ABNORMALITIES OF NEURAL FUNCTION IN THE PRESENCE OF INADEQUATE NUTRITION 



l8 99 



table 3. Neurologic Manifestations oj Riboflavin 

 Deficiency in Animals 



return toward 'normal' upon supplementation, was 

 observed in the pressure-pain threshold measured by 

 means of a sphygmomanometer cuff applied to the 

 calf. Manual speed (involving large movements of 

 the arm and requiring some skill), complex body- 

 reaction times to visual stimuli, and toe-reaction limes 

 exhibited a similar pattern of statistically siuniticant 

 impairments. 



Riboflavin 



Riboflavin participates in an important "roup of 

 respiratory enzymes, the flavoprotcms. The ribo- 

 flavin content of the various parts of the brain is 

 proportional to their respiration rate (139). 



NEUROLOGICAL MANIFESTATIONS OF RIBOFLAVIN DE- 

 FICIENCY in animals. Impairment of nervous function 

 in riboflavin deprivation has been reported in several 

 animal species. The main findings consist of low 

 physical activity, collapse and coma. Anatomical 

 lesions characterized by degeneration of peripheral 

 nerves and the spinal cord have been reported. A 

 summary of the neurologic findings in experimental 

 riboflavin deficiency in animals is given in table 3. 



Administration of riboflavin analogues has been 

 used as a tool for the production of riboflavin defi- 

 ciency (299), resulting in 'hyperirritability.' Other 

 components of the diet appear to be important in the 

 production of the neural manifestations of riboflavin 



deficiency. A high-fat diet favors the development of 

 neurologic symptoms in the rat (64, 239). 



The specificity of the neural manifestations of ribo- 

 flavin deficiency is still a controversial matter. Patek 

 et al. (204) suggested that the spastic paralysis ob- 

 served in their riboflavin-deficient pigs may be due to 

 other concomitant vitamin deficiencies and not to the 

 lack of riboflavin itself. Follis (77, p. 163) considers 

 the pathological alterations (myelin degeneration of 

 some peripheral nerves and of the dorsal columns of 

 the spinal cord) as 'equivocal.' 



RIBOFLAVIN DEFICIENCY AND THE NERVOUS SYSTEM 



in man. In 1938 Sebrell & Butler (235, 236) described 

 the clinical picture of riboflavin deficiency in man. 

 Some of the skin lesions were already known to be 

 present in certain clinical conditions characterized by 

 neurologic symptoms (259, 260). Stannus (261) 

 believed that the neurologic manifestations were the 

 consequence of capillary dysergia. The alteration in 

 nervous function would then be due, not directly to 

 a chemical lesion localized in the nervous cell itself, 

 but to a primary lesion of the capillaries. Recent work 

 on experimental riboflavin dcliciencv in man has 

 given little indication of impairment of nervous func- 

 tions (no, III). 



Work done in this laboratory (134) showed that 

 normal young men suffer no neurophysiological 

 handicap from subsistence for at hast 5 mo. on a diet 



providing 0.31 m« of riboflavin per 1000 Cal. which 

 represents one fifth of the recommended dailv allow- 

 ance (79). 



\ ii otinu Ami 1 \ ia 



The physiological role of nicotinic acid depends 

 on its participation in the molecule of three important 

 coenzymes, the diphosphopyridine and triphospho- 

 pyridine nucleotides (or coenzymes I and III and the 

 more recently discovered coenzyme III. These coen- 

 zymes act as hydrogen acceptors in the dehydrogena- 

 tion of numerous metabolically important sub- 

 stances. 



Only two mammalian species, dog and man, 

 develop characteristic niacin deficiency states (115) 

 which can be easily differentiated from other nutri- 

 tional deficiencies. In man it is generally identified 

 with the syndrome of pellagra, although pellagra 

 represents a complex nutritional deficiency involving 

 nicotinic acid, tryptophan and perhaps factors antago- 

 nistic to nicotinic acid. Experience during the Spanish 

 Civil War and World War II made it clear that most 



