Paradox of the Basal Ganglia Model: The Antidyskinetic Effect of Surgical Lesions in Movement Disorders

The revitalization of pallidotomy for Parkinson's disease (PD) provided a new opportunity to examine the effects of focal lesion of the basal ganglia and the adequacy of current pathophysiological concepts. The accumulated data, both from early surgical experiences as well as contemporary pallidotomy, established a dual, antiparkinsonian and antidyskinetic effect of a similarly placed lesion of the globus pallidum medialis (GPm). Modern studies have shown that pallidotomy induces significant improvement of movement parameters, restores thalamocortical activity, and eliminates Levodopa-induced dyskinesias without causing any major deficit of movement control. In patients with hemichorea-ballism or dystonia, pallidotomy also induce marked amelioration of the dyskinesias. These observations pose two major paradoxes for the pathophysiological model of the basal ganglia (BG) (1) Pallidotomy improves parkinsonism and eliminates dyskinesias and (2) pallidotomy does not produce overt motor or behavioral deficits. In this article, we review the data regarding the antidyskinetic effects of pallidotomy in PD and related movement disorders and discuss a possible solution to the first paradox of the classic basal ganglia model.