



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY III 



if not all the neurologic disorders seen in clinical 

 pellagra are due to other deficiencies. The mental 

 disturbances, however, seem to be more directly re- 

 lated to the deficiency of nicotinic acid and, therefore, 

 form a true part of the picture of 'pellagra 9 in so far 

 as this disease is considered as caused by a deficiency 

 of nicotinic acid. 



Pellagra has been produced experimentally in man 

 in the classic work of Goldberger (89). More recently, 

 Goldsmith and her associates (90) produced perhaps 

 the purest form of nicotinic acid deficiency. No 

 neurologic disturbances were described, but some 

 mental alterations consisting of apathy and depression 

 wen- noted. The specificity of these mental alterations 

 as manifestations of nicotinic acid deficiency is sup- 

 ported b\ the therapeutic effects of this vitamin. 

 Administration of nicotinic acid to pellagra patients 

 produces striking changes in mental condition, while 

 no improvement or even worscnini; of the neurologic 

 manifestations may take place (93, 95; 257, p. 44). 

 These mental disturbances reappear when the drug is 

 stopped (256). 



The mental manifestations of pellagra begin in 

 mi isi of the cases very early and may be mistaken for 

 symptoms of a psychoneurosis. The patients complain 

 of depression, insomnia, feeling of fatigue, fears, 

 anxiety, emotional instability and impairment of 

 memory. Psychosensory disturbances are present in 

 advanced stages of the disease. Mania, hallucinations 

 and delirium may develop. 



In a careful study of the mental disturbances ol 

 pellagra (151), the psychotic manifestations were 

 traced to the organic sensory disturbances which 

 frequently accompany the disease. The clouding oi 

 consciousness facilitates the translation of perverted 

 sensibility into hallucinations. The burning sensations, 

 which so often appear in conjunction with pellagra, 

 probably lead pellagrins on occasion to drown them 

 selves according to the classic pellagrologists. 



I In- role oi niacin, with special reference to the 

 chiatric manifestations of pellagra, was reviewed 

 recently by Gregory (100). Mental signs, 'psycho- 

 neurotic' in character, of mild niacin deficiency, 

 labeled as 'pellagra sine pellagra,' may occur in the 

 absence ol the typical lesions of the skin, mucous 

 membranes and gastrointestinal system. 



Closely related is the syndrome termed 'nicotinic 

 Hid deficiency encephalopathy' (124), considered 

 l>\ some authors as an .nun- form ol nicotinic acid 

 deficient > in conn. isi to the more , (ironic form ol 



pellagi 1 I In syndrome < (.0, 269 isisis <>| clouding 



ofcons< iousness, cogvt heel rigidity, and uncontrollable 

 "i asping and sucking reflexes. 



table 4. Neurologic Manifestations of Pantothenic 

 Acid Di fit u n, 1 in . Inimals 



Pantothenic And 



This vitamin is a constituent of coenzyme .1 which 

 participates in a fundamental way in the intermediary 

 metabolism of carbohydrate and fat (191), and in the 

 synthesis of acetylcholine. Deficiency of pantothenic 

 acid has been produced experimentally in different 

 animal species (table 4) and, more recently, in man. 

 The pig appears to develop the most typical manifes- 

 tations, including the spastic gait described as 'goose 

 Stepping.' The nervous manifestations appear gen- 

 erally in late stages of the deficiency, and for this 

 reason some authors consider them as secondary 

 changes. 



A relationship of pantothenic acid to nervous func- 

 tion in man has been suspected since 194b when 

 Gopalan (<M I reported successful results of the treat- 

 ment of the 'burning feet' sv ndrome with this v itamin. 

 Bean and his associates (11, 1 _• ) demonstrated thai 

 normal young men subsisting oil a diet deficient in 



pantothenic acid or given a pantothenic acid antago- 

 nist (omega-methyl-pantothenic acid) develop a 

 clinical picture in which altered nervous function is 

 clearly manifest. The main signs are torpor, apathy 



and depression, and a neuromotoi disorder with 

 paresthesias and burning sensations. Although there 

 are differences between the typical 'burning feet' and 

 the sv ndrome produced experimentally bv Bean tt at., 

 there is no doubt thai some of the basic neurologi< 

 disturbances ol the 'burning feet' sv ndrome are 

 reproduced in experimental pantothenic acid defi- 

 ciency 



