The Pathology of the Nervous System in Vitamin Deficiencies *

The concept of a positive agent, such as a bacterium or virus, a chemical substance, or a physical agent, producing injury to tissue is so well ingrained in medical thought that it has actually hindered our understanding of the whole problem of avitaminosis. Especially is this true in the more restricted field of the vitamins that are responsible for the maintenance of the health of the nervous system. That the absence from the diet of an agent like an accessory food factor-a vitamin-could produce injury to nervous tissue was unsuspected 45 years ago. This concept has met strong resistance on the part of those who championed an infectious agent as the etiology of beriberi and spoiled maize or a bacterial infection as the etiology of pellagra. It was indeed a great step forward, therefore, when Eijkman2 proved that he could produce a beriberi-like lesion in the fowl with a diet of polished rice, which has since been found lacking in vitamin B1. Since Eijkman's day we have progressed far in our knowledge of deficiency states. We have learned that the so-called polyneuritis of human beriberi is not an inflammatory condition of the peripheral nerves at all (Fig. 1), but a purely degenerative one, affecting first the myelin sheaths and only later the axis cylinders (Fig. 2). There is thus a time when the correction of the deficient diet or, better still, when the necessary vitamin (B1 or thiamin), supplied in pure form and in excess, produces both an amelioration of the clinical symptomatology and a restitution to normal of the pathologic picture. Likewise, beyond the stage of axone destruction a permanent injury remains, even if the process is arrested with the availability of thiamin. This injury consists of the disappearance of the effected fasciculi and their replacement by fibrous connective tissue (Fig. 3). The sensory nerves are more involved than are the motor; the