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Biomedical subjects

J J van Nes

Publications and source records attributed to J J van Nes.

At least 19 recordsLinked to original sources
PubMed2000

Fibrocartilaginous embolism of the spinal cord (FCE) in juvenile Irish Wolfhounds.

This study describes the occurrence of fibrocartilaginous embolism of the spinal cord (FCE) in eight juvenile Irish Wolfhounds that were presented within a period of 16 months (1996-1997). The dogs, seven males and one female between eight and 13 weeks of age, were presented because of an acute onset of abnormal locomotion. Five dogs were euthanized and FCE was diagnosed by the histomorphological presence of focal myelomalacia and Alcian blue-positive-nucleus-pulposus material in the spinal cord vasculature. Three dogs, which were thought to have FCE because of their clinical symptoms, improved with partial or almost complete return to normal locomotion. Although the observed high incidence may be a coincidence, oral information from breeders and lay reports of similar cases in journals for dog breeders from various countries suggest that FCE is a common disorder in young Irish Wolfhounds.

Animals↗
PubMed2000

Cerebellar cortical abiotrophy in two Portuguese Podenco littermates.

Cerebellar cortical abiotrophy in two Portuguese Podenco littermates is reported and discussed. The disease is characterized by progressive cerebellar ataxia with an early onset of two to three weeks. Extensive loss, degeneration, and necrosis of Purkinje cells particularly involved the cerebellar hemispheres. An autosomal recessive pattern of inheritance is suspected.

Animals↗
PubMed1998

A neuronal vacuolar disorder in young rottweiler dogs.

Four rottweiler pups from two litters developed severe progressive signs of spinal ataxia, cerebellar ataxia and tetraparesis/paralysis. The signs started with ataxia of the pelvic limbs at seven to eight weeks of age and progressed to tetraparesis and paralysis within three to five weeks. Postmortem, a vacuolar neuronal disorder was found in the cerebellum, brainstem and the spinal cord, associated with Wallerian type degeneration in the brainstem, cerebellar peduncles and the medullary cord. Electron microscopy revealed empty membrane-bound vacuoles. Immunohistochemistry for PrPSc was negative. The disorder differs clinically and pathologically from other neurological disorders in the breed and a new (familial) neurological disorder in the rottweiler is suspected.

Animals↗
PubMed1997

[Epidemic of nutritional polyneuropathy in the cat. Final report of the investigational team].

In June 1996 companion animal practitioners received a report prepared by the Faculty Investigative Team on the outbreak of polyneuropathy among cats, and at the end of August a 'definitive' bulletin was circulated by Spillers Petfoods. The coccidiostatic drug salinomycin, which was present in the vitamin premix supplied by a third party, was considered the cause of the neuropathy. The investigative team is of the opinion that all veterinary practitioners in the Netherlands should receive a conclusive report about the epidemic because of the unique nature of the epidemic, which despite its sudden outbreak could be well documented, and because aspects of the affair merit the attention of veterinary practitioners.

Animals↗
PubMed1997

Progressive neuronopathy in two Cairn terrier litter mates.

Clinical, histopathological, and EM findings are described for two Cairn terrier litter mates, an 18-months-old male and an 11-month-old female with progressive neuronopathy. The initial clinical signs were characterized by hind limb weakness and ataxia, which deteriorated with exercise. These signs progressed over several months to tetraparesis. Pathological examination revealed extensive chromatolytic degeneration of neurons and moderate secondary Wallerian-type degeneration in the spinal cord and brain stem. Progressive neuronopathy can be differentiated clinically from globoid cell leukodystrophy, another progressive neurological disorder in Cairn terriers, by the exercise-induced deterioration of the neurological signs. Progressive neuronopathy occurs only in Cairn terriers and because of the similarity in age of onset and the occurrence in one litter, an inherited disease is suspected.

Animals↗
PubMed1996

Acute idiopathic polyneuropathy in nine cats.

This report describes nine unrelated cats with acute idiopathic polyneuropathy. All cats presented with acutely developing tetraparesis or tetraparalysis and loss of spinal reflexes. Seven cats recovered completely within 4 to 6 weeks, without any medication. Two years after complete recovery, none of these cats had had a relapse. In the acute stage, two cats were euthanized because of respiratory complications. Postmortem examination was performed on one of these cats and revealed generalized peripheral motor polyneuropathy. The clinical signs in these cats were identical to those of the Guillain-Barré syndrome in humans.

Acute Disease↗
PubMed1991

Familial stomatocytosis--hypertrophic gastritis (FSHG), a newly recognised disease in the dog (Drentse patrijshond).

A newly recognised disease, which we have given the provisional name of familial stomatocytosis-hypertrophic gastritis (FSHG), is described in two families of dogs of the Drentse partrijshond breed. The affected dogs consisted of 3 females and 5 males, 3 to 19 (mean 9.5) months of age at admission. The main clinical problems were diarrhoea, icterus, and ataxia and paresis of the pelvic limbs. Laboratory evaluation revealed abnormal red cell shape (stomatocytosis), increased osmotic fragility, haemolytic anaemia, and increased liver enzymes and serum bilirubin. Gastroscopic and histopathologic examination of the gastric mucosa revealed hypertrophic gastritis resembling Ménétrier's disease in man. Histologic findings in the liver were suggestive of progressive liver disease. Cysts were found in the kidneys of the five oldest patients. Electroneurography in 2 dogs revealed polyneuropathy. In the parents of 2 patients (sister and brother), there were no clinical or laboratory abnormalities. An autosomal recessive hereditary defect of lipid metabolism is suspected.

Animals↗
PubMed1989

Pharmacokinetics of three formulations of diphenylhydantoin in the dog.

The pharmacokinetics of the sodium salt of diphenylhydantoin was studied in three healthy dogs, using three formulations, a capsule, a tablet and a suspension. The results were essentially the same for all three formulations. The serum half life after intravenous injection ranged from 3.1 to 3.6 hours before and 1.3 to 1.6 hours after a two-week period of oral treatment. The bioavailability of the formulations varied from 43 to 54 per cent. Serum levels likely to be required for canine therapy could not be maintained with any of the formulations used in this experiment.

Animals↗
PubMed1986

Progressive ataxia due to central demyelination in Rottweiler dogs.

A clinicopathological study of a neurologic disease in Rottweiler dogs was conducted. Clinical data were available on 16 dogs, 11 of which were examined pathologically. All dogs had a history of progressive gait abnormalities, which had commenced insidiously at an age varying from 1.5 to 3.5 years. In most dogs the fore limbs were affected prior to the hind limbs. At neurologic examination ataxia of all 4 limbs was seen, in some instances accompanied by an apparent paresis. Proprioceptive positioning was delayed whereas spinal reflexes were often hyperactive. Plain and contrast radiographs of the spine did not reveal any compressive lesions in 5 dogs examined. Cerebrospinal fluid analysis in 4 dogs was normal. Electrodiagnostic testing in 3 dogs revealed no abnormalities. At pathologic examination demyelinating lesions were found in the central nervous system. These were largely confined to the cervical spinal cord and brain stem and had a rather characteristic more or less symmetric distribution. Pedigree data suggested that the disease is transmitted genetically.

Animals↗