From recent observations on the production of Parkinson-like syndromes by various "tranquilizers" and ganglion blocking agents and from studies on the distribution of norepinephrine, serotonin, and dopamine in the brain and on the depletion of these substances by reserpine and chlorpromazine, the working hypothesis was formulated that a disorder of catecholamine metabolism may possibly be found in basal ganglia diseases. In order to test this hypothesis, urines of patients were assayed for pressor response with a modification of the rabbit aorta test of Helmer, Sjoerdsma''s qualitative determination of 5-HIAA, and Simola''s iodine reaction. The results on more than 40 cases (including examples of Parkinson s disease, Sydenham''s chorea, congenital chorea, Huntington a chorea, choreoathetosis, dystonia musculorum deformans, Wilson''s disease, and drug-induced parkinsonism) indicate that there is a statistically significant increase in the urine of most of these patients of a substance having pressor action on the rabbit aorta strip and turning purple or red when heated in the presence of iodine (Simola''s reaction). The pressor reaction obtained was always marked and sometimes was in the range expected from pheochromocytoma. At no time did Sjoerdsma s qualitative reaction become positive, indicating the substance studied was not serotonin or its urinary derivative, 5-HIAA, Chemopallidectomy with radioactive palladium in parkinsonian patients released extremely high amounts of this substance in the urine, while similar operations in other regions of the brain did not do so. Thus, the results of this study indicate that a metabolic abnormality is present in a wide variety of basal ganglia diseases. The nature of this abnormality is still definite but it appears to be related to the metabolism of catecholamines. The physiologic and clinical implications are being investigated.