Since Eijkman demonstrated, in 1897, that atrophic degeneration of the medullary sheaths of nerves occurs in hens fed a diet of polished rice, attempts have been made to produce lesions of the nervous system experimentally by deficient diets. The earliest studies were concerned largely with deficiency of the antineuritic vitamin, B1, but in recent years vitamin A and the B2 complex have received attention. These investigations were in the main handicapped by inadequate information regarding the vitamins and by the error of attempting to produce absolute deficiency of the factor studied rather than a partial one. Such animals often died before clear cut lesions developed. Furthermore, drawings and retouched photographs were offered as evidence of nerve and spinal cord lesions, and it was later admitted that at least some of the supposed degenerations were artefacts. So unconvincing was this earlier work, that Grinker and Kandel (1) in 1933, after negative experiments of their own, decided that long standing severe vitamin A, B~, and B complex deficiency causes no well defined histologic changes in the central nervous system.In spite of this criticism, the subject has been pursued by several workers, particularly by Zimmerman and his associates (2-5).