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Affective Spectrum Disorders Obsessive–Compulsive Disorder
Platelet Monoamine Oxidase Activity and Aggressive Obsessions
a report by
Maria Mercedes Perez-Rodriguez,
and Enrique Baca-Garcia
1. Department of Psychiatry, Ramon y Cajal University Hospital, Madrid; 2. University of Alcala, Madrid; 3. Department of Neurosciences,
Columbia University Medical Center, Department of Psychiatry, Fundacion Jimenez Diaz, Madrid, and Department of Psychiatry, Autonoma University of Madrid
Obsessive–compulsive disorder (OCD) is characterised by the repeated activity alleles compared with controls.
However, the results are still
eruption in the mind of unwanted ideas, images or impulses described by inconsistent, with other studies reporting negative results.
the term ‘obsessions’. These obsessions are accompanied by a feeling of
urgency or catastrophe, leading to repetitive, ritualistic behaviours known Biological Markers of Serotonergic Activity in
Compulsions are frequently intended to neutralise the Obsessive–Compulsive Disorder
anxiety caused by the obsessions.
The lifetime prevalence of OCD has been The results of studies analysing biological markers of serotonergic activity
consistently estimated at between 2 and 3.5% across different studies.
are also inconclusive.
Some authors cannot find any association
between cerebrospinal fluid (CSF) 5-hydroxyindolacetic acid (5HIAA)
The most frequent types of compulsion include checking (63%), washing concentration and OCD,
while others report higher levels of CSF 5HIAA
(50%), counting (36%), the need to ask or confess (31%), symmetry and in OCD patients compared with healthy volunteers.
precision (28%) and hoarding (18%). The most frequently reported types 3H-imipramine binding, while some authors find an association between
of obsession are contamination (45%), pathological doubt (42%), OCD and decreased 3H-imipramine binding sites
and an increase
somatic (36%), need for symmetry (31%), aggressive (28%), sexual towards normal levels after treatment,
negative results have also been
(26%) and other (13%).
Most studies using factor-analytic techniques reported.
Challenge studies with serotonergic agents have yielded
on generally recognised OCD scales, such as the Yale-Brown equally inconsistent results.
Obsessive–Compulsive Scale (Y-BOCS),
report three to five major
symptom clusters, including symptom dimensions such as contamination, Platelet Monoamine Oxidase in Obsessive–Compulsive
checking, pure obsessions and hoarding.
Several of these studies include Disorder and Other Psychiatric Disorders
aggressive obsessions as one of the main symptom dimensions that may Although both MAO-A and MAO-B catabolise the biogenic amines
constitute a distinct clinical phenotype in OCD.
noradrenaline, dopamine and serotonin, MAO-B has been more closely
connected to serotonin.
Platelets contain only the B form of MAO, and
The aim of this article is to review the available evidence on the may be used as a model for the study of central serotonergic
association between aggressive obsessions and platelet monoamine mechanisms. Moreover, platelet MAO-B activity has been shown to
oxidase (MAO) activity, and to integrate this evidence with the data correlate with cerebral MAO-B activity.
Low platelet MAO activity has
supporting the serotonergic hypothesis of OCD. been associated with psychiatric disorders such as schizophrenia,
cluster A and B personality
Genetic Studies of Serotonergic Genes in disorders
Alternatively, it has been hypothesised that the
Obsessive–Compulsive Disorder altered platelet MAO levels found in disorders such as schizophrenia may
Functional neuro-imaging has implicated the fronto-subcortical brain circuits in fact be caused by medications such as neuroleptics, with drug-free
– including the basal ganglia, thalamic structures and frontal cortical areas – patients having MAO levels similar to those seen in controls.
in the pathophysiology of OCD.
Response to selective serotonin re-uptake both alcohol use and tobacco use reportedly lower platelet MAO
inhibitors (SSRIs) supports the implication of the serotonergic system in activity,
which may confound the results of some investigations in
The serotonergic hypothesis suggests that a decreased serotonergic which alcohol and tobacco use is not adequately controlled.
input into the frontosubcortical circuits may be permissive for the obsessive
and compulsive symptoms.
Although twin and family studies suggest that In OCD patients, the findings regarding platelet MAO activity have been
genetics may play a role in the aetiology of OCD, the mode of inheritance is inconclusive so far. While Flament et al.
could not find any significant
Based on the existing pharmacological and neuro-imaging differences in platelet MAO activity between OCD patients and age- and sex-
evidence, several genetic studies have explored serotonergic genes as matched controls, Cath et al.
observed that platelet MAO activity was
candidate genes for OCD.
Some authors have also attempted to link the elevated in tic-free OCD subjects compared with patients with tics, patients
OCD spectrum with polymorphisms in serotonergic genes.
with Gilles de la Tourette syndrome without OCD and healthy controls.
However, these results should be considered in light of several limitations.
The gene coding for the enzyme MAO, a serotonergic candidate gene for The subjects in the study by Flament et al. were adolescents. In the study by
OCD, has been the subject of a handful of studies. Some of these studies Cath et al., some patients were treated with antipsychotic medications that
have suggested a sexually dimorphic association between OCD may have an effect on peripheral serotonergic markers, and OCD patients
and polymorphisms of the MAO-A gene.
High-activity alleles of with tics were significantly younger than controls. None of these studies
polymorphisms within the MAO-A gene
have been associated with explored associations between dimensions of OCD and platelet MAO activity.
OCD in males, while females with OCD have higher rates of the low- In a previous study,
we examined platelet MAO activity in 29 OCD
22 © TOUCH BRIEFINGS 2008
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