The pathology of the cranial nerves in tabes dorsalis / by Tom A. Williams.

  • Williams, Tom A. (Tom Alfred), 1870-
Date:
1910
Catalogue details

Licence: In copyright

Credit: The pathology of the cranial nerves in tabes dorsalis / by Tom A. Williams. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    lateral movements could not be accomplished, nor could the raising or lowering of the globes; but the external movements could be performed. The left pupil was larger than the right. There was no reaction to light, and that on attempting convergence and distant regard was defective. The sensibility of the cornea and the reflex lacrymal secretion were present. Bilateral nystagmoid movements occurred. 1 hus, there was complete paralysis of all the acts governed by the third nerve, with the exception of the pupillary reaction upon accommodation, convergence, and distance. Respiration was more rapid than normal—28 per minute. It was interrupted by parox- ysms, especially after excitement. During these, breathlessness and angoisse appeared, a “whooping” cough distressed her, the face reddened, and there was often abundant secretion of tears and saliva. Phonation was rough, bitonal, nasal, and often almost inaudible. The right vocal cord was paralyzed, and the right side of the tongue was atrophied, corrugated, and showed fibrillary twitchings. There was, perhaps, a little facial asymmetry. There were no basal crises nor bulbar trouble other than the foregoing. However, it was a typical case of basal tabes as regards the cranial symptoms. There were no tabetic symptoms in the lower limbs, but the deep reflexes were exaggerated, and the toes sometimes extended when stroking the sole. There were occasional lightning pains, but no visceral incontinences, and no other trouble of the nervous func- tions. Lumbar puncture showed an intense lymphocytosis. The diagnosis was clearly basilar meningitis, superior tabes. During the two years which elapsed before her death few new symptoms appeared. The Jacksonian epilepsy reappeared. It was probably due to an area of cerebral softening found post mortem in the right hemisphere. The ocular palsies improved, although she never succeeded in convergence or holding the eye for more than an instant toward the inner canthus. The atrophy of the tongue, however, persisted. At the avio'psy the meninges did not appear diseased, and the cranial nerves seemed unaltered in volume, except the optic nerve, which had shrunken to about the size of a normal oculomotor. The right angular gyrus showed an old softening about tlie size of a quarter. Under the microscope the spinal cord revealed no degen- eration of the posterior roots nor of the posterior columns, where the internal bandalette was quite intact. The anterior roots were also normal. The optic nerve showed characteristic tabetic atrophy, not a single nerve fiber being preserved. The connective tissue presented a very severe endoneuritis and perineuritis, with arteritis of the type described by Marie and Leri,^® and due to transverse “radiculitis” i* Rev. neurol., 1906.