Immune-mediated polyneuropathy in cats: Clinical description, electrodiagnostic assessment, and treatment

Abstract

Background: Suspected immune-mediated polyneuropathy has been increasingly reported in cats, especially in the last decade, but the condition remains poorly understood.

Objectives: Refine the clinical description and review the classification of this condition based on electrodiagnostic investigation and evaluate the benefit of corticosteroid treatment and L-carnitine supplementation.

Animals: Fifty-five cats presented with signs of muscular weakness and electrodiagnostic findings consistent with polyneuropathy of unknown origin.

Methods: Retrospective, multicenter study. Data from the medical records were reviewed. The owners were contacted by phone for follow-up at the time of the study.

Results: The male-to-female ratio was 2.2. The median age of onset was 10 months, with 91% of affected cats being <3 years of age. Fourteen breeds were represented in the study. The electrodiagnostic findings supported purely motor axonal polyneuropathy. Histological findings from nerve biopsies were consistent with immune-mediated neuropathy in 87% of the tested cats. The overall prognosis for recovery was good to excellent, as all but 1 cat achieved clinical recovery, with 12% having mild sequelae and 28% having multiple episodes during their lifetime. The outcome was similar in cats with no treatment when compared with cats receiving corticosteroids or L-carnitine supplementation.

Conclusions and clinical importance: Immune-mediated motor axonal polyneuropathy should be considered in young cats with muscle weakness. This condition may be similar to acute motor axonal neuropathy in Guillain-Barré syndrome patients. Based on our results, diagnostic criteria have been proposed.

Keywords: feline; juvenile; nerve conduction; neuromuscular; peripheral nerve; weakness.

FIGURE 1

Animal ages at the time of the electrodiagnostic study.

FIGURE 2

Motor nerve conduction study. (A) Distal compound muscle action potential amplitude for each nerve. (B) Motor nerve conduction velocity for each nerve. Reference values are shown in gray.

FIGURE 3

F‐ratio for sciatic‐fibular and radial nerves. Reference values are shown in gray.

FIGURE 4

Histochemical evaluation of muscles of the same cat. (A) Diffuse variability in myofiber size without necrosis or inflammatory cells in the biceps femoralis muscle (hematoxylin and eosin stain, bar = 200 μm). (B) Intramuscular nerve showing fibers loss and fibrosis in the tibialis cranialis muscle (modified Gomori's trichrome stain, bar = 100 μm).

FIGURE 5

Kaplan‐Meier estimate curve of the risk of developing a relapse.

FIGURE 6

Analysis of duration of the studied episode. Four cats are not included: time from examination to recovery could not be estimated for 3 cats because of sequelae and duration of signs at presentation was missing for 1 cat. (A) Distribution of duration of episodes depending on treatment. The 3 cats receiving corticosteroids in the absence of significant improvement after 1 month with L‐carnitine supplementation were excluded. (B) Distribution of duration of episodes for cats with and without history of previous episodes.