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Pallidoluysian atrophy

Dystonia and basal ganglia functional anatomy

Departments of Neurology (Dr. Wooten) and Pathology (Division of Neuropathology) (Drs. Lopes and Vandenberg), University of Virginia Health Sciences Center, Charlottesville and Newport News (Drs. Harris and Reagan), VA.

The clinical correlates of "pure" pallidoluysian atrophy are not well described. A 59-year-old man presented with 20 years of progressive generalized dystonia, dysarthria, gait disorder, supranuclear vertical gaze palsy, and bradykinesia. At autopsy there was severe bilateral atrophy of the external pallidum and subthalamic nucleus with neuronal loss and marked gliosis. This syndrome may epitomize the consequences of "pure" pallidoluysian atrophy. In this case, dystonia appears to occur in the setting of decreased excitation (increased inhibition) of medial pallidal neurons, a pathophysiologic condition common to several hyperkinetic states.

Address correspondence and reprint requests to Dr. G.F. Wooten, Department of Neurology, Box 394, University of Virginia Health Sciences Center, Charlottesville, VA 22908.

Received October 21, 1992. Accepted for publication in final form January 14, 1993.

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