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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    either because it could not be mobilized or because it could not be used by the respective cells. In conclusion, let me say a few words as to what would be expected to result from dietetic treatment in subacute combined degeneration, especially in established cases. Dr. Carmichael has emphasized in his recent work that the peripheral nervous system is largely involved in this disease and that in curative results that are seen nowadays it is primarily changes in the peripheral nervous system that account for the improvement. Similar results have been described by Baker, Bordley and Longcope [5] in a series of cases of subacute combined degeneration. In my experimental animals also, as mentioned above, the afferent peripheral nerves as well as those of the central nervous system show degenerative changes. Whereas certain early changes in the peripheral nerves, such as those found in the ophthalmic division of the trigeminal nerve associated with early xerophthalmia, heal up quickly on giving vitamin A, more severe degenerative changes may take months before the demyelination clears up and the nerve function is completely restored. I mention this fact because, as pointed out by Baker, Bordley and Longcope, many clinicians seem to expect curative results too quickly from the treatment of subacute combined degeneration of the cord. Where fibres in whole areas of the cord have disappeared, it would not be expected that any form of therapy would restore this function. On the other hand, it would be definitely expected that peripheral nerve lesions would clear up. Even in this case, however, if these are severe, such im¬ provement would not be expected until after months of treatment. Baker, Bordley and Longcope say that nine months may be necessary. If continuous dietetic treatment cures, as it is now known to cure, the peripheral nerve lesion, it is probably safe to assume that the cord degenerative changes are stopped. Thus, even in severe cases of subacute combined degeneration, beneficial effects may be expected from this type of treatment, due both to the recovery of peripheral nerves and to the prevention of further central degenerative changes. To sum up the present position in the light of the experimental and clinical work referred to above, it would appear that— (1) The nervous system is greally influenced by nutritional factors, since it is possible to produce in young animals demyelination changes in medullated nerve- fibres of both the central and peripheral systems, which are similar to—probably in many respects identical with-—those of convulsive ergotism, pellagra, lathyrism and subacute combined degeneration, i.e. the well-known toxic degenerations of the nervous system. In these experiments absence of vitamin A and carotene from the diet is the chief factor, but the condition may be hastened by adding cereals or cereal products such as embryo or ergot. (2) Whereas these results probably account largely for the nerve lesions in convulsive ergotism, pellagra, and lathyrism, they cannot alone explain the nerve lesions of subacute combined degeneration, because in this disease the body contains vitamin A. (3) If the animal experiments mean anything in relation to subacute combined degeneration—and the close similarity of the peculiar lesions suggest that they must do so—it can only be assumed that, for some unknown reason, vitamin A cannot be mobilized or cannot carry out its normal function in ordinary quantities in this disease. Beasons have been given to show that some other essential chemical substances in the body are also relatively ineffective in this disease. There is clearly a gap to be bridged between the experimental and clinical knowledge. What is wanted is knowledge as to those conditions which prevent vitamin A from acting in the body in ordinary quantities. I know of no such conditions as yet. Possibly the associated condition, in subacute combined degenera¬ tion of achylia gastrica, may afford the clue to the missing link. However, I have never yet seen this condition in my experimental animals.