BASAL GANGLIA AND MOVEMENT-DISORDERS - AN UPDATE

A model of basal ganglia functioning proposed a few years ago suggests that increased and decreased activity in basal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyski netic movements as seen in Huntington's disease or after treatment wit h L-dopa and neuroleptics, respectively. Although the basic features o f this model have stood the test of time, patterns of electrophysiolog ical activity and changes in indices of GABA-dependent transmission in the external pallidum lead to a reconsideration of the mechanisms res ponsible for these changes in output activity.