A case of homonymous, left-sided inferior tetartanopsia following toxic dose of salicylate of soda / by J. Herbert Claiborne.

  • Claiborne, John Herbert, Jr., 1861-1922.
Date:
[1905]
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Licence: In copyright

Credit: A case of homonymous, left-sided inferior tetartanopsia following toxic dose of salicylate of soda / by J. Herbert Claiborne. Source: Wellcome Collection.

Provider: This material has been provided by UCL Library Services. The original may be consulted at UCL (University College London)

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    salicylic acid or salicylate of sodium, and that the ophthalmo- scopic picture in a minor degree is that produced by quinine. The only ophthalmic sign in my case, two months after the intoxication, was fullness of the veins. The only sign in the fundus remarked at the time of the intoxication was a possible pallor of the discs. A recent communication from the surgeon who first examined this case tells me that he has found the fields, in April of this year, practically the same as I found them twelve months before; the main difference between his result and mine lies in personal equation. He did not, however, find the islets for green and red. The patient writes me he is no longer annoyed by his defect. Brunner, in discussing the mechanism of quinine blindness, suggests the possibility that the blindness has a cerebral origin, the central ganglia of the cortex of the cerebri being affected, and that the loss of function depends upon circulatory disturbances or inflammatory processes in the cerebral cortex of the visual centers. He finally, however, dismisses this possibility, and accepts ischjemia of the retinae, the ultimate result being secondary changes and thickening of the vessel walls. De Schweinitz, in his study of quinine amaurosis, found com- plete atrophy of the visual path, optic nerve, chiasm, and tracts, as far as they could be traced. Both Brunner and de Schweinitz admit that the original eflfect of quinine is upon the vaso-motor centers, and I believe all con- cur in this view. If this is true, then it is not impossible that there may be an acute endovasculitis or thrombosis at the cerebral cen- ters, and that the degeneration of the retina and the visual paths, in quinine amaurosis, may be partly descending, if not entirely so. Holden, in an experimental study on dogs, concludes that the pathological process, following quinine amaurosis, consists in a constriction of the retinal vessels, particularly of the arteries, fol- lowed by an albuminous serous exudation into the nerve fibre layer, and a degeneration of the ganglion cells, together with their axis cylinder processes. Holden subsequently made other experiments, keeping the dogs