Alcohol-related brain damage(Redirected from Alcohol's neurotoxicity)
Alcohol-related brain damage is the damage that occurs to brain structures or function of the central nervous system as a result of the direct neurotoxic effects of alcohol intoxication or acute withdrawal. The frontal lobes are the most damaged region of the brains of alcohol abusers but other regions of the brain are also affected. The damage that occurs from heavy drinking/high blood alcohol levels causes impairments in judgement and decision making and social skills. These brain changes are linked to poor behavioural control and impulsivity, which tend to worsen the existing addiction problem.
The problems of alcoholism are well known, such as memory disorders, liver disease, high blood pressure, muscle weakness, heart problems, anaemia, low immune function, disorders of the digestive system and pancreatic problems as well as depression, unemployment and family problems including child abuse. Recently attention has been increasingly focused on binge drinking by adolescents and young adults due to neurochemical changes and brain damage which, unlike with alcoholism, can occur after a relatively short period of time; the damage is particularly evident in the corticolimbic region. This brain damage increases the risk of abnormalities in mood and cognitive abilities, increases the risk of dementia and additionally binge drinkers have an increased risk of developing chronic alcoholism.
Individuals who are impulsive are at high risk of addiction due to impaired behavioural control and increased sensation seeking behaviour. Alcohol abuse, especially during adolescence, causes a deterioration of executive functions in the frontal lobe. This brain damage from alcohol actually increases impulsivity and therefore worsens the addictive disorder. With prolonged abstinence neurogenesis occurs which can potentially reverse the damage from alcohol abuse.
Signs and symptomsEdit
Alcohol related brain damage causes a wide range of executive function impairments including, impaired judgment, blunted affect, poor insight, social withdrawal, depression, reduced motivation, distractibility, attentional and impulse control deficits.
Dark cell degeneration as well as inhibition of brain neural stem cell proliferation and neurogenesis are among the causes of alcohol related brain damage. Increases in microglia density also occurs in alcohol abusers which is evidence of neurodegeneration. These increases in microglia persist after abstinence from alcohol according to animal research. People with an alcohol use disorder also show an increased expression of proinflammatory cytokine and microglia protein expression.
Adolescents are naturally at increased risk of alcohol abuse due to increased impulsivity and sensation seeking which results in larger intake of alcohol and more frequent binge drinking episodes. Additionally the developing brain of adolescents is significantly more vulnerable to the neurotoxic and neurodegenerative effects of alcohol abuse. It also appears that there is a genetic risk for proinflammatory cytokine mediated alcohol-related brain damage. There is evidence that variants of these genes are involved not only in contributing to brain damage but also to impulsivity and alcohol abuse and all three of these genetic traits contribute heavily to an alcohol use disorder.
Excitotoxicity and kindlingEdit
Binge drinkers and alcoholics with multiple detoxifications have impairments in executive control tasks sensitive to dysfunction of prefrontal cortex. Animal studies show that repeated withdrawals are associated with an inability to learn new information. The mechanism of neurotoxicity and kindling of neurotransmission systems is due to alcohol's acute effects on GABAergic enhancement and NMDA suppression, leading to CNS depression leading to a partial acute tolerance to these effects, followed by a rebound effect, during acute withdrawal due to the partial tolerance that developed. The acute withdrawal/rebound causes the neurotransmission systems to go into a hyper-excitability state; if this hyper-excitability state occurs multiple times, kindling and possible neurotoxicity can occur. There is evidence that excitotoxicity may also occur as a result of repeated withdrawals. Similar to people who have been detoxified multiple times from alcohol, binge drinkers show a higher rate of emotional disturbance.
Alcoholics often present with smaller brain volumes which is probably due to alcohol induced neurotoxicity. Impairments in impulse control in binge drinkers, which is more prominent in female binge drinkers, is due to dysfunction of the frontal lobe. The findings in humans have been largely concordant with animal studies. Such animal studies find that heavy and regular binge drinking causes neurodegeneration in corticolimbic brain regions areas which are involved in learning and spatial memory, such as the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and the hippocampal dentate gyrus. A study in rats found that a heavy 2-day drinking binge caused extensive neurodegeneration in the entorhinal cortex with resultant learning deficits. While brain damage from binge drinking is known to occur as a result of binge drinking patterns, it is unclear how long drinking sessions last and how regular binge drinking is done to cause brain damage in humans. One study found that humans who drank at least 100 drinks (male) or 80 drinks (female) per month (concentrated to 21 occasions or less per month) throughout a 3-year period had impaired decision making skills compared to non-binge drinkers. In the same study, an MRI brain scan found that levels of N-acetylaspartate (NAA) which is a metabolite biomarker for neural integrity was lower in binge drinkers and additionally found that brain metabolism was abnormal and found loss of white brain matter in the frontal lobe and higher parietal gray matter NAA. There was a correlation between binge drinking and poor executive functioning and working memory; frontal NAA loss was associated with impaired executive functioning and processing speed in neuro-performance tests.
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