This phenomenon is less frequently observed in dogs compared with cats, due presumably to the dogs higher tolerance to chronic hyperglycemia.
In concert with neuropathy, microvascular pathologies lead to varying degrees of [[nephropathy and retinopathy.
Hyperglycemia has been show to cause nerve degeneration in many peripheral nerves including sympathetic nerves (motor nerve to muscles) and autonomic nerves. These changes are thought to involve perineurial thickening and swelling, manifesting clinically as a neuropathy of:
- Vagus nerve - cardiac control,
- Vagosympathetic trunk - Horner's syndrome
- Pudendal nerve and pelvic splanchnic nerve - dysuria
- Celiac nerve - loss of intestinal motility control
Clinical signs in affected dogs is weakness, muscle atrophy, ataxia, hyporeflexia, hypotonia and hypotension. Urinary incontinence due to diabetic uropathy is also reported in the dogs, due to progressive demyelination of pudendal and splanchnic nerves and consequential bladder nerve dysfunction.
The diagnosis of diabetic polyneuropathy is based on clinical signs, electromyographic abnormalities, nerve biopsies, and muscle biopsies. Electrodiagnostic abnormalities consistent with a diagnosis of polyneuropathy include spontaneous electrical activity, decreased M-wave amplitude (suggestive of axonal disease), and markedly slow motor and sensory nerve conduction velocities (suggestive of demyelinating disease).
Histopathological findings consistent with canine polyneuropathy are axonal degeneration with segmental demyelination and remyelination.
Treatment is primarily aimed at rectifying the hyperglycemia associated with diabetes.
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