ABSTRACTS - World Psychiatric Association
ABSTRACTS - World Psychiatric Association
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