A 48-year-old woman with a history of chronic alcohol use and alcoholic liver cirrhosis presented with a 6‑month history of dizziness and gait disturbances that had acutely worsened over 5 days. She reported non-spinning dizziness and a unilateral tendency to fall while walking. The medical history included esophageal variceal bleeding, which was treated with endoscopic ligation, poor nutritional intake, and poor treatment compliance. On examination, she was alert but showed an unsteady gait and truncal instability without limb weakness. Routine laboratory tests revealed chronic liver disease without major metabolic derangement. Brain diffusion-weighted imaging revealed symmetric high-signal lesions in the splenium of the corpus callosum, bilateral peritrigonal white matter, periphery of the cerebral peduncle, corona radiata, and centrum semiovale, and this was compatible with Marchiafava–Bignami disease (MBD) in the clinical context of chronic alcoholism and malnutrition (Fig. 1A).^1-3 High‑dose parenteral thiamine and multivitamin supplementation were started immediately. Dizziness and gait disturbance gradually improved over subsequent days. After clinical stabilization and partial neurological recovery, the patient was discharged on oral thiamine, nutritional support, and strict alcohol-cessation counseling.

MBD is a rare metabolic encephalopathy wherein the corpus callosum undergoes inflammatory damage, demyelination, and eventual tissue loss, which most commonly affects individuals with chronic alcoholism and malnutrition.^1,3 Pathologically, cytotoxic edema and blood–brain barrier disruption advances to callosal demyelination and atrophy, particularly in the genu and splenium.^2,3 Clinically, patients present with a wide spectrum of symptoms—from gait disturbance, dysarthria, and cognitive or behavioral changes to coma and seizures, which frequently overlap with other alcohol‑related encephalopathies.⁴ The diagnosis relies on MRI, which typically reveals hyperintense callosal lesions on T2‑weighted and fluid-attenuated inversion recovery sequence, and this is often with spread into the nearby supratentorial white matter (Fig. 1B, 1C).¹ In the absence of standardized treatment, high-dose parenteral thiamine, vitamin supplementation, and alcohol cessation are associated with improved prognosis.^2,3