APOPLEXY
CEREBRAL THROMBOSIS
Chart 20
O’Donnell was brought to the Psychopathic Hospital some six weeks after the paralysis, complaining merely of a slight headache and desirous of treatment. There were no mental symptoms of any sort. Physically, O’Donnell was in general not abnormal (there was a slight pre-systolic murmur and a blood pressure of 190 mm. systolic). The pupils were slightly irregular, the left larger than the right; both reacted sluggishly. Both ears were moderately deaf; the tendon reflexes of the left arm and leg were somewhat more lively than those on the right. The systematic neurological examination otherwise revealed no abnormalities. The urine was negative. The serum W. R. was positive but the spinal fluid reaction was negative. There were but 2 cells per cmm., and there was a very slight trace of albumin.
1. How shall we account for O’Donnell’s transient paralysis? We might invoke brain tumor, alcoholic pseudoparesis, or some form of neurosyphilis. The diagnosis of brain tumor seems quite untenable in view of the absence of premonitory symptoms and in the absence of intracranial pressure. As for alcoholic pseudoparesis it is true that the patient was excessively alcoholic.
However, against these two diagnoses and in favor of the diagnosis of Neurosyphilis, are the positive serum W. R. and the pupillary reactions (although these are short of the true Argyll-Robertson phenomenon). Dizziness with retention of consciousness and associated with the paralyses mentioned suggests rather a subcortical than a cortical lesion. We are inclined to regard this lesion as probably Thrombotic, and to place it possibly in the region of the internal capsule. We are inclined to regard the phenomenon as purely vascular and as not in this case associated with an encephalitis. We are, however, not entirely satisfied with the diagnosis.
2. What shall be said as to treatment? A full-blown left-sided hemiplegia may be produced even when the thrombotic lesion is itself exceedingly small. It is common to explain this on the basis that there is an area of collateral edema about the small necrotic, thrombotic, or hemorrhagic area responsible for the lesion. In short, numerous neurones are functionally rather than structurally affected, or at all events capable of early restitution of function.
3. What is the prognosis in such cases? It appears that now and again patients run for several years without further trouble, both with and without treatment. We are inclined, however, to advocate treatment rather than absence of treatment for a variety of reasons. In the first place, vascular lesions may at any time become associated with meningitic lesions, and treatment by salvarsan may perhaps be counted on to head off this process; secondly, the treatment with iodids may possibly aid in the resolution of a local thrombotic process.
4. What are the prodromal symptoms of cerebrospinal syphilis? According to Nonne, headache, dizziness, sleeplessness, mental symptoms of the irritability group, loss of capacity as to mental work, whether severe or not, and loss of capacity for difficult thinking; also impairment of memory. Nonne does not regard these phenomena as characteristic of syphilitic vascular disease, and calls attention to the fact that in every organic disease the same subjective symptoms occur. The triad—headache, dizziness, and impairment of memory—is for example now counted as a prodromal symptom complex for arteriosclerotic apoplexy (Cramer). Of course, apoplectic attacks occur without such preliminary symptoms: particularly, according to Nonne, the nocturnal attacks.
5. Can the fleeting paralysis be of service in differentiating the diffuse from the paretic form of neurosyphilis? Probably not. In both forms transient paralyses occur as well as the permanent ones. In general, however, the transient paralyses are more frequent in paretic neurosyphilis, whereas the permanent ones occur more often in diffuse neurosyphilis.