Canine polyneuropathy is a neurological disease of dogs characterized by a dysfunction of multiple peripheral nerves.
This disease can be observed as either a primary genetic X-linked condition or as a result of underlying secondary disease such as is commonly observed with peripheral neuropathy associated with diabetes mellitus.
Somatic nerve dysfunctions are most predominant, but autonomic nerves may also be affected.
The cause of this disease is diverse, including infectious, immune-mediated, hereditary conditions or in association with neoplasia, drug reactions and endocrinopathies such as diabetes mellitus, hypothyroidism, insulinoma, multicentric lymphoma or disseminated carcinoma.
Breed-associated polyneuropathy in Rottweiler, Border Collies, Pyrenean Mountain Dog, Leonberger and Alaskan Malamutes have been reported, with onset of disease occurring at 2 to 5 months of age, with variable phenotypic expression ranging from sub-clinical to severely affected forms. In the Rottweiler, laryngeal paralysis appears to occur commonly as a concurrent condition.
Clinical symptoms are associated with peripheral neuropathy signs such as hindlimb ataxia, reduced reflexes, forelimb hemiparesis, paddling-gait, which often progress to paralysis and sensory deficits. Regurgitation, vomiting and coughing may be observed associated with megaesophagus and aspiration pneumonia.
Blood tests, urinalysis and CSF testing are usually unrewarding. Electromyographic evidence of denervation and 52 decreased nerve conduction velocity has been observed in affected nerves.
Diagnosis usually requires tissue biopsy of peripheral nerves. Histopathologically, there are characteristic axonal swelling and pale myelin observed, with giant axons mimicking giant axonal neuropathy, atrophic axons and severe interstitial edema.
Variant forms include chronic inflammatory demyelinating polyneuropathy (observed in a Rottweiler and Miniature Schnauzers), greyhound polyneuropathy and acral mutilation syndrome (sensory neuropathy).
Electromyography studies usually show reduced reduced nerve conduction velocity.
Treatment requires identifying any underlying disease process and address this initially, followed by prednisolone or pulsed dexamethasone therapy.
Dogs with less severe clinical signs often have good quality of life parameters.
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