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Biomedical subjects

M Vandevelde

Publications and source records attributed to M Vandevelde.

At least 145 records · Page 8Linked to original sources
PubMed1980

Multiple sclerosis and canine distemper encephalitis--an epidemiological approach.

The evolution of the incidence of canine distemper encephalitis in dogs in some areas of Switzerland over the past 30 years was studied from the neuropathological records of the School of Veterinary Medicine at Berne and compared with the incidence of multiple sclerosis, as estimated from the clinical records of the Neurologic Hospital at the same University. Even considering incubation times of up to 10 years no epidemiological relationship was found between the diseases. Whereas canine distemper encephalitis has become a rare disease since the second half of the sixties, the multiple sclerosis rate has remained approximately the same. In view of these findings, a causal link between canine distemper infection in dogs and multiple sclerosis in man seems unlikely.

Animals↗
PubMed1980

Chronic canine distemper virus encephalitis in mature dogs.

Five dogs 2 to 8 years old with old dog encephalitis were compared to five other dogs, 4 to 8 1/2 years old, with prolonged multifocal demyelinating distemper encephalitis. The dogs with old dog encephalitis had a diffuse panencephalitis involving most areas of the central nervous system with relative sparing of the cerebellum. The clinical signs were related to the cortical and subcortical lesions. The other dogs had severe focal necrotizing lesions mostly in the cerebellum and in the vicinity of the fourth ventricle; clinical signs were related to brainstem and spinal cord lesions. Viral isolation attempts were unsuccessful in the dogs with old dog encephalitis. In two dogs with multifocal encephalitis, canine distemper virus was isolated in tissue culture. The differences in lesions, clinical signs and observations in vitro indicate differences in pathogenesis between old dog encephalitis and multifocal demyelinating distemper encephalitis although both diseases may be caused by the same agent.

Age Factors↗
PubMed1980

Neuronal ceroid-lipofuscinosis in older dachshunds.

A lysosomal storage disease with accumulation of periodic acid-Schiff- and Sudan black-positive autofluorescent granules in neurons occurred in one 5 1/2- and one 7-year-old dachshund. Ultrastructurally, the storage material consisted of membranous material arranged in stacks and fingerprint patterns. The disease was defined as ceroid-lipofuscinosis, and resembled a previously reported case in an adult dachshund.

Animals↗
PubMed1979

Lead-induced encephalopathy in dogs fed high fat, low calcium diets.

Growing, mongrel dogs were fed high fat (22%), low calcium (.1%) semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity. Seizures were observed in 44% of the lead toxic dogs and microscopic encephalopathy was observed in 89% of the lead toxic dogs. The encephalopathy was characterized by bilaterally symmetrical areas of vacuole formation involving the neuropile especially in a laminar pattern at the tips of the gyri of the cerebral cortex. The spongy state was accompanied by capillary activation and gliosis. These lesions are similar to those reported in accidental lead toxicoses in other species but previous efforts to experimentally induce these lesions in young dogs fed low-calcium, normal-fat (16%) purified diets have been unsuccessful.

Animals↗
PubMed1979

Polioencephalomyelitis in cats.

Six cats with chronic progressive neurologic signs of ataxia, paresis, tremors, pupillary abnormalities and seizures had polioencephalomyelitis of probable viral origin. Lesions were most severe in the spinal cord. The uniformity in distribution and nature of the lesions in all six cats strongly suggested a common cause. The condition was compared with other viral infections of known and unknown cause.

Animals↗
PubMed1979

Polioencephalomalacia associated with canine distemper virus infection.

Eight dogs with severe neurologic signs, including seizures, had polioencephalomalacia of the pyriform cortex, Ammon's horn and deep structures in the temporal lobe. The polioencephalomalacia was considered to be a consequence of canine distemper virus infection based on clinical signs, typical inclusions, the demonstration of viral antigens in the lesions and of characteristic paramyxovirus nucleocapsids by electron microscopy. Little evidence for neuronal destruction by direct viral activity was found. Selective nerve cell necrosis was attributed to ischemia (vascular lesions and seizure induced consumptive anoxia) and immune mechanisms. The selective involvement of the rhinencephalic structures was thought to be related to the mode of entry and spread of the virus.

Animals↗
PubMed1979

Polioencephalomalacia in the dog.

Disturbance of cerebral blood flow from causes such as meningitis, thromboembolic disease and atherosclerosis was considered an important factor in the pathogenesis of polioencephalomalacia in 25 dogs. In dogs with polioencephalomalacia of undetermined cause, the distribution of lesions in neocortex and paleocortex suggested a change of neuronal metabolism secondary to cerebral anoxia/ischemia. Five dogs with canine distemper infection had bilateral necrosis of the hippocampus and pyriform cortex. Convulsions, central visual impairment and hemiparesis were the most prominent neurologic signs.

Animals↗
PubMed1979

Fascicular nerve biopsy in the dog.

A nerve fascicular biopsy technique that preserves the functional integrity of the parent nerve is reported in the dog. Fascicular biopsies from ulnar and peroneal nerves did not produce clinical sensory or motor deficits. Electrodiagnostic testing for the modalities of latency, duration, amplitude, and conduction velocities were not markedly altered after fascicular biopsies. Morphometric analysis of muscle fiber types, delineated by histochemic techniques, revealed no statistical (P greater than 0.05) difference between muscles from biopsied or control limbs. Fascicular biopsies resulted in small neuromas in all dogs.

Animals↗
PubMed1978

Spontaneous lower motor neuron disease in rabbits (oryctolagus cuniculus).

Spontaneous neurologic disease was observed in 6 to 8-week-old rabbits. Both males and females from several different litters were affected but all were sired by the same male. Clinically, the disease was characterized initially by posterior weakness and incoordination which progressed to tetraplegia within 3--4 weeks. With light microscopy there was neuronal degeneration and loss within the ventral horns of the spinal cord and brain stem and type-II fiber atrophy of skeletal muscles. Ultrastructurally the neuronal degeneration was characterized by accumulations of 100 A neurofilaments within the perikaryon. These findings are compared to diseases with neurofibrillary accumulation in animals and man.

Animals↗
PubMed1978

Dysmyelination of the central nervous system in the Chow-Chow dog.

Five Chow-Chow dogs from three different litters had generalized body tremors since birth. Histologically a severe myelin deficiency was found in the central nervous system. The peripheral nerves were normally myelinated. Electron microscopically abnormally thin myelin sheaths and completely naked nerve fibers were found. There were many astrocytes in the myelin deficient areas as well as cells with the characteristic features of oligodendrocytes but also containing fibrils. The present cases are compared to other dysmyelinating diseases and possible pathogenetic mechanisms are discussed.

Animals↗
PubMed1978

Granulomatous meningoencephalomyelitis in six dogs.

An acute progressive CNS disease characterized by fever, nystagmus, head tilt, facial paralysis, circling, and cervical pain was studied in 6 mature dogs. The term "granulomatous meningoencephalomyelitis" was proposed for the disease complex, which was characterized pathologically by disseminated granulomatous lesions having a predilection for brainstem structures.

Animals↗
PubMed1978

Immunofluorescence studies of canine distemper encephalitis on paraffin-embedded tissue.

A paraffin-embedding technique for fluorescent antibody studies of canine distemper encephalitis was developed. Specific fluorescence was demonstrated in all brain tissue from dogs with canine distemper, and when compared with tissue on cryostat sections, the paraffin-embedded tissue showed superior preservation of tissue architecture. The preservation of viral antigen was good, and the appearance of fluorescence in gray- and white-matter lesions was described. In gray matter, extensive fluorescence was found mainly in neurons; fluorescence in white matter was less extensive and was mainly associated with astrocytes.

Animals↗