A clinical lecture on remissions and relapses in insular sclerosis / by Thomas Buzzard.

  • Buzzard, Thomas, 1831-1919.
Date:
[1904]
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Licence: In copyright

Credit: A clinical lecture on remissions and relapses in insular sclerosis / by Thomas Buzzard. 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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    remedies may be assumed to have passed off. In syphilis we have to deal with comparatively gross changes—inflammation, gummata, endarteritis, and the like. For the most part the changes in insular sclerosis may be said to be of gross character. It is true that some observers have pointed to the fact that occasionally the anatomical appearances in insular sclerosis cast some doubt upon the more usually received opinion that the disease is of inflammatory origin. Redlich, for example, amongst others, has found in insular sclerosis nerve fibres profoundly affected along with relatively little- changed neuroglia, and says that vascular changes happen only in a certain number of cases. But, as I have pointed out on another occasion, this is by no means conclusive. Paren- chymatous degeneration of the posterior columns in a case of tabes may be accompanied by gross intracranial endarteritis. Presumably, therefore, a toxin may give rise coincidently to each form, and in some cases of insular sclerosis—or in some localities in a particular case—its influence may fall upon the nerve fibres rather than on the vessels and interstitial tissue. The remarkable variations in the degree of acuteness in insular sclerosis, again, appear to be much more consistent with an infective than an endogenous origin. I have had cases under observation in this hospital in one of which 15 and in another 19 months only had elapsed from the com- mencement of symptoms and death. One that I met with in private (which was not, however, verified by necropsy) lived only 12 weeks. Ribbert examined anatomically one that survived only for three months. More often, as is well known, a far longer period characterises these cases, which may drag on for ten or 20 years or more. We are well accustomed to the differing degree of acuteness in all forms of infective disorder, due probably either to intensity of the infecting agent or diminished power of resistance. In Friedreich’s ataxia, on the other hand, to instance what is probably an example of congenital defect, the course of the disease is practically uninterrupted and chronic in character. I fail also to see adequate grounds for the suggestion which has been more recently offered that insular sclerosis is the result of a toxic influence upon an existing defect of development. The presupposition of such a congenital defect appears to me as unnecessary as it would be in the case of infantile paralysis or of the neuritis which so often is a sequel of diphtheria. The frequency with