1. Was the “nervous prostration” at 46 of syphilitic origin? One cannot give a categorical answer to this question. The high incidence of shock in the family suggests poor stock in which a psychoneurosis is not an unusual phenomenon. The presence of syphilis might act as a debilitating factor or _agent provocateur_, if it were not to cause any demonstrable brain lesion. As pointed out in the case of Harrison (9), however, it is not unusual in neurosyphilis to find a history of symptoms occurring years before the final breakdown and symptoms frequently not recognized as of neurosyphilitic nature. 2. Does the fairly long duration of the psychosis (at least 3 years) explain the marked atrophy? Cases having symptoms even much longer than three years at times show relatively very little atrophy, so that this factor in itself cannot be said to explain the tremendous destruction of tissue. =The THERAPY OF NEUROSYPHILIS has to face not merely variations in the degree of brain wasting and in the degree of meningitis, but also variations in the topographical distribution of lesions. Autopsy.= =Case 103.= To bring out this point we may instance the case of Alfred Weed, a victim of PARETIC NEUROSYPHILIS, dying at the age of 48 years after a course of about seven years. The following is an abstract of the clinical history: A. W. suffered from lues some 24 years before his death at Danvers Insane Hospital in 1907. There is no account of insanity in his family. The patient had been undergoing mental changes for six years before death. At the age of 42 began to take interest in socialism and spiritualism. Would become excited at times and was observed to talk to himself. At times it seemed that he was reacting to visual hallucinations. After eight months he became depressed and apprehensive and developed delusions of poisoning. On admission to the Danvers Insane Hospital in June, 1902, the subject was found to be ataxic, falling in the Romberg position. Pupils were equal but of pin-point size. There was tremor of the facial muscles. The knee-jerks were absent. Speech was ataxic. Memory defective. Depressed. Thought he was to be punished. Refused to eat. Later in the year of admission, patient became more negativistic. He refused to have his clothes brushed. His answers were slow. Mental arithmetic was correctly but slowly done. During January, 1903, the patient was apt to be active and talkative for a time, and then his attitude would suddenly change to one of silence, resistivement and untidiness. From time to time he would be querulous and sulky. In August, 1903, the patient became weaker and could walk with assistance only. Paralysis developed in the left facialis region and in the left external rectus. Pupils were still small, but the left had become smaller than the right. Light reaction tests unsatisfactory. Knee-jerks could not be obtained.