Aetiology

The best argument for considering Tourette syndrome as being genetically transmitted is the high concordance in monozygotic twins (50-70 per cent) compared with dizygotic twins (10-20 per cent). A third of the relatives also have this syndrome, tics, obsessive-compulsive disorder, or attention-deficit hyperactivity disorder, but the uncertain phenotype makes it difficult to test clear genetic models of transmission, although a single major locus is more likely. Homozygosity at such a locus (dosage-effect model) is common in families with this syndrome as a result of assortative mating and is related to the severity of symptoms.(24) Susceptibility genes have not been identified.

The efficacy of neuroleptic treatment has led to the hypothesis that dysfunctional dopaminergic circuits may be implicated, but postmortem studies have not shown consistent abnormalities in D/D2 receptors and in vivo receptor-binding studies have been conflicting. PET studies have suggested decreased metabolism and blood flow in basal ganglia-thalamocortical projection systems, but it is unclear whether these findings are related to the syndrome or merely to tic suppression required for imaging/25) Structural imaging has not demonstrated consistent abnormalities.

The occurrence of tics, obsessive-compulsive disorder, and hyperactivity in children with paediatric autoimmune neuropsychiatric syndromes following b-haemolytic streptococcal infection has opened the possibility that autoimmune mechanisms may be relevant.

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