Introduction In recent years, neurosurgeons have been empirically placing lesions in the globus pallidus and the ventrolateral nucleus of the thalamus (V.L.) in patients with parkinsonism, with resultant diminution of rigidity, hypokinesia, and tremor.10,13,18,42,44,52The role of these structures in the physiology of movement and its distortions is incompletely understood and requires further elucidation. The adventitious appearance of "extrapyramidal" symptoms with the administration of psychotropic drugs has also raised the question of how drugs like chlorpromazine can reproduce the symptom complex of parkinsonism.1,2,49,57 It has been demonstrated that stimulation of globus pallidus,20,54V.L.,3,17,54substantia nigra,3and the cerebral cortex13,16,57all effect an inhibition of the υ-efferent system or of the myotatic reflex. The administration of chlorpromazine also produces υ-inhibition.19,51This inhibition has been recorded by monitoring ventral-root υ-efferent impulses, muscle spindle discharges, or the myotatic reflex in the variously anesthetized and unanesthetized preparation.