Thiamine deficiency in a cat: Resolution of MRI abnormalities following thiamine supplementation

Abstract

Thiamine (vitamin B(1)) is an essential component of a number of metabolic pathways and thiamine deficiency results in a progressive encephalopathy in both humans and animals. Confirming thiamine deficiency is problematic and relies on demonstrating reduced red blood cells transketolase activity, or indirect methods including urinary organic acid analysis and dietary analysis. The characteristic and selective vulnerability of different brain regions in carnivores has been demonstrated by magnetic resonance (MR) imaging in the dog and cat as an aid to diagnosis. A 2-year-old, female, domestic shorthair cat was presented with an acute onset of seizures and ataxia. MR imaging was consistent with thiamine deficiency and supplementation resulted in a progressive clinical improvement. Repeated MR imaging 4 days after starting thiamine supplementation revealed near complete resolution of the MR abnormalities. Repeated MR imaging following appropriate therapy may be useful to further confirm thiamine deficiency.

Suspected acquired hypocobalaminaemic encephalopathy in a cat: resolution of encephalopathic signs and MRI lesions subsequent to cobalamin supplementation

“…26 Reversal of both T2W MRI hyperintensities and clinical signs on thiamine supplementation has previously been described in cases of feline thiamine deficiency. 24 The present report is unique in describing reversible MRI changes in a cobalamin-deficient companion animal. Complete resolution of both imaging and neurological abnormalities was evident at an 8-week follow-up.…”

Hippocampal Necrosis in a Cat from Australia

“…The rapid elevation in ALT did raise concerns about phenobarbitone administration, as this drug has been identified as a potential hepatotoxin [10]. Phenobarbitone would be contraindicated with severe liver disease of any aetiology and so the decision was made to change from anticonvulsant therapy with phenobarbitone to levetiracetam which is excreted predominantly in an unchanged form and considered a safer option for patients with hepatic disease [11]. Although unlikely, a thiamine deficiency was considered possible.…”

A novel encephalopathy in a thiamine-deficient dog resembling human Wernicke’s disease with atypical MRI pattern

“…In humans and dogs affected by TD, MRI findings suggest that both vasogenic and cytotoxic oedema are involved in the pathogenic mechanism of the lesions found in the affected brain areas (Harper and Butterworth, 1997). These pathological alterations are typically seen as bilateral and symmetrical hyperintensities on T2-weighted and FLAIR sequences, both in humans (Manzo et al, 2014) and dogs (Palus et al, 2010;Chisolm-Straker and Cherkas, 2013). Bilateral and symmetrical involvement of specific anatomical areas of the CNS, with anatomical preservation, is typical of metabolic-toxic and degenerative diseases (Gavin and Bagley, 2009;Ricciardi et al, 2014).…”

“…Bilateral and symmetrical involvement of specific anatomical areas of the CNS, with anatomical preservation, is typical of metabolic-toxic and degenerative diseases (Gavin and Bagley, 2009;Ricciardi et al, 2014). Among metabolic disorders, TD has been widely reported as one of the major causes of selective, bilateral gray matter damage detectable during MRI examination in humans (Manzo et al, 2014) and small animals (Garosi et al, 2003;Palus et al, 2010). In dogs, the brain areas typically involved during TD include the red nuclei, caudal colliculi, vestibular nuclei of the brainstem, cerebellar nodulus (Garosi et al, 2003), mesencephalic periventricular grey matter, claustrum, lateral geniculate nuclei, occipital and parietal cortex (Vernau et al, 2013).…”