Subacute combined degeneration due to vitamin B12 deficiency in a chronic alcoholic presenting as paraparesis

Chronic alcohol abuse can damage the central and peripheral nervous systems through direct neurotoxicity and by causing nutritional deficiencies. Vitamin B12 (cobalamin) and thiamine deficiencies are well recognised in people with alcohol use disorder and may result in reversible myelopathy or polyneuropathy. We report a 42‑year‑old man with long‑standing heavy alcohol consumption who presented with progressive numbness and weakness of the lower limbs. Examination revealed symmetric lower‑limb weakness, sensory loss and areflexia without cranial‑nerve or upper‑limb involvement. Laboratory tests showed macrocytosis, mildly elevated transaminases and gamma‑glutamyl transpeptidase, but normal serum creatinine and electrolytes. Ultrasonography revealed hepatomegaly with grade I fatty change. Magnetic resonance imaging (MRI) of the brain was unremarkable, whereas sagittal T2‑weighted images of the spine demonstrated longitudinally extensive hyperintense signal abnormalities in the posterior columns without cord expansion. The clinical presentation and imaging findings were consistent with subacute combined degeneration of the spinal cord due to vitamin B12 deficiency in the setting of chronic alcoholism. The patient improved with parenteral vitamin B12 and thiamine replacement along with gabapentin for neuropathic pain. This case highlights the importance of recognising nutritional myelopathy in chronic alcoholics because early diagnosis and vitamin replacement can prevent permanent neurological deficits.