Like the liver, the brain is commonly affected by long-term alcohol misuse. While neurocognitive dysfunctions are widely known in their most extreme presentations, such as Korsakoff’s syndrome and Wernicke’s encephalopathy (WE), there are other less explicit manifestations of neurocognitive damage which occur more frequently. This chapter explores these conditions under the umbrella term ‘alcohol-related brain damage’ (ARBD), more specifically employing the term Wernicke–Korsakoff’s syndrome (WK) when referring to the acute and chronic effects of thiamine deficiency. The correlation between excessive alcohol consumption and thiamine intake is explored, along with the body’s response of boosting gamma-aminobutyric acid (GABA)–benzodiazepine and NMDA receptors. In acute and non-acute cases of ARBD, prompt diagnosis and treatment are essential due to the risk of long-term cognitive and intellectual damage it can yield. As such, psychosocial treatment in the aftermath of the clinical phase is equally important, focusing on assessment, therapeutic intervention, adjustment, and social integration.