In summary, the scheme of basal ganglia function presented here, in conjunction with known features of anatomical organization and dopamine neurotransmission provides a hypothesis for the pathophysiology of tics. According to the hypothesis, clusters of striatal neurons (matrisomes) become abnormally active in inappropriate contexts leading to inhibition of GPi or SNpr neurons that would normally be active to supress unwanted movements. The inhibition of htese GPi or SNpr neurons would then disinhibit thalamocortical circuits. Leading to the production of tics. Activity-dependent dopamine effects would inappropriately reinforce these activity patterns leading to stereotyped repetion. Over time, exactly which striatal neuronal clusters are overactive may change under various influences so that the produced movement change over time. This hypothesis is testable directly but requires a valid animal model of tics or higher resolution functional imaging techniques. Continuing work on basic basal ganglia physiology, pathophysiology, and functional imaging in TS is advancing our knowledge of neural circuit abnormalities in TS, but much more work is still needed.