Cerebral infarction with associated venous thrombosis in a dog.

317 degeneration to loss of Purkinje cells. In the Purkinje cell layer where neurons were lost, there were empty baskets. Degenerate Purkinje cells were accompanied by axonal torpedoes in the granular layer. The empty baskets indicate Purkinje cell loss normally de~eloped,~ while axonal torpedoes are a nonspecific sign of Purkinje cell degeneration and not a consequence of developmental f a i l ~ r e. ~ Thus, Purkinje cell degeneration in the present cases may have occurred after they attained normal development and reached the proper location. In the present cases, there was a relationship between degree of Purkinje cell degeneration and severity of granular cell diminution. This suggests that granular cell alteration was secondary to Purkinje cell degeneration. Granular cells are formed from the external germinal layer later in gestation than Purkinje cells, and their formation is not complete until the postnatal p e r i ~ d. ~ Investigation of cerebellar mutant mice suggested that there was an interaction between Purkinje cells and the external granular layer, i.e., the number of granular cells formed was appropriate to the number of Purkinje cells nearby.9 In the present dogs, development of granular cells might have been disturbed by degeneration or loss of Purkinje cells. Thus, the hypoplastic process might have contributed to development of the present granular cell lesions. Early regressive changes found in the cerebellar nucleus neurons are regarded as transsynaptic degeneration after the Purkinje cell damage. Involvement of the cerebellar nuclei has been described in Airedale dogs.' The pathological features of the present cases were degen-eration or loss of normally developed Purkinje cells and ensuing granular cell lesion. Thus, cerebellar cortical degener-ation seems appropriate descriptive terminology for the present beagles.