ABSTRACT
Regular heavy consumption of alcohol is associated with a wide range of physical, psychological and social problems. All health-care clinicians should be able to screen for and detect problematic levels of alcohol consumption in their patients, and deliver an effective brief intervention. When patients with alcohol dependence are admitted to hospital there must be an assessment of whether medication is required to prevent withdrawal symptoms and potential delirium tremens and withdrawal seizures. Medically assisted alcohol withdrawal using a long-acting benzodiazepine such as chlordiazepoxide should be carefully monitored and titrated to effect, and the clinician should be aware of the risk of Wernicke-Korsakoff syndrome and other complications. Abstinence from alcohol is usually only the first step in treatment, and effective linkage to community alcohol services is an important step.
Subject(s)
Alcohol Withdrawal Delirium/prevention & control , Alcohol Withdrawal Seizures/prevention & control , Alcoholism/diagnosis , Benzodiazepines/therapeutic use , Alcohol Withdrawal Delirium/etiology , Alcohol Withdrawal Seizures/etiology , Alcoholic Korsakoff Syndrome/diagnosis , Alcoholic Korsakoff Syndrome/etiology , Alcoholic Korsakoff Syndrome/prevention & control , Alcoholic Korsakoff Syndrome/therapy , Alcoholism/complications , Alcoholism/therapy , Community Mental Health Services , Hospitalization , Humans , Referral and Consultation , Risk Assessment , Wernicke Encephalopathy/diagnosis , Wernicke Encephalopathy/etiology , Wernicke Encephalopathy/prevention & control , Wernicke Encephalopathy/therapyABSTRACT
Chronic alcohol use induces silent changes in the structure and function of the central and peripheral nervous systems that eventually result in irreversible, debilitating repercussions. Once identified, nutritional supplementation and cessation measures are critical in preventing further neurologic damage. The proposed mechanisms of neuronal injury in chronic alcohol abuse include direct toxic effects of alcohol and indirect effects, including those resulting from hepatic dysfunction, nutritional deficiencies, and neuroinflammation. Clinical manifestations include cerebellar ataxia, peripheral neuropathy and Wernicke-Korsakoff encephalopathy. Continued exploration of the pathophysiologic mechanisms may lead to the discovery of early interventions that can prevent permanent neurologic injury.
Subject(s)
Alcohol-Induced Disorders, Nervous System/physiopathology , Alcoholism/physiopathology , Alcohol-Induced Disorders, Nervous System/etiology , Alcohol-Induced Disorders, Nervous System/metabolism , Alcohol-Induced Disorders, Nervous System/psychology , Alcohol-Related Disorders/metabolism , Alcohol-Related Disorders/physiopathology , Alcohol-Related Disorders/psychology , Alcoholic Korsakoff Syndrome/etiology , Alcoholic Korsakoff Syndrome/metabolism , Alcoholic Korsakoff Syndrome/physiopathology , Alcoholic Korsakoff Syndrome/psychology , Alcoholic Neuropathy/etiology , Alcoholic Neuropathy/metabolism , Alcoholic Neuropathy/physiopathology , Alcoholism/complications , Alcoholism/metabolism , Alcoholism/psychology , Cerebellar Ataxia/etiology , Cerebellar Ataxia/metabolism , Cerebellar Ataxia/physiopathology , Humans , Neurotransmitter Agents/metabolismABSTRACT
Alcohol consumption is common in Western countries and has been increasing in older adults. Latest figures from Great Britain suggest 75% of those over 65 years drink, an increase from 71% 10 years ago. Chronic heavy intake is a well-established cause of brain atrophy and dementia, with a recent long-term prospective study from the USA reporting a doubling of the odds of later severe memory impairment in those with a history of an alcohol use disorder. Drinking of moderate amounts has been reported to be protective for brain health in a number of epidemiological studies, including some claims of possibly reducing dementia risk. Rigorous recent research has questioned this belief, with new evidence of harmful associations in moderate drinkers compared with abstainers. This has raised suspicion that reported protective effects of moderate drinking were due to confounding by socioeconomic class and intelligence. Clinicians should look out for cognitive impairment in heavy drinkers, considering that abstinence may induce a degree of clinical improvement. Discussions with patients regarding moderate drinking should be informed by recent research. Health benefits of moderate drinking at least for cognitive function are questionable, and if they exist are probably limited to one unit of alcohol daily with respect to other body systems.
