Recent laboratory experiments have produced increasing evidence that nigral-striatal dopamine deficiency causes an inhibitory hyperactivity in the medial globus pallidus (MGP), where it freezes the initiation of movement and thus causes bradykinesia, rigidity and tremor. Surgical lesions in the ventroposterolateral (VPL) pallidum in man not only improve the parkinsonian bradykinesia, but also the tremor, rigidity, and the L-dopa-induced dyskinesias disappear or diminish. The present study shows that VPL pallidotomy improves several psychomotor functions, such as walking speed and manual dexterity. Right-sided VPL thalamotomy also increases the speed and accuracy in verbal performance. Ventrolateral thalamotomy increases bradykinesia. The findings support the concept that the parkinsonian symptoms in man develop in the MGP. Intact pathways from MGP via thalamus to the premotor and motor cortex seem necessary for normal motor functioning. The author also discusses the mechanisms of pallidotomy and thalamotomy.