1. Is not the convulsive episode an alcoholic phenomenon in David Collins entirely separate from the patient’s general and neurosyphilis? Possibly; however, an outbreak of neurological symptoms with spontaneous recovery is not only consistent with the diagnosis of syphilis, but somewhat characteristic of neurosyphilis. We suspect that another attack will occur in David Collins.[12] We shall from time to time make use of the social service to suggest his going under treatment, and shall employ his record of contact with a public institution to drive in our suggestion. Still it is clear that there are numerous cases in the community that are not accessible to social service initiated from a public institution. Accordingly, educational propaganda is necessary for salvage of the middle- and upper-class victims of syphilis. It is a little unfortunate that the ethics of the private practitioner make such salvage of middle- and upper-class persons not very likely. Might it not be that an extension of state medicine to this field would incidentally increase the amount of successful private practice? 2. What may be the cause of such a convulsive episode as that of David Collins? It would appear that the convulsions of general paresis and of neurosyphilis in general often occur without gross structural lesions of the brain. It may be suggested that vascular irritation or parenchymal irritation by spirochetes, acting in appropriate parts of the central nervous system, can produce such convulsions. 3. What is the significance of the unilateral phenomenon in David Collins (left knee-jerk greater than right; left-sided Babinski)? The current explanation of hyperreflexia is that somehow inhibitory impulses from upper portions of the nervous system have ceased to influence the local arcs that mechanize reactions like the knee-jerk and the normal plantar reflex. The phenomena are commonly found in cases with pyramidal tract disorder, and in the case of David Collins one may suspect, therefore, that there was a central disorder affecting the right pyramidal tract above its decussation. One might suspect that the convulsions were initiated by a lesion (whether gross or microscopic in range) in the right side of the cerebrum; but whether in the white matter or in the gray matter must be left doubtful. The clearing up of all symptoms suggests either that the lesion was microscopic in range or that the phenomena were transient and functional.