On the whole, it would seem best to consider the case of Mrs. Bartlett to be one of Cerebral Arteriosclerosis of Syphilitic Origin, and a case in which there is no evidence of meningitis or meningoencephalitis.
1. What is the explanation of the negative spinal fluid W. R.? It may be that none of the W. R. producing bodies have gone over into the spinal fluid. It has been shown by the work of Weston that the W. R. producing body is not identical with the bodies responsible for the other tests in cerebrospinal syphilis. Moreover, it has been clearly shown that these several tests of the spinal fluid do not run at all parallel with one another. Especially is it true that the chemical tests do not correspond at all with the degree or nature of the pleocytosis. On the whole, when involvement of the nervous system is entirely vascular, it is not only theoretically proper but also practically common, to find a spinal fluid negative to several tests.
2. Omitting consideration of the syphilitic gold sol of this case, what conclusion could be drawn from the albumin and globulin findings? It would not be warrantable to assume syphilis since it is a common finding after cerebral hemorrhage due to non-syphilitic arteriosclerosis to find excess albumin and also globulin in the spinal fluid. Occasionally, also, pleocytosis occurs in cases of cerebral hemorrhage even when the hypothesis of an active meningitis can be excluded. We may recall in this connection the pleocytosis in so-called meningitis sympathica of certain brain tumors. (See also the case of Milton Safsky (48), a case of brain tumor in which there was an excess of albumin, a large quantity of globulin, and a pleocytosis of 146 cells per cmm.)
3. What can be expected from treatment in these cases of vascular cerebral syphilis? The condition offers very little opportunity for therapeutic results. However, antisyphilitic therapy is indicated to prevent if possible further progress of the lesions. Since the lesions are, however, vascular, and since it must remain a question how far these vascular lesions are due directly to spirochetal action, and since in any event it may be difficult to reach the spirochetes thus active, perhaps it is best to place most reliance on potassium iodid. In any event, potassium iodid should be given. Salvarsan and mercury are also indicated. It is common to warn against administration of large doses of salvarsan in this type of case on the ground that further vascular ruptures may be produced. (See Friedberg, 108.)
4. If we conclude that the aphasia of the Bartlett case is due to vascular disease, can we conclude a relation between this vascular disease and vascular tension? It is not safe to draw such a conclusion. The Bartlett case itself showed low blood pressure. To be sure, some cases of neurosyphilis show high blood pressure from which one draws the à la mode clinical conclusion to the effect that the kidneys are probably involved in the arteriosclerosis; but other cases do not show a high blood pressure but may in fact show a low blood pressure. The vascular disease doubtless responsible for the aphasia in the Bartlett case is probably not at all an effect of blood pressure conditions, but is, on the contrary, an effect of local syphilitic vascular lesions.
PARETIC NEUROSYPHILIS (“general paresis”) is often marked by APHASIA.
Case 22. Meyer Levenson, a traveling salesman of 36 years, had for the last two or three years been undergoing a change of disposition, quite interfering with his work. He had begun to take unreasonable aversions to people, had become irritable and emotionally depressed, and often fell to weeping without cause.
About nine months before hospital observation, it seems that a trunk-cover had fallen on Levenson’s head, and there is some question as to whether he did not have a convulsion at that time. However, a month later he had a definite seizure, followed by speech disorder, a slight paralysis, and a staggering gait. Four weeks later, however, he had gotten over these post-convulsive difficulties and had gone back to work.
At his work, he became tired easily, his gait and speech did not seem entirely normal, and there was a considerable memory disorder. After five more months, another attack of a convulsive nature, with twitching of hands and face and tongue-biting occurred, and the attending unconsciousness remained for two days. Again improvement followed, though without ability to return to work. Four (?) months later there were several severe convulsions and Levenson would remain unconscious for a day or two at a time. Restlessness, irritability, and irrational talking followed.
Physically, the patient was fairly well developed and nourished; blood pressure 168 systolic, 68 diastolic; pupils reacted very sluggishly to light. There was a marked motor aphasia, which the patient recognized as a speech difficulty. On the whole, however, Levenson was very euphoric and was entirely sure that he was improving and would surely get well.