Feline polyradiculoneuritis

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Acute idiopathic polyradiculoneuritis is a common inflammatory disease primarily affecting the ventral nerve roots and peripheral nerves. It is common in dogs and rare in cats. Clinical signs often develop 7-14 days after a raccoon bite or scratch ( Coonhound paralysis); however, other affected animals have no exposure to raccoons. A similar syndrome can develop in dogs and cats within 1-2 wk of vaccination. An immune-mediated reaction to raccoon saliva or other antigen is suspected. Typically, flaccid paresis begins in the pelvic limbs and progresses within 1-2 days to tetraparesis and, in some cases, facial and laryngeal weakness. Occasionally, the thoracic limbs are initially affected. Death from respiratory paralysis can occur in severe cases. Spinal cord reflexes are weak to absent, and severe muscle atrophy is evident within 10-14 days. Pain perception is intact and some dogs may appear hyperesthetic. Mentation and appetite are not affected. Urination, defecation, and tail movement usually remain normal. Analysis of CSF collected from the lumbar subarachnoid space shows increased protein with a normal cell count. Electromyography shows denervation, and nerve conduction studies show marked dispersion and prolonged latency of F-waves, indicative of slowed conduction in the ventral roots. There is no effective treatment other than nursing care, and corticosteroids are not helpful. Most affected animals begin to improve spontaneously within 3 wk, with complete recovery by 2-6 mo. Animals with severe signs and marked muscle atrophy may recover incompletely. Relapses can occur, especially in hunting dogs that frequently encounter raccoons. Pathologically there is inflammation, demyelination, and varying degrees of axonal degeneration in the ventral nerve roots and peripheral nerves.

Chronic relapsing idiopathic polyradiculoneuritis is a rare disease associated with inflammation of the nerves and nerve roots. It affects mature dogs and cats. Exercise intolerance, ataxia, and weakness develop slowly over several months. Some animals have spontaneous temporary remissions. Spinal cord reflexes are decreased, and cranial nerves may be affected. In severe cases, decreased sensation is evident. Diagnosis is based on nerve biopsy. There is non-suppurative inflammation; axonal degeneration; and demyelination of nerves, nerve roots, and, in some cases, dorsal root ganglia. The cause is unknown, although immune-mediated mechanisms are suspected. Corticosteroids are helpful in some cases, but the disease tends to slowly wax and wane, gradually becoming more severe over months to years.

Chronic inflammatory demyelinating polyneuropathy is fairly common in adult dogs and cats. Onset of tetraparesis with hyporeflexia is insidious and is sometimes accompanied by cranial nerve dysfunction. Electromyography is usually normal, but nerve conduction velocities are slowed with temporal dispersion. Nerve biopsy shows multifocal paranodal demyelination. Clinical signs usually improve with the administration of corticosteroids (eg, prednisone 1-2 mg/kg/day), although signs may relapse when therapy is stopped. The aetiology is unknown.

Trigeminal neuritis (idiopathic trigeminal neuropathy) is common in dogs and uncommon in cats. It is characterized by acute onset of flaccid jaw paralysis. Affected animals cannot close the mouth and have difficulty eating and drinking. Horner’s syndrome, facial paresis, and decreased facial sensation are also possible. The cause is unknown. Pathologically, there is bilateral non-suppurative inflammation and demyelination in the motor branches of the trigeminal nerve. Affected animals usually recover spontaneously within 3-4 wk. Fluid and nutritional support may be necessary.