ABNORMALITIES OF NEURAL FUNCTION IN THE PRESENCE OF INADEQUATE NUTRITION 1903 



peripheral and the central nervous system. The 

 medulla oblongata, pons, cerebellum and cranial 

 sensory nerves are especially liable to suffer severe 

 damage. In young ducks a vitamin-A deficient diet 

 produces buckling and twisting of the spinal cord, 

 hemorrhages and necrosis of the gray and white 

 matter, and degeneration of fiber tracts and nerve 

 cells (75). Vitamin A deficiency produces an eleva- 

 tion of the pressure of the cerebrospinal fluid in 

 dogs (165) and in calves (178). This effect, however, 

 does not appear to be necessarily related to the 

 osseous thickening, since in calves papilledema and 

 high pressure decrease rapidly when vitamin A is 

 given. It has been suggested that the phenomenon 

 may be due to an alteration of the ependyma which 

 is of epithelial origin and, like other epithelia, depends 

 for normal function on an adequate supply of vita- 

 min A. 



Vitamin A participates in the resynthesis of rhodop- 

 sin (288). Accordingly, its deficiency impairs dark 

 adaptation. Morgan (181 ) has shown, by means of a 

 behavioral technique in which albino rats were re- 

 quired to choose between a lighted and a dark panel, 

 that the brightness of the test p. itch at which the 

 animals discriminated accurately after a given time 

 spent in the dark was substantially higher in the 

 vitamin-A deficient than in the control animals 

 receiving a supplement of cod liver oil. 



In man the increase in the lighl threshold of the 

 dark-adapted eye was reported alter distressingly 

 variable lengths of vitamin deprivation (192). Careful 

 studies made in Great Britain (114) indicate thai 

 vitamin A deficiency is much less readily induced in 

 hitherto well-fed adults than has been previously 

 supposed. A large rise in the rod threshold, deter- 

 mined after 20 min. of dark adaptation, was obtained 

 only in 3 out of 16 subjects, at about to, 12 and 20 

 mo., respectively, from the start of the experiment. 

 Their cone-rod transition time was lengthened. This 

 feature of vitamin A deficiency may occur at the 

 same time as the deterioration of the rod threshold 

 or may precede it. A fall of the average plasma level 

 to below 50 iu per 100 ml (normal average, 120 11 ) 

 preceded the deterioration of dark adaptation by a 

 few weeks. 



Electrophysiological!)-, the functional capacitv of 

 the rods may be assessed on the basis of an electro- 

 retinogram. The electroretinographic tracing repre- 

 sents the action-potential response of the rods of the 

 retina in a dark-adapted eye exposed to a flash of 

 light. When the vitamin A content of the blood 

 reaches a critically low level (about 20 iu per 100 ml 



of plasma) patients develop night blindness and the 

 electroretinogram becomes suddenly extinguished or 

 the b-wave becomes very small (56). This is a re- 

 versible phenomenon, representing a functional 

 (biochemical) change rather than a structural lesion. 

 The electroretinographic response returns to normal 

 in the course of treatment with vitamin A. 



Vitamin E (Tocopherol) 



The relationship between vitamin E deficiency 

 and certain alterations of the reproductive system, 

 musculature and vascular system is well established, 

 but its role in the metabolism of the nervous system 

 is not clear (157). Histopatholodcal changes in the 

 nervous system of vitamin E deficient animals have 

 been observed only in a limited number of specie-, 

 and there is much disagreement as to the specificity 

 of the lesions and their causal relationship to the 

 deficiency of tocopherol. Lesions of the fibers of the 

 dorsal columns and the dorsal roots are prominent 

 (60, 148) and account for the ataxia observed in 

 tocopherol-deficient rats. The lesions ,,i ,|„. anterior 

 horn neurons described by Einarson sV Ringsted (6i 

 were denied by other authors, and Malamud et al. 

 , ;i concluded that no constant lesions can be 

 found either in the lower or upper motor neuron 

 svsiem. The pathological changes in the musculature 

 do not appear to be correlated with neurological 

 lesions, and it is generally accepted at present that 

 the changes in skeletal musculature are myogenic. 

 In the chicken (202, 2051, the syndrome of •nutri- 

 tional encephalomalacia' is characterized by motor 

 incoordination and ataxia, spasticity of the legs, head 

 retraction and opisthotonus, tremors, somnolence, 

 stupor, and death. Pathological examination shows 

 alterations especially in the cerebellum, which include 

 changes in the libers and cells, with degeneration of 

 the Purkinje cells, and the small cells of the granular 

 layer. It is doubtful whether these lesions are a direct 

 consequence of the vitamin E deficiency. They mav 

 be a consequence of vasomotor disturbances (296). 

 Similar alterations were found in the spontaneous 

 disease of chickens called 'crazy chick disease' which 

 m, iv be considered as a subacute avitaminosis E. 

 This disease has a seasonal occurrence, with ischemic 

 necrosis, extensive fibrosis of the cerebellum ( 1 28 1 

 and degeneration of the Purkinje cells (293). Tremors 

 and incoordination were described in the vitamin-E 

 deficient rat (152) and some changes in behavior 

 were noted (16). The existence of changes in the 

 central nervous system of rats deficient in vitamin E 



