The author gives the historical background of the surgical therapy of the extrapyramidal diseases, from Horsley (1890) to Bucy and Buchanan (1931) and other neurosurgeons who adopted the attack on the "pyramidal" tract, and, afterwards, beginning with Meyers (1940), the operations at the level of the basal ganglia. The good results of pallidectomy and thalamectomy on the parkinsonian tremor and rigidity imposed a reformulation of concepts on the physiopathology of the extrapyramidal system. The author discusses the site of the lesion responsible for the parkinsonian symptomatology, accepting the view that the dyskinesia and the rigidity are caused by a lesion of the substantia nigra, in the same way as lesions of the subthalamic nucleus are responsible for the hemiballism. The author criticizes the classificai concept of the prevailing pallidal site of the lesion and the erroneous jacksonian interpretation of the phenomena. The experimental and surgical contributions to the study of the pathological physiology of the medial pallidum and the ventrolateral nuclei of the thalamus are emphasized. The parkinsonian tremor can be regarded as the result of hyperactivity of the pontomesencephalic reticular formation (Jenkner and Ward), owing to the loss of the inhibitory drive of the locus niger, associated to the sparing of the pallidothalamic facilitation. In the periphery the tremorogenic reticulospinal impulses follow the α route. The parkinsonian rigidity would depend on the same encephalic pathologic processes, but its peripheral physiopathogenesis is controversial. Some authors believe that it results from γ hyperactivity, associated to oversensibility of the inhibitory pathways of the motoneurons (HufSchmidt's 5 system). Other investigators, however, have brought to light experimental data pointing to the partial paralisys of the γ sytem, associated to hyperactivity of the α drive. Finally, the author refers to some theories which try to explain the basic mechanism of the physiopathologic process in the extrapyramidal diseases, especially in parkinsonism: abnormal discharges of degenerating neurons (Cooper), oversensibility of the deafferented nuclei (Jenkner and Ward), imbalance between damaged and preserved neural structures (Alberts et al.).