Pathology of the Axons

Degeneration of the axons occurs in a number of diseases: traumatic, demyelinating, infectious, metabolic, and ischemic. The injured axons swell, become fusiform, and disintegrate into small argyrophilic fragments that are gradually removed by macrophages. Early degeneration of axons is readily detected with immuno-histologic stain using antibodies against P-amyloid precursor protein (P-APP) (Fig. 2.4).The P-APP- immu-noreactivity of damaged axons precedes changes observed in conventional histologic stain.

Axonal spheroids are round, homogenous, or slightly granular eosinophilic and argyrophilic structures commonly found in traumatic shearing injuries and at the edge of infarcts. They consist of axoplasm extruded from the disrupted ends of the axons (see Fig. 2.4).

Axonal torpedo, a fusiform enlargement of the proximal portion of the Purkinje cell axon, frequently occurs in cerebellar cortical degenerations (see Fig. 2.4).

Dystrophic axonal spheroids are distinctive histo-logic features of infantile neuroaxonal dystrophy. They also may occur in congenital biliary atresia, mucoviscido-sis of children, and in nucleus gracilis of elderly subjects.

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