1902 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY III 



(108, 198, 199). A lack of myelinization was observed 

 in chick embryos, with reduction of nucleic acid in 

 the spinal cord, the spinal ganglia and the sympathetic 

 ganglia (5, 69). The neurologic picture of pernicious 

 anemia in man indicates alterations of both the poste- 

 rior and lateral columns of the spinal cord (141, 146) 

 with ataxic gait, positive Romberg signs, absence of 

 knee and ankle jerks, presence of extensor plantar 

 reflexes, absence of abdominal reflexes, tenderness of 

 the calf muscles, and sensory loss. The pathological 

 findings show degeneration of the white matter in the 

 thoracic segments of the spinal cord, affecting first 

 the myelin sheath and later the axis cylinder. Retro- 

 grade degeneration ma\ be seen in the Betz cells of 

 1 he motor cortex and in the cells of Clarke's column. 

 Demyelinization of the peripheral nerves of the lower 

 limbs has been observed as well as ocular disturbances 

 (dimness of vision, diplopia, nystagmus and pupillary 

 anomalies). Menial symptoms are seen (257, p. no), 

 with variable intensity and order of presentation. 

 They \.ii\ from slight disorders of mood or mental 

 slowness to maniacal episodes, confusion and progres- 

 sive menial enleeblement. 



There is evidence that the neurologic and mental 

 disturbances of pernicious anemia are not the conse- 

 quence of the anemia itself, but rather a consequence 

 of some metabolic disturbance in the nervous tissue 

 caused by the vitamin deficiency. Scheinbcrg (230) 

 observed a decrease both in the oxygen and the glu- 

 cose consumption of the brain of pernicious anemia 

 patients. Administration of B 12 produced an improve- 

 ment of (he mental disturbances and an increase of 

 the oxygen consumption. More recent observations 

 indicate thai vitamin Bit deficiency may be associated 

 with an alteration of pyruvate metabolism (59). 



I he metabolic defect of the brain in pernicious 

 anemia results in alterations of the electroencephalo- 

 gram (227). W'iih the improvement of the mental 

 Condition produced bv ihe adminislration of vitamin 

 B,,, there is also .1 tendency for the electroencephalo- 

 graphic rhythms to become normal. Walton tt a/. 

 I j(|o| have also luimd I lie l.l.t \ to be made normal by 

 administration of vitamin Bu in pernicious anemia 

 patients. 



Nutritional Neuropathies 



This term is applied to a varietv of neurological 

 Iromi a sociated with nuiriiion.il deficiencies. 



I >' < *n< h syndrome .1 :iated with malnutrition was 



observed in the course of the Spanish Civil War 



(94, 95) A list of the main clinical features is given in 



table 6. Xeurologic and Other Clinical Features 

 of Nutritional Neuropathy in Madrid* 



Paresthesias 98 



Causalgic symptoms 53 



Neurasthenia 88 



Visual disturbances 42 



Sensations of coldness . . 51 



Disturbances of gait 58 



Glossitis 47 



Dysphagia 21 



Menstrual disorders 31 



Urgency of micturition 39 



Polyuria 33 



Nycturia 18 



Diarrhea 35 



Constipation lb 



Pernio 11 



* Frequency of occurrence in 98 cases studied by Grande 

 & Peraita (95). 



tabic 6. Thiamine, riboflavin and nicotinic acid were 

 ineffective in its treatment, but good results were ob- 

 tained with yeast, both fresh and autoclaved. The 

 conclusion was drawn that the parcsthctic-causalgic 

 syndrome was a nosological entity different from 

 pellagra but frequently associated with this disease, 

 and that it was due to a deficiency of some thermo- 

 stable factors or factors of the vitamin B complex. 

 Later Gopalan (91 I in India recorded therapeutic 

 success with pantothenic acid in patients with similar 

 symptoms. After World War II numerous reports 

 dealt with related syndromes (44, 55, 88, 95, 249, 

 252, 257). 



from a physiological point of view this syndrome 

 is of interest in that the nutritional deficiency re- 

 sponsible for iis development appears to affect prefer- 

 entially sensory functions and the autonomic system, 

 in particular, the vasomotor innervation. There is a 

 striking contrast between the neurologic manifesta- 

 tions of beriberi and those of the 'burning feet' 

 syndrome 12071. 



I 'itamin .1 



There is no evidence of the involvement of vitamin 

 A in neuronal metabolism or in the formation and 

 maintenance of myelin (295). It is of interest in the 

 present contexl on two accounts: a) the mechanical 

 production of nervous lesions in vitamin A defi- 

 ciency, resulting from disproportionate growth of 

 the bonv Structures which surround the central 

 nervous system; and /< 1 the role of vitamin A in the 

 function of the rods of the retina. 



In a series of studies carried over a period of some 

 20 years, Mellanbv 11(171 provided experimental 

 evidence that ill puppies vitamin A deficiency causes 

 a general thickening and dysplasia of bone. The 

 hvpertrophy and (he altered shape of bones result in 

 widespread mechanical lesions, involving both the 



