Open Menu Close Menu Open Search Close Search
Print Friendly, PDF & Email

Clinical Case Challenge: Feline with Severe Neurological Signs

 

CLINICAL PRESENTATION

A 6-year-old rescued cat, fed mainly with canned fish, was admitted as an emergency to the Neurology Department at Cummings Veterinary Medical Center for severe neurological signs. The general clinical examination was unremarkable. The neurological examination revealed neck ventroflexion, bilateral ataxia, depression and no menace response with normal pupillary light reflexes.

Please watch the following videos:

What is the most likely anatomical localization?

Answer: bilateral central vestibular

What is your more likely differential diagnosis?

1.     Metabolic: thiamine deficiency

 

2.     Toxic: metronidazole intoxication (if the animal was treated with a high and chronic dose of metronidazole)

 

Diagnostic Findings

CBC and chemistry did not show any relevant changes. The MRI of the brain revealed bilateral and symmetrical, well-defined lesions on T2WI (less obvious but also hyperintense on FLAIR, PD or GRE); rounded, strong signal intensities at the lateral geniculate; caudal colliculi; vestibular and fascial nuclei. There was also a patchy ill-defined T2 hyperintensity within the hyppocampus and certebral cortex. (Please see images). The images were consistent with thiamine deficiency.

T2w transverse- bilateral, symmetrical, well-defined hyperintensities at lateral geniculate nuclei. T2w transverse- bilateral, symmetrical, well-defined hyperintensities at lateral geniculate nuclei.

 

T2w transverse- bilateral, symmetrical well defined hyperintensities at vestibular nuclei. T2w transverse- bilateral, symmetrical well defined hyperintensities at vestibular nuclei.

 

T2w transverse- bilateral, symmetrical well defined hyperintensities at fascial nuclei. T2w transverse- bilateral, symmetrical well defined hyperintensities at fascial nuclei.

 

T2w transverse- bilateral, symmetrical well defined hyperintensities at caudal colliculi nuclei. T2w transverse- bilateral, symmetrical well defined hyperintensities at caudal colliculi nuclei.

 

Treatment

Clinical resolution is possible if the case is diagnosed early enough. Supplementation with thiamine at 50mg per cat until resolution of the symptoms and further 25mg a day for several weeks until the diet is restored can lead to complete recovery.

 

Discussion

Thiamine is water-soluble vitamin B1 that acts as an essential cofactor for carbohydrate metabolism. Thiamine-dependent biochemical processes include the citric acid cycle and pentose phosphate pathway, which are major energy production processes in the central nervous system (CNS). Carnivores must obtain thiamine from the environment due to impaired autosynthesis and minimal storage. Causes of thiamine deficiency include consumption of raw fish that often contains thiaminase, cooked food in which the thiamine has been destroyed due to heating, or meats preserved with sulphite that inactivates thiamine (canned food). However, a poor absorption secondary to an underlying gastro-intestinal disease could also lead to thiamine deficiency.

 

Clinical signs of thiamine deficiency include anorexia, depression and neurological signs like bilateral vestibular signs, vision loss, mydriasis without pupil light reflexes, incoordination, ataxia, and opisthotonus.

 

Further Reading

-Thiamine deficiency in dogs and cats Jessica E. Markovich, DVM, DACVIM; Cailin R. Heinze, VMD, MS, DACVN; Lisa M. Freeman, DVM, PhD, DACVN J Am Vet Med Assoc. 2013 Sep 1;243(5):649-56

 

Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA 01536

 

-Outbreak of thiamine deficiency in cats associated with the feeding of defective dry food. Chang YP1,2,3, Chiu PY2,3, Lin CT2,3, Liu IH4,5, Liu CH J Feline Med Surg. 2017 Apr;19(4):336-343