Most forms of dyskinesia categorized as extrapyramidal are associated with widespread neuropathological changes. In these disorders the basal ganglia suffer severe pathological alterations, but specific brain stem nuclei frequently are affected also. Although neuropathological studies have indicated that lesions involving the basal ganglia are probably responsible for most forms of human dyskinesia, attempts to produce similar dyskinesia in animals by creating lesions in these structures have been notoriously unsuccessful.65,73,113 Recent neurosurgical experiences further indicate that most patients with dyskinesia are benefited symptomatically by lesions involving particular portions of the basal ganglia.35,37,41,42,72,81 Rarely do lesions in these structures exaggerate prior disturbances. While these clinical findings are not adequately supported by anatomical evidence, they appear to confirm earlier experimental studies.
Experimentally, almost all lesions consistently provoking dyskinesia in animals have involved brain stem nuclei, the cerebellum, or pathways originating from the cerebellum. These experiences, together with the numerous unsuccessful efforts
MALCOM B. CARPENTER. Brain Stem and Infratentorial Neuraxis in Experimental Dyskinesia. Arch Neurol. 1961;5(5):504–524. doi:10.1001/archneur.1961.00450170042006