CT/MRI Society Case of the Month
Publication Date: 2008-06-20
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History
8-year old male, castrated mixed breed dog with a history of acute collapse. On physical examination at the rDVM, the dog had weak pulses, pale mucous membranes, tachycardia, and dehydration. The dog was fluid resuscitated and admitted to the Animal Medical Center for further evaluation. The dog was quiet, alert and responsive on admission with normal hydration status. Neurologic exam was initially normal but the dog deteriorated over the next 24 hours. The dog became recumbent and minimally responsive to stimuli on physical examination.
Findings
Images: Top Row: T2-weighted images of the brain from the level of the caudate nucleus to the rostral mesenchephalon. Middle Row: T1-weighted images at the same level as above. Bottom Row: Fluid attenuated inversion recovery (FLAIR) images at the same level as above. NOTE: These regions did not contrast enhance (not shown). No abnormal contrast enhancement was identified on post-contrast T1-weighted images.
Bilateral, focal T2-hyperintensities are present within the left and right thalmus. The region is oval and more discrete on the right and larger yet more poorly marginated on the left. These areas are mildly hypointense on T1-weighted images and remain hyperintense on FLAIR images.
Diagnosis
Most consistent with a metabolic encephalopathy. Considering the history, myelinolysis following correction of an electrolyte disorder (namely hyponatremia) was considered most likely. Toxicity, seizure-edema, or vascular compromise could not be completely ruled out.
Discussion
Bloodwork from the rDVM revealed profound hyponaturemia. By the time the dog was admitted to AMC, all electrolytes were normal. CSF tap after the MRI was normal. Myelinolysis is a noninflammatory, demyelinating brain disease caused by rapid correction of chronic hyponatremia. A delay in neurologic deterioration is noted after correction. The syndrome is analogous to central pontine myelinolysis in people with a similar history. Most dogs with experimentally induced changes had extrapontine lesion, with the thalamus being most affected. The exact pathogenesis of the lesion is unknown but a primary degeneration of glial cells in the absence of vascular changes is identified histologically. Acute shifting of serum osmolality occurs in chronically hyponaturemic dogs given IV fluids over a short period of time. Potential causes of the initial hyponaturemia in this dog include hypoadrenocorticism and pseudoaddison’s disease (Whipworm infection). The dog of this report died over the next 12 hours after the MRI. A necropsy was not performed. Reports in the literature describe some dogs that recovery fully and others that do not.
Notes from Dr. DeLahunta on the case: I agree with the presumptive diagnosis of myelinolysis. In dogs the diencephalon is more commonly affected than the pons which is the site or predilection in humans. Keep in mind that any severe osmolality change that is too rapidly corrected can cause this lesion. It has been seen in dogs that are either hyponatremic or hypernatremic. My differential diagnosis for that MR image lesion would be metabolic abnormality or toxicity less likely vascular- ischemia. The Leigh-like syndrome that occurs in the Alaskan husky has diencephalic lesions very similar to that in your dog. Both Jon Levine at Texas AM and Kerry Smith Bailey at Cornell recently identified in dogs a toxin that caused somewhat similar bilateral lesions in the caudate nuclei. I would not have considered polioencephalomalacia as that lesion with thiamin deficiency or hypoxia affects the lateral geniculate nuclei and not the central region of the diencephalon - in addition to the cerebral cortex and other brain stem nuclei.
References
- O’Brien DP, Kroll RA, et al. Myelinolysis after correction of hyponatremai in two dogs. Journal of Vet Intern Med. 8;1, 1994. pp. 40–48.
- Churcher RK, Watson ADL, et al. Suspected Myelinolysis following rapid correction of hyponatremia in a dog. J Am Anim Hosp Assoc 1999; 35:493-7.
- Martin RJ. Central pontine and extraponine myelinolysis: the osmotic demyelination syndromes. J Neurol Neurosurg Psychiatry 2004; 75 (suppl III): iii22-28.