, Ayhan Algül 

GATA Haydarpasa Education Hospital, İstanbul, Turkey 

E-mail: asil.budakli@gmail.com 

Background: Priapism is pathologically prolonged and painful penis erection, usually without sexual desire or stimulation. Priapism is 

classified as veno occlusive low flow (ischemic) and arterial high flow (non ischemic). The low flow–ischemic type is the most common 

type of priapism and if it is untreated, leads to irreversible ischemic cavernosal tissue changes. The causes include generally certain 

medications, although the mechanism for drug-induced priapism is unknown (1-4). 

Here we discuss, in light of the literature, a 62-year-old- male paranoid schizophrenic patient, who had been treated with oral 

zuclopenthixol since 1995 and developed an acute and painful erection. 

Case: It was revealed that the patient, who presented with priapism, that hadcontinued for a week, took zuclopenthixol 20 mg a day for 

2 days prior to the veno occlusive priapism. 

After emergency urological treatment, the psychiatric examination revealed paranoid psychosis. Zuclopenthixol was stopped and 

risperidone 6 mg/day and biperiden 4 mg/day were prescribed. A week later he was discharged from hospital. 

Discussion: In many cases it has been reported that psychotropic drugs may cause priapism. Some of them are trazadone, chlorpromazine, 

haloperidol, zuclopenthixol, olanzapine, ziprasidone, and clozapine (3). Although the mechanism of priapism associated with antipsychotics is not 

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 

of zuclopenthixol to induce priapism is thought to be due to its antagonist activity on alpha-1 adrenergic receptors (1,3). 

Therefore it is important that clinicians must take notice of side effects of antipsychotics, including rarely seen ones. 

Key words: Zuclopenthixol, priapism, side effect, drug induced, antipsychotics 

References: 

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 

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): 

699-73.Epub 2008 Jun 10. 

3. Sood S, James W and Bailon MJ. Priapism associated with atypical antipsychotic medications. a review. Int Clin Psychopharmacol 2008; 23: 9-17 

S167


4. Şükrü Kartalcı, Işıl Göğceğöz Gül, Rıfat Karlıdağ, Birgül Elbozan Cumurcu Recurrent priapism during quetiapine treatment case report; Bulletin of Clinical 

Psychopharmacology, Vol: 20, N.: 4, 2010 327-328 


[PP-078] Ref. No: 113 

Prescribing patterns and inappropriate use of medications in patients referred to 

doctors in Ardabil City of Iran 

Firouz Amani, Amin Shaker 

Iran- Ardabil University of Medical Sciences, Iran 

E-mail: biostat.f@gmail.com 

Objective: To determine the drug use patterns and descriptive analysis of prescriptions among patients who visited doctors in Ardabil City. 

Methods: A retrospective study was carried out on 2000 randomly selected prescriptions from all registered prescriptions in Ardabil City 

using data from two insurance organizations. Data were obtained on demographics, prescribing indicators and potentially inappropriate 

medications. The collected data were analyzed by descriptive statistical methods using SPSS software. 

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 

years ranging from 1 to 91. On thousand three hundred and six (65.3%) of all prescriptions were from general practitioners and others from 

specialists. The mean number of drugs per prescription was 3.58±1.3 ranging from 1 to 9. Dexamethasone, with 219 (24.7 %) prescriptions, 

was the most commonly prescribed medication. The total number of medications prescribed in all the prescriptions was 7158 while the 

mean number of medications per encounter was 3.6. Antibiotics, with 52.8% of the prescriptions, were the most prescribed drug group. 

Conclusion: The results showed that the mean of prescription drugs per encounter and the rate of prescription injection drugs were more 

than the global standards. Also, the pattern of prescription drugs was inappropriate. It is necessary to reduce irrational prescription of 

drugs to patients by monitoring and control indicators of medical doctors who prescribe higher numbers of prescriptions. 

Key words: Pattern, drug utilization, inappropriate medications 


[PP-079] Ref. No: 305 

Bipolar affective disorder and normal pressure hydrocephaly: A case report 

Kader Semra Karataş 1 , Jülide Güler 1 , Özgür Bilgin Topçuoğlu 2 , Ebru Damla Bostancı 1 , Beliz Soyer 1 

1Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Psychiatry, İstanbul, Turkey 

2Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Neurology, İstanbul, Turkey 

E-mail: drsemraocak@yahoo.com 

Background: The subject of this study was how affective disorders are related to structural changes in the brain. The use of lithium in 

affective disorders can cause pseudotumor cerebri, which has been reported in the literature, although there is no information about the 

occurrence of normal pressure hydrocephalus. We detected normal pressure hydrocephalus in a patient diagnosed with bipolar affective 

disorder 10 years ago and treated with lithium. 

Case: A 55 year-old woman, housewife, not working, lives in Istanbul with her husband and children. She was diagnosed with bipolar 

affective disorder 10 years ago and treated with lithium. She had hand tremors, weakness and dizziness and was admitted to hospital. 

The patient was dehydrated, walking with small steps, showed balance difficulty and urinary incontinence. The patient was admitted 

to the psychiatric unit. A neurology consultation and cranial MRI were requested. The patient was thought to have normal pressure 

hydrocephalus. Lumbar puncture was performed twice. The patient was diagnosed with arrested hydrocephalus; CSF flow could not be 

identified. A CSF dynamic MRI was requested and the patient was transferred to neurosurgery. 

Discussion: There are publications about the relationship between structural brain abnormalities and affective disorders. Hydrocephalus, 

by definition, is the accumulation of CSF in the ventricular system due to an imbalance between production and absorption of CSF. 

Presenting symptoms include memory impairment, urinary incontinence symptoms, and ventriculomegaly (2,3). The etiology of 

normal pressure hydrocephalus can include head trauma, metabolic problems, endocrinopathies, infectious and immunological 

conditions; danazol, tamoxifen, oxytocin, tetracycline, indomethacin, lithium, drugs such as retinol are mentioned (2.4). Normal pressure 




hydrocephalus is not known to be associated with lithium in the literature. Lithium is known for its relationship with pseudotumor cerebri. 

Taking into account the patient saw benefits from lithium, it was decided to postpone to a change to the mood stabilizer. 

Key words: Bipolar affective disorder, lithium, normal pressure hydrocephalus, structural brain abnormalities 

References: 

1. Arnone D, Cavanagh J, Gerber D, Lawrie SM, Ebmeier KP, Mclntosch AM. Magnetic resonance imaging studies in bipolar disorder and schizophrenia: meta-analysis. 

BJPsych 2009; 195:194-201. 

2. Görgülü O, Yurt A, Özer FD, Turan Y. Normal basınçlı hidrosefali ön tanılı 26 hastanın analizi. Demans Dergisi 2003; 3:117-120. 

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. 

Arch Gen Psychiatry. 2008;65:1017-32. 

4. Levine SH, Puchalski C. Pseudotumor cerebri associated with lithium therapy in two patients. J Clin Psychiatry. 1990; 51:251-3. 


[PP-080] Ref. No: 307 

Agmatine attenuats cognitive impairment and oxidative damage following chronic 

unpredictable mild stress: A behavioral, biochemical, and histological study 

Salih Gümrü 1 , Emre Yarcı 1 , Özer Şehirli 1 , Yusufhan Yazır 2 , Tijen Utkan 3 , Feyza Arıcıoğlu 1 

1 Department of Pharmacology and Psychopharmacology Research Unit, Marmara University, Faculty of Pharmacy, Istanbul, Turkey 

2 Department of Histology and Embryology, Kocaeli University, Medical Faculty, Kocaeli, Turkey 

3 Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey 

E-mail: salihgumru@gmail.com 

Agmatine (l-amino-4-guanidinobutane) is an endogenous polycationic amine synthesized by the decarboxylation of arginine by the 

enzyme arginine decarboxylase and hydrolysed by agmatinase. Agmatine has been quantified in nearly all organs including brain. It 

has been proposed to act as a novel neuromodulator in the mammalian brain. Previous studies have shown that endogenous agmatine 

interacts with a number of receptor subtypes such as, imidazoline, 2-adrenergic and N-methyl-D-aspartate. It also blocks other ligandgated 

cationic channels, including nicotinic receptors, and inhibits all three isoforms of nitric oxide synthase. Although there are papers 

showing that agmatine may have a modulator role in learning and memory, the question of whether it is able to reverse impaired learning 

and memory still remains. This study was planned to investigate the effect of agmatine on cognitive functions and oxidative damage 

following chronic unpredictable mild stress (CUMS). 

Rats were allocated to the following study groups: animals not exposed to CUMS (control group, n=12), animals exposed to CUMS for 

5 weeks (CUMS group, n=12), animals exposed to CUMS and treated with agmatine (CUMS+Agmatine Group, n=12). The control and 

CUMS groups were injected with saline and the CUMS+Agmatine group was injected with agmatine 40 mg/kg, i.p. daily throughout the 

experiment. CUMS was applied according a previous study with a minor modification. Briefly, the CUMS and CUMS+Agmatine groups 

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 

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 

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 

per day and the same stressor was not applied continuously for 2 days so that animals could not predict the occurence of stimulation. 

After 5 weeks, animals were tested in the passive avoidance (PA) and Morris’s water maze (MWM) tasks to evaluate learning and memory 

functions. At the end of the experiment, the brains of the rats were either removed freshly for malondialdehyde (MDA), glutathione (GSH) 

levels and myeloperoxidase (MPO) activity or removed with 4% paraformaldehyde perfusion for c-fos, glial fibrillary acidic protein (GFAP) 

and brain-derived neurotrophic factor (BDNF) determination immunohistochemically in cortex and hippocampus. 

There was a significant defect in cognitive functions of the CUMS group whereas agmatine treatment significantly reversed this effect 

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 

with agmatine treatment, which were considered markers of oxidative damage. In the immunohistochemical experiments, it was found 

that c-fos and GFAP were overexpressed and BDNF was decreased in the CUMS group whereas data for the agmatine treatment group 

were similar to those of the control group. The findings of the current study clearly showed beneficial effects of agmatine on cognitive 

impairment and oxidative damage in CUMS. 

Key words: Agmatine, BDNF, c-fos, chronic unpredictable mild stress, GFAP, malondialdehyde, glutathione, myeloperoxidase 


S169


[PP-081] Ref. No: 308 

Ceruloplasmin levels before and after treatment in patients with depression: 

A case-control study 

Mehmet Cemal Kaya 1 , Yasin Bez 1 , Salih Selek 2 , Haluk Asuman Savaş 3 , Hakim Çelik 2 , Hasan Herken 4 

1 Dicle University School of Medicine, Department of Psychiatry, Diyarbakir, Turkey 

2 Harran University School of Medicine, Department of Psychiatry, Sanliurfa, Turkey 

3 Gaziantep University School of Medicine, Department of Psychiatry, Gaziantep, Turkey 

4 Pamukkale University School of Medicine, Department of Psychiatry, Denizli, Turkey 

E-mail: mcemalkaya@yahoo.com 

Objective: Ceruloplasmin is a serum protein synthesized by hepatocytes and involved in both copper and iron metabolism. It is an 

acute phase reactant and has antioxidant capacity (1). Deficiency of ceruloplasmin is thought to cause neural cell damage secondary to 

decreased mitochondrial energy production and increased lipid peroxidation, and iron associated free radicals (2,3). Ceruloplasmin, an 

antioxidant agent, has previously been investigated in some psychiatric disorders like schizophrenia and obsessive compulsive disorder 

(4). Studies about ceruloplasmin in depression are relatively scarce (5). In this prospective study, we aimed to determine the serum 

ceruloplasmin levels of depressive patients before and after treatment, to compare them those of healthy control subjects and to assess 

any possible association of ceruloplasmin levels to treatment response. 

Methods: Among the admissions to the Psychiatry Outpatients Clinic of Gaziantep University Medical Faculty Hospital 19 (8 males, 11 

females) patients who were diagnosed with major depressive disorder according to the DSM-IV criteria and 40 (17 males, 23 females) 

healthy control subjects have been included in the study. The patients received naturalistic antidepressant treatment during the 8 weeks 

period after the diagnosis. The serum ceruloplasmin levels and the Hamilton Depression Rating Scale (HAM-D) scores of the patients 

were measured before and after the 8 week period of antidepressant treatment. Blood collection for ceruloplasmin measurement was 

done only once for the healthy control subjects. The measurement of ceruloplasmin levels was conducted according to the standard 

procedures. 

Results: The ceruloplasmin levels of patients both before and after antidepressant treatment were significantly higher than those of 

control subjects (t=7.569, p



[PP-082] Ref. No: 159 

Foetality in schizophrenia 

Elif Mutlu, Mehmet Emin Ceylan, Agah Aydın 

Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

E-mail: elifmutlu@yahoo.com 

Objective: The aim of this study was to evaluate common morphological and neurological features of schizophrenia from an ontogenetic 

perspective and to propose a new conceptual approach to schizophrenia, in which early foetal marks persist without diminishing in 

comparison to other people. 

Material and Methods: Fifty patients diagnosed with schizophrenia from the Bakırköy Research and Training Hospital for Psychiatry, 

Neurology and Neurosurgery were chosen for the study group. The control group consists of fifty healthy male subjects. The ages of 

all subjects varied between 18 and 65. All of the subjects were informed about the study and their written consents were obtained. 

Sociodemographic data of all subjects were recorded and the Waldrop Minor Physical Anomalies Scale, the NES ( neurological evaluation 

scale), and the Edinburgh Handedness Inventory were applied. 

Results: We found significantly higher scores among schizophrenic patients in comparison to healthy subjects both in the NES total and 

all four sub-categories of the scale. The minor physical anomalies scores, head circumference, and hypertelorism were significantly higher 

in the schizophrenic group. In addition, for hand-eye dominancy, we observed more tendency to be crosswise. 

Conclusion: Some characteristics of schizophrenia such as hypertelorism, large head circumference, high palate, thin muscle and 

bone structure, primitive reflexes, mental and behavioral characteristics could be evaluated as a separate ontogenetic entity.Evaluating 

schizophrenia within the context of a neurodevelopmental hypothesis, as an evolutionary process, in which foetal traits persist, would 

contribute to our understanding of the disorder’s ambigous nature and phenomenology. 

Key words: Schizophrenia, foetality, ontogenesis 


[PP-083] Ref. No: 182 

Metabolic changes in the acute phase with olanzapine treatment 

Mehmet Ak 1 , Abdullah Bolu 1 , Süleyman Akarsu 1 , Deniz Sezlev 2 , Tülin Yanık 2 , Özcan Uzun 1 , Fuat Özgen 1 , Aytekin Özşahin 1 

1Department of Psychiatry, Gulhane Military Medical Faculty, Ankara, Turkey 

2METU, Faculty of Science, Biology department, Ankara, Turkey 

E-mail: drmehmetak@gmail.com 

Introduction: Atypical antipsychotics are used in treatment of psychotic disorders and severe behavior disorders. Despite the lack of extra 

pyramidal side effects, they cause metabolic disorders (such as hyperlipidemia, weight gain, glucose intolerance), which are important 

causes of mortality (1). The exact mechanisms of these side-effects of atypical antipsychotics have not been identified so far and therefore 

and protective measures could not be established (2). In this study we aimed to examine the acute phase changes in blood lipid profile 

and body mass index while using olanzapine. 

Materials and Methods: Twenty four patients, who were diagnosed with first-episode psychotic disorder and received olanzapine 

treatment in the Department of Psychiatry, Gulhane Military Medical Faculty, were enrolled in the study. The serum lipid levels and fasting 

blood sugars were measured before the treatment and four weeks after the treatment; body mass index was calculated and the data 

obtained were compared. 

Results: The comparison of pre- and post-treatment data showed significant increases in the weight gain, measurement of waist 

circumference, body mass index, total cholesterol, and VLDL levels (p


References: 

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) 

70–85. 

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. 

3. Chagnon YC. Susceptibility genes for the side effect of antipsychotics on body weight and obesity.Curr Drug Targets 2006; 12: 1681-1695 

4. Evans WE, Johnson JA. Pharmacogenomics: the inherited basis for interindividual differences in drug response. Annu Rev Genomics Hum Genet 2001; 2: 9-39 


[PP-084] Ref. No: 183 

Do cultural factors effect clinical manifestations of OCD? Clinical features of 

a Turkish sample 

Ramazan Konkan 1 , Ömer Şenormancı 1 , Oya Güçlü 1 , Erkan Aydın 1 , Mehmet Z. Sungur 2 

1 Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

2 Marmara University School of Medicine, İstanbul, Turkey 


Objective: In the present study we evaluated the clinical characteristics of OCD patients monitored in an outpatient program and 

compared them with other cultures. 

Method: The study included 116 OCD patients who presented to the clinics at the Bakirköy Research and Training Hospital for Psychiatry, 

Neurology and Neurosurgery, met the inclusion criteria, volunteered to participate in the study after being diagnosed and were referred 

by two psychiatrists. The diagnosis was confirmed using the Structured Clinical Interview Form for the DSM-IV Axis I Disorders (SCID-I). An 

inquiry form was developed for obsessive compulsive symptoms based on the obsessions and compulsions included in the Yale-Brown 

Obsession Compulsion Scale (Y-BOCS) according to their incidence and a sociodemographic form from the SCID-I clinical interview guide. 

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 

common obsessions were impurity-contamination (49.1%), followed by doubt (20.7%) and religious (11.2%) obsessions. Secondary 

obsessions included doubt (53.4%), impurity-contamination (14.7%) and sexual obsessions (9.5%), respectively. In tertiary obsessions, 

21 patients reported presence of symmetry-exactness (18.1%), 13 patients reported doubt (11.2%), 10 patients reported sexual (8.6%) 

obsessions, and 43 patients (37.1%) had no tertiary obsessions (Table 1). Ninety-six percent of patients had accompanying compulsions. 

The most common compulsions were cleaning and washing (53.4%), checking (26.7%) and repetitive ritual behavior (7.8%).DISCUSSION: 

The most common obsession in the present study was impurity/contamination with a rate of 49.1% in line with the literature, followed by 

doubt obsessions of 20.7%. The most common compulsion reported in literature is washing accompanied by obsession of contamination, 

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 

checking (26.7%) and repetitive ritual behaviors (7.8%). Although the first two obsessions and compulsions are in line with the literature, 

the tertiary obsessions reported as aggressive or sexual obsessions in the literature were replaced by religious obsessions (11.2%) in our 

sample. An intercultural study showed that religious obsessions were the most common obsessions with 60% in the Egyptian sample, 

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. 

Studies on Jewish populations showed similar results with the Muslim populations, with a religious obsession rate of 50%. We believe that 

the rate of religious obsession is associated with our country’s position, being at the junction of Western and Eastern cultures. Relatively 

lower rate of sexual obsessions compared to the literature may result from the fact that obsessions related with sexuality may be more 

difficult to report than other obsessions in our population. 

Key words: Clinical manifestation, cultural differences, OCD 





[PP-085] Ref. No: 196 

Reliability and validity of Turkish version the Brief Fear of Negative Evaluation 

Scale II (BFNE-II) among male patients with alcohol dependency 

Cüneyt Evren, Selime Çelik, Reşide Aksoy, Turan Çetin, Müge Ülkü, Sera Yiğiter, Elif Mutlu 

Bakırköy Training and Research Hospital for Psychiatry, Neurology and Neurosurgery, Alcohol and Drug Research, Treatment and Training Center (AMATEM), İstanbul, Turkey 

E-mail: cuneytevren@yahoo.com 

Background and Objective: The construct of fear of negative evaluation consists of feelings of apprehension about others’ evaluations, 

distress over these negative evaluations, and the expectation that others will evaluate one negatively (1). The Brief Fear of Negative 

Evaluation Scale (BFNE) is a measure of a person’s tolerance for the possibility they might be judged disparagingly or hostilely by others 

(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 

alcohol dependent inpatients. 

Methods: Participants were 155 consecutively admitted male alcohol dependents. Patients were investigated with the BFNE-II, the Social 

Phobia Scale (SPS), the Social Interaction Anxiety Scale (SIAS) and the Liebowitz Social Anxiety Scale (LSAS). The BFNE-II was repeated in 

136 of these 155 patients after 2 weeks. 

The BFNE is composed of 12 items describing fearful or worrying cognition. Eight of the twelve items describe the presence of fear or 

worrying, while the remaining four items describe the absence of fear or worrying (3). In the BFNE-II (4) reversed items are corrected. 

Results: The Turkish version of the BFNE-II was found to be compatible with the original scale. In alcohol dependents the internal 

consistency coefficient (Cronbach’s alpha) was 0.91 for the BFNE-II. For each of the items, the corrected item-total correlation values were 

between 0.57 and 0.84 (p


when meeting and talking with other people”’ (1). Thus the two companion measures were designed to distinguish between scrutiny fears 

and concerns about interaction. The scales correspond to the DSM-III-R descriptions of Social Phobia--Circumscribed and Generalised 

types, respectively. In this study, the reliability and validity of the Turkish translation of the Social Phobia Scale (SPS) and Social Interaction 

Anxiety Scale (SIAS) in male alcohol dependent inpatients were determined. 

Method: The study was conducted with hospitalized patients between August 2008 and March 2009 in the Bakirkoy State Hospital 

for Mental Health and Neurological Disorders, AMATEM (Alcohol and Drug Research, Treatment and Education Center) in Istanbul. 

Participants were 155 consecutively admitted male alcohol dependents. Diagnoses of alcohol dependence and social anxiety disorder 

were made with the SCID-I modules of these disorders. Patients were investigated with the SPS, the SIAS (2), the Brief Fear of Negative 

Evaluation II (BFNE-II) and the Liebowitz Social Anxiety Scale (LSAS). 

Results: The Turkish versions of both the SPS and the SIAS were found to be compatible with the original scales. In alcohol dependents, 

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 

item-total correlation values were between 0.21 and 0.68 (p



[PP-088] Ref. No: 217 

Venlafaxine-mirtazapine combination in the treatment of post traumatic stress disorder 

Abdullah Bolu, Süleyman Akarsu, Cemil Çelik, Barbaros Özdemir, Kamil Nahit Özmenler 

Department of Psychiatry, Gulhane Military Medical Faculty, Ankara, Turkey 

E-mail: abdullah_bolu@yahoo.com 

Introduction: Posttraumatic stress disorder (PTSD) is an incapacitating clinical syndrome characterized by intrusive recollections, 

emotional numbing and withdrawal, cue-related responses, and psychological and physiological hyperarousal. In the treatment of PTSD 

pharmacotherapy must be supported with psychotherapy to increase the success of treatment. In this study we aimed to evaluate the 

effect of venlafaxine-mirtazapine combination in the PTSD patients, who did not respond to antidepressant treatment at 

adequate dose for an adequate duration. 

Material and Methods: The hospital records of the patients who were diagnosed with PTSD according to DSM-IV diagnostic criteria and 

did not respond to adequate doses of an antidepressant treatment for adequate duration were examined retrospectively. Data of the 

patients (n=28), whose treatment were venlafaxine- mirtazapine combination, were obtained. These data were IES-R, Hamilton Anxiety 

scale and Hamilton Depression Scale scores. 

Results: IES-R score, Hamilton Anxiety, Hamilton depression scores of 28 patients who were diagnosed with PTSD were evaluated. A 

significant decrease in IES-R total, IES-R avoidance, Hamilton Anxiety and Hamilton depression scores (p> 0.05) with adequate dose and 

duration of venlafaxine-mirtazapine treatment were detected. The same change was not accompanied in IES-R hyperarousal and IES-R 

intrusive test scores. 

Conclusion: Post-traumatic stress disorder treatment takes longer and sometimes becomes chronic. According to the results of this study, 

venlafaxine- mirtazapine combination can be used in the treatment of PTSD patients who did not respond to antidepressant treatment 

at adequate doses for an adequate duration. 

Key words: Mirtazapine, posttraumatic stress disorder, PTSD, venlafaxine 

References: 

1. McDougall SJ, Widdop RE, Lawrence AJ (2004) Medial prefrontal cortical integration of psychological stress in rats. Eur J Neurosci; 20: 2430-2440. 

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 

repeated stress. Exp Neurol; [Epub ahead of print]. 

3. Kılıçoğlu A. Stress and effects of brain: A review. New Symposium Journal; July 2007, Volume 45, İssue 3 


[PP-089] Ref. No: 221 

Efficacy and 3-month follow-up of repetitive transcranial magnetic stimulation 

(rTMS) in treatment resistant depression: Three cases 

Onur Durmaz, Mehmet Alpay Ateş, Mesut Çetin, Servet Ebrinç, Cengiz Başoğlu, Ayhan Algül 

Department of Psychiatry, GATA Haydarpasa Training Hospital, Istanbul, Turkey 

E-mail: drodurmaz@gmail.com 

Introduction: rTMS(Repetitive Transcranial Magnetic Stimulation) is an effective non-invasive cortical stimulation method that is being used 

in the treatment of drug resistant major depressive disorder. The underlying mechanism of effect of rTMS has not been fully understood 

yet. Neuromodulation, neuroplasticity, and cortical excitability are the most accepted theories (1). Even though the post-treatment effect of 

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 

treatment with 3 month follow-up after treatment in 3 outpatient cases diagnosed with drug resistant unipolar major depression. 

Case 1: A 33 year-old female patient was diagnosed with major depressive disorder and received venlafaxine 300 mg/day for two years. 

An add-on 15 sessions of DLPFC rTMS (20 Hz, 110% MT, 1000p/d) was applied due to insufficient medication response. The MADRS and 

HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after treatment. The MADRS scores were 

found to be 37, 11, 2 and 4, while the HAM-A scores were found to be 35, 9, 5 and 6, respectively. 

Case 2: A 35 year-old male patient was diagnosed with major depressive disorder since age 12 and received escitalopram 20 mg/day for 

three months. An add-on 15 sessions of DLPFC rTMS (20 Hz,110% MT,1000p/d) was applied due to insufficient medication response. The 

S175


MADRS and HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after treatment. The MADRS 

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. 

Case 3: A 44 year-old male patient was diagnosed with major depressive disorder since age 15 and received venlafaxine 375 mg/day and 

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 

medication response. The MADRS and HAM-A scales were assessed before and the day following treatment and then 1 and 3 months after 

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. 

Conclusion: Maintenance of improvement in major depression treatment has been another concern apart from efficacy of current 

interventions. rTMS is an effective method as monotherapy and also as add-on treatment of depression. In this study each of three 

patients responded favorably to rTMS. In the post-treatment course, significiant improvement was maintained at the 3-month follow-up. 

Given its relatively benign side effect profile, long lasting therapeutic effect, and more practical non-invasive application than ECT, we 

conclude that rTMS can be considered as an optional treatment before ECT in treatment-resistant depression patients. 

Key words: rTMS, resistant depression, treatment, follow-up, maintenance 

References: 

1. Pell GS, Roth Y, Zangen A.Modulation of cortical excitability induced by repetitive transcranial magnetic stimulation: Influence of timing and geometrical 

parameters and underlying mechanisms. Prog Neurobiol. 2010 Nov 5. 

2. Bortolomasi M, Minelli A, Fuggetta G, Perini M, Comencini S, Fiaschi A, Manganotti P.Long-lasting effects of high frequency repetitive transcranial magnetic 

stimulation in major depressed patients. Psychiatry Res. 2007 Mar 30;150(2):181-6. 

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 

transcranial magnetic stimulation for treatment-resistant depression in a clinical setting. J ECT. 2011 Mar;27(1):18-25. 


[PP-090] Ref. No: 225 

The effects of brain-derived neurotrophic factor Val66Met polymorphism on 

executive functioning in patients with obsessive-compulsive disorder 

Raşit Tükel 1 , Hakan Gürvit 2 , Berna Özata 1 , Banu Aslantaş Ertekin 1 , Erhan Ertekin 1 , Bengi Baran 2 , Şükriye Akça Kalem 2 , 

Nalan Öztürk 1 , Güher Saruhan Direskeneli 3 

1 Istanbul University, Istanbul Faculty of Medicine, Department of Psychiatry, İstanbul, Turkey 

2 Istanbul University, Istanbul Faculty of Medicine, Department of Neurology, İstanbul, Turkey 

3 Istanbul Faculty of Medicine, Department of Physiology, Istanbul University, İstanbul, Turkey 

E-mail: rtukel@gmail.com 

Objective: In the present study, we investigated the association between the brain-derived neurotrophic factor (BDNF) Val66Met 

polymorphism and performance on tests measuring executive functions in a sample of patients with obsessive-compulsive disorder 

(OCD). 

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 

Yale-Brown Obsessive-Compulsive Scale and the Hamilton Depression Rating Scale. Patients also performed the Wisconsin Card Sorting 

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 

lexical fluency) and the Stroop Test. Genomic DNA was extracted from whole blood. The single nucleotide polymorphism (G/A) leading 

to amino acid substitution at the 66 codon in the BDNF gene (dbSNP number rs6265) was screened by a polymerase chain reaction 

and restriction digestion analysis in the DNA samples. The performance of the patients on the neuropsychological tests of executive 

functioning was compared between the patients with Val/Val genotype and Met carriers. 

Results: Subjects with Val/Val genotype and Met carriers (Met/Met or Val/Met genotypes) did not differ on socio-demographic and clinical 

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 

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 

to the Val/Val group. There were no significant differences in the WCST and the Verbal Fluency Test performances between the two groups. 

Conclusions: These findings suggest that the BDNF Met allele may be associated with poorer performance on neuropsychological tests 

of executive functions in OCD patiens. 

Key words: Brain-derived neurotrophic factor, executive functions, obsessive-compulsive disorder, polymorphism 





[PP-091] Ref. No: 228 

Diagnostic confusion about OCD and schizophrenia: A case report 

Sevgi Gül Kabak, Mustafa Burak Baykaran, Selma Bozkurt Zincir 

Erenköy Mental Health Training and Research Hospital, İstanbul, Turkey 


Introduction: Both obsessions and delusions are based on wrong, absurd and extreme ideas and it is thought that they could be 

separated on the basis of the presence of insight. Between obsessions and delusions there is the protection of insight and the ability to 

resist compulsive thoughts and/or behaviors. The insight of obsessive patients against obsessions may be protected or completely lost 

(1). In this paper, the diagnostic process in a patient with OCD, who also had delusions, is discussed. 

Case: A 30 year-old, married, female patient applied to the hospital with complaints of unhappiness, suspiciousness, self-reproach, thoughts 

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 

years ago she had sexual feelings towards her female collegues and she thought that her feelings were mutual and her thoughts could be 

read by them. During psychiatric examination, her thought content had Schneiderian symptoms such as paranoia, thought withdrawal, 

thought insertion, and reference delusion. Just after the hospitalization and evaluation, the patient was medicated with 6 mg/day risperidone 

and 2 mg/day biperiden for a preliminary diagnosis of schizophrenia. Later the preliminary diagnosis was changed to atypical obsessivecompulsive 

disorder and her treatment was changed to sertraline 200 mg/day, quetiapine 300 mg/day and clonazepam 2 mg/day. Due to the 

fact that after a 10-day period of improvement, her reference delusion and fear of death had restarted, and inappropriate affect was detected, 

a treatment regimen of pimozide 2mg/day, sertraline 200mg/day, clomipramine 75mg/day, clonazepam 2mg/day had been prescribed. 

The difference between the facts and the idea had been discussed through a cognitive approach. After 12 days, her affect recovered and 

obsessive thoughts decreased, therefore the patient was discharged from hospital on the previously mentioned treatment. After 2 months, 

there had been no psychotic symptoms, she had been able to cope with distress better and her psycho-social functioning had been fine. 

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 

symptoms and 4% schizophrenia was reported in another study. Thomsen and Jensen demonstrated that 5% of 135 OCD patients, who 

applied to the hospital for the first time, were later diagnosed as schizophrenic (3). Despite the psychotic nature of OCD that has been 

noticed for a long time, modern classification systems still refer to OCD as an anxiety disorder. Although the DSM-IV mentions poor 

insight in OCD, there has been no objective description for what degree of insight should be accepted as poor. The diagnostic criteria and 

treatment of schizo-obsessions and whether the patients who have schizophrenia and OCD comorbidity should be considered as schizoobsessive 

disorder are still under discussion(2). 

Key words: Comorbidity, differential diagnosis, obsessive compulsive disorder, schizophrenia 

References: 

1. Aydın A. Ceylan ME. Türkcan A. Şizofrenide Obsesif Kompulsif Fenomenler: Bir Gözden Geçirme. Klinik Psikofarmakoloji Bülteni 2008;18:222-234 

2. Demir EY. Aslan S. Şizo-Obsesif Bozukluk: Tanı, Sınıflandırma ve Tedavi. Türkiye’ de Psikiyatri 2005;7(1):38-43 

3. Güleç G. Güneş E. Yenilmez Ç. Obsesif Kompulsif Belirtileri Olan Şizofreni Hastalarının Şizofreni ve Obsesif Kompulsif Bozukluk Hastaları İle Karşılaştırılması. Türk 

Psikiyatri Dergisi 2008;19(3):247-256 


[PP-092] Ref. No: 232 

Is vaginismus a specific phobia? 

Ramazan Konkan 1 , Meltem Bayrak 1 , Oya Güçlü 1 , Ömer Şenormancı 1 , Mehmet Z. Sungur 2 

1 Bakırköy Research and Training Hospital for Psychiatry, Neurology and Neurosurgery, İstanbul, Turkey 

2Marmara University School of Medicine, İstanbul, Turkey 


Objective: Although vaginismus is classified under the title of “sexual pain disorders”, its etiological roots are still controversial. It has been 

suggested that vaginismus should be considered as a phobic reaction resulting in an avoidance behavior due to a dominant fear of pain. It 

has also been argued that, in patients with vaginismus, other fears usually accompany the fear of pain during coitus. Excessive sensitivity 

particularly in the genital area is said to prevail in vaginismus. In our study, patients with vaginismus were compared to a healthy group 

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in terms of commonly seen phobias, amplified perception of somatic sensations and sensitivity to pain 

Method: As a part of a different aspect of a vaginismus trial 40 subjects with vaginismus, who was referred to the Sexual Functioning 

Disorders outpatient clinic and agreed to take part in the study and 50 women of the control group who described penile penetration 

difficulty and pain during coitus, were evaluated. The participiants were evaluated using a sociodemographic form developed by the 

researchers, the SCL-90-R (Symptom Checklist-90-Revised), and the Somatosensory Amplification Scale Halam and Hafner (1977) fear 

checklist. The data were analysed using the SPSS for Windows 10.0 statistical packet program and P



[PP-094] Ref. No: 291 

Switching to fluoxetine due to sertraline-induced urinary incontinence: A case report 

Pınar Güzel Özdemir 1 , Adem Aydın 1 , Mustafa Güleç 2 , Emine Füsün Akyüz Çim 1 

1 Yuzuncu Yil University, Medical Faculty, Department of Pyschiatry, Van, Turkey 

2 Ataturk University, Medical Faculty, Department of Pyschiatry, Erzurum, Turkey 

E-mail: pguzelozdemir@yahoo.com 

Urinary incontinence is involuntary leakage of urine. It is not life-threatening but adversely affects the quality of life (1). The patient usually 

complains about frequent or periodic urinary incontinence in small amount or just leakage. 

Here we report a case of urinary incontinence induced with sertraline and resolved after sertraline was discontinued. 

Case: A 38 year-old married female patient presented to our clinic with complaints such as boredom, avolution, and depression. In 

her history, there was no psychiatric treatment or treatment with any other medications. On her psychological examination, she was 

cooperative, oriented, replying to questions briefly and properly. Her affect was depressive. The patient was diagnosed with depressive 

disorder and prescribed sertraline 50mg/day. She was suggested to come to the clinic for follow up after 3 weeks, however she came back 

a week later complaining of urinary incontinence. Without any pressure feeling, she developed urinary incontinence which negatively 

affected her daily activities. Her medication was changed to fluoxetine 20mg/day from sertraline 50mg/day. Her urinary incontinence 

complaint disappeared 2 days after. On the follow-up the patient did not have any urinary incontinence. 

We presented a case report of urinary incontinence, which developed after starting sertraline. In the literature, there are case reports 

about sertraline induced urinary incontinence and switching to fluoxetine (1,2). 

Despite extensive research, the mechanism of enuresis has not been clarified in detail. Continence is maintained by alpha-adrenergically 

mediated constriction of the bladder sphincter (3). Sertraline has alpha-adrenergic blockage, which may partially explain urinary incontinence 

in our case. 

Enuresis is usually underdiagnosed because of clinicians do not ascertain about it or the masking of this side effect by multiple drugs such 

as antimuscarinic or noradrenergic agents (3). 

Fluoxetine may be a choice in sertraline induced urinary incontinence cases in the treatment of depression and anxiety disorders. Larger 

case series are needed on this issue. 

Key words: Urinary incontinence, sertraline, fluoxetine 

References: 

1. Votolato NA, Stern S, Caputo RM: Serotonergic antidepressants and urinary incontinence Int Urogynecol J Pelvic Floor Dysfunct 2000;11:p 386–8. 

2. Maalouf Fadi T, Gilbert Andrew R. Sertraline-Induced Enuresis in a Prepubertal Child Resolves after Switching to Fluoxetine. J Child Adolesc Psychopharmacol 

2010;20:161 

3. Andersson KE: Advances in the pharmacological control of the bladder. Exp Physiol 1999;84:195–213 


[PP-095] Ref. No: 292 

The relationship between the serum bilirubin levels and metabolic syndrome 

in schizophrenia patients 

Filiz Karadağ 1 , Hasan Herken 1 , Bünyamin Kaptanoğlu 2 , Yaşar Enli 2 , Özgür Kalkancı 1 , Ceyhan Balcı Şengül 3 , Hüseyin Alaçam 1 

1 Pamukkale University Medical Faculty Psychiatry Department, Denizli, Turkey 

2 Pamukkale University Medical Faculty Biochemisry Department, Denizli, Turkey 

*Denizli State Hospital, Denizli, Turkey 

E-mail: filizlal@yahoo.com 

Objective: Especially with the use of atypical antipsychotics, the increase of the metabolic side effects constitutes a major problem 

in schizophrenia patients. Serum bilirubin levels have been reported to be associated with insulin resistance, abdominal obesity, and 

metabolic syndrome (MS) (1,2). However, the relationship between MS parameters and bilirubin levels has not been investigated in 

schizophrenia patients. It has been reported that antipsychotic drugs do not cause significant changes in serum bilirubin levels (3). 

The objective of this study was to investigate the association between bilirubin levels and the parameters associated with MS in 

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schizophrenia patients. 

Methods: Ninety one schizophrenic patients (38 female, 53 male) receiving antipsychotics for at least one year were included in the study. 

The parameters associated with MS were as follows: Body mass index, body weight, waist circumference, systolic and diastolic blood 

pressure, fasting blood glucose, insulin, serum triglycerides, HDL cholesterol levels, and the insulin resistance as calculated by using the 

value HOMA (homeostasis model assessment). The criteria were based on ATP-III criteria for metabolic syndrome (Adult Treatment Panel 

III). Statistical analysis was performed by using SPSS 17.0 (for Windows). 

Results: Serum triglyceride levels were inversely correlated with serum direct bilirubin (p=.006) and positively correlated with indirect/ 

direct bilirubin ratio (p =. 002). Serum HDL levels (p=.018) showed a significant positive correlation with indirect/direct bilirubin ratio. 

Waist circumference (p=.048) showed a significant negative correlation with serum total bilirubin. The levels of insulin (p =.038) and value 

of HOMA (p =.015) were inversely correlated with serum direct bilirubin. 

The rate of metabolic syndrome was significantly lower in the patients with highest quartile (75-100) of the serum direct bilirubin levels 

than the other quartiles (p=.022). 

In these patients, the ratio of the patients that meet criteria for metabolic syndrome according to levels of the fasting triglyceride (p=.013) 

and HDL (p=.040) was significantly lower than others. Additionally, the means of body weight (p=.026), waist circumference (p=.022), and 

serum triglyceride levels (p=.039) of these patients were found significantly lower. 

Conclusions: In this study we found that bilirubin levels are associated with metabolic syndrome and its parameters and high levels of 

serum direct bilirubin may be associated with the lower risk for MS in schizophrenia patients; similar to the healthy individuals (1,2,4). 

Our study is the first study investigating this issue. Our results may be important for the following aspects: High serum direct bilirubin 

levels may serve as an easily applicable, inexpensive marker indicating lower MS risk for schizophrenic patients. Additionally, it may be 

possible to prevent antipsychotics induced metabolic side effects by avoiding the drugs with higher risk for MS, in the patients with low 

levels of direct bilirubin. Due to the relatively limited number of patients and cross-sectional nature, our results required to be confirmed 

by longitidunal studies with larger samples. 

Key words: Schizophrenia, metabolic syndrome, bilirubin, antipsycotic drug 


[PP-096] Ref. No: 293 

Olanzapine abuse: A case report 




Introduction: Olanzapine is a thienobenzodiazepine which specifically blocks 5-HT2A and D2 receptors and additionally blocks 

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, 

Conley & Carpenter 2005). Olanzapine has consistently been found to be significantly superior to placebo and comparable with, or 

superior to, haloperidol for the treatment of overall, positive, and negative symptoms of schizophrenia. In this case, we want to report a 

case of olanzapine abuse. 

Case Report: A 48-year old, primary school graduate, married, female patient was admitted to our psychiatry clinic with tachycardia, 

insomnia, and anxiety. In psychiatric assessment, she mentioned that her symptoms have been similar for 15 years and in the last 3 years 

she has used citalopram 40 mg/d and olanzapine 10 mg/d and after this treatment her symptoms decreased. During psychiatric treatment 

when her consequent doctor wanted to stop the olanzapine treatment, she did not succeed and the patient had anxiety, insomnia, and 

anger and reported decreased symptoms after using the drug again 

Discussion: Besides medications with obvious abuse potential such as benzodiazepines and methyphenidate and other stimulants, abuse 

of a number of commonly prescribed psychiatric medications has been reported. The abuse of anticholinergic drugs was first reported 

in 1960 with the description of a patient, who increased her trihexyphenidyl to achieve antidepressant and euphoriant effects. Recently, 

abuse of quetiapine for its sedative and anxiolytic effects has been reported. The abuse risk of quetiapine has been also reported in our 

country and Kaya et al. studied the abuse risk of quetiapine with prisoners. In the literature there are only two cases of olanzapine abuse. 

Key words: Abuse, olanzapine 





[PP-097] Ref. No: 123 

Various reasons for self-destructive acts and objects used to commit them in 1991 


Irkutsk Regional Psychoneurologic Dispensary 


Objective: The objective of the research was to study and assess the reasons for self-destructive acts committed by the individuals that 

underwent outpatient forensic psychiatric examination in 1991 and to give a brief characteristic of the objects used to commit the selfdestructive 

acts. 

Methods: The statistical method and comparative analysis were employed to study the historical data of 30 archive acts of outpatient 

forensic psychiatric examinations covering the period of January-March, 1991. 

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 

reasons for committing self-destructive acts by the examined individuals who underwent outpatient forensic psychiatric examination in 

1991 included the following: Conflicts with people around them (in 12 patients), conflict situations with parents and other close relatives 

(sister, brother, wife) (in 5), conflicts with inmates in place of imprisonment (in 4), conflict situations during military service (for example, 

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, 

ongoing investigation (in 1), conflict with loved ones (woman) (in 1), protest (investigator refused to allow relatives to visit the patient) (in 

1), and severe headache in combination with high blood pressure (the suicide was attempted to ease the pain) (in 1). Also according to 

the archive documents of forensic psychiatric examination 18 out of 30 individuals used sharp, cutting, or piercing objects (razor, kitchen 

knife, or pen knife, glass, fragment of a broken mirror, wire, sharpened coin, cigar case, etc.), 3 individuals used washing line or belt, 3 

patients used a medicine in tablet form, 1 individual used a medicine in liquid form, and 1 patient used the effect of low temperatures 

(long deliberate stay in cold weather in winter). 

Conclusion: The research findings demonstrated that the most common reasons for self-destructive acts committed by the examined 

patients in 1991 were conflict situations with individuals, out of prison, and in the society rather than conflicts in place of imprisonment 

or in place of military services. The objects used to commit self-destructive acts included: Sharp, cutting, or piercing objects (most often 

razor and kitchen knife), washing line, and a medicine in tablet form (antibiotics, phenazepam, cyclodolum, etc.). 

Key words: Self-destructive acts, outpatient forensic psychiatric examination, archive documents 


[PP-098] Ref. No: 296 

Topiramate induced acute psychotic disorder 

Serkan Barlak, Alpay Ateş, Cengiz Başoğlu, Servet Ebrinç 

Department of Psychiatry, GATA Haydarpasa Training Hospital, Istanbul, Turkey 

E-mail: drserkanbarlak@yahoo.com.tr 

Introduction: The use of topiramate has increased in recent years. It is now used in several specialties to treat a wide range of medical 

conditions. A small number of case reports describes psychosis as an adverse event of topiramate. While using topiramate as an option 

for treatment-resistant epilepsy, clinicians need to be aware of the possibility of topiramate-induced psychosis in patients who have 

not previously had a psychotic episode. Although there is a small literature in neurology journals regarding psychiatric adverse events 

in epileptic patients, the psychiatric literature is silent about the topic. We report a patient without a previous history of psychosis, who 

developed psychosis after use of topiramate. 

Case: The patient on multiple antiepileptic drugs with refractory tonic-clonic epilepsy was prescribed topiramate. The patient developed 

definite psychotic symptoms including auditory halucinations and paranoid-persecutory delusions and other behavioral symptoms 

fifteen days after beginning topiramate. The psychotic and other psychiatric symptoms resolved quickly with discontinuation of 

topiramate and by using a second-generation antpsychotic drug. 

Discussion: Topiramate was originally discovered as an oral hypoglycaemic, afterwards was approved as an anticonvulsant agent and is 

now used as an adjunct to various treatments. The several mechanisms of action include inhibition of sodium conductance, decreased 

frequency of generated action potentials, activated gamma-aminobutyric acid activity, inhibition of AMPA receptor, and weak inhibition 

of carbonic anhydrase (1). The mechanism underlying psychotic symptoms induced by topiramate is not clear, but overactivity of 

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ascending dopaminergic pathways due to GABAergic inhibition of the substantia nigra has been proposed (3). The true prevalence of 

topiramate-induced psychosis is not known. Although there have only been a few case reports of topiramate-induced psychosis, an 

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 

population as studies of topiramate exclude patients with past psychiatric history and past psychiatric history is the most important 

predictor for psychiatric adverse events. As epilepsy could overlap with psychiatric conditions at a rate of 50-60% including mood, anxiety, 

and psychotic disorders, clinicians should be cautious in diagnosing drug–induced psychosis. 

Key words: Topiramate, antiepileptic, drug-induced psychosis 


[PP-099] Ref. No: 170 

Glass-aating behaviour with radiological findings: A pica case 




Pica is the persistent, compulsive ingestion of non-nutritive substances, which includes eating disorders with unusual cravings. Etiologies 

of consumption of common and bizarre substances range from mineral deficiencies and helminthic infestations to cultural preferences. 

Recently, pica has been linked to obsessive-compulsive (OCD) spectrum disorders. 

Although there are few epidemiological studies and likely underreporting by embarrassed patients, pica exists in all ages, races, genders, 

and geographical regions. Lower socioeconomic groups, young children, pregnant women, or nursing mothers with increased nutritional 

demands are at higher risk, as well as those with brain damage, epilepsy, mental retardation, psychosis, or dementia. 

Case Report: A 32-year-old, primary school graduate, unemployed, male patient referred to psychiatry clinic with glass eating behavior 

for 10 years. There was not any history of psychiatry referral before the development of glass eating craving. He was referred to psychiatry 

clinic with this craving and had difficulty to quit eating glass. In psychiatric examination we found cleaning and control obssessions. 

The cranial MRI showed decrease in size of in corpus callosum, enlargement in Sylvian fissure and sulcus, asymmetry in III. and lateral 

ventricules. 

Discussion: In literature we did not a pica case like this one regarding glass eating. Even most pica cases are associated with element 

deficiency in our case there was not any deficiency. Because of obsessive symptoms, it might be associated with obsessive spectrum 

disorders with radiological findings. In OCD spectrum disorders, pica should also be considered and radiological investigation must 

always be done. 

Key words: Obsessive compulsive spectrum, pica, corpus callosum 


[PP-100] Ref. No: 209 

The use of bupropion in treatment Kleptomania’s: Two cases 

Özyıl Öztürk Sarıkaya 1 , Demet Güleç Öyekçin 2 

1Bursa Devlet Hastanesi, AMATEM Birimi, Bursa, Turkey 

2On Sekiz Mart ÜTF Psikiyatri AD, Çanakkale, Turkey 

E-mail: ozyilsarikaya@yahoo.com 

Objective: Kleptomania is an impulse control disorder, which is characterized by one’s uninterrupted impulse of stealing objects 

that needed neither for use nor for value, in a repetitive uncontrollable manner (1). Studies stated that those with kleptomania are 

accompanied by other psychiatric conditions such as mood disorders, other impulse control disorders, or substance abuse and addiction 

(2). 

For the treatment, selective serotonin reuptake inhibitors, mood stabilizers, and opioid receptor antogonists have been shown to be 

effective. In recent years, treatment for pathological gambling and trichotillomania as other impulse control disorders in which naltrexone 

and bupropion were studied for effective treatment of pathological gambling and trichotillomania, bupropion has been found to be as 

effective as naltrexone (3-4). 




The effectiveness of bupropion for treatment of kleptomania, which is classified as an impulse control disorder, is discussed on two cases 

in this report. 

Case 1: A 34 year-old married, women, graduated from high school presented with fatique, stress, lack of motivation, and complaints of 

staying in house, which lasted for the last two months in March, 2011. She had been stealing objects which were not important for her 

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 

not leave the house. 

She had substance abuse history and had been treated for major depression. 

SCID-I revealed she had major depressive disorder recurring type and kleptomania. 

For treatment, bupropion was given 150 mg/day initially, then increased to 300 mg/day. The depressive symptoms were apperently 

reduced in 8th week of the treatment. In 12th week, psychiatric examination revealed that functionalty, stealing impulse, and behaviour 

healed clearly. 

Case 2: A 25 year-old single,women, graduated from high school presented with hypersomnia, eating too much, lying, suicide thoughts, 

and stealing things that she didn’t need. Kleptomanic behaviour had begun one year ago. 

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 

had been shopping compulsively for 3-4 years. 

SCID-I revealed that she had major depressive disorder recurring type and kleptomania. 

Bupropion 150 mg/day was started initially, then 300 mg/day was given for treatment. The depressive symptoms were reduced markedly 

in the 10th week of the treatment. Desire and impulses to steal, hyperphagia, and suicide thoughts were found to be treated. 

Discussion: There are studies (3-4) showed bupropion to be effective for treatment of pathological gambling and trichotillomania, both 

of which are impulse control disorders. We investigated the effectiveness of bupropion treatment in two cases, who had kleptomania 

and co-existing mood disorder. To our knowledge this is the first case report bupropion is used for kleptomania treatment. Larger and 

controlled studies on kleptomania would make it possible to understand the pharmacotherapy and etiology of this disorder better. 

References: 

1. Hocaoğlu Ç, Kandemir G. The use of SSRI (Selective Serotonin Reuptake Inhibitors) in kleptomania’s treatment: case reports. Bulletin of Clinical Psychopharmacology 

2004;14:204-8. 

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. 

3. Bhanji NH, Margolese HC. Alternative pharmacotherapy for trichotillomania: a report of successful bupropion use. J Clin Psychiatry 2004;65(9):1283. 

4. Dannon PN, Lowengrub K, Musin E, Gonopolski Y, Kotler M. Sustained-release bupropion versus naltrexone in the treatment of pathological gambling: a 

preliminary blind-rater study. J Clin Psychopharmacol 2005; 25(6):593-6. 


[PP-101] Ref. No: 251 

A randomized, double-blind, placebo-controlled trial of celecoxib augmentation of 

sertraline in the treatment of a drug-naïve women with major depression 

Farshad Hashemian 1 , Marzieh Majd 1 , Seyed Mohammad Hosseini 2 , Ali Sharifi 1 , Maryam Vahdat Shariat Panahi 3 , Ofogh Bigdeli 1 

1 Department of Clinical Pharmacy, Islamic Azad University, Pharmaceutical Sciences Branch, Tehran, Iran 

2 Department of Psychiatry, Hamedan University of Medical Sciences, Hamedan, Iran 

3 Islamic Azad University, Tehran Medical Branch, Iran 

E-mail: majd.marzie@gmail.com 

Objectives: A growing body of evidence strongly suggests that inflammatory process and immune responses are involved in the 

pathophysiology of depression. While depression itself is considered a heterogeneous disorder, the involvement of immune system 

further complicates the matter. 

Meanwhile, several antidepressant medications (e.g. fluoxetine) have been reported to exert immunomodulatory properties, which may 

affect human immune system and may partly contribute to their efficacy. Moreover, it must be noted that immune response/system 

profoundly varies between the genders due to differences in sex hormones. However, there have been no controlled studies investigating 

the benefits of celecoxib augmentation therapy in treatment-naïve women with depression. 

To increase the homogeneity of the study population, the present study was designed to examine the antidepressant effects of celecoxib 

augmentation of sertraline in the treatment of female drug-naïve patients with depression for 8 weeks. 

Methods: Forty female patients diagnosed with first episode of major depression according to DSM-IV-TR criteria were recruited for this 

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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 

50 years, and 5. Hamilton depression rating scale (17 items) score ranging from 18 to 36. The patients with history of other psychiatric 

disorders, significant suicidal ideation, liver and kidney dysfunction, and cardiovascular disorders were excluded. The patients were 

randomly assigned into two equal groups receiving either sertraline 50-100 mg/day plus celecoxib 100 mg twice daily or sertraline 50-100 

mg/day plus placebo twice daily. The participants were assessed by Hamilton depression and anxiety rating scale at baseline, and 4th and 

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 

Registry of Clinical Trials (IRCT registration number: IRCT201009043106N3). This study was approved by Azad University Pharmaceutical 

Sciences Ethics Committee (No: 4114). 

Results: No significant differences were observed between two groups regarding demographicals characteristics and the Hamilton 

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 

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 

group showed significantly greater decrease in Hamilton scores compared to placebo (P< 0.05) at the end of week 4. The mean decrease 

in Hamilton score was greater in the treatment group compared to placebo over 8 weeks, although it was not statistically significant. In 

addition, remission rate (HamD scores



[PP-103] Ref. No: 298 

Adult primary enuresis nocturna: A case report 

Yücel Yılmaz, Ömer Yanartaş, İshak Saygılı, Aytül Gürsü Hariri 

Erenkoy Mental Health Training And Research Hospital, Istanbul, Turkey 

E-mail: yilmazyucel@live.com 

Introduction: Nocturnal enuresis (bed-wetting) is a hereditary, medical condition, which effects both children and adults (1). Beside this 

there is few studies on pevalance of enuresis nocturna (EN) among adults. EN cases are seldomly reported. Although most of the patients 

recover spontaneusly from EN, in the resistant cases illness persist through adulthood (2). The patients who have frequent bed-wetting in 

their childhood have greater risk for persistence of symptoms (3). 

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 

since his early childhood. He reports that he never had a long period free from bed-wetting at nights. He was suffering from bedwetting 

only at nights and never had daytime wetting. The patient reported that bedwetting becomes more frequent when he was under stress or 

felt unhappy about something and decreased in frequency when he felt less stressed out. While his military service, for a short period his 

symptoms had stopped when his millitary service was over his symptom has started again. In last six months, after he has suffered from 

thoughts of worthlessness, relationship issues with his father, and some economic problems his bed-wetting frequency increased. After 

his first application to the Erenkoy Mental Health Training And Research Hospital outpatient clinic, a consultation with a neurologist and a 

urologist was planned. He had been examined separately by a urologist, a neurologist and a psychiatrist. Several investigations had been 

performed in which they could not detect any organic disease. These investigations included urine analysis, abdominal USG, cranial MRI, 

and EEG. According to the results of these investigations, organic etiology was ruled out and 25 mg/day imipramine had been commenced. 

Later we increased imipramine dosage to 50 mg/day and added behavioral homework to the treatment. In his familiy history, there were 

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 

treatment response of the patient was good; his compliance with pharmacological treatment and behavioral therapy techniques was good. 

Discussion: Our case, according to DSM-IV-TR diagnostic criteria, was fulfilling the criteria for enuresis nocturna and major depressive 

disorder on axis I. His problems about his functionality and his relationship with his father have caused an increase in his depressive 

symptoms and his bed-wetting. We think that patient’s good response to treatment is related to his high motivation in his first psychiatric 

application and his compliance with behavioral threapy. It is compatible with literature data that the relatives of the patient have similar 

symptoms. 

Key words: Enuresis nocturna, imipramine, behavioral therapy 

References: 

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 

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 

enuretic adults. Urology 2009; 74: 915–919 

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 


[PP-104] Ref. No: 311 

Major depressive disorder and the 5-HTTLPR in Spanish and Mexican populations 

Pedro Dorado 1 , Hugo Trejo 2 , Elisa Alonso 2 , Eva Peñas Lledó 1 , Adrián Llerena 1 , Marisol López 3 

1Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain 

2National Institute of Neurology and Neurosurgery Manuel Velasco Suárez. Mexico City, Mexico 

3Metropolitan Autonomous University-Campus Xochimilco, Mexico City, Mexico 

4Co-Principal Investigators 


Preliminary evidence of an increased risk of suffering from MDD for individuals carrying the 5HTTLPR S allele was described in 70 Spanish 

patients [1]. 

The present study aimed to analyze the potential relevance of the 5-HTTLPR genotypes and the risk of suffering from MDD in Mexicans 

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and Spaniards. 

One hundred and twenty-two (70 previously analyzed) white Spanish and 101 Mexican Mestizo patients with a diagnosis of MDD (DSM- 

IV) were studied. Additionally, 327 Spaniards and 153 Mexican Mestizo healthy volunteers were also studied by a previously reported PCR 

method [1]. Genotypes and allele frequencies were compared between MDD patients and HVs by two-tailed Fisher’s test. 

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 

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. 

26.1% for 5HTTLPR LL, LS, and SS genotypes, respectively. The frequencies of 5-HTTLPR genotypes of the four groups (MDD and HV from 

Spain and Mexico) corresponded to those predicted by the Hardy–Weinberg law. 

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 

with the HV group in Spaniards and Mexicans, respectively. 

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 

higher (p



Present data support CYP2C9 and CYP2C19 genotyping prior to phenytoin treatment in order to prevent adverse events. Consistently, for 

patients carrying CYP2C9 and CYP2C19 defective alleles, valproate instead of phenytoin should be recommended to treat SE. 

Grant: The study has been partly supported by the Institute of Health Carlos III-FIS and the European Union (FEDER) Grants, PI10/02010 

and CP06/00030 (P Dorado) and from PRIS Extremadura, Consejería de Sanidad y Dependencia, FundeSalud PRIS10043. This study was 

coordinated in the networks CIBERSAM and CAIBER, which are initiatives of ISCIII (Spain). 


[PP-106] Ref. No: 314 

Influence of CYP2D6 genetic polymorphism on fluoxetine and amitriptyline 

clinical response 

M. López 1 , E. Peñas Lledó 2 , H. Trejo 1 , P. Dorado 2 , J. Guerrero 2 , M. E. Alonso 3 , A. Llerena 2 

1Metropolitan Autonomous University-Campus Xochimilco, Mexico City, Mexico. 

2Clinical Research Centre (CICAB), Extremadura University Hospital and Medical School, Badajoz, Spain 

3National Institute of Neurology and Neurosurgery Manuel Velasco Suárez. Mexico City, Mexico 


Cytochrome P450 2D6 (CYP2D6) is involved in the metabolism of many antidepressants. It is characterized by a high individual variability 

in catalytic activity mainly due to >75 CYP2D6 alleles that determine metabolizer status. The role of CYP2D6 genetic polymorphism in 

the metabolism of amitriptyline and fluoxetine was previously demonstrated [LLerena et al, 2004]. Herein, we analyzed the relevance 

of CYP2D6 genetic polymorphism for the clinical response to the antidepressant drugs fluoxetine and amitriptyline. Sixty-five patients 

(DSM-IV) diagnosed with major depression and a score equal or greater than 17 on the Hamilton-Depression (HAM-D) were prospectively 

studied. They were treated either with fluoxetine or amitriptyline under antidepressant monotherapy. The informed written consent was 

obtained from all patients. Clinical Response was evaluated with HAM-D. The patients were evaluated every month. A two months period 

evaluation is reported here. The patients with a 50% decrease on HAM-D were considered as “responders.” CYP2D6 genotyping was 

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 

and second month evaluation showed that 41 patients remained (8 more dropped-out). Among responders there were 56.6% and 60% to 

fluoxetine, and 50% and 70% to amitriptyline, at first and second follow up evaluations, respectively. The responders were characterized 

by presenting one or two CYP2D6 active genes. Furthermore, the number of active genes was related to better clinical response in both 

drugs. The percentage of responders was higher for those with two active genes than for patients carrying just one: (a) fluoxetine, 81 % 

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 

ultrarapid metabolizers (n=3 UMs; those with more than two CYP2D6 active genes) were found to drop out during the first month. The 

only poor metabolizer patient in the study (PM; with none CYP2D6 active genes) was found among “non-responders” in both follow-up 

evaluations. The number of CYP2D6 active genes seems to be related to clinical response to the antidepressant drugs amitriptyline or 

fluoxetine. Among responders, the frequency of patients carrying two CYP2D6 active genes is higher than those with one copy. Moreover, 

UMs and PMs were not found in this group. 

Grants: Supported by grants from the Spanish Ministry of Health Instituto de Salud Carlos III and EU-FEDER PI10/02758, CP06/00030 (PD); 

AEXCID (9IA006) Junta de Extremadura and EU-FEDER (BS10023) and Consejo Nacional de Ciencia y Tecnología de México (Nº 59366). This 

work was coordinated by Network Red Iberoamericana de Farmacogenética y Farmacogenómica (CYTED206RT0290). 


[PP-107] Ref. No: 137 

Evaluation of insight and functional recovery in patients with schizophrenia 

Aykut Karahan, Ahmet Tiryaki, Baykal İskender, Evrim Özkorumak 

Karadeniz Teknik Üniversitesi, Tıp Fakültesi, Psikiyatri Ana Bilim Dalı, Trabzon, Turkey 

E-mail: baykal.iskender@gmail.com 

Objective: Despite the fact that functional remission is the most important goal for the treatment of schizophrenia, standard definitions 

have not yet been made due to differences in measurement methods, the variability in the course of the disease, cognitive levels of the 

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patients, and psycho-social factors. Nevertheless, there exists an accumulation of knowledge regarding factors, which influence functional 

remission. Insight levels of patients influence their level of functionality, while causing problems in treatment adherence and social 

adaptation. The purpose of this study was to examine the factors which influence schizophrenia patients’ levels of insight and functional 

remission. 

Methods: In this cross-sectional descriptive study, 70 outpatients between the ages of 18-65, who applied to the Karadeniz Technical 

University, Psychiatry Clinic and were diagnosed with schizophrenia according to DSM-IV, were evaluated. The patients who reported they 

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 

injury and/or any disease which affects the central nervous system, whose Clinical Global Impression (CGI) disease severity low score was 

above four, who were taken as inpatients to the hospital in the last two months or whose treatment was changed were excluded from 

the study. The patients were evaluated by using respectively socio-demographic data collection form, clinical interview structured for 

DSM (SCID-I), the Positive and Negative Syndrome Scale (PANSS), Calgary Depression Scale (CDS), the Functional Remission of General 

Schizophrenia Scale (FROGS), Schedule for Assessing the Three Components of Insight (SAI-E), and cognitive test battery. 

Results: Insight levels of the patients determined through the SAI-E, were found to be highly correlated with the PANSS positive, negative, 

and general psychopathology, Stroop Test, Controlled Word Association Test (FAS), and Trail Making Test A-B scores. In the regression 

analysis, PANSS total score, Stroop Test, and FAS scores were the predictors of insight.The FROGS functional levels of patients were found 

to be related with occupational status, sex, age of onset of illness, comorbid psychiatric illness, PANSS positive, negative, and general 

psychopathology, CDS, SAI-E, FAS, Trail Making Test, Stroop Test, and Wisconsin Card Sorting Test. In the regression analysis, occupational 

status, comorbid obsessive compulsive disorder, PANNS negative and general psychopathology, and FAS scores were the predictors of 

patients functional status. 

Conclusion: Although insight levels of patients are basically related to cognitive functions, it has been reported in previous studies that 

clinical symptoms can cause changes in the levels of insight depending on the course of the disease. The relationship between insight 

and depression can vary depending on the severity of the depression, patients’ defense mechanisms, and internalized stigma levels. The 

effects of clinical symptoms of schizophrenia, levels of cognitive function, and levels of insight and employment status on the patients’ 

functionality levels are prominent. 

Key words: Schizophrenia, functional remission, insight, cognitive functions 


[PP-108] Ref. No: 205 

Comparison of superoxide dismutase, glutathione peroxidase, and adenosine 

deaminase activities between respiratory and nocturnal subtypes of patients with panic disorder 

Osman Özdemir 1 , Yavuz Selvi 1 , Halil Özkol 2 , Yasin Tülüce 2 , Lutfullah Beşiroğlu 1 

1 Department of Psychiatry,Yuzuncu Yil University, Van, Turkey 

2 Department of Medical Biology, Yuzuncu Yil University, Van, Turkey 

E-mail: drosmanozdemir@yahoo.com 

Background: Panic Disorder (PD) is a heterogeneous disease and panic attacks are divided according to the different symptom clusters as 

respiratory, nocturnal, nonfearful, cognitive, and vestibular subtypes. Oxidative stress (OS) is produced by free radicals which are named as 

reactive oxygen species (ROS). They can be evaluated indirectly by measurement of some antioxidant enzyme levels such as superoxide 

dismutase (SOD), catalase (CAT), or glutathione peroxidase (GSH-Px). PD is known to be associated with a high frequency of comorbid 

immunological and increased expression of T lymphocytes compared to controls. Adenosine deaminase (ADA) has been accepted as an 

important enzyme in the maturation and function of T lymphocytes. The aetiology of panic disorder is yet to be fully understood. There 

is mounting evidence indicating that ROS may have an important role in the pathogenesis of PD. 

Objective: In the present study we aimed to compare SOD, GSH-Px, and ADA activities in panic disorder patients with/without nocturnal, 

respiratory subytypes, and healthy subjects. Thus to evaluate the effects of OS and inflammatory process on pathogenesis of PD and to 

determine biological parameters in the subtypes of PD. 

Methods: The study comprised of 60 patients with PD and 30 healthy control subjects. Panic Attack Symptom Checklist (PASC), Panic and 

Agoraphobia Scale (PAS), Hamilton Depression Rating Scale (HAM-D), and Hamilton Anxiety Rating Scale (HAM-A) were administered to the 

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 

following five symptom criteria during an individual’s most recent severe panic attack: Feeling of choking or smothering sensations; shortness 

of breath; chest pain or discomfort; numbness or tingling sensations; and fear of dying. The nonrespiratory subtype is operationalized as that 

which does not meet the mentioned symptom criteria. The biochemical analyses were made after all the blood samples were collected. The 




laboratory analyses of investigation were conducted in Department of Medical Biology, Faculty of Medicine, at the University of Yuzuncu Yil. 

Results: We found that SOD and GSH-Px blood activities of patients were significantly lower, and ADA activities of patients were higher 

than the healthy controls. All of the activities were not significantly different between respiratory and nocturnal subtypes. There were 

no significant relationships between the duration of illness and Panic-Agoraphobia (PAS) scores of patients with nocturnal subtypes. 

Hamilton Depression Rating Scale (HAM-D) and Hamilton Anxiety Rating Scale (HAM-A) scores of the patients with nocturnal subtype 

were significantly higher than the patients without nocturnal subtype. When examining the correlations between these variables and 

enzyme levels, there was only a positive correlation between duration of disease and serum activities of GSH-Px. 

Conclusion: In conclusion, SOD and GSH-Px ADA activities of the patients with PD are different from healthy subjects. Our results suggest 

that oxidative and inflammatory processes may play role in pathophysiology of PD. These findings may support the idea that both 

nocturnal and respiratory subtypes of PD have different symptom clusters of the same disease. 

Key words: Panic disorder, subtypes, oxidative stress 

Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):188-9 

[PP-109] Ref. No: 106 

The neural and cognitive effects of Bacopa Monniera: An fMRI study 

Chris Neale 1 , Andrew Scholey 1 , Matthew Hughes 1 , Patrick Johnston 2 

1 Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University of Technology, Melbourne, Australia 

2 Department of Psychology, University of York, York, England 

E-mail: chrisneale@swin.edu.au 

Objectives: Bacopa Monniera is an ayurvedic herbal medicine used in Indian medicine as a memory tonic. Animal models have shown 

that it is an antioxidant (1), a memory enhancer (2), and an antidepressant (3). Human trials have had variable results, but spatial memory, 

attention, and information processing tasks seem to be affected by Bacopa. 

Given the improvements shown the RVIP task as a result of a 12 week Bacopa intervention, an fMRI methodology was employed to see 

how Bacopa affects the brain during this task. The improved performance in these tasks suggests Bacopa may modulate task specific brain 

regions. This investigation looks at the effects of Bacopa on the BOLD signal in the RVIP task over a 90 day intervention. 

Method: The study utilized a double blind, placebo controlled, crossover design where all participants completed a 90 day course of 

both Bacopa (300mg daily) and placebo during the study. The participants were aged between 40 and 65 years and in good health. 

Interventions were separated by a 120 day washout period. Scans were undertaken on a 3T Siemens TRIO magnet before and after each 

90 day intervention where participants would complete two runs of the task per scan visit. 

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 

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 

are repeated 3 times per condition in each of two experimental runs per scan. 

Results: Data collection is ongoing at present. Baseline data show a bilateral increase in BOLD activation in the precentral gyrus and 

precuneus with activation extending to the left inferior frontal gyrus (n=7, p=.005) when compared with control using a task greater than 

baseline mask. Behavioural data suggest fewer ‘hits’ in the active task compared to control task. 

Conclusions: The methodology of the study sets a gold standard for clinical trials using nutraceuticals and fMRI. Given the ongoing nature 

of the study, conclusions are merely speculative at this point. However, the task looks to be a sensitive reflection of sustained attention. 

We anticipate that the 90 day intervention of Bacopa will affect the BOLD signal in these particular regions of interest. 

Key words: Bacopa monniera, fMRI, nutraceuticals, human cognition 

References: 

1. Bhattacharya et al (2000) Antioxidant Activity of Bacopa Monniera in Rat Frontal Cortex, Striatum and Hippocampus. Phytotherapy Research, 14, 174 – 179 

2. Hota et al (2009) Bacopa monniera leaf extract ameliorates hypobaric hypoxia induced spatial memory impairment. Neurobiology of Disease, 34 (1) 23-39 

3. Sairam et al (2001) Prophylactic and curative effects of Bacopa monniera in gastric ulcer models. Phytomedicine, 8 (6) 423-430 


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[PP-110] Ref. No: 98 

Methlyphenidate induced thrombocytopenia in a pediatric patient with 

ADHD and stuttering 

Serdal Özdemir, Fatma Ayık Özdemir 

İnönü Üniversitesi Tıp Fakültesi Turgut Özal Tıp Merkezi Psikiyatri AD, Malatya, Turkey 

E-mail: serdoktor@yahoo.com 

Stuttering and attention deficit hyperactivity disorder (ADHD) can be seen together. Anemia or thrombocytopenia, rarely even pancytopenia 

may occur as a side effect of medications used to treat both disorders. Thrombocytopenia, although it may be seen in some cases using 

methylphenidate, occurs rarely. An 8 year-old boy was brought to our outpatient clinic by his family with the complaints of stuttering, attention 

deficit, and hyperactivity. After the psychiatric evaluation and history were conducted and psychometric tests were applied. One month later 

methylphenidate 18mg/day was started for the treatment of ADHD. Soon after initiation of medication, petechia developed on both lower 

extremities of the patient. CBC showed isolated thrombocytopenia and te patient was followed by hematology clinic. On the 6th day upon 

stopping mehtlyphenidate, the thrombocyte count returned to normal. We also discussed possible mechanisms of thrombocytopenia. 

Key words: Isolated thrombocytopenia, petechia, methylphenidate 


[PP-111] Ref. No: 245 

Use of mirtazapine and olanzapine in treatment of major depressive disorder with 

psychotic features developed during pregnancy: A case report 

Mustafa Güleç 1 , Yavuz Selvi 2 , Ünsal Aydınoğlu 1 

1 Atatürk Üniversitesi Tıp Fakültesi, Psikiyatri Anabilim Dalı, Erzurum, Turkey 

2 Yüzüncü Yıl Üniversitesi Tıp Fakültesi, Psikiyatri Anabilim Dalı, Van, Turkey 


Objctive: To contribute to the of treatment of major depressive disorder with psychotic features developing during pregnancy 

Case: A 25 year-old, married, female patient was 13 weeks pregnant and diagnosed with major depressive disorder (MDD) with psychotic 

features. She was a housewife with primary school degree and was admitted to inpatient unit. The obstetrician did not find any fetal 

anomalies. The patient was put on mirtazapine and olanzapine, doses of which ranged between 15-30mg/day and 5-10 mg/day, 

respectively during her two months hospitalization. In her follow up, 15 days after discharge, olanzapine dose was decreased to 5 mg/day, 

but mirtazapine was continued at 30mg/day until delivery. To decrease neural tube defect risk folic acid 5mg/day was prescribed during 

the treatment, as well. She gave birth to a live and healthy baby on the expected due date during her outpatient treatment. 

The information regarding the safety of use of mirtazapine and olanzapine during pregnancy primarily rely on case reports. While 

there were no fetal abnormalities in majority of cases regarding olanzapine use (1,2), there are some reports including hip dysplesia (3), 

meningocele ve ankyloblepharon (4), atrioventricular channel defect and unilateral pes equinovarus (5). However, more cases and studies 

are needed to explore, whether these cases were coincidental or due to teratogenic effects of olanzapine. Currently available publications 

(6,7,8,9) report that major malformation risk in general population does not increase with the use of mirtazapine during pregnancy. The 

reports from our country are parallel to the reports in the literature (10,11). 

Results: Even in majority of cases no fetal abnormalities were reported regarding olanzapine use during pregnancy, large case series are 

needed to have more evidence for stronger judgments. Also even mirtazapine does not look like a teratogenic agent, is should be used 

with caution during pregnancy and babies that are exposed to mirtazapine should be followed closely. 

Key words: Depression, pregnancy, safety, mirtazapine, olanzapine, teratogenicity 

References: 

1. Littrell KH, Johnson CG, Peabody CD, Hilligoss N. Antipsychotics during pregnancy. Am J Psychiatry 2000; 157(8):1342 

2. Mendhekar DN, War L, Sharma JB, Jiloha RC. Olanzapine and pregnancy. Pharmacopsychiatry 2002; 35(3):122-123 

3. Spyropoulou AC, Zervas IM, Soldatos CR. Hip dysplasia following a case of olanzapine exposed pregnancy: a questionable association. Arch Womens Ment Health 

2006; 9(4):219-222 

4. Arora M, Praharaj SK. Meningocele and ankyloblepharon following in utero exposure to olanzapine. Eur Psychiatr 2006; 21(5):345-356 




5. Yeshayahu Y. The use of olanzapine in pregnancy and congenital cardiac and musculoskeletal abnormalities. Am J Psychiatry 2007; 164(11):1759-1760 

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 

7. Way CM. Safety of newer antidepressants in pregnancy. Pharmacotherapy 2007; 27(4):546-552 

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 

outcomes. J Clin Psychiatry 2006; 67(8):1280-1284 

9. Einarson TR, Einarson A. Newer antidepressants in pregnancy and rates of major malformations: a meta-analysis of prospective comparative studies. 

Pharmacoepidemiol Drug Saf 2005; 14(12):823-827 

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; 

19(2):235-328 

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 

2005; 272(4):298-300 


[PP-112] Ref. No: 253 

Effects of group musical therapy on inpatients with schizophrenia: A preliminary study 

Selma Bozkurt Zincir 1 , Ümit Başar Semiz 1 , Aynil Yenel 1 , Emel Başoğlu 1 , Mustafa Bilici 1 , Cumhur Tulay 2 

1 Erenköy Mental Health Training and Research Hospital, İstanbul, Turkey 

2 Science, Culture, and Art Society (BIKSAD) 


Background: Since ancient times, music has been used as a therapy method and has been considered to have some good effects on 

the human body and mental health (1, 2, 5). Music might have beneficial effects on human life such as physiological functions, quality of 

life, and psychosocial functioning. There is a wide acceptance about musical therapy practices for various disorders. This generalization 

may mean that schizophrenia patients could have some benefits from musical therapy, too (1- 3). There is not enough scientific evidence 

emphasizing the efficacy of musical therapy which is applied to severe mental disorders and has recovery potential for some deficits (2, 4). 

Objectives: The first aim of this study was to examine the feasibility of music therapy for inpatients with schizophrenia, who need acute 

care and also to explore its effects on mental health, general psychosocial functioning, and satisfaction with patient care. 

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 

schizophrenia inpatients. Both groups received medication and standard care for their disorder. Additionally, the study group underwent group 

music therapy with classical Turkish music tones for twelve sessions over four weeks. The assessment included measures of psychotic symptoms 

using the Positive and Negative Syndrome Scale (PANSS), the Brief Psychiatric Rating Scale (BPRS), and quality of life and subjective satisfaction 

with musical experiences. All of the measurement tools were applied before the randomization and weekly until the study was completed. 

Results: This study demonstrated that music therapy for schizophrenia inpatients, who need acute care because of psychotic excitation, 

is feasible. The comparison of the groups also showed that music therapy has significant advantages on improvement of interpersonal 

relationships and general psychosocial functioning. 

Conclusions: This study is the first musical group therapy trial with classical Turkish music tones in schizophrenic patients. Musical activity 

diminishes negative symptoms, reduces social isolation, and improves patients’ abilities to adapt to the social environment in the community after 

discharge from the hospital. Therefore, music therapy may increase the therapeutic alliance of schizophrenic patients in the long term. 

Key words: Music therapy, schizophrenia, inpatient, quality of life 

References: 

1. Altınölçek H. Türklerde psikiyatrik hastaların rehabilitasyonunda müziğin terapötik etkileri. Popüler Psikiyatri Dergisi 2006; 34: 16- 19. 

2. Talwar N, Crawford MJ, Maratos A, Nur U, McDermott O, Procter S. Music therapy for inpatients with schizophrenia: Exploratory randomised controlled trial. British 

Journal of Psychiatry 2006; 189: 405- 409. 

3. Ulrich G, Houtmans T, Gold C. The additional therapeutic effect of group music therapy for schizophrenia patients: A randomised study. Acta Psychiatrica 

Scandinavica 2007; 116: 362- 370. 

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 

Neurosciences 2002; 56: 187- 193. 

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. 


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[PP-113] Ref. No: 255 

Clinical correlations of childhood trauma and dissociation in a sample of female 

inpatients diagnosed with schizophrenia spectrum disorders and severe 

nonpsychotic disorders: the preliminary data 

Selma Bozkurt Zincir, Ümit Başar Semiz, Aysun Demir, Yücel Yılmaz, Sevgi Gül Kabak 

Erenköy Mental Health Training and Research Hospital, Istanbul, Turkey 


Background: There is recent increasing interest in the relationship between early childhood trauma and the risk of developing psychotic 

experiences later in life (2,3). Although a large number of studies of psychiatric patients, a majority of whom have a psychotic disorder, 

indicate that the prevalence of childhood trauma in this group is high, whether childhood trauma is of etiological importance in psychosis 

remains controversial (1, 2, 4). 

Objectives: In the present study, we aimed to investigate the possibility of a link between psychotic disorders and childhood traumatic 

experiences by comparing trauma exposure in a group of female patients with a diagnosis of psychotic disorders to a group diagnosed 

with severe non-psychotic disorders. The secondary purpose of this study was to examine the clinical correlations between trauma 

exposure, dissociative phenomena, and psychiatric symptomatology and psychosocial functioning for these two groups. 

Methods: Patients with psychotic disorders, mostly schizophrenic (n=54), and with a non-psychotic diagnosis (n=24), were recruited 

at the Women’s Clinic of the Istanbul Erenköy Mental Health Hospital. The data were collected through a semi-structured interview for 

demographic, psychiatric, and trauma histories. Psychotic symptoms were measured by using the Positive and Negative Symptom Scale 

(PANSS). At the main interview, the Childhood Traumatic Questionnaire (CTQ), Dissociative Experiences Scale (DES), Traumatic Experiences 

Checklist (TEC), and SCL-90-R were administered to all participants by psychiatrists, who were blind to trauma history. 

Results: In this preliminary study, high prevalence rates of childhood traumatic experiences and dissociative phenomenon were found in 

a sample of consecutively admitted moderately ill psychotic inpatients. Another finding of the present study was that emotional abuse 

during childhood was most strongly correlated with the experience of dissociative symptoms in adult schizophrenia patients. Additionally, 

in this group a history of trauma was significantly related to somatization, poor communication skills, and depressive symptoms. 

Conclusions: The results of this study are consistent with previous studies raising the possibility that such trauma is of etiological 

importance in schizophrenia and other related disorders (4-6). 

Key words: Childhood trauma, dissociation, psychosis, schizophrenia 

References: 

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 

disorders an exploratory study. J Nerv Ment Dis 2006; 194: 135- 138. 

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 

sample of patients with non-psychotic diagnosis. Journal of Trauma & Dissociation 2006; 7(3): 7- 22. 

3. Lysaker PH, LaRocco VA. The prevalence and correlates of trauma-related symptoms in schizophrenia spectrum disorder. Comprehensive Psychiatry 2008; 49: 330- 334. 

4. Larkin W, Read J. Childhood trauma and psychosis: Evidence, pathways, and implications. J Postgrad Med 2008; 54(4): 287- 293. 

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. 

6. Morgan C, Fisher H. Environmental factors in schizophrenia: childhood trauma- a critical review. Schizophrenia Bulletin 2007; 33(1): 3- 10. 


[PP-114] Ref. No: 256 

Comparison of neurocognitive skills between generalized anxiety disorder 

and premenstrual dysphoric disorder patients: A controlled study 

Selma Bozkurt Zincir, Aynil Yenel, Selvinaz Çınar Parlak, Gülnihal Şimşek, Arzu Bayrak, Dicle Bilge, Ümit Başar Semiz, Mustafa Bilici 

Erenköy Mental Health Training and Research Hospital, Istanbul, Turkey 


Background: Recently, there has been increased interest in the ability of female reproductive hormones to impact psychoneurological 

processes involving the interplay of several body systems. This lends reliability to the view of premenstrual dysphoric disorder (PMDD) 




as a disorder founded in real biochemical disturbances (1,2). Although the effects of the menstrual cycle on emotional state and 

cognitive function have been only recently systematically studied, they have long been recognized. Previously published studies yielded 

inconsistent data in terms of cognitive tests throughout the cycle phases (1, 3, 4). 

Objective: This study aimed to compare the effects of cyclic reproductive hormonal changes on cognitive, emotional, and behavioral function 

in childbearing age female patients with generalized anxiety disorder (GAD) and those with premenstrual dysphoric disorder (PMDD). 

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 

higher on the Hamilton Anxiety Scale (HAM-A) score. An age matched healthy control group (n = 40) was also included in the study. The 

psychiatric rating scales were applied twice according to the menstrual phases. The frontal assessment battery, Stroop test, and Weschler 

verbal memory tests were applied for the evaluation of neurocognitive changes with respect to follicular and late luteal phases. 

Results: There was a significant increase in dysphoric mood during the luteal phase in women with PMDD compared to their follicular phase 

and compared to the GAD women and the control group. Taken together with the repeated measures and the data analysis, the GAD group 

had significantly worse performance regarding overall neurocognitive functions in their luteal phase (particularly memory skills, attention, 

and psychomotor function) as compared to the PMDD group, whereas the control group had significantly better performance overall. 

Conclusions: Even though neurocognitive impairments seen in the women with PMDD were partly due to the dysphoric mood during 

the late luteal phase, it seems to be related to the physiological and psychoneurological processes in which female reproductive 

hormones may have a central role. 

Key words: Neurocognitive functions, premenstrual dysphoric disorder, generalized anxiety disorder, female reproductive hormones 

References: 

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. 

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 

and without PMDD (Premenstrual Dysphoric Disorder). Horm Behav. 2008; 54: 185- 193. 

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. 

4. Morgan M, Rapkin AJ, D’Elia L, Reading A, Goldman L. Cognitive functioning in premenstrual syndrome. Obstet Gynecol. 1996; 88: 961- 966. 

5. Resnick A, Perry W, Parry B, Mostofi N, Udell C. Neuropsychological performance across the menstrual cycle in women with and without premenstrual dysphoric 

disorder. Psychiatry Research 1998; 77:147- 158. 


[PP-115] Ref. No: 259 

Evaluation of olfactory function and olfactory bulb volume in major depressive disorder 

Meral Akbıyık, Oğuz Karamustafalıoğlu 

Şişli Etfal Research and Teaching Hospital, Department of Psychiatry, İstanbul, Turkey 

akbiyikmeral@gmail.com 

Objective: The purpose of this study was to assess olfactory function and olfactory bulb volume in patients with major depressive 

disorder (MDD) in comparison to normal subjects. 

Method: Twenty treatment-free premenopausal, 25-45 year-old women diagnosed with long-term, severe MDD at the Şişli Etfal Research 

and Teaching Hospital psychiatric outpatient clinics and 20 healthy women matched by age, education, smoking behavior, and frequency 

of upper respiratory tract infection participated in this study. 

Odor threshold, discrimination, and identification functions were assessed by Sniffin’ sticks. Olfactory bulb volumes were calculated by 

manual segmentation of acquired T2-weighted coronal slices according to a standardized protocol. 

Results: When OB volumes of patients and controls were analyzed with a two-way Analysis of Covariance, with age and education as the 

covariate and group as a factor, the patients had significantly larger OBs than the controls (right p=0.011; left p


[PP-116] Ref. No: 261 

Fluoxetine induced hypomanic shift in a bulimic patient: A case report 

Mustafa Özten, Atila Erol 

Department of Psychiatry, Sakarya University, Faculty of Medicine, Sakarya, Turkey 

E-mail: drozten@yahoo.com 

In the psychopharmacological treatment of bulimia nervosa (BN), antidepressants have a positive effect on mood and reduce the related 

preoccupation with body weight and the number of binge eating episodes. Research with antidepressants such as imipramine, desipramine, 

trazodone, phenelzine, amitriptyline and mianserin has been conducted to investigate their efficacy in the treatment of bulimia. A higher dose 

of the fluoxetine (60 mg/day) was shown to be effective in BN and has received FDA approval. Comorbidity of eating disorders with mood, 

anxiety, and substance use disorders is common. The presence of additional psychiatric disorders impairs compliance with treatment and makes 

treatment difficult by increasing severity and chronicity. The treatment of bulimia nervosa with fluoxetine is adversely affected by the presence 

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. 

When using fluoxetine in patients with a history of bipolar mood disorder (BiPMD) or a positive family history of BiPMD, clinicians need to be 

careful because of the possibility of a manic shift. There is not any developed algorithm for psychopharmacological treatment with comorbidity 

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 

available. Negative effects on weight gain or other negative interactions of mood stabilizers in BN, makes it difficult to use them. Like other 

antidepressants SSRIs may also cause a manic shift. The use of antidepressant doses of fluoxetine for mood and anxiety disorders are known to 

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 

disorder, is recommended. Using high dose fluoxetine in BN also increases the possibility of manic or hypomanic shifts. The use of fluoxetine 60 

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 

the treatment demonstrated that 60 mg of fluoxetine did not result in a significant decrease in symptoms and adequate treatment response. 

Retrospectively inadequate response to the treatment was associated with the presence of comorbid BiPMD. 

Key words: Bulimia nervosa, fluoxetine, hypomania, mania 


[PP-117] Ref. No: 262 

Schizophrenia and Mega Cisterna Magna: A case report 

Semra Karayılan, Atila Erol 

Department of Psychiatry, Sakarya University Faculty of Medicine, Sakarya, Turkey 

E-mail: skryln@gmail.com 

The cerebellum, which is known in general as an organ to control coordination, balance, and fine motor movements, has been demonstrated 

to have an important role in cognitive functions by using anatomical and functional imaging methods. The anomaly of mega cisterna magna 

is one of the various lesions of the posterior fossa which can influence cerebellar functions like cerebellar hypoplasia/agenesis, vermis 

hypoplasia/agenesis, Dandy-Walker malformation or variant, persistent Blake’s pouch, arachnoid cyst, Joubert syndrome, and tumors of the 

posterior fossa. Mega cisterna magna (MCM) is a developmental malformation of the posterior fossa, where morphologically the vermis and 

cerebellar hemispheres are intact. Associated structural brain anomalies are common with mega cisterna magna and especially, MCM may 

be a component of the Dandy-Walker variant (with cerebellum hypoplasia) or Dandy-Walker syndrome (with cerebellum agenesia). Our 

knowledge about the relationship between this anomaly and psychiatric disorders is limited to very few case reports available. In this article, 

we report a case of schizophrenia associated with mega cisterna magna. A 35-year-old married patient (house wife, graduated from primary 

school) was brought to our clinic by her relatives with complaints of disorganized and inappropriate speech, strange behavior, and fear of 

people. She had auditory and visual hallucinations and delusions of reference and persecution. Up to five months ago she had no psychiatric 

or neurological symptoms or history. Her symptoms began with social isolation, decrease of self-care, and positive psychotic symptoms. 

Neurological examination and EEG examination were normal, but mega cisterna magna was discovered in her cranial magnetic resonance 

imaging scan. The patient was treated with risperidone 6mg/day for four weeks and was discharged after remission of psychotic symptoms. 

The prevalence and prognostic significance of MCM has not been defined completely yet. Memory and verbal fluency were found to be lower 

in cases of mega cisterna magna than in controls. Schizophrenic patients are known to have problems of memory and verbal fluency, too. 

The role of the cerebellum in schizophrenia has been highlighted by Andreasen’s hypothesis of ‘cognitive dysmetria’. This hypothesis suggests 




that the cerebellum has a role in the general dyscoordination of sensorimotor and mental processes which are seen in schizophrenic patients. 

The following observations demonstrating the involvement of the cerebellum are determined in studies of schizophrenic patients: high 

prevalence of neurological soft signs, dyscoordination, abnormal posture, balance problems, impaired eye blink conditioning and impaired 

adaptation of the vestibular-ocular reflex. Abnormal cerebellar activations have been showed in functional imaging studies. In the context of 

this case, the relationship of schizophrenia with cerebellar anomalies was reviewed. 

Key words: Schizophrenia, mega cisterna magna, cerebellum, brain imaging methods 


[PP-118] Ref. No: 263 

Congenital hypogonadism and comorbid anorexia nervosa in a male patient: 

A case report 

Mustafa Özten, Atila Erol 

Department of Psychiatry, Sakarya University, Sakarya, Turkey 

E-mail: drozten@yahoo.com 

Male hypogonadism results from a failure of the testes to produce adequate androgen. Patients have low circulating testesterone in 

combination with clinical symptoms such as osteopenia, increased adiposity, decreased muscle mass, decline in energy and stamina, 

decreased cognitive function, decreased libido and erectile dysfunction. The cause may be primary (genetic anomaly) or secondary (defect in 

hypothalamus or pituitary), but often presents with the same symptomatology. Hypogonadal patients who are both symptomatic and who 

have clinically significant alterations in laboratory values are candidates for treatment. Testosterone replacement therapy is widely applied. 

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 

disease and the causes of its appearance. Social, genetic, psychological factors, personality traits and a history of trauma are considered to 

play a role in the development of anorexia nervosa (AN). In addition, steroid hormones affect the development of eating disorders and eating 

behavior. Homosexuality, asexuality and sexual role disorders are known to be more common in male patients with AN. AN is associated 

with notable medical complications and affects many systems like a general medical disease. One of the systems that is affected by AN is 

the genitourinary system; hypogonadism is one of the known complications of AN. Endocrine abnormalities such as hypogonadotropic 

hypogonadism mediate some of the clinical manifestations. Most of the endocrine changes that occur in AN are physiological adaptations 

to starvation and are usually reversible with weight gain. Prolonged AN or cachexia can cause hypogonadism. In this article we report a 

man, who had suffered from hypogonadism since infancy with no treatment and developed AN at age 18. Congenital hypogonadism with 

comorbid AN is a rare illness. As a result of the interaction of hypogonadism with anorexia nervosa the patient developed a sexual identity 

crisis, which is important in its clinical and theoretical aspects, since he suffered from delayed puberty, no secondary sexual characteristics, 

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 

hypogonadism and anorexia nervosa. Hypogonadism with comorbid anorexia nervosa has not been listed as a case in the Turkish indices yet. 

Key words: Anorexia nervosa, congenital hypogonadism, male patient 


[PP-119] Ref. No: 275 

Review of diagnosis and treatment of pregnant psychiatric patients in a state hospital 

Kader Semra Karataş, Jülide Güler, Aytül Hariri 

Erenkoy Mental and Nervous Diseases Training and Research Hospital, Department of Psychiatry, İstanbul, Turkey 

E-mail: drsemraocak@yahoo.com 

Background: Because of the physiological changes during pregnancy there are changes of pharmacokinetic and pharmacodynamic 

characteristics, and there are differences in the treatment of psychiatric disorders in this period. 

Objective: The aim of this study was to evaluate the sociodemographical features, diagnoses, and treatments of 20 pregnant psychiatric 

inpatients that were hospitalized between August 2010 and August 2011. 

Method: The sociodemographical features, diagnoses, and treatments of the patients were evaluated retrospectively. 

Results: The percentages of diagnoses of the patients were as follows: schizophrenia 27.3%, bipolar affective disorder manic episode 

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22.7%, bipolar affective disorder depressive episode 9.1%, unipolar depression 27.4%, and obsessive compulsive disorder, dissociative 

disorder, and schizoaffective disorder, each 4.5%. When the treatments of the patients were evaluated according to their diagnosis 

we found that 13.6% of schizophrenia patients were treated with ECT, 9.09% with haloperidol and 4.5% with atypical antipsychotics; 

the patients with bipolar depression were treated with mood stabilizers and ECT plus mood stabilizers at the same rate of 4.5%; 18.1% 

of the patients with mania were treated with ECT plus haloperidol; and of the unipolar depressed patients 13.6% were treated with 

psychotherapy and 9.09% with ECT and haloperidol. 

Conclusion: ECT was used commonly as a treatment option in our patient group. ECT treatment was added onto haloperidol treatment 

in severe cases. This treatment is consistent with the recommendations of the APA and with those in the literature. 

Key words: Pregnancy, mental illness, treatment, ECT, antipsychotic drugs 


[PP-120] Ref. No: 278 

Peripheral edema associated with mirtazapine: Presentation of a case 

Birmay Çam 1 , Hüseyin Kurt 2 

1Gönen Devlet Hastanesi Psikiyatri Kliniği, Gönen, Balıkesir, Turkey 

2Gönen Devlet Hastanesi İç Hastalıkları Kliniği, Gönen, Balıkesir, Turkey 

E-mail: birmaycam@mynet.com 

In the medical literature, occurrence of edema during treatment with mirtazapine is stated as the least frequently reported side effect. A 

case of edema occurring during mirtazapine treatment is reported below. 

Case: A 34 year-old female patient was admitted to the psychiatric ward with a diagnosis of recurrent depressive disorder. There were no specific 

findings in the patient’s medical history other than high blood pressure and irregularly administered antihypertensive drugs. There was no use 

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 

mg daily. Mirtazapine 15 mg daily was added to the medical treatment, as the depression and insomnia continued. The day after beginning 

the treatment with mirtazapine pretibial edema developed. The CBC, ALT, AST, GGT, ALP, bilirubin, albumin, urea, creatinine, Na, K, Cl, Ca, urine 

analysis, thyroid function tests and chest X-ray were repeated and all were within normal limits, as before. Cardiac insufficiency, cirrhosis, nephrotic 

syndrome, and venous insufficiency, all of which can cause edema, were ruled out by the internal medicine consult. The patient was not in the 

premenstrual period and not pregnant. It was also reported that such a side effect was observed during the administration of escitalopram to the 

patient. The edema was assessed as being due to mirtazapine. The edema decreased three days after the cessation of the mirtazapine treatment 

and the administration of furosemide 40 mg/day at the recommendation of internal medicine. It disappeared ten days later. Escitalopram 10 

mg daily and hydroxyzine 25 mg daily were continued. The patient, whose depressive symptoms decreased and anxiety disappeared, has 

continued to be followed up as an outpatient after discharge. The patient’s depressive symptoms did not recur and her blood pressure remained 

within normal limits although she did not receive any antihypertensive treatment. She had no edema at her two month follow up visit. Her CBC, 

electrolytes, biochemical and thyroid function tests, and urine analysis all remained within normal limits. 

Discussion: In our case, the occurrence of edema simultaneously with the administration of mirtazapine, the exclusion of systemic 

diseases that can cause edema, the lack of continuation or recurrence of the edema even as the patient remained on escitalopram 

between the previous and the current depressive episodes, and finally the disappearance of the edema right after the cessation of 

mirtazapine treatment made us to think that the edema was caused by mirtazapine. In the medical literature, it is reported that MAOIs, 

escitalopram, and sertraline can cause edema. Kutscher et al. reported that peripheral edema occurred in a male patient of 60 years of age 

after the use of mirtazapine and disappeared right after the cessation of mirtazapine treatment (1,2,3,4). More detailed studies should be 

conducted to explore and understand this issue better. 

Key words: Edema, mirtazapine 

References: 

1. Remick RA,Froeze C,Keller FD(1989)Common side effects associated with monoamine oxidase inhibitors.Prog Neuropsychopharmacol Biol Psychiatry 13:497-504. 

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. 

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 

Danub. Mar;23(1):120-2. 

4. Kutscher EC,Lund BC,Hartman BA(2001)Peripheral edema associated with mirtazapine. Ann Pharmacother.35(11):1494-5. 





[PP-121] Ref. No: 280 

Abuse of tianeptine: A case report 

Hüsameddin Özer, Atilla Erol 

Sakarya Teaching and Research Hospital, Psychiatry Clinic, Sakarya, Turkey 

E-mail: husamozer@mynet.com 

Tianeptine is an atypical antidepressant, which modestly enhances the mezolimbic release of dopamine. Tianeptine is an antidepressant 

that is accepted as not being abused by patients. However, there have been some case reports regarding abuse and/or addiction to it. 

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 

141 cases of abuse were reported between 1989 and 2004. The patients usually sought and experienced a psychostimulant effect. The 

stimulant effect of tianeptine has been specifically emphasized in some case reports of tianeptine abuse in the literature. 

In this poster, a twenty year-old female patient, who received tianeptine treatment for depression and developed tianeptine dependence 

is presented. In our case, the patient was taking sixty pills daily. Although she took sixty pills, her biological tolerance was excellent and 

hepatic and hematological parameters were not affected, similar to the findings of other reports in the literature. 

This case emphasizes that while prescribing tianeptine treatment clinicians should be careful using it in patients with substance abuse 

problems, as reported by other case reports in the literature. 

Key words: Tianeptine abuse, tianeptine dependence 


[PP-122] Ref. No: 282 

GWAS with AHP based SNP prioritization approach to identify SNP biomarkers 

for Alzheimer’s disease 

Onat Kadıoğlu 1 , Gürkan Üstünkar 2 , Yeşim Aydın Son 3 

1 Middle East Technical University, Bioinformatics Graduate Program Ankara, Turkey 

2 Middle East Technical University, Informatics Institute Department of Information Science, Ankara, Turkey 

3 Middle East Technical University, Informatics Institute Department of Health Informatics, Ankara, Turkey 

E-mail: onat.kadd@gmail.com 

Genome wide association studies (GWAS) is defined as search for biological variance associated with certain phenotypes and diseases 

among individuals in a population depending on statistical analysis. Combined p-value approach has been introduced recently and 

is defined as the second-wave GWAS. It helps mapping of significant SNPs to genes and pathways to evaluate SNP-gene-disease 

associations. Identification of enriched genes and pathways significantly associated with diseases can be performed via this approach. 

The major bottleneck of current standard GWAS approaches is the prioritization of statistically significant results. Our group has recently 

developed a novel Analytical Hierarchical Process (AHP) based on a structured SNP prioritization algorithm. SNPs are scored according 

to their biological relevance in terms of their genomic location and functional consequence, evolutionary conservation, and genedisease 

association. The recently developed METU-SNP application integrates GWAS, combined p-value while utilizing AHP based SNP 

prioritization algorithms. Combined p-value and AHP prioritization approach for GWAS of Alzheimer’s Disease (AD) has been utilized for 

the SNP-disease association of AD for the first the time in this study with METU-SNP software. 

The results from the analysis of two different sets of AD genotyping data with the newly proposed AHP based prioritization yield promising 

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 

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 

37 of them map to AD linked genes. Glycolysis and gluconeogenesis, leukocyte migration, axon guidance, actin filament polymerization, 

cell adhesion, DNA fragmentation during apoptosis, fatty acid metabolism, and negative regulation of cell proliferation are common 

pathways residing at top 100 pathways according to combined p-value for pathways that are observed in GWAS results of both data sets. 

GWAS of both data with METU-SNP confirms the literature for AD associated genes; A2M, ABCA1, ACE, APOA1, APP, CHRNA7, IL1A, 

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 

associated at PharmGKB database. Moreover, CT and TT genotype of rs6313 at HTR2A gene indicates resistance to the treatment with 

antipsychotic drugs for AD patients presenting delusional symptoms. As presented here METU-SNP is a powerful tool with a novel AHP 

based prioritization algorithm implemented, which can lead to discovery of new associations at SNP, gene, and pathway level. In near 

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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 

medicine approaches with application in pharmacogenomics and psychopharmacology. 

Key words: AHP, Alzheimer’s disease, biomarker, GWAS, personalized medicine, pharmacogenomics, SNP prioritization 


[PP-123] Ref. No: 287 

A case report of a relapse in a major depression patient with valsartan/hydrochlorothiazide 

Alev Büyükkınacı, Devrim Öztürk Can, Gökçe Silsüpür 

Boylam Psychiatry Hospital, Ankara, Turkey 

E-mail: alevkilicoglu@gmail.com 

It is known that some drugs can cause depression. In particular, there is evidence that barbiturates, vigabatrine, topiramate, flunarizine, 

corticosteroids, mefloquine, efavirenz, and interferon alpha have been shown to cause depression (1). Angiotensin II is a strong 

vasopressor with various physiological effects especially regulating blood pressure. It regulates water retention and aldosterone secretion. 

Angiotensin II has two known receptors, AT1 and AT2. Valsartan is a non-selective angiotensin AT selective blocker, which prevents 

angiotensin binding to AT2 receptors and controls hypertension in this way (2). It has been shown that angiotensin converting enzyme 

polymorphism is related to relapse in major depression patients after partial sleep deprivation and this was related to its effect on the 

dopaminergic system (3). This finding shows that drugs targeting the angiotensin system may effect depression. Here we present a case 

with recurrent depression who was in remission and relapsed after she was given an antihypertensive medication containing valsartan 

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 

other episodes in 1997, 2001, and the last one in 2003. After having used venlafaxine and paroxetine, she was given citalopram in 2003 at 

40 mg/day, which she has been using until now. She did not have any depressive attacks after 2003. She was given an antihypertensive 

containing valsartan and hydrochlorothiazide 3 months before she presented to our clinic. After taking the medication she had reluctance, 

despondency, intense feelings of guilt with statements like “she will not be even accepted to hell.” There were no stressors that the patient 

or her relatives defined. The patient was admitted to our clinic after her symptoms increased the month prior to her admission. Since there 

were published articles on depression triggered by valsartan and similar antihypertensives and since the patient’s symptoms started after 

taking the medication, we continued on her drug regimen with citalopram 40 mg/day and changed her antihypertensive medication to 

a calcium channel blocker, amlodipine. After 2 weeks her symptoms started to decrease. We concluded that her depression was triggered 

by valsartan. This case is important for showing that medications affecting the angiotensin system can trigger depression and there is a 

need to study the role of the angiotensin system in the etiology of depression. 

Key words: Valsartan, antihypertensives, depression, relapse 

References: 

1. Celano CM, Freudenreich O, Fernandez-Robles C, Stern TA, Caro MA, Huffman JC. Depressogenic effects of medications: a review.Dialogues Clin Neurosci. 

2011;13(1):109-25. 

2. Black HR, Bailey J, Zappe D, Samuel R.Valsartan: more than a decade of experience. Drugs. 2009;69(17):2393-414. 


[PP-124] Ref. No: 158 

Monosymptomatic hypochondriacal psychosis: A case report 

Yasemin Şimşek, Gökçe Elif Sarıdoğan, Ebru Şahan, Melike Nebioğlu, Cem Cerit, Mecit Çalışkan 

Haydarpaşa Numune Hastanesi Psikiyatri Kliniği, İstanbul, Turkey 

E-mail: cemcerit@yahoo.com 

Introduction: The somatic type of delusional disorder is also recognized as monosymptomatic hypochondriacal psychosis. According 

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 

physical defect or a general medical condition (1). The most substantial characteristic of the aforementioned disorder is the demand of 

the patient attributing the symptoms to a serious physical illness, and seeking medical advice continuously in an effort to find transient 




relief by being informed of the absence of a disease (2). 

Case Presentation: A 26- year old, female patient was admitted to an outpatient psychiatric clinic with complaints of having a possible ocular 

disease, which may cause blindness. Her symptoms included her irises deviating involuntarily, her eyes moving incoherently, and having a 

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 

complaints of dysmorphism and tremor in her hands and having a serious disorder relevant to her hands for which she was seen by several 

specialists although she wasn’t convinced by their answers. Although, thereafter she was hospitalized and was treated with several mood 

stabilizers and antipsychotic medications for the following three years in outpatient clinics, a full remission could not be achieved. 

She was hospitalized again. Her physical and neurological examination didn’t reveal any biological anomalies. It was noticed that she was 

touching her eyes constantly and her speech was focused on her bodily sensations so that she couldn’t maintain her attention on any 

other topic. In the contents of her thoughts, she had somatic delusions as defined above. She was treated with pimozide, started with 2mg 

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, 

increased interest, improved self-care, decrease in the amount of her speech and becoming more functional. 

Discussion: Because there was no increase in psychomotor activity and the content of speech was solely about the sensations in her eyes, 

we did not diagnose her with an affective disorder. We arrived at the diagnosis of monosymptomatic hypochondriacal psychosis after 

evaluating the cues such as the worry about having an eye disease, not being persuaded with the medical examinations and diagnosis, 

lack of any other psychotic symptoms, delusions being only about bodily sensations, several admissions to non-psychiatric physicians, 

and her resistance to treatment with multiple drugs. In the literature there are cases reporting surgery, which was not required, such as an 

operation to treat a patient stating that he had a lumbar nerve root compression (3). In the present case the patient presented to internal 

medicine and ophthalmology clinics at the beginning insisting that she needed an eye operation. In a study on 23 patients it has been 

reported that these cases have responded well to pimozide (4). 


[PP-125] Ref. No: 288 

Amisulpride in the treatment of treatment resistant tic disorder: A case report 

Onat Yılmaz, Mehmet Alpay Ateş, Gülşah Meral, Cengiz Başoğlu, Ayhan Algül, Servet Ebrinç, Mesut Çetin 

GATA Haydarpasa Training Hospital, Department of Psychiatry, Uskudar, Istanbul, Turkey 

E-mail: onatyilmaz@yahoo.com 

Introduction: Tics are sudden, recurrent, involuntary motor movements or vocalizations caused by involuntary contractions of motor 

or vocal muscles. Typically these disorders are characterized by early childhood onset and are more common in the male population. 

Genetic, neurobiological, neurochemical and environmental factors play a role in the pathogenesis, and malfunctioning of the basal 

ganglia is thought to be responsible for the disease. The presence of abnormalities in the EEG of some patients, worsening of the tics with 

administration of dopamine agonists, and improvement of tics with antidopaminergic agents are some of the known biological evidence. 

Amisulpride, with a pure antidopaminergic activity, and thus being used effectively in the treatment of Tourette’s syndrome, makes it a 

candidate to treat other tic disorders, as well. In this report, an adult patient diagnosed with “Tic Disorder Not Otherwise Specified,” who 

was previously treated with several antidepressant and antipsychotic drugs, is cured with amisulpride. 

Case presentation: A 21-year-old single male patient was admitted to the hospital complaining of impairment in interpersonal relations, 

difficulties in social adaptation due to the involuntary repetition of certain movements. His complaints had started at the age of nine after 

his uncles were killed. Though the patient was tried on different treatment regimens, but he had no benefits. Because of his tics, he hardly 

finished his primary school education and was not able to work for a long time. 

In history there were no perinatal or neonatal complications and he was born by spontaneous vaginal birth. As the sixth of eleven children, 

his developmental history was normal. There was no family history of any mental illness, epilepsy, alcoholism, or movement disorder. 

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 

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 

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 

months. 

Discussion: Contrary to the antipsychotics effecting both D1 and D2 receptors in the nigrostriatal pathway, antipsychotics of the 

benzamide group, which work as selective D2 receptor antagonists, are effective in the treatment of tic disorders. As the most preferred 

drug in this group, amisulpride causes less extrapyramidal side effects by selectively acting on the limbic regions rather than striatal 

regions. In the literature, there are case reports of amisulpride’s effective use in tic disorders. 

Clinicians should keep in mind that, with less side effect risk compared to conventional antipsychotics and the benefits of its mechanism 

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of action, amisulpride might be the drug of choice in tic disorders. On the other hand, larger controlled clinical trials should be planned 

on this issue. 

Key words: Tic disorders, echopraxia, amisulpride, side effect 

References: 

1. Turan M, Çilli AS. Tik bozuklukları. Genel Tıp Derg. 1999;9(3):117-21 

2. Fountoulakis KN, Lacovides A, Kaprinis GS. Successful treatment of Tourette’s disorder with amisulpride, Ann Pharmacother. 2004; 3: 901. 

3. Leysen JE, Janssen PMF, Heylen L, Gommeren W, Van Gompel P, Lesage As.Receptor interactions of new antipsychotics: relation to pharmacodynamic and clinical 

effects. Int J Psychiatry Clin Pract; 1998; 2(Suppl.1): 3-17. 

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. 

2009; 47:1: 16-18. 


[PP-126] Ref. No: 290 

Evaluation of patients with obstructive sleep apnea syndrome referred to the sleep 

disorders unit of a university hospital 

Evrim Özkorumak 1 , Haluk Hıdıroğlu 2 , Ahmet Tiryaki 1 , İsmail Ak 1 

1 Karadeniz Technical University, Psychiatry Department, Trabzon, Turkey 

2 Ataköy State Mental Health Hospital, Trabzon, Turkey 

E-mail: evrimozkorumak@yahoo.com 

Introduction: Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive episodes of apnea and hypopnea, and decrease in 

oxygen saturation (1). The relationship of OSAS and other medical conditions has been explored in the research literature while the relationship 

between OSAS and mental health has not been sufficiently investigated yet. The aim of this study was to determine the distribution of mental 

disorders and the type of distribution of mental disorders within clinical features of OSAS from the point of view of psychiatry. 

Method: The patients, who were referred to the sleep disorders unit of Karadeniz Technical University, Faculty of Medicine Hospital for 

1 year were considered the population for this study. A total of 102 patients, with a diagnosis of OSAS according to polysomnography 

and patients with no exclusion criteria composed the sample of the study. The patients were classified according to the ICSD-2 (The 

International Classification of Sleep Disorders) with polysomnography. Sociodemographical and clinical features of the patients were 

recorded. The Montgomery Asberg Depression Rating Scale, the Beck Depression Inventory and the Epworth Sleepiness Scale were 

administered. Psychiatric diagnoses were made by interviews based on the DSM-IV Axis I Disorders (SCID-I). 

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 

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 

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 

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 

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 

score was significantly higher in severe OSAS patients (p=0.002). The relationship of mild and moderate OSAS with BMI was significant 

(p=0.010). The median age of severe OSAS patients was significantly higher than mild OSAS patients (p=0.0529). 

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 

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. 

Discussion: There are many risk factors for OSAS. Male predominance is present for adult OSAS patients. The number of male patients was 

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 

obese in our group. The detected depression rate was correlated with many studies which reported higher depression rates in OSAS (2-5). 

In this study the rate of anxiety disorders was higher than in the healthy population while being similar or lower than the rate estimated 

in previous studies with OSAS patients. 

Conclusion: Mental disorders associated with medical diseases are important clinical syndromes effecting morbidity and mortality. 

Recognizing the symptoms and signs of OSAS is important. Regarding this issue, further studies with larger samples comparing different 

subgroups are needed. 

Key words: Obstructive sleep apnea, mental diseases 





[PP-127] Ref. No: 286 

Clozapine use in idiopathic tardive dystonia and paranoid schizophrenia comorbidity: 

A case report 

Mustafa Güleç, Elif Oral, Esat Fahri Aydın 

Department of Psychiatry, Medical Faculty, University of Atatürk, Erzurum, Turkey 


Objective: To present brief idea about a suitable and safe antipsychotic usage in patient with schizophrenia and tardive dystonia. 

Method: Results will be discussed. 

Results: 

Case: A 42-year-old woman with diagnose of first episode and drug naïve schizophrenia presented with involuntary movements in her 

orobuccal region, including tongue and lips. At first administration, routine biochemical and hematological assessments were normal, and 

patient had positive and negative features of schizophrenia. According to the information received her relatives, although she has not taken 

any antipsychotic medication, her involuntary movements has been risen 18 month earlier her antipsychotic treatment. These movements 

were consulted with neurology clinic. Her brain MRI, EEG, and further assessments including detailed neurological examination, jaw MRI was 

normal, and specialist of neurology suggested that the clozapine usage may be helpful because of the possible idiopathic tardive dystonia. 

Clozapine medication was started with gradually, although there was not enough proof about prior antipsychotic usage and anatomical 

or functional deficit. During her hospitalization, all of the involuntary movements were recovered with 200 mg/day clozapine, and more 

than 35% percent decrease was observed at her positive (SAPS) and negative (SANS) scale assessments with 600 mg /day clozapine. In this 

period, there was no side effect except moderate sialorrhea. Etiology of the idiopathic tardive dystonia is still remaining unclear, and data 

for treatments is receiving from the case reports. There is some evidence about efficacy of clozapine treatment (1,2). In addition, there is a 

consensus about that clozapine can cause extrapyramidal side effects rarely and effective treatment option for schizophrenia as well (3). On 

the other hand, tendency of the general psychiatry practice would prefer to this molecule in the resistant schizophrenia which is describe as 

show no remission despite of two different kinds of antipsychotic usage for minimum six weeks (4). In this case, clozapine usage in the first 

line seems to be necessary because of the idiopathic tardive dystonia. It may be clarified with further studies whether this case was remitted 

incidentally or this remission was related with antagonistic effects of clozapine on the receptors of D1. 

Conclusion: Clozapine may be a first line treatment option for the drug naïve patients with first episode schizophrenia and tardive 

dystonia. However, we need further studies performed with wide case series to achieve this kind of opinion. 

Key words: Tardive dystonia, neurological, schizophrenia, clozapine, safety, efficacy 

References: 

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 

2010; 34(1):238-239. 

2. Aukst-Margetic B, Margetic B. Treatment of generalized tardive dystonia with clozapine. Psychiatr Danub 2008; 20(3):329-331. 

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 

Database Syst Rev 2010; (11):CD006633. 

4. Kane J, Honigfeld G, Singer J, Meltzer H. Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine. Arch Gen Psychiatry 

1988; 45(9):789-796. 


[PP-128] Ref. No: 306 

The clinical use of Buprenorphine-Naloxone in the opioid-dependent patient 

with Hepatitis C 

Tuğba Kara, Arzu Çiftçi 

Bakirkoy Research and Training Hospital for Psychiatry and Neurology, Istanbul 

E-mail: tugbakara111@yahoo.com 

Introduction: Guidelines for the treatment of opioid dependence which developed by organizations such as American Society 

of Interventional Pain Physicians (ASIPP) and the American Psychiatric Association (APA) recommend extensive treatment with 

S201


pharmacological treatments such as methadone, buprenorphine, buprenorfine-naloxone as well as psychosocial therapy. Buprenorphine- 

Naloxone therapy is being used effectively as an alternative treatment to entering patients into a methadone outpatient clinics (1). The 

clinical relevant effect of buprenorphine depends on m-opioid receptor agonism (2). 

Case: 16-years-old male patient with opioid dependence diagnosed according to DSM-IV criteria entered CEMATEM ( Child and 

Adolescent Alchol and Substance Treatment Centre ) clinic for out-patients in Bakirkoy Research and Training Hospital for Psychiatry and 

Neurology and a week later the patient has been hospitalized. Liver enzyme levels were normal and opiat value was found as positive in 

sub-threshold in routine controls and after 6- 8 hours Buprenorfin-Naloksan combination (Suboxone) treatment was received the patient 

experienced withdrawal symptoms.In patient’s routine blood tests, hepatitis C virus (HCV) was determined and the patient developed 

significiantly elevated liver enzyme levels during buprenorphine-naloxone treatment. 

Conclusions: Although Buprenorphine has been used clinically in the early 1970s, it’s metobolism has not been fully unterstood already 

(3). Buprenorphine was mainly metobolized by N-dealkylation and glucuronidation of buprenorphine and norbuprenorphine by CYTP450 

isoforms in liver ( 4). For non-hepatitis subjects, buprenorphine treatment showed no evidence of altered liver enzyme levels. 

In contrast, AST and ALT levels increased significantly with buprenorphine treatment among patients with a history of hepatitis (5). 

Liver enzym values significiantly elevated in this case with hepatitis C received Buprenorphine-Naloxone combination treatment. 


[PP-129] Ref. No: 105 

The use of z hypnotics in the management of insomnia in forensic psychiatric 

units in Oxford, England 

Hasanen Ali Altaiar 

Oxford Health NHS Trust, Littlemore Hospital, Oxford, ox4 4xn, UK 

E-mail: hasanen.al-taiar@oxfordhealth.nhs.uk 

Objectives: Insomnia has an estimated prevalence of 30% in general population and its prevalence is higher among psychiatric patients. In 1987 a 

survey showed around half of psychiatric patients received a hypnotic medication. Also people with mental health problems have an increased risk of 

developing dependence on hypnotics. “Z-drugs” are benzodiazepine like medications and are used as primary pharmacological treatment for insomnia. 

They include zolpidem, zaleplon, and zopiclone. Zopiclone is not available in the US, although its active stereoisomer, eszopiclone is available. NICE 

guidelines recommend trying non-pharmacological interventions such as sleep hygiene prior to considering “z drugs.” The symptoms, findings of 

evaluation, and the reasoning behind prescribing “z drugs” should be documented in medical and nursing notes. The maximum duration should not be 

longer than 2 weeks when “z drugs” were used. 

The aims of this study included: To review if ‘z-drugs’ were prescribed according to the NICE guidelines, whether “insomnia” was documented in patient 

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 

drug” to another. 

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= 

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. 

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 

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 

and documentation was found in one case, too. The maximum duration was not documented and there was no revision in original orders. 

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 

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. 

Checking for the response to the treatment and conducting the study in general wards beside forensic units would have improved this study and 

provided more patients, who were prescribed those medications. 

The majority of forensic patients are on high doses of antipsychotics or rapid tranquilizers, which might help to cope with insomnia. We found that 

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 

prescribe Z hypnotics, when needed. The use of sleep hygiene in treatment of insomnia should be encouraged for all patients. 

Key words: Z hypnotics, forensic, psychiatric, z drugs, Oxford 



[PP-130] 

Pathological gambling: A case report 

Mehmet Fatih Tastan, Haluk A. Savas 

Gaziantep University, Medical School, Department of Psychiatry, Gaziantep, Turkey 

E-Mail: mfatihtastan@yahoo.com, drhaluksavas@hotmail.com 



Pathological gambling(PG), is a disorder which is growing everyday with the increasing prevalence of opportunities for play, usually properly diagnosed, 

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 

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 

Disorders Not Elsewhere Classified” has been included under the heading. Physiological symptoms of DSM-3-R were included in the PG, “the excitement is 

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 

hearing restlessness or irritability, such as” withdrawal symptoms participated in the diagnostic criteria. We present a case of PG, 28 year old male patient 

who is treated with quetiapin and cognitive behavioral treatment (CBT). With CBT, we did daily psychotherapeutic interview and patient had discovered 

his cognitive distortion. Also we saw that SSRIs, Naltrexone, Lithium and Carbamazepine could be used in PG treatment. Patient was externed after 11 

days hospitalizing. At the controls we obtained that patient had not gamble again. As a result this was the effect of Cognitive Behavioral Treatment. 

Key words: Pathological gambling, cognitive behavioral treatment, cognitive distortion 


S203

(±)-3-4-methylenedioxymethamphetamine S36 

1-benzylpiperazine S36 

5-HT1B A-161T S108 

Absence convulsion S118 

Absenteeism S150 

Abuse S180 

Academic achievement S154 

Academic performance S58 

Acceptance S105 

Access S156 

Access to health care S156 

Addiction S54, S42, S83, S109, S151, S155 

ADHD S57, S66, S73, S96, S97, S136, S148 

Adolescence S96 

Adolescents S126, S153 

ADRA2A S148 

Adult ADHD S159 

Adult attention deficit hyperactivity disorder S163 

Affective disorder S161 

Agmatine S166, S169 

Agranulocytosis S46 

AHP S198 

Alcohol S155 

Alcohol abuse S173, S174 

Alcohol dependence S108 

Alexithymia S56 

Alkaline phosphatase S116 

Alloxan S116 

Alzheimer’s disease S52, S198 

Amenorrhea S135 

Amisulprid S160, S200 

Amplified perception of somatic sensations S178 

Amygdala S110, S133 

Anger S138 

Animal model of depression S140 

Anorexia S92 

Anorexia nervosa S130, S195 

Antidepressant S38, S39, S43, S51, S81, S121, S136, S140 

Antiepileptic S182 

Antihypertensives S198 

Antioxidant S170 

Antioxidant vitamins S74 

Antipsychotic S63, S135, S144, S149, S167 

Antipsychotic development S50 

Antipsychotic drug S180, S196 

Antisocial personality disorder S163 

Anxiety S69, S163, S132, S133, S141, S155 

Anxiety disorders S40, S67, S68 

Anxiety models S69 

Anxiety symptom levels S153 

Archive documents S181 

Aripiprazole S135, S144, S152 

Assessment S150, S151, S155 

Atherosclerosis S143 

Atomoxetine S136 

Attachment S56 

Attention deficit hyperactivity S58 

Attention deficit hyperactivity disorder S95, S139 

Atypical antipsychotics S63, S144, S164, S171 

Augmentation S126 

Autism S72 

Avoiding behavior S122 

Bacopa monniera S108, S153, S189 

Basal ganglia hemorrhage S157 

BDNF S91, S169 

Behavioral therapy S185 

Bilirubin S180 

Binge eating S54 

Biogenic amines S51 

Biological rhythm S88, S89 

Biomarker S102, S198 

Bipolar S36, S57, S149 

Bipolar affective disorder S169 

Bipolar disorder S39, S59, S98, S100, S124, S126, S140, S142, S158 

Blood level S142 

Blood sugar S111 

Body dysmorphic disorder S143 

Brain imaging methods S195 

Brain injury S136 

Brain microdialysis S36 

Brain-derived neurotrophic factor S176 

Bright light S89 

Bulimia S92 

Bulimia nervosa S95, S194 

Buprenorphine S35 

Bupropion S113, S121, S143 

C-fos S169 

Cabergoline S124 

Calcium S72, S123 

Cannabis S37, S83, S130 

Cannabis dependency S159 

Caregiver burden S141 

Catatonia S162 

CBT S105, S106, S111 

Cerebellar cognitive affective syndrome S138 

Cerebellum S138, S195 

Cerebral ischemia S112 

Ceruloplasmin S170 

Subject Index 

Character S34, S54 

Chemotherapy S132 

Chest pain without cardiac etiology S138 

Child S36, S57 

Childhood trauma S79, S86, S192 

Children S74, S75, S97, S139 

Cholinesterase inhibitors S136 

Choreoathetoid movement S152 

Chronic schizophrenia S125 

Chronic unpredictable mild stress S166, S169 

Chronotherapeutics S89 

Cigarette S156 

Clinical characteristics S82 

Clinical manifestation S172 

Clozapine S46, S126, S201 

CNR1 1359 G/A S108 

Co-morbidity S96, S97 

Cognition S34, S91, S153 

Cognitive behavior therapy S40, S41 

Cognitive functions S83, S136, S138, S158, S188 

Cognitive processing of emotions S56 

Cognitive side effects S149 

Combination drug therapy S40 

Community care S129 

Comorbidity S92, S95, S177 

Complementary and alternative medicine S65 

Confidence interval S104 

Congenital hypogonadism S195 

Corpus callosum S182 

COX-2 inhibitor S184 

Craving S156 

CRH S51 

Crisis team S129 

Cultural differences S172 

Cytochrome P450 2C9 S132 

Cytokines S70 

D-serine S50 

Death S155 

Deep brain stimulation S61 

Dementia S62, S134 

Depression S36, S38, S39, S43, S57,S60, S60, S64, S65, S70, 

S77, S78, S81, S82, S85, S87,S89, S130, S132, S139, S141, S145, 

S155, S161, S162, S163, S170, S178, S184, S190, S193, S198 

Depression treatment S58 

Depressive symmptom levels S153 

Descriptive statistics S104 

Development S74 

Diabetic rats S116 

Differential diagnosis S177 

Diltiazem S119 

Dissociation S192 

Dissociative disorder S159 

Dissociative symptoms S146 

Divorce S144, S184 

Don Juanism S52 

Dopamine S49, S63 

Dopamine agonists S124 

DRD2 TaqIA S108 

Drug S100, S103 

Drug discovery S62 

Drug induced S167 

Drug-induced psychosis S182 

Drug interactions S97 

Drug safety S48 

Drug utilization S168 

Dual diagnosis S109 

Duloxetine S115, S139 

E-selectin S143 

Eating disorders S54, S92, S93, S94, S130 

Eating pattern S125 

Echopraxia S200 

Ecstasy S36 

ECT 196 

Ecuadorian population S132 

Edema S196 

Education S65 

Education factors S128 

EEG S110, S133 

Effectiveness S151 

Efficacy S38, S136, S201 

Electroconvulsive therapy S174 

Electromagnetic induction S117 

EMDR S106, S127 

Emotion regulation S40 

Emotionality S34 

Enuresis nocturna S185 

Environmental risk S52 

Erectile dysfunction S137 

Escitalopram S160 

Essential fatty acids S66 

Estrogen S77 

Euthymia S158 

Evidence based treatment S41 

Executive functions S176 

Exercise S91 

Extrapyramidal side effects S144, S165 

Eye movement desensitization and reprocessing S123 

Fear of negative evaluation scale S173

Female adolescents S125 

Female reproductive hormones S193 

Fish oil S135 

Flight safety S103 

Fluanxol S129 

Fluoxetine S113, S130, S147, S179, S194 

FMRI S62, S108, S189 

Foetality S171 

Follow-up S176 

Forced swimming test S166 

Forensic S202 

Forensic psychiatric examination S128 

Functional outcomes S136 

Functional remission S188 

Functioning S86 

GABA S51 

Galactorrhea S147, S160 

Ganser Syndrome S159 

Gating S49 

Gender S140 

Generalized anxiety disorder S193 

Generalized convulsion S118 

Genes S52 

Genetic S68S 100 

Genetic association S46 

Genetic polymorphism S131, S132 

Genomic diagnostics S157 

GFAP S169 

Ginseng augmentation therapy S114 

Glia S50, S51 

Glossodynia S161 

Glutamate S40, S49, S50, S51, S69, S70 

Glutathione S169 

Glycine S50 

GOT S116 

GPT S116 

Guidelines S98, S100 

GWAS S157, S198 

Hallucination S121 

Haloperidol S129 

Happiness S34 

Harm minimization S42 

Health S34 

Hematological S130 

Heroin S109 

Hippocampal neurogenesis S91 

HIV/AIDS S42 

HLA-system S46 

Hoarding S134 

Homework assignments S41 

HPA axis S51 

Human characteristics S34 

Human cognition S108, S189 

Huntington’s disease S152 

Hyperammonemic encephalopathy S164 

Hyperprolactinemia S124, S135, S160 

Hypersexual disorders S52 

Hypersomnia S44 

Hypochondriasis S105 

Hypoglycemia S78 

Hypomania S194 

Hyponatremia S139, S141 

Hypothalamic-pituitary-thyroid axis S77 

ICAM-1 S143 

Imipramine S185 

Immunosuppresive treatment S161 

Impulse control disorder S53 

Impulsivity S94 

In vitro analysis S115 

Inappropriate medications S168 

Individualized medicine S101 

Inflammation S184 

Information processing disorder S49 

Inpatient S191 

Insight 188 

Insomnia S139 

Insulin S78 

Insulin resistance S78 

Interethnic differences S131 

Iron deficiency S74 

Isolated thrombocytopenia S190 

Ketamine S49, S69 

Lack of self confidence S111 

Lactation S48, S71, S71 

Lamotrigine S142 

Lateral ventricle S61 

Learning S112 

Leukopenia S127 

Lipid peroxidation S140 

Lithium S169 

Lithium carbonate S161 

Locomotor activity S141 

Long QTc S119 

Losartan S132 

Lung functions 141 

Magnetic resonance imaging S61 

Maintenance S176 

Maintenance phase S100 


Subject Index 

Major depressive disorder S115 

Male patient S195 

Malondialdehyde S169 

Management S95 

Mania S157, S194 

Manic episode S124 

Marital conflict S144, S184 

Mechanism of action S63 

Medical care S156 

Medical decision support systems S157 

Medical diseases S67 

Medical marijuana S37 

Medication S40, S43 

Mega cisterna magna S195 

Melatonin S75 

Mental diseases S200 

Mental disorder S144, S184 

Mental health S154 

Mental illness S196 

Mental symptom S123, S135 

Mentalizing S56 

Metabolic syndrome S180 

Metabolic S171 

Metabolic side effect S140 

Methadone S35, S114 

Methadone substitution therapy S137 

Methylphenidate S139, S190 

Metoprolol S119 

METU-SNP S102, S157 

MGLU receptors S70 

Middle-aged male S139 

Mindfulness S40, S105 

Mirtazapine S139, S175, S190, S196 

Mixed mania S98 

Modafinil S44 

Models S49 

Molecular diagnostics S102 

Mood S89, S91, S153 

Mood disorder S77, S79, S134, S149, S162 

Mood stabiliser S149 

MRI S62 

Music therapy S191 

Myeloperoxidase S46, S169 

NADPH-oxidase S46 

Neuroactive steroids S50, S51 

Neurocognitive functions S193 

Neurodegeneration S90, S91 

Neurodevelopment S49 

Neurodevelopmental disorders S75 

Neurogenesis S193 

Neuroimaging S36, S62, S148 

Neuroleptic malignant syndrome S125 

Neurological S201 

Neurological co-morbidity, treatment S97 

Neurological deficits S164 

Neuromodulation S117 

Neuropathic pain S59 

Neuroplasticity S90 

Neuroprotection S112 

Neuroprotective effect S90 

Neuroregeneration S91 

Neurotrophic factors S70 

Neutropenia S127 

Nicotine S112 

Nitric oxide S50 

NMDA S40, S70 

NMDA receptor S49, S69 

Non-seasonal affective disorder S89 

Normal pressure hydrocephalus S169 

Nutraceuticals S108, S153, S189 

Nymphomania S52 

Obesity S94 

Obsessive beliefs S137 

Obsessive compulsive behavior S126 

Obsessive compulsive disorder S71, S134, S176, S177 

Obsessive compulsive spectrum S182 

Obstructive sleep apnea S200 

Occupation S58 

OCD S59, S137, S172 

Olanzapine S171, S180, S190 

Olfaction S193 

Oman S145 

Omega fatty acids S75 

Omega-3 fatty acids S64 

Ontogenesis S171 

Opioid dependence S35 

Opioid withdrawal syndrome S114 

Orally disintegrating olanzapine S115 

Outpatient forensic psychiatric examination S181 

Oxford S202 

Oxidative stress S170, S189 

Oxytocin S76, S133, S118 

P value S104 

Pain S54, S55, S81, S82 

Pain reflex 141 

Pain threshold S178 

Paliperidone S165 

Panic disorder S78, S106, S122, S137, S189, S71

Panic symptoms S122 

Paroxetine S156 

Pathological gambling S53, S174 

Pattern S168 

Pentylenetetrazol (PTZ) S118 

Perinatal depression S64 

Persistent symptoms S86 

Personality S34 

Personality disorder S178 

Personalized medicine S102, S157, S198 

PET S62 

Petechia S190 

Pharmacogenetics S63, S101 

Pharmacogenomics S102, S157, S198 

Pharmacological treatment S93 

Pharmacology S93 

Pharmacotherapy S53, S93 

Phobias S178 

Physical activity S91 

Physical health monitoring S149 

Physical symptom S123, S135 

Pica S182 

Pilots S103 

Piracetam S146 

Placebo S38, S123, S135 

Polymorphism S63, S100, S108, S176 

Polypharmacy S164 

Post traumatic stress disorder S141 

Post-partum blues S163 

Post-traumatic stress disorder (PTSD) S123, S175 

Pregnancy S35, S48, S71, S190, S196 

Pregnant women S149 

Premenstrual dysphoric disorder S193 

Premenstrual syndrome S123, S135 

Priapism S167 

Progesterone S77 

Progressive muscle relaxation S132 

Psychiatric S202 

Psychiatric disorders S37, S48, S62, S74, S77 

Psychiatry S65, S74, S101, S109 

Psychopathology S125 

Psychopharmacotherapy S71 

Psychosis S83, S167, S178, S192 

Psychospiritual interventions S42 

Psychostimulants S44 

Psychosurgery S61 

Psychotherapy S53, S95, S105, S106, S151 

Psychotic disorder S80, S162 

Psychotropic drugs S48, S88, S90, S103 

Psychotropics S140 

PTSD S59, S106, S175 

Quality of life S132, S191 

Quantitative EEG S58 

Questionnaire S151 

Racine scale S118 

Radial-arm maze S112 

Rape S127 

Rapid antidepressant efficacy S69 

Rat S68 

Rat behaviour S36 

Rational drug use S102 

Rats S141 

Reaction time S113 

Reboxetine S130 

Reference memory S112 

Referral pathways S129 

Rehabilitation S86 

Relapse S149, S198 

Religious beliefs S155 

Renal transplantation S161 

Repetitive transcranial magnetic stimulation (rTMS) therapy S58 

Resistant depression S176 

Risk factors S137 

Risky behavior S153 

Risperidone S135 

RTMS S176 

Safety S190, S201 

Schizophrenia S49, S50, S59, S61, S63, S77, S80, S86, S126, 

S129, S134, S143, S157, S164, S171, S177, S180, S188, 

S191, S192, S195, S201 

Scientific basis S63 

SCL-90 S144 

Seasonal affective disorder S89 

Self-destructive acts S181 

Self-perception S138 

Serotonin S49, S63 

Serotonin syndrome S36 

Sertraline S179 

Serum drug levels S149 

Sexual dysfunction S80, S103 

Sexual trauma S167 

Side effect S63, S103, S127, S130, S161, S167, S200 

Sigma receptor S112 

Single Nucleotide Polymorphisms (SNPs) S102 

SLC6A2 S148 

Subject Index 

Sleep S43, S89 

Sleep deprivation S87, S89 

Smoking cessation S162 

SNP genotyping S157 

SNP prioritization S198 

SNRI S55 

Social anxiety S173, S174 

Social behaviour S76 

Social Phobia Scale S174 

Social Interaction Anxiety Scale S174 

Sodium valproate S164 

Somatic symptoms S139 

Somatization S56, S105 

Somatoform S105 

Soviet times S128 

SPECT S62 

Spinal Cord Injury 141 

SSRI S55, S103 

St. John’s Wort S65 

Stress S111 

Structural brain abnormalities S169 

Substance abuse S83, S130 

Substance P S51 

Substance use S125, S159 

Subtypes S189 

Sucrose preference S166 

Sudden cardiac death S119 

Suicide rate S145 

Switching S130 

Synaptic plasticity S91 

Tardive akathisia S144 

Tardive dyskinesia S165 

Tardive dystonia S201 

Tardive syndromes S144 

Temperament S54 

Ten year period S145 

Teratogenicity S190 

Terlipressin S141 

Testicular mutilation S134 

Testosterone S77 

Thalamic EEG S118 

The quran reciting S145 

Therapeutic relationship S41 

Therapy S109, S123 

Thinking S34 

Thrombocytopenia S130 

Thyroid hormones S77 

Tianeptine abuse S197 

Tianeptine dependence S197 

Tic disorders S200 

TMS S59 

Topiramate S182 

Tourette’s disorder S160 

Transcranial magnetic stimulation (TMS) S60, S117 

Transcultural psychiatry S37 

Transcultural psychiatry in USA S37 

Transgenic S68 

Translational medicine S157 

Trauma S56, S80, S123, S127 

Treatment S87, S89, S93, S96, S101, S105, S126, S151, S174, S176, S196 

Treatment outcome S41 

Treatment principles and pitfalls S41 

Treatment resistance S86 

Treatment resistant depression S85 

Turkish American cases S37 

Typical and atypical antipsychotics S110 

Typical antipsychotics S164 

UGT1A4 S131 

Unintended pregnancy S163 

Units S202 

Urinary incontinence 

Vaginismus S178 

Vagus nerve stimulation S60 

Valproic acid S126 

Valsartan S198 

Varenicline S162 

VCAM-1 S143 

Venlafaxine S127, S175 

Ventricular arrhythmias S119 

Vigilance-promoting agents S44 

Visual and auditory tasks S113 

Vitamin D S72, S116 

Volumetry S193 

Vorbeireden S159 

Weight loss S139 

Well-being S34 

Wellness S34 

Wender-Utah rating scale S163 

Z hypnotics S202 

Zinc deficiency S116 

Zinc supplementation S73 

Ziprasidone S119 

Zuclopenthixol S167 

Zuclopenthixol acetate S125 

γ –hydroxybutyrate S44

Abalı O. S97 

Abnavi M. A. S155 

Abolghasemi S. S111 

Abtahi M. M. S111 

Adler L. A. S135 

Adzlin U. B. S42 

Aghamohammadi A. S122, S134, S163 

Ahl J. S115 

Ak İ. S200 

Ak M. S54, S127, S171, S174 

Akarsu S. S171, S175 

Akbıyık M. S193 

Akça Ö. F. S72 

Akdeniz F. S142 

Akkaya C. S81 

Aksoy A. S150, S151 

Aksoy R. S173 

Aksoy Ş. G. S158 

Aksoy U. M. S158 

Alaçam H. S179 

Alev L. S114, S115, S135 

Algül A. S59, S167, S175, S199 

Allahtavakoli M. S112 

Alnıak İ. S152 

Alonso M. E. S131, S185, S187 

Alowesie R. M. S136 

Alpkan L. R. S141 

Altaiar H. A. S202 

Altın M. S114, S115, S135 

Altındağ A. S55 

Altınok Ü. S141 

Altuğ A. S149 

Altunkaynak Y. S144 

Amani F. S168 

Anderson I. S38 

Annagür B. B. S94 

Ansari A. S145 

Antón J. M. S186 

Arıcan H. A. S149 

Arıcıoğlu F. S70, S166, S169 

Arun K. S47 

Ashna S. M. S117 

Askari K. S111 

Aslan S. S85 

Asvadi I. T. S132 

Atagün M. İ. S141 

Atagün Z. S141 

Ateş M. A. S167, S175, S181, S199 

Atila Erol S194 

Atmaca M. S121 

Ay M. E. S108 

Ay Ö. İ. S108 

Aydemir M. Ç. S101, S138 

Aydemir Ö. S90 

Aydın A. S87, S130, S146, S171, S178, S179 

Aydın E. S121, S136, S172 

Aydın E. F. S201 

Aydın M. D. S60 

Aydın S. S58 

Aydınoglu U. S125, S143, S147, S190 

Ayhan Bilgiç S73 

Ayhan M. G. S135 

Aziz S. A. S137 

Baharudin A. S137 

Bahçeci B. S65, S126 

Bakar A. K. B. A. S42 

Baker G. B. S35, S50, S68 

Bakım B. S59 

Balaban Ö. D. S141 

Balıbey H. S91, S123, S162 

Balikci A. S123 

Baran B. S176 

Barlak S. S181 

Başabak A. S150, S151 

Başoğlu C. S175, S181, S199 

Başoğlu E. S191 

Bayar N. S162 

Baykaran M. B. S140, S177 

Bayrak A. S192 

Bayrak M. S177 

Author Index 

Beatson S. S128 

Beltrán L. S131 

Benson S. S152 

Beşiroğlu L. S188 

Bez Y. S98, S170 

Bigdeli O. S113, S183 

Bilge D. S192 

Bilgin A. A. S160 

Bilici M. S142, S191, S192 

Boardman B. K. S135 

Bolu A. S171, S175 

Bora S. S109, S117, S133 

Bostancı E. D. S168 

Bozkurt A. S127, S174 

Brueckl T. S44 

Budaklı A. A. S167 

Buturak Ş. V. S60 

Büyükkınacı A. S198 

Büyükşahin F. S162 

Can D. Ö. S198 

Canan F. S125, S143, S147 

Cascorbi I. S45 

Cengiz F. F. S138, S166 

Cerit C. S198 

Cetin M. S78, S175, S199 

Ceylan M. E. S133, S134, S171, S178 

Chichinadze K. S140 

Cho S. S148 

Choi J. S. S139 

Cloninger C. R. S34 

Cumhur Tulay S191 

Cumurcu B. E. S158 

Çalışkan M. S198 

Çam B. S160, S196 

Çelenk S. S163 

Çelik C. S175 

Çelik H. S170 

Çelik S. S173 

Çetin T. S173 

Çetingüç M. S102 

Çiftçi A. S201 

Çim E. F. A. S179 

Çoban A. A. S153 

Dalkilic A. S37, S93 

Deldar A. S135 

Demir A. S125, S142, S192 

Demir S. S158 

Demirel B. S163 

Demirgoren S. S133 

Deveci E. S77 

Dilbaz N. S124 

Diler R. S. S36, S57 

Direskeneli G. S. S176 

Doğan S. S52 

Doksat K. M. S56 

Domac F. M. S125 

Domianidze T. S140 

Dorado P. S131, S185, S186, S187 

Döke M. A. S156 

Döm H. A. S156 

Duran S. S138 

Durell T. M. S135 

Durmaz O. S175 

Dursun S. S50, S68 

Durukan İ. S66 

Ebrinç S. S71, S175, S181, S199 

Efe M. S108 

Eker E. S51 

Elbi H. S67 

Elboğa G. S55 

Enli Y. S179 

Erbas O. S109, S117, S118, S133 

Erdal M. E. S108 

Erdem M. S80, S174 

Eren İ. S99, S162 

Ermis A. S133 

Erol A. S92, S129, S156, S180, S182, S194, S195, S197 

Ersoy M. A. S85 

Ertekin B. A. S176 

Ertekin E. S176

Etli T. S162 

Evren C. S80, S154, S173 

Evren M. B. S162 

Evren V. S117 

Farjad S. S112 

Felati N. M. A. S145 

Girit O. C. S133, S134 

Glaser P. E. S135 

Golchin M. T. S132 

Göka Erol S138 

Gönen M. S157 

Guerrero J. S187 

Gulec M. S130 

Guveli H. S126 

Güçlü O. S121, S136, S172, S177 

Güçlü O. G. S144 

Gül I. G. S158 

Güleç H. S55 

Güleç M. S78, S89, S179, S190, S201 

Güler J. S161, S162, S168, S195 

Gümrü S. S169 

Günay H. S68 

Güner S. S106 

Gürol D. T. S154 

Gürvit H. S176 

Güven M. S83 

Habil M. H. S42 

Hamdikene M. S115 

Hariri A. G. S142, S185, S195 

Hasankhani H. S144, S184 

Hashemian F. S113, S183 

Hashmi S. S. A. S145 

Hegazy R. R. S141 

Hergüner A. S139 

Hergüner S. S139 

Herizchi S. E. S132 

Herken H. S108, S170, S179 

Hıdıroğlu H. S200 

Hızlı G. S58 

Hisim O. S133 

Hnidek . S48 

Hobbs D. S114 

Hocaoglu C. S64, S126 

Hofmann S. S40 

Horacek Jiri S49 

Hosseini S. M. S183 

Höschl C. S48, S49 

Hudson A. L. S35 

Hughes M. S108, S189 

Ibrahim N. S137 

Ismail I. E. S141 

İnanlı İ. S162 

İpekçioğlu D. S134 

İskender B. S187 

İşmen M. S150 

Jaafar N. R. N. S137 

Jan F. S148 

Jarrott B. S112 

Javadpour A. S155 

Johnston P. S108, S189 

Jung H. Y. S139 

Kabak S. G. S177, S193 

Kadıoğlu O. S197 

Kalem Ş. A. S176 

Kalkancı Ö. S179 

Kaptanoğlu B. S179 

Kara T. S152, S201 

Karadağ F. S62, S154, S179 

Karadayı G. S149, S151 

Karadere M. E. S163 

Karagianis J. S114 

Karahan A. S187 

Karalar B. S150 

Karaman U. S149 

Karaman Z. S149 

Karamustafalıoğlu O. S193 

Karataş K. S. S159, S168, S195 

Karayılan S. S129, S194 

Karimi S. S144, S184 

Karlıdağ R. S158 

Author Index 

Kartalcı Ş. S158 

Kavzoğlu S. Ö. S142 

Kaya M. C. S66, S170 

Kaya N. S127, S135, S149 

Kaya Z. E. S124 

Kazantzis N. S41 

Kazemi M. S144, S184 

Kazemi S. S144, S184 

Kechrid Z. S115 

Kenar J. S159 

Kenawy S. A. S141 

Kennedy V. S148 

Kesebir S. S140, S142 

Khananashvili M. S140 

Kheirabadi G. R. S116 

Kılıç S. S104 

Kılınç E. S134 

Kırlı S. S39, S81 

Kim B. S148 

Kim J. S148 

Kim M. H. S124 

Kirsch I. S38 

Koca E. K. S125 

Koç C. S150, S151 

Konkan R. S121, S136, S144, S172, S177 

Korkmaz S. S121 

Kuloglu M. S121 

Kumsar N. A. S156, S180, S182 

Kurt H. S196 

Kuru T. S163 

Kültür S. E. Ç. S73 

Labadze I. S140 

Lalies M. S35 

Lazarashvili A. S140 

Lee H. W. S139 

Lee J. Y. S139 

Lledó E. P. S131, S185, S186, S187 

Llerena A. S45, S131, S185, S186, S187 

López M. S131, S187, S185 

Machín E. S131 

Mackay M. S50 

Maden O. S127 

Mahmodi G. S111, S155 

Majd M. S113, S183 

Maner F. S53, S133, S134, S158, S178 

Maracy M. R. S116 

Martin P. R. S35 

Matitaishvili T. S140 

Mazlum B. S74 

Mcgough J. J. S135 

Melledo J. M. S50 

Meral G. S199 

Meyers A. S115 

Min S. S124 

Mislan N. S137 

Mitchell N. D. S50, S69 

Mohamadzadeh S. S154, S155 

Mohr P. S48 

Mokri A. S113 

Molavi H. S111 

Monroy N. S131 

Moshtaghian J. S111 

Mutlu E. S171, S173, S178 

Nachnani M. S128 

Nasiripour A. A. S155 

Neale C. S108, S152, S189 

Nebioğlu M. S198 

Negahban T. S145 

Nuray Atasoy S76 

Oakes T. M. M. S115 

Oral E. S88, S201 

Ortega A. S131 

Ozşahin A. A. S125, S127 

Ögel K. S105, S149, S150, S151, S153, S154 

Öneş K. S141 

Öyekçin D. G. S182 

Özata B. S176 

Özbek K. S114, S115 

Özçelik N. B. V. S61 

Özçetin A. S103 


Özdemir B. S175 

Özdemir F. A. S190 

Özdemir O. S188 

Özdemir P. G. S146, S179 

Özdemir S. S190 

Özen N. E. S68 

Özer H. S197 

Özgen F. S171 

Özkol H. S188 

Özkorumak E. S64, S187, S200 

Özmen M. S90 

Özmenler K. N. S175 

Özşahin A. S171, S174 

Özten M. S194, S195 

Öztürk M. S57 

Öztürk N. S176 

Palenicek T. S49 

Panahi M. V. S. S183 

Paparrigopoulos T. S42, S43 

Papavasiliou A. S44 

Park K. C. S124 

Parlak S. Ç. S192 

Peker G. O. S117, S133 

Perdeci Z. S162 

Perreault A. S35 

Pieri M. C. S109 

Pigott T. A. S135 

Piri I. T. S132 

Prakash A. S115 

Ranjkesh M. S116 

Rashid R. A. S42 

Raskin J. S114 

Rubin R. L. S135 

Sabri A. A. A. S145 

Sabri Hergüner S74 

Saglam S. S121 

Sahmelikoglu O. S133 

Salehi M. S116 

Sanaat Z. T. S132 

Sarıdoğan G. E. S198 

Sarıkaya Ö. Ö. S182 

Sarkis E. S. S135 

Sarp K. S126 

Sarp N. S153 

Savaş H. A. S170 

Saygılı İ. S164, S165, S185 

Sayyadi A. R. S145 

Scholey A. S108, S152, S189 

Seifertova D. S48 

Selek S. S170 

Selvi Y. S88, S146, S188, S190 

Semerci B. S96 

Semiz Ü. B. S164, S165, S191, S192 

Sezlev D. S171 

Shabanloui R. T. S132 

Shafaie J. S112 

Shaker A. S168 

Sharaf O. A. S141 

Sharifi A. S113, S183 

Sheehan D. S115 

Shin J. S124 

Shin M. S148 

Shohrati M. S113 

Sidi H. S137 

Silsüpür G. S198 

Sinani G. S125, S143, S147 

Sinici E. S127 

Soldatos C. R. S43 

Son Y. A. S101, S156, S197 

Sonmez E. O. S127 

Sook A. J. S124 

Soyer B. S159, S168 

Spaniel F. S49 

Stough C. S152 

Sundar A. S. S46 

Sungur M. Z. S41, S121, S136, S172, S177 

Sünbül E. A. S138, S166 

Author Index 

Sünbül M. S138 

Şahan E. S198 

Şehirli Ö. S169 

Şengül C. B. S100, S108, S179 

Şenormancı G. S144 

Şenormancı Ö. S53, S121, S136, S144, S172 

Şimşek G. S192 

Şimşek Y. S198 

Tabatabayi M. S. S113 

Taner E. S63 

Taner H. A. S160 

Taner Y. S160 

Tarhan N. S58 

Tellioglu T. S37 

Terán E. S131 

Tezcan A. E. S140 

Thirunavukarasu M. S46, S47 

Tıkır Baise S138 

Tiryaki A. S187, S200 

Toğul H. S160 

Topçuoğlu Ö. B. S168 

Toprak B. S140 

Torres E. L. S186 

Tosun M. S84 

Trejo H. S185, S187 

Treuer T. S114 

Tuncel Y. Y. S156 

Turan T. S76 

Tükel R. S176 

Tülüce Y. S188 

Türkbay T. S95 

Türker T. S162 

Uğur M. S75 

Uguz F. S70, S135, S146 

Uhr M. S44 

Ulusoy S. S152 

Utkan T. S166, S169 

Utkan T. S169 

Uz Y. S125 

Uzun Ö. S171 

Ülkü M. S173 

Ünal A. S97, S161, S162 

Ünay D. S62 

Ünübol B. S161, S162 

Ünübol H. S161, S162 

Üstünkar G. S156, S197 

Valesova V. B. S49 

Valzdorf E. S128, S129, S181 

Williams D. W. S135 

Würz A. S104 

Yaci H. S125 

Yanartaş Ö. S164, S165, S185 

Yang Y. S148 

Yanık T. S171 

Yarcı E. S169 

Yavuz K. F. S152, S163 

Yazır Y. S169 

Yeloglu Ç. H. S126 

Yenel A. S191, S192 

Yeroham R. S150 

Yeşil B. S158 

Yılbaş B. S157 

Yıldız M. S86 

Yılmaz O. S199 

Yılmaz Y. S164, S165, S185, S192 

Yiğiter S. S173 

Yousefi F. S154 

Yucel A. S130 

Yuksel R. N. S124 

Yüce M. S96 

Yücel B. S94 

Yükselir C. S174 

Zafari M. S111, S122, S134, S155, S163 

Zakaria H. B. S42 

Zaki H. F. S141 

Zepeda N. S35 

Zincir S. B. S79, S165, S177, S191, S192

SYMPOSIA

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