Multihormonal islet cell carcinoma in a greater bushbaby (Galago crassicaudatus argentatus).

the synthesis or assembly of the molecules of compact myelin. Blakemore et a1.l reported that protein and lipid analyses of myelin from affected white substance were not abnormal except for some lowering of total protein content. Internodal myelin and much of that surrounding the paranodes appears normal. Some circumferential thinning of myelin sheaths has been described, but no lesions of the inner or outer tongues were reported.’ The longest focal lesions are well short of the length of any internode thus emphasizing their paranodal character. Although Blakemore et a1.l reported some specialized contact points between processes and axon, it may be that the profuse process proliferation interferes with the establishment of the normal array of axoglial tight junctions.’.o This may breach the integrity of the axoglial space and cause conduction abnormalities.’ Fluid distending interlamellar and adaxonal spaces may account for the marginal vacuolation seen in many foci. Some eventual disruption of formed compact myelin in the affected paranodes could explain the lux01 fast blue-positive granules seen in many foci. The large cells, called hypertrophic oligodendrocytes by Blakemore et al.’ resemble the immature oligodendrocytes of active myelination. Perhaps an inability to switch off the proliferation of fine processes explains the continuing cytologic picture of high metabolic activity shown by these cells. The shape and dimensions of the focal lesions are related to the three dimensional anatomy of white substance. Peters et aL5 have observed that nodes of Ranvier frequently appear in groups in transverse sections and propose that each group reflects sheaths formed by the ultimate processes of one of the several major processes of an oligodendrocyte. Each focal lesion is thus a clump of affected paranodes. There are no large confluent lesions; each group of abnormal paranodes remains discrete. The relatively late onset and progressive nature of the disease may reflect the slow persistent proliferation of fine processes with consequent failure to adequately ensheath the growing axon and to establish normal axoglial tight junctions.