\ii. i;kfk('ts of i)i;fi('Ii;.\(v 527 



Mackenzie ct al. ''■'■' l\i])|)('iili('inu'r,"' Marliii ami Mooic,' .Moiiiiici/ ' and 

 INIuson and l*]mm('l.' 'The liist cNidcnce of paresis is a waddlinj; and sliiihtly 

 incoordinatetl jj;ait; later tliere is i)r()n()iin( ed straddlinji; of the liind iefi;s, 

 hj'perflexion of dij^its, fial)l)iness and weakness of the mus( ulatuic in\-olving 

 the adductor tlii.iih muscles particularly dia<;,i>;in,ti i»f the hind le<2;s, ina- 

 bility to walk or stand, distinct ataxia, pronounced muscle atrophy, de- 

 formity of feet, and i>;eneral aud localized sensory disturbaucos. The ani- 

 mals are Inmip-liacked, unkempt in appearance; ulcerations of the skin 

 are common. ^V\\o skt^letal muscles are atrophic, somewhat dry or gi'itty, 

 and somewhat brownisli in color. Once the adult paresis is well-established, 

 prolonged \-itamin E therapy does no more than arrest tlie process and 

 improve the growth and well-being of the rat; that is, there results a per- 

 manent paralysis of about the degree present at the beginning of 

 therapy.'' • ''• "" This is ciuite different from the rabbit, where paresis can 

 be made to disappear and reappear repeatedly by careful regulation of the 

 vitamin E intake,*'^ and the late-lactation paralysis in rats where E therapy 

 is of little or no avail once sj'^mptoms appear. 



The histopathologic picture (Fig. 4) differs from that of late-lactation 

 paralj'sis chiefly in the relatively smaller number and widely scattered lo- 

 cation of affected muscle fibers. Edema, fragmentation, and leucocytic infil- 

 tration are less conspicuous features. Necrosis tends to involve longer fiber 

 segments, but the degenerative and regenerative processes, although proceed- 

 ing perhaps at a somewhat slower rate, are cjuite similar to those characteriz- 

 ing late-lactation paralysis. Sarcolemma nuclei appear to undergo amitotic 

 proliferation and become irregularly distributed in the fiber, followed by 

 the appearance of coarse interfibrillar granules and vacuoles, loss of cross 

 striations, breakdown of fibrillar substance, and remo\-al of debris by in- 

 vading macrophages. The latter are often marked by accumulations of 

 acid-fast pigment which commonly appears in the degenerating hbers. 

 Usually the point of segmental degeneration is marked by an area of high 

 cellular concentration which, as in the case of early dystrophy, contains 

 considerable numbers of free muscle nuclei with theii' iiuestment of sarco- 

 plasm and strongly basophilic multinucleate sti'ands which rei)r(^sent early 

 phases of a regenerative reaction. The basophilic strands gi\-e rise to slend(>r 

 muscle fibers possessing I'ows of (entrally i)laced nuclei, arising ])resinnal)ly 

 through i-apid amitotic diN'isions; such fibei's are ([uite common, and de- 

 generating fibers absent, in muscles from animals gi\-en \-itamin E therapy 



"* C. G. Mackenzie, J. IV M;ickenzie, and V.. \. .Mc( 'olluni, I'roc. .Soc. Expll. Biol. 



Med. 44, 95 (1940). 

 '^M. Monnier, CoDipl. retid. sac. phijs. ct lii.st. nut. ((icncvc) 57, 252 (1940); Inlcni. Z. 



Vitaminfursch. 11, 235 (1941). 



