The treatment of subacute combined degeneration / by Edward Mellanby.

  • Mellanby, Edward, Sir, 1884-1955
Date:
[1933?]
Catalogue details

Licence: In copyright

Credit: The treatment of subacute combined degeneration / by Edward Mellanby. Source: Wellcome Collection.

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    THE TREATMENT OF SUBACUTE COMBINED DEGENERATION By Professor Edwabd Mellanby, M.D., F.R.S. >: I AM reluctant to precede Dr. Carmichael in opening this discussion because the work I wish to describe is mainly of an experimental nature, and although it is difficult to avoid the conclusion that the results have some bearing on the aetiology and treatment of subacute combined degeneration of the cord, the evidence at present available is by no means conclusive. Indeed, the facts to be described may only add to the difficulty of the situation. However, there have been so many examples in recent years where experimental and clinical investi¬ gators have met together and discussed—with fruitful results—problems of disease, from what appear at first sight to be points of view with very little in common, that we can probably afford to be optimistic even on the present occasion. Some essential points to be borne in mind in considering this disease are that it is a condition of nerve degeneration in the spinal cord and peripheral nerves, that the nerve changes are primarily those affecting the myelin sheaths, that the degener¬ ative changes are unaccompanied by inflammatory reactions and with little or no neuroglial overgrowth, and that subacute combined degeneration is classed with pellagra, convulsive ergotism, and lathyrism, as toxic and not infective in character. If the spinal cord of a patient deceased of any of these diseases was presented to a pathologist for diagnosis, he would probably have some difficulty in deciding which was responsible for death. A further point of fundamental importance is that all recent wTork has emphasized the fact that subacute combined degeneration of the cord is a metabolic disease. Its close association with pernicious anaemia—now controllable by liver and its water-soluble extracts or by desiccated pig’s stomach,—and the general view, although there are still great differences of opinion as to the means of so doing, that these degenerative nerve changes can also be prevented and relieved, if present, by dietetic means, support the idea of a nutritional basis being involved. If, in addition, it is possible by dietetic means to produce and prevent experi¬ mentally comparable lesions in the spinal cords and peripheral nerves of animals, involving demyelination of conducting nerves in the absence of inflammatory reaction and neuroglial overgrowth, it will be agreed that such an experimental basis may afford a means of adding valuable knowledge to the metabolic processes which underlie the disorder. I wish, therefore, to give a bird’s-eye view of evidence which demonstrates not only that the spinal cord is within the pale of nutritional influences, but also that the so-called toxic degeneration of the nervous system can be produced by certain ordinary foodstuffs and can be prevented by specific food ingredients ; that, in other words, there are neurotoxic agents in food which can only act and hasten demyelinative changes in nerves in the absence from the diet and from the body of certain essential protective factors in food.