Peer-reviewed veterinary case report
Hereditary nerve disease causing paralysis in young cats
By Carmichael, K P et al.·Published in Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc·1993·College of Veterinary Medicine, United States·View original on PubMed →
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Original publication title: Neuroaxonal dystrophy in a group of related cats.
- Species:
- cat
Plain-English summary
A group of related cats aged 6 to 9 months suddenly developed problems with their back legs, starting with difficulty walking (hind limb ataxia) that progressed to weakness and paralysis. This condition, resembling a hereditary disorder known as feline hereditary neuroaxonal dystrophy, was linked to specific changes in their brain and spinal cord. Unfortunately, there is no known treatment for this condition, and the affected cats may face serious mobility challenges. Owners of affected cats should consult their veterinarian for guidance on managing symptoms and providing supportive care.
People also search for: cat hind leg weakness · feline hereditary neuroaxonal dystrophy · cat paralysis treatment · young cat walking problems
Abstract
A syndrome resembling previously described feline hereditary neuroaxonal dystrophy (FHND) was diagnosed in a litter of cats. The disorder was characterized by a sudden onset of hind limb ataxia that slowly progressed to hind limb paresis and paralysis. The cats were between 6 and 9 months old when clinical signs were first noted. Histologically, there was marked ballooning of axonal processes, with spheroid formation and vacuolation in specific regions of the brain and spinal cord. Some dystrophic axons contained a central periodic acid-Schiff (PAS)-positive core. Neuronal loss and gliosis were seen in certain brain stem nuclei, spinal cord nuclei, and the cerebellum. Ultrastructurally, there was hypomyelination and dysmyelination of affected axons. The PAS-positive core in dystrophic axons corresponded ultrastructurally with accumulations of electron-dense, flocculent, amorphous material. In addition, these axons contained membrane-bound osmiophilic bodies and large nonmembrane-bound vacuoles. The syndrome in this report differs from the previously described FHND in that no inner ear involvement was seen and onset of clinical signs occurred at a later age. In addition, although some of the affected cats did have diluted coat colors, abnormal coat color was not always associated with clinical disease. This disease is similar to juvenile neuroaxonal dystrophy in children and to neuroaxonal dystrophies described in horses, dogs, cattle, and sheep.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/8286459/