J Vet Intern Med. 1994 Jan-Feb;8(1):40-8.

Myelinolysis after correction of hyponatremia in two dogs.

O'Brien DP, et al

Abstract

Two dogs developed delayed neurological deterioration after rapid correction of severe hyponatremia. Sequential magnetic resonance imaging showed the development of lesions in the thalamus. One dog was necropsied, and the lesions were characterized by myelinolysis with sparing of axons and neurons. The second dog gradually recovered with no detectable neurological deficits. The syndrome seems analogous to central pontine myelinolysis in human beings. Guidelines for correction of hyponatremia to prevent development of myelinolysis are given.

J Am Anim Hosp Assoc. 1999 Nov-Dec;35(6):493-7.

Suspected myelinolysis following rapid correction of hyponatremia in a dog.

Churcher RK, Watson AD, Eaton A.

Abstract

A dog developed signs of neurological dysfunction five days after rapid correction of severe electrolyte derangements, including hyponatremia, caused by gastrointestinal parasitism (i.e., trichuriasis). History, laboratory findings, and onset of neurological signs following correction of hyponatremia led to a diagnosis of myelinolysis. Myelinolysis is a noninflammatory, demyelinating brain disease caused by sudden, upward osmotic shifts in central nervous system plasma, often a result of rapid correction of chronic hyponatremia. The pathogenesis is complex, but recovery is possible. Iatrogenic damage due to myelinolysis can be avoided by adherence to therapeutic guidelines for correction of chronic hyponatremia.

Can Vet J. 2003 Jun;44(6):490-2.

Neurologic complications following treatment of canine hypoadrenocorticism.

MacMillan KL.

Abstract

After treatment for hypoadrenocorticism, an 18-month-old dog exhibited marked ataxia and intermittent muscle tremors, progressing to head pressing, dysphagia, and quadraparesis. Serum sodium increased by 38.9 mmol in 48 hours, suggesting myelinolysis. The dog made a complete recovery after intensive treatment.