Clinical and morphologic features of a progressive polyneuropathy in y
oung mature Alaskan Malamutes are described. Clinical signs included p
rogressive paraparesis, synchronous pelvic limb gait, exercise intoler
ance, hyperesthesia, hyporeflexia, muscle atrophy, and tetraplegia. El
ectromyographic testing revealed diffuse fibrillation potentials and p
ositive sharp waves in limb muscles, especially in muscles below the e
lbow and stifle. Pathologic findings in skeletal muscles and periphera
l nerves included neurogenic muscle atrophy, focal or diffuse loss of
myelinated nerve fibers, myelinoaxonal necrosis, and variable demyelin
ation or remyelination. Ultrastructural changes included axonal degene
ration, presence of numerous Bungner bands, and denervated Schwann cel
l subunits. The nature and distribution of abnormal electrophysiologic
and pathologic findings were suggestive of a distal sensorimotor poly
neuropathy, which we have termed idiopathic polyneuropathy of Alaskan
Malamutes to distinguish this condition from hereditary polyneuropathy
of Norwegian Alaskan Malamutes, last described in 1982. Copyright (C)
1997 by the American College of Veterinary Internal Medicine.