Biochemical factors

Although a variety of biological aetiologies have been proposed in OCD since 1860, (33) modern neurobiological theories began with the clinical studies showing that clomipramine and other serotonin reuptake inhibitors (SRIs) had a unique efficacy in treating the disorder. This inspired a 'serotoninergic hypothesis' of OCD (see ChaptĀ§L4.8). In children, the involvement of the serotonin system in the pathophysiology of OCD is supported by one study in which improvement of obsessive-compulsive symptoms during clomipramine treatment was closely correlated with pretreatment platelet serotonin concentration, (34) and reports of decreased density of the platelet serotonin transporter in children and adolescents with OCD but not in those with Tourette's disorder. (35) However, the delayed and incomplete action of serotonergic drugs, suggesting multiple effects on other neurotransmitters as well, and numerous biochemical studies of OCD patients and controls have not yet indicated a single biochemical abnormality as a primary aetiological mechanism in OCD.

In Tourette's disorder, multiple neurochemical systems have been implicated by pharmacological and metabolic studies, but dopaminergic involvement is a prime candidate, especially in view of the dramatic improvement of tics with dopamine receptor antagonists. Furthermore, the frontal-subcortical circuits seem to represent the anatomic region implicated in the disorder, and dopamine plays an important role in the neurotransmission of those areas. (36)

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