A case of toxic amblyopia : with autopsy and microscopical examination of the specimens / by G. E. de Schweinitz.

  • De Schweinitz, G. E. (George Edmund), 1858-1938.
Date:
[1897]
Catalogue details

Licence: Public Domain Mark

Credit: A case of toxic amblyopia : with autopsy and microscopical examination of the specimens / by G. E. de Schweinitz. 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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    the usual or constant starting-point of this lesion in so-called intoxica- tion-amblyopias. Certainly, degeneration of the ganglion-cells could not have been the cause of the atrophy of the macular fascicle in the present case, nor in several others which have been reported, notably those of Sachs, who, like myself, carefully examined the ganglion-cells of the macula and found them normal. Neither can disease of these cells be held responsible for the atrophy of the optic nerve which occurs in quinine-toxsemia, if I may judge from the examination of a large series of sections in which no notable changes in the ganglion-cells can be demonstrated. In quinine and salicylic-acid amblyopia, and as I expected I would find in filix mas amblyopia, but I was not successful in securing atrophy, the primary changes are vascular, sometimes, in the earlier stages, of the nature of a pure ischsemia, and later, if the influence of the poison con- tinues, these functional vascular changes, if I may so express myself, become organic ones. Endovasculitis, thickening of the vessel-walls, etc., appear, associated with degeneration and atrophy of the nervous tracts which they supply. Sometimes a single tract is attacked, as in the tobacco and alcohol- amblyopias, and, again, an entire nerve, as in ^;ninine-amaurosis. Why certain tracts or areas are affected to the exclusion of others, we do not know. Perhaps the process depends upon nutritional disturbances sim- ilar to those which occur in certain tracts of the cord in pernicious ansemia, and which subsequently develop into atrophies resembling those seen in locomotor ataxia. The belief of Sachs, that the earlier stages of these intoxication- amblyopias must be sought for in vascular disturbances, has a good deal to recommend it, and seems borne out by the action of other toxic agents. What exactly is the active principle which produces these nutritional disturbances we do not know. Sometimes it is tobacco, some- times tobacco and alcohol combined, sometimes it is other poisons, as opium, hashish, iodoform, etc., and sometimes it is a toxin, as, for example, the toxin of diabetes. I have long ago contended that I did not believe it was tobacco alone, or its active principle, nicotine, which was the essential poisonous agent, but that one or more of the many principles freely present in tobacco-smoke, or some toxic influence which they liberate in the system, must be held accountable for the disease. Sachs contends that even in the tobacco cases certain complex chemical combinations occur in the stomach, and there is a resulting transformation of the normal gastric juices into acids of the fatty type which combine with nicotine to form substances which are more injuri- ous than the simple tobacco-bases themselves. Experimental work now being carried on in Chicago under the direction of Dr. Casey Wood indicates that certain stomachic toxins are capable of causing in animals blindness, probably of the type under consideration.