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Abstracts of the Invited Speakers [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 Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S42 [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 S42 Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org
Bulletin of Clinical Psychopharmacology, Vol: 21, Supplement: 2, 2011 - www.psikofarmakoloji.org Abstracts of the Invited Speakers 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 Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S42-3 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. Bulletin of Clinical Psychopharmacology 2011;21(Suppl. 2):S43 S43
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SYMPOSIA

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