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    Necrotizing meningoencephalitis associated with cortical hippocampal hamartia in a Pekingese dog

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    A 4-year-old male Pekingese dog was referred to the clinic with a history of recurrent seizures and progressive abnormal gait and behavior, which did not respond to treatment. At necropsy, a large cortical defect in the right temporo-parietal cortex, malacia of subcortical white matter, right basal nuclei, and capsula interna, as well as abnormalities of the right hippocampus were observed. Histological examination of the brain revealed moderate to severe nonsuppurative meningoencephalitis in the left cerebral hemisphere and extensive infarction-like lesions with milder inflammation in the right hemisphere. In the right hippocampus, the pyramidal cells were arranged in a gyrus-like pattern and intermingled with gemistocytic and fibrillary astrocytes. The histopathological features of the inflammatory lesions were consistent with necrotizing meningoencephalitis and resembled those described in so-called Pug dog encephalitis. The hippocarnpal changes were interpreted as dysplasia (monolateral hippocarnpal cortical hamartia), unrelated to clinical signs and necrotizing inflammatory lesions

    Fibrocartilaginous embolism in 75 dogs: Clinical findings and factors influencing the recovery rate

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    The records of 75 dogs with fibrocartilaginous embolism of the spinal cord were evaluated retrospectively. The diagnosis was confirmed histopathologically in 21 dogs (group A) and remained suspected in 54 patients (group B). The two groups were compared. Particular emphasis was placed on the description of physiotherapy procedures, recovery rates and prognostic criteria. Results demonstrated that fibrocartilaginous embolism affected mainly middle-aged, large- or giant-breed dogs. Clinical signs were peracute in onset, non-progressive and often asymmetric. Cerebrospinal fluid analysis was normal in the majority of dogs. Intramedullary swelling was the only abnormality detected on myelograms of these patients. A positive correlation was found between a poor prognosis and the involvement of intumescences, symmetrical clinical signs and decreased deep pain sensation. However, physio/hydrotherapy instituted immediately after the diagnostic work-up seemed to have a major influence on the recovery rate

    HYDROCEPHALUS WITH PERIVENTRICULAR ENCEPHALITIS IN THE DOG

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    A 3-month-old female Dalmatian dog and a 2.5-month-old Poodle dog were referred with a sudden onset of neurological syndrome consistent with hydrocephalus. Clinical signs included depression, severe ataxia, eye abnormalities and skull enlargment in one case. Postmorten examination revealed severe internal hydrocephalus with cavitation of the cerebral white matter associated with necrotizing and inflammatory lesions of the periventricular nervous tissue. Although no bacteria were isolated from cerebrospinal fluid and no infectious agents were detected in the brains, an infectious etiology was postulated

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

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    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

    Cerebellar granuloprival degeneration in an Italian Hound

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    A severe atrophy of the cerebellum was observed in a 7-monthold male Italian hound with a history of progressive ataxia and head tremor from the age of 3 months. On clinical examination, signs included severe hypermetric gait, head tremors and proprioception deficits in all limbs. At necropsy, a pronounced symmetrical reduction in size of the cerebellum was the only gross lesion observed. Histological examination of the cerebellum revealed marked thinning of the granular and molecular layers with almost complete loss of granule cells. Purkinje cells had normal morphology and distribution. These findings differ from those of previous reports of cerebellar cortical abiotrophy in dogs, which were mainly characterized by prominent Purkinje cell degeneration and loss

    "Necrosis of hippocampus and piriform lobe:clinical and neuropathological findings in two Italian cats"

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    The present paper reports the clinical and neuropathological findings in two cats with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and piriform lobe. The cats were presented because of acute onset of behavioural changes and complex partial seizures. The neurological examination suggested a forebrain lesion. The results of blood examination were within the normal range, and the cerebrospinal fluid (CSF) analysis and computed tomography (CT) scan in one cat did not show any abnormality. Despite therapy with diazepam (Valium; Roche) there was deterioration of the clinical signs and the cats were euthanased. The neuropathological examination revealed hippocampal necrosis that included the piriform lobe
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