MORBID ANATOMY 



1719 



Purkinje's cells, in the cerebellum, and in the cortical cerebral 

 cells. 



If these accounts are confirmed, they might be found to stand 

 in relationship to the angio-neurotic process in the skin, the con- 

 gestion of the alimentary canal, the vertigo, and the mental 

 condition. 



However, all these points are at present extremely obscure, and 

 are only brought forward here because they appear to require 

 investigation. 



The lesions found in post-mortems in cases of acute pellagra, in 

 oar opinion, apparently support the theory of some protozoan 

 parasite, as suggested above, acting upon the central nervous 

 system and the autonomic nervous system. 



Morbid Anatomy. — The principal point in studying the morbid 

 anatomy of pellagra is to attempt to distinguish between the ap- 

 pearances truly produced by the disease and the signs caused by 

 complications. As we are unacquainted with either the aetiology 

 or the pathology of pellagra, this is most difficult, and only an 

 attempt, which may possibly be fallacious, can be made. 



The Essential Lesions. — Our experience would indicate that in acute cases 

 the body need not be emaciated, and that no trace of the erythema may be 

 visible, but that the lines of demarcation can, as a rule, be easily seen on the 

 arms, legs, and neck, as well as thickened or pigmented areas of the epidermis, 

 bullae, etc. 



In these cases there may be fluid, and at times haemorrhages under the 

 cerebral dura mater, oedema and thickening of the pia-arachnoid , which, 

 however, is not adherent to the cortex. The cerebro-spinal fluid is usually, 

 but not always, increased in amount. In the cord there may be subdural 

 haemorrhages, sometimes extensive, especially in the region of the lower 

 cervical and upper dorsal cords, and there may be congestion of that area 

 of the cord; otherwise the naked-eye appearances of brain, spinal cord, and 

 nerves, may be normal. 



Sometimes the alimentar5'' canal is almost normal, but this is rare, and 

 usually there is more or less congestion and at times even ulceration of the 

 mucosa of the small intestine, and the valves of Kekring may show small 

 haemorrhages. The ileum may be thinned, and Peyer's patches may be 

 diminished in number and atrophied (these lesions are, of course, found in 

 many diseases). The large bowel may be thickened, congested, and ulcer- 

 ated, but the ulcers need not contain amoebae. Pancreas, liver, and kidneys 

 may show signs of cirrhosis (the above intestinal lesions are often associated 

 with polyfibrosis) . The mesenteric glands may be enlarged and congested. 

 The spleen may or may not be slightly enlarged, and the suprarenal capsules 

 may be larger than normal, and the cortex may be black, while the medulla 

 is whitish in colour; but, on the other hand, the capsules may appear to 

 be perfectly normal. In chronic cases the body is often emaciated and anaemic, 

 the skin rough, hypertrophied in places and atrophied in others, the changes 

 being marked on the face, neck, arms, hands, legs, and feet. The subcutaneous 

 fat is diminished. The muscles, heart, liver, spleen, and kidnej^'s, are all 

 atrophied ; the stomach is usually normal, but the intestines may be atrophied, 

 as described above, and the rectum may be ulcerated. The nervous system 

 shows a diffuse leptomeningitis, with marked thickening in places ; the frontal 

 convolutions may be atrophied in some cases and the motor convolutions in 

 others. The bloodvessels may show calcareous degeneration, and there may 

 be sclerosis of the postero-lateral and postero-median columns of the cord, 

 and in the dorsal region there may be also lateral sclerosis. The posterior 



