VII. VITA MIX A DKKK IKXCY IN ANIMALS 119 



workers. Accordinu to I'cilmaii the sites of these hony nodiik^s are deter- 

 niiiUHl l)y the t'orinatioii of islands or huds of \ascuhii' coiniect i\'e ti.ssiie. A 

 gootl list of references accompanies his artich'. 



MeUaul^y,'-"' who worked almost exclusi\-ely with dogs, attributes the 

 skeletal changes result ini; from \itamin A deficiency solely to its effect 

 upon ''the position and actixity of osteoclasts and osteoblasts." Although 

 in general he found great diminution in osteoclasis while osteoblastic acti\-- 

 ilies I'emained essentially unchanged, thus accounting for the greatei' thick- 

 ness of })()ues and alterations in contours, he made no attempt at correlation 

 with endochondral bone growth or with normal growth i)at terns. 



After \itamin A therai)y, bone growth seciuences return to noi'mal. The 

 order of resumption of the normal processes concerned has not been deter- 

 mined. Melianby-'' has described only the early return of normal osteoblastic 

 and osteoclastic activities of l)one formed during the deficiency state. That 

 prompt return to normal of epiphyseal cartilage setiuences in the rat takes 

 place has been shown by Wolbach and Bessey"* by the fact that vitamin A 

 therapy begun 7 to 10 days before the usual onset of paralyses prevents 

 sufficient disparity of growth re([uired for pressure effects of bone upon the 

 nervous system. Rats prevented from paralyses in experiments of this type 

 have nevertheless shown slight buckling of nerve roots within the spinal 

 canal. The epiphyseal cartilage cells in all layers return to normal by 

 resumption of mitotic activities, growth, and maturation. U, as occurs in 

 long-continued vitamin A deficiency, a plate of bone has formed on the 

 diaphyseal side, it becomes perforated and blood vessels penetrate the 

 spaces occasioned by the degeneration of mature cartilage cells.* 



3. Bone C.howtii and thf: Nervous System 



Xo proof exists that degeneration of the nervous system results from 

 vitamin A deficiency. The long-contimied deficiency in fully grown animals 

 does not result in disabilities of nervous origin or demonstrable lesions of 

 the nervous system, in yoiuig animals, during the period of rapid growth, 

 damage to the nerxons system results from compression of brain, spinal 

 cord, and nerx'e roots caused by the retarded skeletal growth already 

 described. 



The cranial cax'ity and spinal canal fail to enlarge sufficiently to accom- 

 modate the central neivous system, which continues to grow at a normal 

 rate. The result in the cranial cavity is compression of the brain and its 

 dislocation toward the foi'amen magnum and multii)le luMuiations of the 

 cerebrum and cerebellum into the venous sinuses of the dura at sites of 



28 K. Mellanf)y, A Story of Nutritional Research: The litTcct of Some Dietary Fac- 

 tors on Bone.s and the Nervous System. Williams and Wilkins ('ompan\-, Balti- 

 more, 1950. 



