Alcohol misuse remains one of the most important modifiable risk factors for death and disability. In neurology, it is linked to central nervous system damage, ranging from acute encephalopathies and withdrawal complications, strokes and trauma, to chronic cognitive syndromes and structural damage affecting the cerebellum and corpus callosum. The clinical presentation is often non‑specific, and concomitant metabolic disturbances, liver disease, infections, and trauma may delay proper diagnosis. This article provides a concise, practical review of the most clinically relevant clinicopathological phenotypes associated with long‑term alcohol misuse and nutritional deficiencies. Issues discussed include key mechanisms (direct neurotoxicity of ethanol and its metabolites, oxidative stress, neuroinflammation, impaired energy metabolism, and thiamine and magnesium deficiency) as well as the clinical picture and diagnostic approach to Wernicke encephalopathy and Korsakoff syndrome, Marchiafava–Bignami disease, alcohol‑related cerebellar degeneration, and cortical laminar necrosis including Morel’s laminar sclerosis. Typical features on magnetic resonance imaging and principles of differential diagnosis with stroke, central nervous system infection, and metabolic encephalopathy are summarised. Long‑term consequences of prenatal alcohol exposure, referred to as foetal alcohol spectrum disorders, are also discussed. In acute presentations, immediate intravenous thiamine administration before glucose, together with the simultaneous correction of metabolic abnormalities, is emphasised as a time‑critical intervention. For chronic syndromes, sustained abstinence, rehabilitation, and psychological support remain the cornerstone of care.

alcohol, Wernicke encephalopathy, Korsakoff syndrome, Marchiafava–Bignami disease, foetal alcohol spectrum disorders