S. A. K. Wilson in 1912 called attention to a particularly important syndrome, designated by him as "progressive lenticular degeneration" and characterized by dysarthria, dysphagia, general tremors of the extremities, forced laughing and crying, muscular rigidities and contractures, with a slight intellectual impairment. Interesting features of this disease complex are that it is familial in type, but not hereditary, comes on early in life, usually progressing to a fatal termination, and is associated with a cirrhosis of the liver which is not alcoholic in origin. At autopsy degenerations of the nucleus lentiformis have been found. J. Ramsey Hunt in 1916 called attention to the association of both paralysis agitans and Huntington's chorea with lesions in the globus pallidus. Oppenheim has recently differentiated a striatum syndrome to which he gave the name "dystonia musculorum." Difficulties in writing, tremors, disturbance of the gait, rigidities, tonic and clonic movements of the muscles and other neurological symptoms are present. Several cases reported by Abrahamson in 1920 showed definite emotional disturbances. Cecile and Oskar Vogt have recently (1919) studied the striatum lesions from a standpoint of both pathology and symptomatology. As summarized by Lhermitte[166] their work shows that athetosis, paralysis agitans, Huntington's chorea, dystonia musculorum, probably paralysis agitans and various other neurological syndromes are to be attributed directly to conditions involving the striate bodies. Prominent among these are softenings and hemorrhages which may result from arteriosclerosis. In view of these facts a careful study of the focal lesions associated with the arteriosclerotic disorders is exceedingly important. The pathological processes involved have been carefully studied by Heubner and others. He was originally of the opinion that cerebral arteriosclerosis was always of specific origin. Baumgarten, however, subsequently showed that this was not the case. The more characteristic changes in the larger vessels manifest themselves in the form of patches of atheromatous thickening so common at autopsy. As a result of degenerative changes in the elastica and media, and a consequent weakening of the vessel wall, intimal thickening takes place. This is not the circular, uniform, concentric involvement found in syphilitic processes but a localized proliferation of the intima at some one point. There may be an infiltration of colloid and calcareous material in the media. This leads to further intimal thickening. In the smaller vessels arteriocapillary fibrosis has been described—a uniform thickening of the vessel walls with a connective tissue formation. Endarteritis obliterans, first described by Friedländer in 1876, is probably always of syphilitic origin.