Rare Case: Vitamin A Deficiency Causes Brain Compression in Domestic Cat

MRI, CT and Histopathological Findings in a Cat with Hypovitaminosis A

Irene Espadas, Emanuele Ricci, Fraser McConnell, Daniel Sanchez-Masian

Background

Vitamin A (retinol) is a vital micronutrient essential for vision, immunity, and neurological health. Felids, unable to convert β-carotene to vitamin A, are particularly susceptible to dietary deficiency. While hypovitaminosis A is well recognized in wild felids, it is rarely reported in domestic cats. Deficiency can result in progressive neurological dysfunction and bony changes in the skull leading to brain compression. This case presents the first comprehensive clinical, imaging, and histopathological description of hypovitaminosis A in a domestic cat.

Methods / Case Description

A seven-year-old, male domestic longhair cat was presented with a five-week history of lethargy, heat-seeking behavior, progressive ataxia, and visual impairment. The cat had been fed exclusively on a home-cooked chicken-based diet for five years. Neurological examination revealed multifocal central nervous system (CNS) deficits, including cerebellovestibular ataxia, tetraparesis, visual impairment, and absent menace response. Diagnostic imaging (MRI and CT) was performed under general anesthesia, followed by biochemical testing and postmortem histopathology.

Results

MRI revealed diffuse thickening and sclerosis of the calvarium, especially the occipital and temporal bones, with compression of the cerebellum and brainstem. The frontal lobes were reduced in size, the tentorium cerebelli was thickened, and mild ventriculomegaly was evident. CT confirmed generalized skull hyperostosis. Plasma retinol was markedly low at 0.1 µmol/L (reference 0.86–2.2 µmol/L), confirming hypovitaminosis A. Postmortem examination revealed diffuse skull hyperostosis causing frontal lobe compression and reduced cerebral volume. Histopathology demonstrated white matter spongiosis, Wallerian degeneration in the corona radiata and optic nerves, and meningeal thickening with mineralization. An incidental finding of systemic mastocytosis involving the spleen and liver was also noted.

Limitations

This report describes a single case, limiting generalizability. The animal was euthanized following anesthetic complications, precluding longitudinal evaluation or response to vitamin A supplementation. While the dietary etiology was presumed, hepatic retinol storage and other metabolic factors were not fully assessed. The incidental systemic mastocytosis may have influenced systemic findings but was not linked causally to hypovitaminosis A.

Conclusions

This case highlights that hypovitaminosis A, though rare, should be considered in domestic cats exhibiting multifocal CNS signs and diffuse skull hyperostosis, particularly when dietary history suggests inadequate vitamin A intake. Early identification and supplementation are crucial, as chronic deficiency can lead to irreversible neurological damage. The study underscores the importance of balanced nutrition in feline diets and demonstrates how MRI and CT can reveal characteristic calvarial and CNS changes associated with retinol deficiency.

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