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Movement disturbances, including tics, dystonia, and dyskinesias, are often overlooked yet disabling consequences of chronic cocaine abuse. The persistence of these motor control deficits implies that prolonged cocaine exposure has lasting effects on the nigrostriatal dopamine system, though this hypothesis has not been explicitly tested in humans. Accordingly, the overarching goal of this proposal is to translate basic science findings to human addicts through functional neuroimaging in order to characterize sensorimotor network changes which may underscore cocaine-related motor disturbances. This functional MRI investigation will examine the behavioral and neurofunctional changes that occur in chronic cocaine users relative to controls performing a visually-cued motor task (Aim #1) and a memory-cued motor task (Aim #2). Through these aims I seek to translate previous basic science research to a human model of sensorimotor disturbance in chronic cocaine addicts. As the average young user in the cocaine boom of the 1980s reaches the middle age, during which may movement disorders first become clinically detectable, the neurobiologic basis for movement dysfunction in these patients may be of increasing public priority.