Case 34. John Bennett, 28, was brought to the Psychopathic Hospital much confused. His brother, who came with him, said that he had been a very heavy drinker but had given up drinking about four months before. He had recently had a cold but was otherwise in good health up to the night before admission. On this night, Bennett had become suddenly excited and went into his mother’s room, at the common home, and began to curse her. However, he was put to bed safely, but on the next morning began to moan continuously. After some hours of moaning, he was brought to the hospital. Here he remained difficult to manage, being irritable, noisy, and resistive. Questions he either would not or could not answer, and there was even no evidence that he understood questions. However, within a few hours, it was clear that he was slowly coming out of the confused state. On the following day, it was possible even to rouse him and get his name. The confusion gradually cleared still further and, by the end of three days, he had become mentally absolutely well so far as could be determined.
He then informed us that he had had a chancre about five or six months before, followed by a secondary skin eruption; that he had received four injections of salvarsan (the last, a month before admission) and three injections of mercury. At about the time of the last injection of salvarsan, he had developed headache with pain and slight stiffness in the back of his neck; and a fortnight later, he began to have dizzy spells, followed during the last week by difficulty in hearing. There was amnesia for everything that happened after his spell of sudden excitement on the evening before admission, and this amnesia was never lifted for the four days that followed.
Physically, Bennett was very well built and muscular. Nor were there any evidences of disease outside the nervous system. There was some slight stiffness of the neck and slight pain on movement of the head, which probably ought to be attributed to meningitis. The neurological examination showed tendon reflexes all normal, and normal sensations. There were, in fact, no neurological signs except that both pupils were dilated; the left was larger than the right. Both pupils reacted to light but reacted very poorly. They reacted much better to accommodation.
The W. R. proved to be positive, as might well be expected in a man whose infection had taken place less than six months before. The globulin and albumin of the cerebrospinal fluid were in great excess, of a degree which we clinically express by ++++. The W. R. of the fluid also was strongly positive down to 0.1 of a cmm. The gold sol reaction was the “paretic” type, and there were 228 cells per cmm.
1. How early may clinical evidence of neurosyphilis set in after infection? Craig found one case of “brain syphilis” occurring one month after infection. Frye claims a case of tabes dorsalis developing six weeks after infection. Craig states that he has had three cases of brain syphilis occurring within six months, and six within a year of infection.
2. What effect did the salvarsan injections have in causing or preventing the symptoms in this case? Nonne sums up the neurorecidive question as follows: Since the introduction of salvarsan therapy for neurosyphilis, paralyses of various cranial nerves are seen more frequently. This higher frequency is in part only apparent since more attention has been paid of late to auditory and labyrinthine disorders. On the whole, however, it must be considered that salvarsan does mobilize spirochete foci which without salvarsan therapy would perhaps have remained latent. Probably we are here dealing in some instances with fresh infections of neurosyphilis, in other cases with a Herxheimer reaction. Ehrlich believed that these latent foci occur particularly in places with stagnant blood current; as, for instance, in the narrow bony canals. This hypothesis, sufficient in some instances, is less satisfactory for cases of peripheral neuritis, for example.
3. What treatment is indicated? Intensive antisyphilitic treatment is strongly indicated. Whatever may be the truth concerning the production of neuro-recurrences (“neurorecidives”) it is certain that the symptoms usually vanish with a continuance of salvarsan therapy. The important point is to give efficient treatment, and in a case like Bennett’s improvement is fairly certain unless some serious insult occurs before the remedial efforts have been given time. It is still an open question whether intraspinous treatment is more efficient in such cases than intensive intravenous injections of salvarsan. In Bennett’s case diarsenol was injected intravenously twice a week in 0.6 gm. doses, reënforced with intramuscular injections of mercury salicylate and potassium iodid by mouth. Under this treatment improvement began slowly and in a few months he was symptomatically well and after three months his tests were practically negative.
JUVENILE PARETIC NEUROSYPHILIS (“juvenile paresis”) with OPTIC ATROPHY.
Case 35. Mary Coughlin, a blind girl of 16 years, was brought to the hospital in a state of great excitement, laughing and crying alternately. The neurologist is entitled to think of blindness, and particularly of the optic atrophy which Mary showed, as probably due to syphilis. However, there was no history of syphilis in the father, who died in an accident at the age of 40, or the mother, who died at 45, of heart trouble. An elder sister was married and well; two younger sisters were living and well. The fifth sibling, a boy, had died in infancy. There had been no miscarriages. In fact, the only point in favor of syphilis was the somewhat far-fetched point that the younger brother of the patient had died in infancy.
The patient’s history was rather suggestive of some other diagnosis. Her birth had been normal, she walked and talked at 13 months, was at school from six to twelve, reaching the seventh grade, and was considered bright. At three years of age, she had been run down by a car and dragged under the fender for a considerable distance. Her head was hurt but the patient did not lose consciousness in the accident. Fainting spells began at 11, in which spells the patient would lose consciousness for a minute or two. About this time, the patient’s eyesight had begun to fail, and for some four years she had been entirely blind. Headaches had come on of late.