Abstract

A northern fur seal pup estimated to be approximately 6 months old, stranded and was admitted into rehabilitation. Head bobbing, intention tremors and ataxia that were far more pronounced on land than in the water led to suspicion of cerebellar disease. All lab work and other physical examination findings were within normal limits. Radiographs of the head and thorax and ultrasound of the caudal brain and abdomen were within normal limits. MRI was performed using T1W (pre and post gadolinium administration), T2*W, T2W and FLAIR sequences and revealed a normal cerebellum and bilaterally symmetric lesions affecting the rostrolateral aspect of the caudate nucleus. Characterization of the changes among the MRI sequences indicated active inflammation or necrosis limited to the rostrolateral aspect of the caudate nucleus bilaterally. Differential diagnoses included hypothiaminosis, toxin induced inflammation (including but not limited to domoic acid toxicosis) or immune mediated disease.

Based on imaging alone the cause of the changes to the caudate nuclei could not be determined. Similar imaging findings affecting only the caudate nucleus with a bilaterally symmetric distribution were not identified in the literature in any species, marine mammal or terrestrial.

Supplementation with vitamin B did not alter the clinical signs. Prednisone therapy was administered for three weeks and resulted in a mild improvement in signs. Termination of the steroid therapy resulted in marked deterioration and progression of the clinical signs that led to the decision to euthanize the patient.

The clinical signs were more suggestive of cerebellar disease than forebrain disease, and the imaging findings were unexpected. A literature search revealed that canines show similar clinical signs when their caudate nuclei are altered experimentally using drugs, suggesting that the clinical signs were consistent with the lesions observed in this very unusual case.