Platelet Monoamine Oxidase Activity and Aggressive Obsessions

Maria Mercedes Perez-Rodriguez, Manuelo Arrojo, Jeronimo Saiz-Ruiz, Enrique Baca-Garcia
European Psychiatric Review, 2008;1(1):22-23
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Obsessive–compulsive disorder (OCD) is characterised by the repeated eruption in the mind of unwanted ideas, images or impulses described by the term ‘obsessions’. These obsessions are accompanied by a feeling of urgency or catastrophe, leading to repetitive, ritualistic behaviours known as ‘compulsions’.1,2 Compulsions are frequently intended to neutralise the anxiety caused by the obsessions.2 The lifetime prevalence of OCD has been consistently estimated at between 2 and 3.5% across different studies.3–5

The most frequent types of compulsion include checking (63%), washing (50%), counting (36%), the need to ask or confess (31%), symmetry and precision (28%) and hoarding (18%). The most frequently reported types of obsession are contamination (45%), pathological doubt (42%), somatic (36%), need for symmetry (31%), aggressive (28%), sexual (26%) and other (13%).1 Most studies using factor-analytic techniques on generally recognised OCD scales, such as the Yale-Brown Obsessive–Compulsive Scale (Y-BOCS),6 report three to five major symptom clusters, including symptom dimensions such as contamination, checking, pure obsessions and hoarding.7 Several of these studies include aggressive obsessions as one of the main symptom dimensions that may constitute a distinct clinical phenotype in OCD.7

The aim of this article is to review the available evidence on the association between aggressive obsessions and platelet monoamine oxidase (MAO) activity, and to integrate this evidence with the data supporting the serotonergic hypothesis of OCD.

Genetic Studies of Serotonergic Genes in Obsessive–Compulsive Disorder

Functional neuro-imaging has implicated the fronto-subcortical brain circuits – including the basal ganglia, thalamic structures and frontal cortical areas – in the pathophysiology of OCD.8 Response to selective serotonin re-uptake inhibitors (SSRIs) supports the implication of the serotonergic system in OCD.9 The serotonergic hypothesis suggests that a decreased serotonergic input into the frontosubcortical circuits may be permissive for the obsessive and compulsive symptoms.8 Although twin and family studies suggest that genetics may play a role in the aetiology of OCD, the mode of inheritance is still unknown.10 Based on the existing pharmacological and neuro-imaging evidence, several genetic studies have explored serotonergic genes as candidate genes for OCD.10,11 Some authors have also attempted to link the OCD spectrum with polymorphisms in serotonergic genes.12

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