In a retrospective study of twenty-nine spinal tumours in dogs and cats approximately equal numbers of extradural and intradural tumours were found. The most prominent tumour type was the group of primary tumours of bone which included osteosarcomas, fibrosarcomas, hemangiosarcomas and multiple cartilagenous exostoses. Primary sarcomas of the spinal cord were the next most prominent type of tumour identified. A close clinicopathological correlation was found for tumour localization; however, intradural and extradural tumours could not be differentiated clinically. In comparison with extramedullary tumours which were evenly divided between acute and insidious onset, the majority of animals with intramedullary tumours had acute onset of neurological signs. In general, the intramedullary tumours had the shortest duration of clinical signs (1.7 weeks) whereas the extradural tumours had a mean duration of 3-4 weeks and intradural-extramedullary tumours had the longest mean duration (5-7 weeks). Contrast radiography was the most useful diagnostic aid. It confirmed the regional localization in twenty-two of twenty-four animals and the topographic localization in nineteen of twenty-four animals.
Facial nerve paralysis of acute onset is reported in seven mature dogs, five of which were cocker spaniels. The clinical signs were characterised by ear drooping, lip commissural paralysis, sialosis, and collection of food on the paralysed side of the mouth. All dogs showed absent menace responses and trigeminofacial/acousticofacial reflexes. Horner's syndrome was not present in any dog. In four dogs, bilateral facial paralysis developed. The facial paralysis was unrelated to otitis media. Electrodiagnostic studies revealed denervation potentials and absent evoked muscle potentials. Facial nerve biopsies from two cases showed nerve fibre degeneration and apparent loss of larger diameter myelinated fibres. The condition has been termed idiopathic facial paralysis since the aetiopathogenesis is presently unknown.
Seven Domestic shorthair cats with a lysosomal storage disorder analogous to human Niemann-Pick disease type C,from a breeding colony were studied to characterize the neurological manifestations of this disorder. Affected cats were identified by means of liver biopsies at 4 to 6 weeks of age. Neurological examinations were performed at 2 week intervals from the onset of clinical signs. All cats displayed signs referrable to the cerebellum, with a subtle intention tremor noticed initially at 8 to 1 2 weeks of age; the disease was rapidly progressive. The tremor became more pronounced, menace response was lost, and severe dysmetria ysosomal storage diseases are inborn errors of metabo-L lism in which specific deficiencies of degradative enzymes cause substrate accumulation and resultant cellular and clinical dysfunction.' The sphingomyelin lipidoses, better known as Niemann-Pick disease, encompass a heterogeneous group of lysosomal storage disorders characterized by the accumulation of variable amounts of sphingomyelin and other lipids in organs of the reticuloendothelial system. Nervous system involvement may or may not be present. Six types of Niemann-Pick disease, designated types A through F, and inherited as autosomal recessive traits are recognized in human beings. They are classified according to the age of onset and progression of disease, degree of hepatosplenomegaly, extent of nervous system involvement, and level of sphingomyelinase activity. I A recently proposed classification scheme for the sphingomyelin lipidoses addresses disparities in sphingomyelin accumulation and sphingomyelinase activity.293 Group 1 includes sphingomyelinase deficient types A, B, and F. Types C, D, and E are included in group 2, and do not have consistent decreases in sphingomyelinase activity. The two groups are further divided into subacute (S), acute (A), and chronic (C) forms based on the age of onset and severity of symptoms and prognosis.Niemann-Pick disease type C (NPC) is included in group 2s and is manifested by progressive neurological deterioration and hepat~splenomegaly.~.' The lipid storage pattern in NPC disease is complex. Neurovisceral accumulation of sphingomyelin, cholesterol, glycolipid, and bis(monoacy1-glycero1)phosphate is characteristically noted.',* Neuroaxonal dystrophy also occurs, and is considered the hallmark of neurological disease.6 The biochemical defect responsible for lipid accumulation is not completely understood, but deranged cholesterol metabolism, with a resultant increase in unesterified intracellular cholesterol, has been documented in fibroblasts from affected individuals.' Studies suggest that intracellular translocation of cholesterol from lysosomes to other cell compartments is impaired.' Cholesterol accumulation may impair lysosomal function, resulting in the heterogeneous pattern of lipid acc~mulation.~ A model of NPC has been reported in mice." Lowenthal et a1 recently also described the disease in a Domestic shorthair cat noted to be ataxic at 6 weeks of age.' Neurological exami...
Abstract. A 1.3-year-old Great Dane dog had a chronic progressive neurologic disease clinically expressed as a distal symmetrical polyneuropathy characterized by weakness and bilateral atrophy of bulbar and distal appendicular musculature. Qualitative and quantitative studies showed neurogenic atrophy of muscles below the elbow and stifle. There was Walleriantype degeneration, Schwann cell proliferation and cell bands of Biingner, and marked depletion of medium (5 to 8 pm) to large (9 to 15 pm) diameter myelinated fibers in the distal parts of appendicular and laryngeal nerves. Sensory (saphenous and superficial radial) and autonomic (sympathetic and dorsal vagal trunk) nerves were affected to a lesser degree. A distribution of distal axonal degeneration suggested a dying back process. The disease differed from classical dying back disorders by absence of axonal degeneration in selected pathways of the central nervous system.
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