ArticleCase reports in neurological medicine2026
Insights Into Subacute Combined Degeneration of the Cord: 'Rabbit Ear Sign' as a Radiodiagnostic Clue in Case of Vitamin B12 Deficiency Associated With Schizophrenia.
Article in Case reports in neurological medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- Insights Into Subacute Combined Degeneration of the Cord: 'Rabbit Ear Sign' as a Radiodiagnostic Clue in Case of Vitamin B12 Deficiency Associated With Schizophrenia.Case reports in neurological medicine · 2026Article
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Abstract
Background: Subacute combined degeneration manifests as the degeneration of the dorsal and lateral columns of the spinal cord. Typical symptoms include sensory deficits, weakness, ataxia, and disturbances in gait which can progress to spasticity and paraplegia. Prolonged vitamin B12 deficiency can result in irreversible neurological damage and psychiatric manifestations such as depression, irritability, hallucinations, dementia, and delirium in the affected individuals. To date, only a few cases of schizophrenia with vitamin B12 deficiency with SCD have been reported in the literature. Objective: To report a case of vitamin B12 deficiency with neuropsychiatric manifestations and rabbit ear sign as a radiological clue supporting subacute combined degeneration of the cord in vitamin B12 deficiency. Case Description: A 44-year-old male, who is a smoker and was diagnosed with schizophrenia 18 months ago, presented with a gradual, symmetrical, and painless weakness affecting all four limbs over the past 6 months. Neurological examination revealed spastic quadriparesis with impaired dorsal column. Laboratory tests were suggestive of mild to moderate anemia with a peripheral blood smear showing macrocytosis. Neuroimaging of the craniocervical junction revealed a characteristic "rabbit ear sign" or "inverted V sign". Although serum vitamin B12 and folate levels were within normal range, homocysteine levels were significantly elevated, leading to a diagnosis of subacute combined degeneration (SCD) of the spinal cord secondary to vitamin B12 deficiency. Methylmalonic acid testing was unavailable locally; however, marked hyperhomocysteinemia (> 15 μmol/L) with neuropsychiatric manifestations and anemia strongly supports functional vitamin B12 deficiency, as neurological features may occur in the absence of overt macrocytosis. Vitamin B12 replacement resulted in marked improvement in functional status of the patient, in terms of spasticity, as well as, motor, sensory and psychiatric symptoms. Conclusion: This case highlights the need to evaluate vitamin B12 deficiency in young patients with neuropsychiatric symptoms, even with mild to moderate anemia, as early replacement can prevent irreversible neurological damage from SCD.
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