TOURETTE SYNDROME AND RELATED TIC DISORDERS

Each movement is preceded by certain preliminary sensory signals and is in turn followed by sensory impressions at the end of the action. Each movement is the result of a voluntary capitulation to a demanding and relentless urge accompanied by an extraordinarily subtle sensation that provokes and fuels the urge. Successively sharper movements build up to a cli-max—a climax that never comes (1). A MODEL NEUROPSYCHIATRIC DISORDER Biological models allow investigators to extrapolate from simple to complex systems, to generate and test hypotheses, and to grasp schema that are within range of our intellect, as we reach to conceptualize things beyond this range. Tourette syndrome (TS) is a ‘‘model neuropsychiatric disor-der’ ’ (2,3) that seems tantalizing in its simplicity. The ge-netic basis is stronger than any common neuropsychiatric disorder other than Huntington disease. The age of onset and the sex distribution of TS are strong clues that neurode-velopmental and hormonal processes are causative in TS. Emerging evidence suggests a role of epigenetic (e.g., hy-poxia) or ‘‘environmental’ ’ (e.g., group A streptococcal in-fections) factors in the origin of at least some cases of TS, again making TS an ideal model for ‘‘nature-nurture’ ’ inter-actions in the pathogenesis of brain disorders. The clinical presentation and responsivity to dopamine antagonists pro-vide strong clues that the critical substrates of TS fall within the basal ganglia, a system implicated in an increasing num-ber of neuropsychiatric disorders and perhaps the one most studied and best understood in the neuropsychiatric litera-ture. The familial and phenomenologic links to obsessive-compulsive disorder (OCD) have led many investigator