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Cerebellar cortical atrophy in an adult Japanese macaque.

Cerebellar atrophy-hypoplasia-degeneration as a congenital or acquired lesion has been reported in many species [I, 6, IlJ but we were unable to locate any report of naturally occurring cerebellar atrophy in a monkey. An adult male, Japanese macaque (Macacafuscata) about 5 years old had a pronounced intention tremor of its head. The tremor was exaggerated with any excitement, which sometimes caused him to fall over backwards. He was capable of voluntarily stopping these ataxic movements, but only momentarily. Locomotion was otherwise normal. There was no clinical evidence of blindness. He was one of several macaques imported from Japan and had been housed in the Metro Toronto Zoo for several months. His weight was normal (13.6 kilograms) and other than the nervous disorder, he seemed in good health. Previous clinical observations and history were unknown. The monkey was killed with an overdose ofketamine hydrochloride and barbiturate, and necropsied. No lesions were seen. The cerebellum appeared to be of normal size, but was not weighed. Microscopically there was generalized depletion and degeneration of Purkinje cell neurons in the cerebellar cortex of all folia and depletion of the cells of the internal granular layer (fig. 1,2). There was moderate increase in the number of Bergmann cells in the Purkinje cell and molecular layers (fig. 2). Folia were generally thin and there was spongy degeneration of the central white matter of several folia (fig. 3). Organic mercurial poisoning (Minamata Disease) of human and non-human primates [10, II Jand other mammals [II] generally includes neuronal degeneration and perivascular cuffmg in both the cerebrum and the cerebellum [10, II]. Furthermore, in monkeys, the cerebral cortex has severest lesions and the Purkinje and the granular cell layers of the cerebellum are not affected in either acute or chronic organic mercurial poisoning [IOJ. In monkeys, cerebellar degenerative lesions may be sequels to infection with viruses of the tick-borne encephalitis complex, which have a special predilection for the Purkinje cells of the cerebellum and develop after apparent recovery from clinical encephalitis [13]. There are, however, perivascular cuffings and other residual encephalitic lesions in addition to degenerative cerebellar lesions [13]. Feline panleukopenia virus in cats and ferrets [9], bovine viral diarrhea-mucosal disease virus in cattle [7] and rat virus in rats [8] are a few of the viruses that have a predilection for the cerebellum. This results in cerebellar hypoplasia if infection occurs during the perinatal period. To date, no virus with such specificity is known to affect monkeys naturally. Cases of heredodegenerative diseases of the cerebellum have been describedin man [I, 5], dogs [2, 3], horses [4J and possibly cattle [l2J. In our case, a specific cause could not be determined. Although this may have been an acquired lesion, there is also the possibility that this is an hereditary cerebellar atrophy/abiotrophy similar to that in man.