Alcohol use disorders and the brain

Abstract

A diagnosis of alcohol use disorder is associated with a higher risk of dementia, but a dose–response relationship between alcohol intake consumption and cognitive impairment remains unclear. Alcohol is associated with a range of effects on the central nervous system at different doses and acts on a number of receptors. Acute disorders include Wernicke's encephalopathy (WE), traumatic brain injury, blackouts, seizures, stroke and hepatic encephalopathy. The most common manifestations of chronic alcohol consumption are Korsakoff's syndrome (KS) and alcohol‐related dementia (ARD). There is limited evidence for benefit from memantine in the treatment of ARD, but stronger evidence for the use of high‐dose parenteral thiamine in the progression of neuropsychiatric symptoms for WE.Accumulating evidence exists for pharmacological treatment in the prevention of hepatic encephalopathy. Rehabilitation of people with ARD may take several years, and requires an approach that addresses physical and psychosocial factors.

Investigating the causal nature of the relationship of subcortical brain volume with smoking and alcohol use

“…It had previously been hypothesised that alcohol can cause cell death or reduced cell density, subsequently resulting in volume loss 46 . For instance, chronic alcohol consumption is known to induce the release of tumour necrosis factor alpha (TNF-α), a cytokine involved in potentiating neuro-inflammation which can cause neuronal death 47 . We found only weak evidence that more alcoholic drinks per week decreases amygdala, pallidum, and thalamus volume.…”

Las otras dianas del trastorno por uso de alcohol: Afectaciones sistémicas derivadas del consumo excesivo de alcohol

“…In fact, the debate on the potential benefits of alcohol consumption dates back to the late 1970s, when The Lancet published an inverse association between alcohol consumption and coronary heart disease mortality. The effect was attributed to the beneficial properties of moderate wine consumption (Leger et al, 1979). Four decades later, the results of a…”

Ascorbic Acid Deficiency Prevalence and Associated Cognitive Impairment in Alcohol Detoxification Inpatients: A Pilot Study

“…Malnutrition contributes to acute alcohol-related cognitive impairment in patients with alcohol use disorder (AUD) through several mechanisms, not limited to thiamine deficiency or thiamine dysmetabolism [ 1 , 2 , 3 ]. Those acute cognitive impairments relate to several functions (episodic memory and executive functions) and are observed immediately after alcohol withdrawal, early in abstinence.…”

“…Those acute cognitive impairments relate to several functions (episodic memory and executive functions) and are observed immediately after alcohol withdrawal, early in abstinence. They are most often transient and usually decrease under appropriate treatment (healthy nutrition, alcohol abstinence and neuropsychological training) [ 3 , 4 , 5 ] within days or weeks. The relevance of nutritional support in the care of patients with AUD undergoing detoxification is not only intended for the prevention of Wernicke encephalopathy and Korsakoff syndrome.…”

“…Additionally, its effect is discussed in cognitive impairment in elderly populations or in patients with neurodegenerative diseases [ 16 , 17 , 18 , 19 ]. Because ascorbic acid (AA)’s cognitive protective role could be mediated by its demonstrated effect to attenuate the excitotoxicity of glutamate [ 19 , 20 , 21 ], which is involved in alcohol withdrawal [ 3 ], the impact of AAD could be more pronounced in patients with AUD. In the general population, risk factors for AAD and insufficiency (AAI) were identified.…”