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.
4. Can the dysdiadochokinesis be used to indicate cerebellar lesion in David Collins? Possibly; but it does not appear that the difficulty in executing successive movements was unilateral. It seems impossible to bring into close topographical relation the basis for the Babinski and left-sided hyperreflexia, and the basis for the dysdiadochokinesis. Alcohol is sometimes asserted to exert an especial effect upon the cerebellum.
5. Must we suppose structural lesions, either (a) of the nature of cell losses demonstrable microscopically, or (b) of the nature of secondary degenerations demonstrable by Weigert myelin sheath methods, in the case of David Collins? It appears that we do not need to assert the existence of such lesions.
6. Could the hyperreflexia and the Babinski reaction be due to local spinal cord disease? Possibly; but the existence of other neurological symptoms (lingual and manual tremor, speech defect to test phrases, ataxic handwriting, and dysdiadochokinesis) makes it probable that there were lesions, or at any rate disordered functions, within the cranium; and there appears to be no basis for asserting local spinal cord disease.
Differential diagnosis between NEUROSYPHILIS and ACUTE ALCOHOLIC PSYCHOSIS.
Case 62. Joseph Buck was a chef of 60 years who came in, seeking advice because his memory was getting poor; he was unable to remember names and what he was about to do. He was tremulous and had much pain in his limbs. He had been drinking heavily for weeks,—probably ten weeks; in fact, he described himself as having had “the shakes” and as having lately seen animals and people that were unreal. He had had the shakes before and the condition had lasted for two to three days after alcohol was discontinued.
Physically, Buck was tall, well developed, although poorly nourished, with a skin suggesting alcoholism. There was a slight acne over the back and chest; there was a slight enlargement of the heart, with blood pressure, systolic, 180, diastolic, 120. There was a corneal opacity of the left eye, which the patient said was the result of syphilis following a chancre, which he had acquired at the age of 27. There was also a ptosis of the upper lid of the left eye. The right pupil was irregular and reacted to light sluggishly, and with a very small excursion. The patient was slightly deaf in both ears. The deep reflexes were all lively and equal. The tremor was most marked in finely coördinated movements. There was a slight swaying in the Romberg position but the sign could not be said to be present. The gait was unsteady. There was a marked tenderness over the nerve trunks.
So far as mental examination went, it seemed that the patient’s claim of amnesia was subjective. There was certainly no more amnesia than a slight difficulty in recalling details. The diagnosis of alcoholism with convalescence from delirium tremens would certainly seem to have been sufficient for the phenomena, and the suggestion of alcoholic neuritis only confirmed the picture. To be sure, one might expect a diminution or absence of deep reflexes; still, these reflexes may be overactive in an irritative stage of the disease.
Naturally, however, the history of syphilis and the pupillary phenomena and ptosis, made the consideration of neurosyphilis necessary. Both serum and fluid W. R.’s proved positive; there was an excessive amount of albumin and globulin, the gold sol reaction was typically “paretic,” and there were 377 cells per cmm.