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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    (b) When cereal is replaced by potatoes, even when the diet is deficient in vitamin A, it is much more difficult to produce nerve lesions, and often the animals remain normal. (c) The reason why yellow maize does not produce nerve degeneration is because it contains carotene as its pigment. White maize, not containing carotene, allows these changes to develop. (d) Although the nerve degeneration changes described are not prevented by adding calcium salts to the diet, it seems probable that a great deficiency of calcium in the diet makes such changes worse. A diet containing only a small quantity of milk, or separated milk, and rich in cereals brings about abundant nerve degeneration, and since additional calcium in the form of calcium carbonate reduces this in amount, it is probably the result of a calcium deficiency. These animals develop very soft bones containing but little calcium salts, and quickly become paralysed. It is probably this condition which accounts for Stockman’s recent results, in which he obtained demyelination changes in the cord of animals receiving diets rich in maize and other cereals, and deficient in calcium-containing foods. Distribution of central nervous lesions.—In the absence of vitamin A and carotene, the nerve degenerative changes are especially seen in the spino-cerebellar tracts, the posterior tracts, and the anterior lateral columns. It is probable that the fibres principally affected are ascending, and that the crossed pyramidal tract usually escapes. The distribution of the degenerating fibres varies at different levels of the cord [2]. Above the medulla, spino-cerebellar fibres entering the cerebellum via both the inferior and the superior peduncles show degenerative changes. Other tracts affected include the fillet and the posterior longitudinal bundle. Above the mid-brain the number of fibres showing myelin degeneration is greatly reduced, but it is quite clear from the behaviour of the animals that the higher parts of the brain do not escape the harmful effect of these diets. These animals when affected are stupid and incapable of fixing their attention on any definite object. In some cases, at least, the cerebral nerve-cells suffer degenerative changes, but this part of the nervous system has not yet been properly examined. Other nerve-cells, such as Clarke’s column cells, Purkinje’s cells, cells of the dentate nucleus, and, to a less extent, the anterior horn cells, are all apt to show chromatolysis, shrinking, excentric nuclei, and many glial cells in the immediate vicinity. Changes in the peripheral nerves.—A more recent development of this experimental work is the discovery that the peripheral nerves are also involved in similar degenerative changes [4]. It would indeed appear that most afferent nerves suffer myelin degeneration. Thus the vestibular and cochlear divisions of the eighth, the optic nerve, the ophthalmic division of the fifth and the sciatic nerves when stained by the Marchi or Scharlach method show characteristic degeneration. At least in the early stages, and before paralysis develops, the efferent nerves seem to escape. This fact becomes evident on examination of the anterior and posterior roots of the cord. As a general rule, the anterior roots of animals brought up on these vitamin A-deficient diets are free from degenerating fibres while the corresponding posterior roots are greatly affected. These changes in the afferent nerves are probably of great significance, especially in relation to the increased susceptibility of epithelial surfaces to infection which develops when diets are deficient in vitamin A [4]. Have the foregoing facts any relation to subacute combined degeneration of the cord ?—Here again, as has happened on several occasions in recent years, we see a series of morbid lesions produced experimentally in animals by certain defined conditions showing a close similarity to a well-recognized disease found in man, and it is our duty to see whether the aetiology of the animal and human diseases respectively bear any relation to one another.