Aetiology
OCD most probably results from a confluence of aetiologies. Genetic factors are important, as monozygotic twins are much more likely to exhibit OCD symptoms than dizygotic twins.[11] First-degree relatives of OCD patients have a higher risk of developing the disorder than the general population.[12] Evidence exists that the disorder is transmitted in an autosomal dominant fashion.[13][14][15][16] Candidate genes are related to the serotonin, dopamine, and glutamate neurotransmitter systems.[17] The OCD Collaborative Genetics Study aims to clarify the role that genetic factors play in the development of OCD.[18] A recent animal study has shown that deletion of genes for a glutamatergic postsynaptic scaffolding protein results in excessive grooming behaviour in mice.[19]
Learning theories explain that, by temporarily reducing anxiety, compulsions are self-reinforcing.[17] Cognitive theory suggests that obsessions represent catastrophic misinterpretations of a person's thoughts, images, and impulses.[20][21][22] Several faulty cognitions in OCD have been described that are related to the overestimation of threat, intolerance of uncertainty, importance of thoughts, control of thoughts, and perfectionism.[23] In addition, there is an association between pregnancy and the development of obsessive-compulsive symptoms. In one study of 59 female OCD patients, 39% of participants described an onset of OCD symptoms during pregnancy.[24] Rarely, striatal lesions or head trauma result in the development of OCD.[10]
Pathophysiology
The efficacy of serotonin reuptake inhibitors in the treatment of OCD illustrates that serotonergic dysfunction plays a role in the pathophysiology of OCD.[25] Low prolactin response to meta-chlorophenylpiperazine (m-CPP) serotonin stimulation has been implicated as a predictor of poor response to selective serotonin-reuptake inhibitors (SSRIs).[26] The dopamine and glutamate neurotransmitter systems have also been implicated.[17] Functional neuroimaging studies have shown a hypermetabolic brain circuit involving the orbital-frontal cortex, anterior cingulate, thalamus, and striatum.[17] Preliminary evidence suggests that activity of these areas is altered in both adults and children with OCD.[27] SSRIs or cognitive behavioural therapy have been shown to result in a normalisation of metabolic rate in this circuit.[28][29] In a subset of patients, OCD symptoms can be caused or exacerbated by an autoimmune reaction in which antibodies to beta-haemolytic streptococci cross-react with proteins in the basal ganglia; this phenomenon has been termed PANDAS (paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection).[30] Studies examining the compulsive hoarding subtype of OCD have indicated that this subtype may result from a different neurobiological mechanism, as patients with compulsive hoarding were found to have a lower (as opposed to higher) metabolic rate in the posterior cingulate gyrus and cuneus, and also had lower metabolic rates in the dorsal anterior cingulate gyrus.[31]
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