VII. EFFECTS OF DEFICIENCY 535 



lor some time.'"^ Bird and Culton'"^ dcscrilx' more severe manifestations 

 of a similar disorder in which edema of brain and kinj^s, marked distention 

 of heart and pericardium, generahzed ascites, and coronary and intestinal 

 hyperemia usually terminate in stupor and death of the chicks. Xo histo- 

 pathologic study of the localized lesions of exudative diathesis has been 

 reported. 



(3) Nutritional Enccphalomalacia. This disorder of the nervous system, 

 as described by Pappenheimer et aZ."'**'' ""^' '"^ and by Adamstone,'"^ is 

 characterized by motor incoordination, ataxia, head retraction, coarse 

 tremors, opisthotonos, prostration with legs spastic and claws strongly 

 fiexed, somnolence, stupor, and death. At necrospy there is gross swelling, 

 flattening, irregular distortion, and greenish-brown discoloration of the 

 cerebral con\'olutions. Similar lesions frequently occur in the cerebrum, 

 midbrain, and medulla. They vary from small focal areas to large confluent 

 patches of ischemic necrosis. The cerebellar lesions, microscopically, show 

 edema and disruption of cellular and fibrillar elements of the gray matter, 

 degenerative necrosis of Purkinje cells and the small cells of the granular 

 layer, capillary thrombi which are especially abundant where the blood 

 vessels make a pronounced right-angle turn at the Purkinje cell level, and 

 small hemorrhages in the cortical white matter. Although capillar}^ throm- 

 bosis seems to be the primar}^ cause of the ischemic necrosis, it is possible 

 that some of the symptomatology may be secondary to prolonged vasocon- 

 striction or vasomotor paralysis of largerblood vessels. ^°^ During spontaneous 

 or induced recovery there is active ingrowth of new blood vessels, gliosis 

 and reparative reorganization in the softened tissues, and appearance of 

 phagocytes with brownish pigment. The symptoms and lesions described 

 are identical to those of "crazy chick disease," long recognized bj'^ poultry- 

 men in brooder-stage cliicks**^' ^'"' 



Jungherr,^"" who has given particular attention to the seasonal occurrence 

 and histopathology of this spontaneous disease, which is often a more 

 chronic disorder than that produced experimentally, reports that in associa- 

 tion with, and sometimes independent of, this ischemic necrosis there occurs 

 extensi\'e fibrosis of the cerebellum. Furthermore, the ischemic and fibrotic 

 lesions are often associated with large areas of increased vascularity in the 

 medulla, the midbrain, and the thalamus, accentuated by adventitial cell 

 proliferation and intervascular gliosis, which he regards as a "new morpho- 

 logic expression of subacute E-avitaminosis in chickens." 



'o< H. Dam, /. Nutrition 27, 193 (1944). 



»o^ H. R. Bird, and T. G. Culton, Proc. Soc. Exptl. Biol. Med. 44, 543 (1940). 



"« A. M. Pappenheimer and M. Goettsch, J. Exptl. Med. 53, 11 (1931). 



1" A. Wolf and A. M. Pappenheimer, /. Exptl. Med. 54, 399 (1931). 



los F. B. Adamstone, Arch. Pathol. 31, 603 (1941); 43, .301 (1947). 



