Periventricular spread of primary central nervous system T-cell lymphoma in a cat.

A 9-year-old domestic shorthaired cat with clinical signs of neurological disease was determined to have primary T-cell lymphoma of the central nervous system (CNS) on necropsy examination. Microscopically, neoplastic lymphocytes were distributed in the CNS parenchyma bilaterally around the cerebral ventricles, third ventricle, mesencephalic aqueduct, fourth ventricle and central canal of the spinal cord. The neoplastic infiltration was associated with complete loss of ependymal cells and marked astrocytosis. A large, solitary neoplastic lesion was present in the parenchyma around the central canal of the spinal cord at the level of the 13th thoracic vertebra. Immunohistochemically, the majority of neoplastic cells expressed CD3 and many also labelled for proliferating cell nuclear antigen (PCNA) and Ki-67. This is, to our knowledge, the first report of periventricular spread of primary CNS T-cell lymphoma in animals.

Histopathological and ultrastructural features of feline hereditary cerebellar cortical atrophy: a novel animal model of human spinocerebellar degeneration.

Human spinocerebellar degeneration is one of the intractable diseases. We studied the detailed neuropathology of cats with hereditary cerebellar degeneration obtained from the experimental breeding. The findings included almost total loss of Purkinje cells with an increase in Bergmann's glia in the cerebellar hemisphere, preservation of some Purkinje cells in the vermis and moderate neuronal depletion of the olive nucleus. Cerebellar and pontine nuclei were normal. The cerebrum and spinal cord as well as the peripheral nervous system appeared normal. Electron microscopic examination revealed swelling of the distal dendrites of Purkinje cells in the less-affected nodule of the vermis, and clusters of presynaptic boutons without any synaptic contact in the severely affected folia where Purkinje cell bodies and dendrites disappeared. Prolonged existence of presynapses in the molecular and Purkinje cell layers was confirmed by positive immunoreactivity to anti-synaptophysin. Quantitative analysis using electron microscopy demonstrated an apparent increase in the density and mean size of presynapses in the molecular layer of the severely affected folia. These findings indicate that degeneration of Purkinje cells started at the most distal part of the dendrite in this animal model of cerebellar degeneration, and that presynapses, axon terminals of the granular cells and basket cells can exist for a long time even after complete degeneration of the Purkinje cells. Further investigation of this novel animal model may promote a better understanding of pathogenesis of human hereditary cerebellar degeneration.

Clinical and pathological findings of a Yorkshire terrier affected with necrotizing encephalitis.

A three-year-old, male Yorkshire terrier was presented with blindness, circling, hind limb weakness, and convulsive seizure for the past 3 months. Characteristic clinical findings were chronic, progressive neurological signs involving cerebrum and brain stem, an elevation of brain-type isoenzyme of serum creatine kinase, appearance of high voltage slow activity in electroencephalogram, and multifocal lesions in the cerebral hemispheres on magnetic resonance imaging. Necrotizing encephalitis of Yorkshire terrier was diagnosed after postmortem pathological examination. This is the first case report of the disease in Japan.