A diffuse, bilaterally symmetrical leucoencephalopathy was observed in a 2-month-old female crossbred puppy with a clinical history of progressive tetraparesis with front limb hypermetria, head tremor and seizures. Severe myelinolytic lesions with significant macrophage infiltration were confined to the white matter, mainly of the cerebellum and spinal cord. Moderate loss of myelin with severe gliosis predominated in the cerebrum. Axonal degeneration and axonal loss accompanied myelin degeneration. This disease was classified as a leucodystrophy. The clinical signs and certain features of the lesions (morphology and distribution), differed from those in previously described degenerative myelinolytic diseases in animals. The possible occurrence of the disorder in a littermate suggested a genetic basis.

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The effect of levamisole on the canine central nervous system.

Levamisole was given orally to 3 groups of dogs, totaling 56 animals. Drug administration period varied from 1 to 120 days. All animals were killed and the central nervous system was examined histologically. Lesions were found in 44 of 56 dogs. These consisted of disseminated perivascular cuffing with mononuclear cells throughout the brain and meninges. The severity of the perivascular cuffing varied considerably and could not be correlated to the length of the drug administration period nor to any other variables. There was no damage to the neural tissues associated with the perivascular cuffing. There was evidence of regression of the lesions whether levamisole treatment was continued or not. The changes observed in this study were considered to be related to the known immunomodulating properties of levamisole. The pathogenesis of this change in uncertain.

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Identification of canine glial cells by nonradioactive in situ hybridization.

Studies on the development of the canine central nervous system and on demyelinating diseases demand unequivocal identification of the glial cells. For that reason, nonradioactive in situ hybridization (ISH) was performed in primary dog brain cell cultures (DBCC) and in brain sections of neonatal dogs. Specific RNA probes were used to detect messenger RNA (mRNA) coding for proteolipid protein (PLP), myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP). PLP and MBP are markers for oligodendrocytes, GFAP for astrocytes. Oligodendrocytes positive for PLP and MBP mRNA were found in both DBCC and brain sections of neonatal dogs. Astrocytes expressing GFAP specific mRNA were detected in DBCC and in brain sections. These cells were evenly distributed in the white matter with additional accumulation in the membrana limitans gliae superficialis, around the ventricles and blood vessels. ISH clearly improves the study of oligodendrocytes in brain sections as, in contrast to the immunohistochemical methods, this technique allows to identify individual cells.

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Multisystem neuronal degeneration in cocker spaniels.

Four young Cocker Spaniels had slowly progressive neurologic signs with ataxia and mental deterioration. Pathologically, the lesions consisted of diffuse nerve cell loss, gliosis, axonal degeneration, and some demyelination in several areas of the brain. Pedigree analysis strongly suggests a hereditary cause for this disease, which is classified as a multisystem neuronal degeneration. This disorder has not been previously reported and has some resemblance to certain degenerative neurologic diseases found in humans. The clinical differential diagnosis includes cerebellar degeneration and lysosomal storage diseases. A definitive diagnosis requires postmortem examination.

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Congenital tremor with spongy degeneration of the central nervous system in two puppies.

Two crossbred puppies exhibited a generalized tremor that was accentuated by excitement or voluntary movement. Hypermetria was also present. Neurohistologic examination showed a bilaterally symmetric spongy condition, predominantly of the gray matter in the brain and spinal cord. These two dogs were different, both in their clinical presentation and histologic appearance, from other reported cases of spongy degeneration. The clinicopathologic correlation between spongy degeneration and tremor is unclear. Spongy degeneration should be included in the differential diagnosis of tremor syndromes in puppies.

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A tremor syndrome with a central axonopathy in Scottish terriers.

A central axonopathy in 2 male and 1 female Scottish Terrier puppies from 3 different but related litters is reported. Clinical signs consisting of severe whole-body tremors and ataxia were first detected at the age of 10 to 12 weeks. They worsened with activity and excitement and diminished during rest or sleep. Two dogs also had paraparesis. In 1 dog the neurological deficits progressed over several months. Neuropathological examination revealed widespread axonal changes, vacuolation, and gliosis in the white matter of the central nervous system.

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PubMedDate not supplied

Necrosis of hippocampus and piriform lobe in 38 domestic cats with seizures: a retrospective study on clinical and pathologic findings.

The clinical records of 38 cats (1985-1995) with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and occasionally the lobus piriformis were evaluated retrospectively. There was no sex or breed predisposition. Most cats were between 1 and 6 years of age (mean age 35 months) and had either generalized or complex-partial seizures of acute onset and rapid progression. The seizures had a tendency to become recurrent and to present as clusters or even status epilepticus later in the course of the disease. Fourteen cats died spontaneously, and 24 were euthanized. Histopathologic examination revealed bilateral lesions restricted to the hippocampus and occasionally the lobus piriformis. The lesions seemed to reflect different stages of the disease and consisted of acute neuronal degeneration to complete malacia, affecting mainly the layer of the large pyramidal cells but sometimes also the neurons of the dentate gyrus and the piriform lobe. The clinical, neuropathologic, and epidemiologic findings suggest that the seizures in these cats were triggered by primary structural brain damage, perhaps resulting from excitotoxicity. The cause remains unknown, but epidemiologic analysis suggests an environmental factor, probably a toxin.

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PubMedDate not supplied

[A comparative study of two methods of cytological evaluation of spinal fluid in domestic animals].

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