By Abouzeid, Ola Abdelaziz.
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EM, x 3500 Fig. 14 a-d. Invasion of phagocytes into the myelin sheaths (myelin stripping) in acute multiple sclerosis. a Same lesion as described in Fig. 13; a phagocyte between the axon and the myelin sheath (arrow) Toluidine blue,x 1000. b,c21-year-old malewithsubacuteMS, leading to death 14 months after onset of the disease; relapsing disease course with rapid progression during the last 4 months; active lesion in the brain stem. b Phagocyte with debris, invaded between lamellae of the myelin sheath (arrow).
1980). During the following remission there is some perivascular accumulation of IgG but not of fibrinogen. It is at present not resolved to what extent perivascular IgG in this stage of the disease is derived from the circulation or locally produced in perivenous plasma cells. With the onset of a relapse of the disease in the chronic stage, some perivascular accumulation ofIgG and fibrin is noted which is, however, much less pronounced compared with that in the acute disease episode and restricted to the demyelinating plaques.
Fig. 18 a-g. Legend e page 52 51 All these observations suggest that in EAE myelin is the primary target in the pathogenesis of plaque formation. As myelin and oligodendrocytes share some antigens, these cells may be secondarily destroyed to a variable extent in an immunological attack directed against myelin. This view is further supported by the fact that sensitization with oligodendrocyte preparations results in a disease morphologically identical to that found after sensitization with white matter or myelin (Raine et al.