FELINE POLIOENCEPHALOMYELITIS

(Feline Nonsuppurative Meningoencephalomylelitis)

RICHARD A. LECOUTEUR, B.V.Sc., Ph.D.
Diplomate, American College of Veterinary Internal Medicine (Neurology); Neurology/Neurosurgery

GEORGINA CHILD, B.V.Sc.
Diplomate, American College of Veterinary Internal Medicine (Neurology)

Etiology and Pathogenesis. Feline polioencephalomyelitis is a chronic, slowly progressive encephalomyelitis of unknown etiology described in immature and mature cats.  Histopathologically, the disease is characterized by neuronal degeneration and perivascular cuffing by mononuclear cells. Demyelination and axonal loss are most conspicuous in the ventral and lateral columns of the spinal cord and most severe in the thoracic spinal cord segments. Lymphocytic meningitis, neuronophagia, and glial nodules also have been described, and lesions may be found in the cerebral cortex, diencephalon, midbrain, and medullary nuclei.

The pathogenesis of the disease is unknown. A viral etiology is suspected on the basis of the histopathologic changes, although a specific viral agent has not been isolated.  The chronic clinical course, distribution of lesions, and lack of inclusions distinguish this disease from rabies, pseudorabies, and FIP, Feline panleukopenia virus, FeLV, and arboviruses have been suggested as possible agents in the pathogenesis of lesions. Further virologic and serologic tests are needed to determine the role of viral infection in the pathogenesis of this disorder. It has been proposed in a recent study that a tick-borne virus may be the causative agent in Sweden.

Clinical Findings. Clinical signs include ataxia, paraparesis, tetraparesis, hypermetria, head tremors, and localized hyperesthesia. Spinal reflexes, pupillary light reflexes, and postural reactions may be normal or depressed. Two animals have been described as having episodes of hallucinations, clawing, hissing, and biting at imaginary objects during sleep. These "seizures" preceded other clinical signs by more than 2 years in one cat. Clinical signs usually are indicative of multifocal CNS disease but may be suggestive of focal transverse myelopathy in the thoracolumbar region or lumbar enlargement. Clinical signs are slowly progressive over several months.

Diagnosis. Antemortern diagnosis is difficult and is made by ruling out other multifocal CNS diseases. Two affected cats have been reported to be leukopenic, and one affected cat had an elevated CSF protein concentration (40 mg/ml).

Treatment. Treatment of affected cats has not been reported.


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