The disturbed movements seen in disorders of the basal ganglia, such as Huntington's disease and parkinsonism, emphasize the importance of the basal ganglia for nonnal motor control. Understanding of the pathophysiÂ ology of these disorders has been limited because most proposed models of basal ganglia function fail to explain adequately how disturbances in the structure and function of neuronal populations and alterations in neuroÂ chemistry result in abnormal motor behavior. This lack of adequate models, in tum, is related to deficiencies in our understanding of the neuronal interactions that mediate normal movement. A useful model for basal ganglia function should describe the circuitry involved in normal movement and provide a rationale for the signs produced by pathologic processes. The model should be consistent with current knowledge of the anatomy, physiÂ ology, and neurochemistry of the basal ganglia. The model should account also for the responses of patients with basal ganglia disorders to various pharmacological and surgical manipUlations. The anatomy, pharmacology, and physiology of the basal ganglia have been reviewed extensively (Baldessarini & Tarsy 1980, Barbeau 1979, DenÂ ny-Brown 1962, Fallon & Moore 1978, Graybiel & Ragsdale 1979, HorÂ nykiewicz 1979, Iversen 1977, Jung & Hassler 1960, Oberg &
Annual Review of Neuroscience – Annual Reviews
Published: Mar 1, 1983
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