Alcohol-related dementia Wikipedia

Alcohol-related dementia (ARD) has received little recognition as a distinctive clinical entity, predominantly due to doubts regarding the etiopathogenesis and lack of pathophysiological profile typical for ARD. Recently, researchers have showed interest owing to its magnitude, ageing of population and focus of health bodies on alcohol-related issues across the world (3). There are doubts and debates concerning https://ecosoberhouse.com/ ARD whether the cognitive impairment or dementia is due to direct ethanol neurotoxicity, or representation of another underlying pathology (thiamine adeficiency) or if it is multifactorial (neurotoxicity as well as multivitamin deficiency) (4). Alcohol related brain damage tends to be more common in people in their 40s and 50s and comprises about 10% of the cases of young onset dementia diagnosed.

  • It can affect several areas of the brain, but it most commonly affects the mammillary bodies found on the hypothalamus.
  • This was supported by a recent SPECT (single-photon emission computed tomography) study that reported reduced regional cerebral blood flow in the frontal cortices, basal ganglia, and thalami of patients with ARD [42].
  • Treatment typically involves the use of thiamine supplements in oral or injected forms.
  • Everyday Health follows strict sourcing guidelines to ensure the accuracy of its content, outlined in our editorial policy.

Compared to Alzheimer’s dementia, the ARD group performed better on confrontational naming, category fluency, general knowledge (semantic tasks) and verbal memory (15, 51). However, moderate alcohol drinking was shown to reduce likelihood of verbal memory impairment in one study (52). The Wernicke’s encephalopathy is likely to be the main underlying pathology in both KS and ARD.

Overview of Alcohol-Related Dementia

Finally, as the addition of new analyses of existing and ongoing cohort studies will also be affected by the previously noted limitations, there is a need for future studies to address these limitations. Dementia caused by alcoholism can appear to people of all ages, and it usually starts as a result of abusing alcohol regularly for many years. Alcohol addicts develop the Wernicke’s encephalopathy first, and then this causes the Korsakoff syndrome. Ultimately, the serious memory problems caused by Korsakoff syndrome will lead to alcoholic dementia. The Wernicke’s encephalopathy appears because heavy drinkers lose thiamine from the body as a result of frequent and long binge drinking episodes. Most alcohol addicts do not replenish this vital substance (either through diet or supplements), and as a result, alcoholic dementia can appear.

Excessive, prolonged consumption can cause a vitamin deficiency, which can cause parts of the brain to deteriorate. Even with treatment, some symptoms, such as gait changes, confabulation, or memory loss, may not improve. A thiamine deficiency over a long period of time can cause brain atrophy or damage.

Effects on the Brain

In cases where they suspect Korsakoff syndrome, a doctor will likely recommend long-term use of thiamine, possibly combined with other vitamins and magnesium. Experts recommend that screeners check anyone with memory loss for alcohol use. Alcohol-related dementia is a type of brain disorder where a person develops issues with thinking or processing and memory. There are two main subtypes, including Wernicke’s encephalopathy and Korsakoff syndrome, though experts may refer to them together as Wernicke-Korsakoff syndrome. The answer depends on several factors, but two of the more researched factors include the amount of alcohol consumed and whether someone is an APOE ε4 gene carrier. At the current time there are no acceptable criteria to definitively define alcohol-related dementia.

The GP may refer the person for managed withdrawal of alcohol, counselling and prescribe medication to stop the withdrawal symptoms and reduce the urge to drink alcohol. In addition, if the GP suspects that there may be cognitive damage they may refer the person for an assessment of the cognitive damage and for ongoing support if needed. Cox regression was used in all analyses, with age as the timescale to model the associations with hazard of incident dementia. Participants were censored at date of record of dementia, death, or 31 March 2017, whichever came first. Models were first adjusted for sociodemographic factors, then additionally for health behaviours, and finally for health status. For a clear diagnosis, the person needs to have these symptoms even when they have stopped drinking and are not suffering from the effects of alcohol withdrawal.

Risk Factors Identified For Early-Onset Dementia

According to Julia Martinez, chair of the Psychological and Brain Sciences Department at Colgate University, it is possible to have neurocognitive issues after consuming a large amount of alcohol over a brief period. “Education is modifiable because you can always incorporate learning new things into your life, like taking a new class, learning a new language, learning how to play a alcohol and dementia musical instrument, or learning a new dance,” says Hara. Marixie Ann Manarang-Obsioma is a licensed Medical Technologist (Medical Laboratory Science) and an undergraduate of Doctor of Medicine (MD). Considering these controversies surrounding the concept of ARD, we have tried to review the nosology, prevalence, presentation, underlying pathology and management of ARD in this paper.

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