Tourette syndrome (TS) has long been thought to involve dopaminergic disturbances, given the effectiveness of antipsychotics in diminishing tics. Molecular-imaging studies have, by and large, confirmed that there are specific alterations in the dopaminergic system in TS. In parallel, multiple lines of evidence have implicated the motor cortico-basal ganglia-thalamo-cortical (CBGTC) loop in TS. Finally, several studies demonstrate that patients with TS exhibit exaggerated habit learning. This talk will present a computational theory of TS that ties together these multiple findings.

The computational theory builds on computational reinforcement-learning models, and more specifically on a recent model of the role of the direct and indirect basal-ganglia pathways in learning from positive and negative outcomes, respectively.

A model defined by a small set of equations that characterize the role of dopamine in modulating learning and excitability in the direct and indirect pathways explains, in an integrated way: (1) the role of dopamine in the development of tics; (2) the relation between dopaminergic disturbances, involvement of the motor CBGTC loop, and excessive habit learning in TS; (3) the mechanism of action of antipsychotics in TS; and (4) the psychological and neural mechanisms of action of habit-reversal training, the main behavioral therapy for TS.

A simple computational model, thoroughly grounded on computational theory and basic-science findings concerning dopamine and the basal ganglia, provides an integrated, rigorous mathematical explanation for a broad range of empirical findings in TS.

The author has not supplied his declaration of competing interest.