Habit learning in Tourette syndrome: a translational neuroscience approach to a developmental psychopathology.
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BACKGROUND: The etiology of Tourette syndrome (TS) involves disturbances in the structure and function of the basal ganglia. The basal ganglia mediate habit learning. OBJECTIVE: To study habit learning in persons with TS. DESIGN: Patients with TS were compared with normal controls in performance on a probabilistic classification, or habit-learning task (weather prediction). SETTING: University research institute. PARTICIPANTS: One hundred twenty-three children and adults, 56 with a diagnosis of TS and 67 healthy control subjects. MAIN OUTCOME MEASURES: Habit learning was assessed by the extent of improvement in accuracy of predictions and reaction times over trial blocks during performance of the weather prediction task. Declarative learning was assessed by performance on 3 tasks that required intact declarative memory functioning. RESULTS: Children with TS were impaired at habit learning relative to normal controls (P = .01). This finding was replicated in the independent sample of adults with TS (P = .01). The rate of learning correlated inversely with the severity of tic symptoms across both samples (r = -0.34; P = .01). Thus, impaired learning accompanied more severe symptoms. Measures of declarative memory functioning, in contrast, were normal in the TS groups. CONCLUSIONS: Striatal learning systems are uniquely dysfunctional in both children and adults with TS. The correlation of habit learning with symptom severity suggests that the number and severity of tics are a function of the degree to which the system for habit learning is dysfunctional. Thus, both the deficits in habit learning and the tic symptoms of TS are likely to be consequences of the previously reported anatomical and functional disturbances of the striatum in children and adults who have TS. The existence of a well-developed animal model for this learning system, which permits study of the neural and molecular bases of habit learning, has important implications for the neurobiological study of TS and for the development of new or improved therapeutics for this condition.
