Presentation
History of occasional seizures. Other dogs in the litter are affected. Mild obtundation, ataxia, tetraparesis.
Patient Data
Multifocal, bilateral, symmetrical, well-defined, T2 hyperintensities are present in the thalamus, internal capsule, caudate nuclei, frontal lobes, and brainstem. Mild, focal T2 / FLAIR hyperintensity is present in the white matter of the dorsal right parietal and occipital lobes. Focal T2 / FLAIR hyperintensity is present in the cerebellum. There is mild peripheral enhancement of the thalamic lesions.
Case Discussion
Alaskan Husky encephalopathy is caused by a genetic mutation (homozygous mutation in the SLC19A3.1) that encodes a thiamine transporter protein. This gene is specifically expressed in the CNS and is presumed to cause a local thiamine deficiency. Although the disease was previously hypothesized to be a mitochondrial encephalopathy secondary to Leigh syndrome, no such mutations were found in AHE affected dogs. The histologic lesions of symmetric polioencephalomalacia are similar between dogs affected with thiamine deficiency and AHE, however the lesion distribution differs. The bilaterally symmetric distribution is however indicative of a toxic or metabolic disease.
The Alaskan Husky is not recognized as a pure breed by the American Kennel Club, though it is bred for racing purposes.
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