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Tourette

Mechanisms by which microglial abnormalities contribute to disease are likely to be shared across distinct etiologies and traditional diagnoses. For instance, abnormal synaptic pruning was observed both in animals inoculated with GAS (which may capture key elements of the pathophysiology of PANDAS) and in mice that develop excessive grooming after inactivation of the progranulin gene. In both cases, increased synaptic pruning cooccurs with microglia activation.

A review of clinical observations and literature reports leads to the hypothesis that, via a process analogous to Sydenham’s chorea, infections with group A β-hemolytic streptococci, among others, may trigger autoimmune responses that cause or exacerbate some cases of childhood-onset obsessive-compulsive disorder (OCD) or tic disorders (including Tourette’s syndrome).