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ABSTRACTS - World Psychiatric Association

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cologic treatment options are now available to treat BED. These<br />

agents include selective serotonin reuptake inhibitors, the anti-obesity<br />

agent sibutramine, and the anticonvulsant topiramate. This paper<br />

reviews the current clinical evidence for these and other medications<br />

in the treatment of BED.<br />

TL5.<br />

ENVIRONMENTAL CAUSES OF MENTAL DISORDER<br />

M. Rutter<br />

Institute of Psychiatry, London, UK<br />

Half a century ago, there was a general acceptance of the view that<br />

environmental causes of mental disorder were strong and determinative.<br />

That view has been seriously challenged and it has become clear<br />

that the strong and deterministic notion of environmental causation<br />

was extremely misleading. Nevertheless, powerful research strategies<br />

have demonstrated the reality and importance of environmental causation.<br />

This paper reviews the challenges and how they have been<br />

met; summarises the ways in which the early views have had to be<br />

modified; and indicates the current state of the art and the challenges<br />

that remain. Six issues constitute the main focus: a) the identification<br />

of key elements of risk, together with the appreciation that the casual<br />

effects may be prenatal as well as postnatal, and include both physical<br />

and psychosocial hazards; b) the recognition that with multifactorial<br />

disorders there cannot be any single “basic” cause; rather the<br />

need is to identify key individual causal components and the direct<br />

and indirect pathways involved in the causal process; c) the reality of<br />

reverse causation, as exemplified by child effects on parenting; d) the<br />

need to consider possible genetic mediation of risks associated with<br />

specific environments; e) the role of “natural experiments” in testing<br />

causal inferences; f) the heterogeneity of response to environmental<br />

risk, the reality of resilience and the importance of the effects of environments<br />

on biology and the need to consider how “environments get<br />

under the skin”.<br />

TL6.<br />

THE CAUSES OF SCHIZOPHRENIA: THE STRIATUM<br />

AND THE STREET<br />

R.M. Murray<br />

Institute of Psychiatry, London, UK<br />

Much evidence suggests that the final common pathway to at least the<br />

positive symptoms of schizophrenia is dopamine dysregulation in the<br />

striatum. It is clear that an individual can develop this dysregulation<br />

consequent upon a number of different aetiological factors. Firstly, we<br />

have known for many years that inheritance contributes, and the evidence<br />

from the plethora of molecular studies over the last 6 years suggests<br />

that in most cases this operates through the interaction of a number<br />

of genes of small effect. However, in a small proportion of cases, a<br />

copy number variation may play a major role possibly through impairing<br />

neurodevelopment. Certainly, some pre-schizophrenic children<br />

have cognitive and neuromotor impairments, and at first presentation,<br />

many individuals with schizophrenia have obvious brain structural<br />

and neuropsychological abnormalities. Furthermore, the risk-increasing<br />

effect of obstetric complications has been demonstrated for schizophrenia,<br />

and these are known to be associated with both structural<br />

brain and cognitive abnormalities and with dopamine dysregulation.<br />

Thus, a second aetiological pathway implicates deviant neurodevelopment.<br />

The excessive use of stimulant drugs and cannabis also<br />

increases risk of schizophrenia, and once again this appears to be via<br />

their effect on striatal dopamine. Finally, there is increasing evidence<br />

implicating exposure to a number of social factors, including migration,<br />

urbanisation, and possibly childhood maltreatment. Of course,<br />

in many patients, more than one of these risk pathways is involved,<br />

and a combination of genetic, developmental and social factors project<br />

the individual over the threshold into illness.<br />

TL7.<br />

LONG-TERM MANAGEMENT OF DEPRESSION:<br />

THE ROLE OF PHARMACOTHERAPY<br />

AND PSYCHOTHERAPIES<br />

M.E. Thase<br />

University of Pennsylvania School of Medicine and Philadelphia<br />

Veterans Affairs Medical Center, Philadelphia, PA, USA<br />

This paper deals with the treatment of recurrent major depressive disorder,<br />

focusing on strategies for prevention. There is broad consensus<br />

in practice guidelines that virtually all patients who respond to antidepressant<br />

medications should receive a 6 to 9 month course of continuation<br />

phase therapy to reduce the risk of relapse and that patients<br />

who have experienced three or more lifetime depressive episodes<br />

should receive a longer course of maintenance phase therapy to prevent<br />

recurrent illness. For those who do not obtain a full remission<br />

during acute phase therapy, there is increasing evidence that simply<br />

continuing the incompletely effective strategy is not sufficient to offset<br />

the risk of relapse. With respect to maintenance phase therapy,<br />

there are surprisingly few studies of truly long-term courses of pharmacotherapy<br />

(i.e., across 2 or more years). It does appear that all<br />

medications with established short-term efficacy are also significantly<br />

more effective than placebo for prevention of relapse or recurrence.<br />

There is also evidence that various forms of cognitive behavior therapy<br />

(CBT) have some degree of enduring prophylactic efficacy and<br />

may reduce the risk of recurrent illness following withdrawal of antidepressant<br />

medications. Although studies of interpersonal psychotherapy<br />

(IPT) have yielded mixed results, the value for ongoing<br />

monthly sessions of IPT – in lieu of pharmacotherapy – has been<br />

shown in studies of adults under the age of 70, particularly when therapeutic<br />

focus is maintained on key areas of interpersonal vulnerability.<br />

Areas of controversy are also discussed, including questions pertaining<br />

to tachyphylaxis and whether or not the benefit-risk profile of<br />

longer-term antidepressant therapy has been exaggerated.<br />

TL8.<br />

WHAT IS A MOOD STABILIZER<br />

P.E. Keck, Jr.<br />

Lindner Center of HOPE and University of Cincinnati College<br />

of Medicine, Cincinnati, OH, USA<br />

The term “mood stabilizer” first entered the scientific lexicon in 1960,<br />

and did not refer to lithium, but rather to an obscure first generation<br />

antipsychotic agent then in development. This may have been prescient,<br />

however, as pharmacologic agents from different classes and<br />

different therapeutic designations have increasingly come to be<br />

described as mood stabilizers. Mood stabilizers have, in turn, been<br />

conceptualized as treatments for bipolar disorder, although the<br />

course of major depressive disorder for many patients suggests that<br />

this latter illness could benefit from mood stabilizing concepts as<br />

well. This paper considers the question of what a mood stabilizer is in<br />

the context of definitions formulated by investigators in the field of<br />

bipolar disorder, and in the light of evidence from randomized, con-<br />

2 <strong>World</strong> Psychiatry 8:S1 - February 2009

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