J.J. van Nes

Salinomycin-induced Polyneuropathy in Cats: Morphologic and Epidemiologic Data

In April 1996, an outbreak of toxic polyneuropathy in cats occurred in the Netherlands. All cats had been fed one of two brands of dry cat food from one manufacturer. Chemical analyses of these foods, stomach contents, and liver and kidney of affected cats revealed contamination with the ionophor salinomycin. Epidemiologic and clinical data were collected from 823 cats, or about 1% of the cats at risk. In 21 affected cats, postmortem examination was performed. The affected cats had acute onset of lameness and paralysis of the hindlimbs followed by the forelimbs. Clinical and pathologic examination indicated a distal polyneuropathy involving both the sensory and motor nerves.

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 Ménétriers 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.

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.

Sensory neuronopathy in dogs: A study of four cases

A neurological disease which selectively affects the primary sensory pathways was observed in 4 dogs. Clinical signs were dominated by ataxia due to impaired position sense. Deficient or abnormal pain sensation was also observed. Difficulty in eating probably arose from oral and lingual sensory deficit. The lesions were characterized by degeneration and loss of central and peripheral primary sensory axons, with a predilection for large myelinated fibres. The concept of a sensory neuronopathy was supported by the finding of neuronal degeneration and loss in dorsal root ganglia seen in 2 dogs. The cause of the disease is not known. The presence of mononuclear inflammatory cells in acute lesions suggests an infectious or autoimmune disease. Toxic and genetic factors are also to be considered.

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. Inmunohistochemistry 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.

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

Summary 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.

Cerebellar cortical abiotrophy in two portuguese podenco littermates

Summary 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.Summary 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.

Hereditary necrotising myelopathy in Kooiker dogs

A retrospective clinicopathological study of a neurological disorder in 22 Kooiker dogs (Dutch decoy dog) was made. The disease was found to occur equally in both sexes and clinical signs began at three to 12 months old. Physical examination revealed a progressive paresis of the hindlimbs. Post mortem examination showed symmetrical areas of malacia in the ventral, lateral and dorsal white matter of the spinal cord. In one dog dorsal white matter was spared. Cervical segments C4 to C8 were involved in all subjects. Rostral and caudal to these areas, Wallerian degeneration was prominent. The disease has much in common with similar myelopathies in the Afghan hound and the rottweiler. Indications of heritability were the similarity in clinical and pathological findings, the age of onset of the disease, and the significantly higher inbreeding coefficient in the patients than in the breed population (P = 0.001). All patients were descended from one pair. Segregation analysis suggested inheritance involving a simple autosomal recessive trait.

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.

Clinical application of neuromuscular electrophysiology in the dog: A review

Summary A review of the literature concerning the application of electromyography and electroneurography in canine neurology is presented. Measurements of amplitude and duration of motor unit potentials in normal dogs varied largely in the various reports. It was therefore concluded that these measurements are of limited clinical value. The results of motor and sensory nerve conduction studies in normal dogs are summarised. The differences between the methods used are discussed. It is concluded that variations in reported normal values are due mainly to differences in method. The application of electromyography and electroneurography in neuromuscular disorders in the dog is systematically presented, based upon the reported diagnoses. The considerable number of first descriptions of newly‐recognised and described neuromuscular diseases appears to be related to the introduction of neuromuscular electrophysiology into veterinary medicine.