ABNORMALITIES OF NEURAL FUNCTION IN THE PRESENCE OF INADEQUATE NUTRITION 



I 901 



Vitamin B e (Pyridoxins) 



In spite of the fact that vitamin B 6 was identified 

 20 years ago (20), its participation in biochemical 

 reactions taking place in the nervous system has been 

 made clear only in the last few years. The most im- 

 portant function of vitamin B 6 is related to the role of 

 pyridoxal phosphate in the metabolism of amino acids 

 and proteins (273) and, more specifically, in the 

 reactions of transamination and decarboxylation 

 (cf. 276). 



It is likely that in pyridoxine deficiency the original 

 defect consists of some alteration in the ability of the 

 nerve cell to handle the amino acids, particularly the 

 glutamic acid and its amide, but there is no definite 

 evidence regarding the biochemical changes ulti- 

 mately responsible for the alterations in excitabilit) 

 of the brain. 



MANIFESTATIONS OF DEFICIENCY IN ANIMALS. The 



neurologic manifestations are among the 1110-1 

 characteristic and constant signs of pyridoxine defi- 

 ciency in animals. Typical convulsive seizures can be 

 produced in rats (38). The lits resemble typical human 

 epilepsy and appear in the rat after some 20 wk. of 

 maintenance on the deficient diet. Similar seizures 

 have been obtained by the administration of antago 

 nists of pyridoxine (desoxypyridoxinc, isonicotinic 

 acid hydrazide, and semicarbazidc). The neurologic 

 signs in vitamin B 6 deficiency are summarized in 

 table 5. 



Other neurological symptoms are not so character- 

 istic as the convulsive seizures and consist mainh ol 

 incoordination of movements, spastic gait and paral- 

 ysis. The convulsive seizures are related to an in- 

 crease of the irritability of the brain (46). The electro- 

 shock threshold of pyridoxine-deficient rats is rapidly 

 elevated by administration of pyridoxine. 



MANIFESTATIONS OF DEFICIENCY IN MAN. The produc- 

 tion of convulsive seizures in man by deficiency of 

 vitamin B 6 was first reported by Snyderman el a!. 

 (254, 255) in a defective infant fed a synthetic diet. 

 The convulsions were promptly corrected by the 

 intravenous administration of pyridoxine chlor- 

 hydrate. Convulsive seizures were observed by various 

 authors in infants fed commercial formulas (41, 

 158, 176). Hunt et nl. (116) reported a case of recur- 

 rent convulsive seizures controlled by the adminis- 

 tration of pyridoxine. Livingston et at. (150) observed 

 no improvement in cases of epilepsy of various types. 

 Neurological manifestations of pyridoxine defi- 

 ciency have been induced repeatedly by giving 

 pyridoxine antagonist Deficiency symptoms, includ- 



table 5. Xeurologic Manifestations of Pyridoxin* 



Deficiency in Animals 



ing polyneuritis, were produced by administration 

 of desoxypyridoxine and controlled by pyridoxine 

 treatment t ^78). Convulsive seizures produced in 

 man and animals (2 1 7) by administration of isoniazide 

 respond to pyridoxine therapy. The central nervous 

 s\Mem syndrome which accompanies vitamin B 6 

 deficiency in infancv is considered to include the fol- 

 lowing manifestations (42): hyperirritability, gastro- 

 intestinal distress, increased startie responses and 

 convulsive seizures. Changes in the EEG, consisting 

 of increased voltage and slow waves, were reported 

 during seizure^ 1 p 1, but no abnormalities are found 

 during the interseizurc periods. 



Vitamin />',_■ (Cyanocobalamine) 



This vitamin is concerned with the biosynthesis 

 of the methyl groups but perhaps not with the process 

 of transmethylation itself (272). It appears to In- 

 important also for the reduction of coenzyme .1 and, 

 therefore, it may be involved in the intermediate 

 metabolism of carbohydrate and fat. The importance 

 of vitamin B,.> for the nervous system is demonstrated 

 by the neurologic disturbances characteristic of 

 pernicious anemia, fundamentally a deficiency of 

 B12 (17). Jewesbury (118) proposed to call the neu- 

 rologic syndrome of pernicious anemia the "vitamin 

 Bj.. deficiency neuropathy." 



Deficiency of this vitamin may cause important 

 congenital defects and structural alterations of the 

 nervous organs. Newborn rats from dams kept on a 

 diet devoid of vitamin B 12 develop hydrocephalus 



