Alcohol-related brain damage: Difference between revisions
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'''Alcohol-related brain damage''' alters both the structure and function of the [[Human brain|brain]] as a result of the direct [[Neurotoxicity|neurotoxic]] effects of [[Alcoholic drink|alcohol]] intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the [[Frontal lobe|frontal lobe,]]<ref name=":0">{{Cite journal|last=Oscar-Berman|first=Marlene|date=June 2003|title=Alcoholism and the Brain|url=http://0-search.ebscohost.com.libus.csd.mu.edu/login.aspx?direct=true&db=hxh&AN=13839618&site=eds-live|journal=Alcohol Research & Health|volume=27(2)|pages=125-133|via=}}</ref> [[limbic system]], and [[Cerebellum|cerebellum,]]<ref name=":2">{{Cite journal|date=2014-01-01|title=Neuropathology of alcoholism|url=https://www.sciencedirect.com/science/article/pii/B9780444626196000355|journal=Handbook of Clinical Neurology|language=en|volume=125|pages=603–615|doi=10.1016/B978-0-444-62619-6.00035-5|issn=0072-9752}}</ref> with widespread [[cerebral atrophy]], or brain shrinkage caused by [[Neurodegeneration|neuron degeneration]]. |
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'''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.<ref name="pmid19410598"/> |
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Frontal lobe damage becomes the most prominent as alcoholics age and can lead to impaired neuropsychological performance in areas such as problem solving, good judgement, and goal-directed behaviors.<ref name=":0" /> Impaired emotional processing results from damage to the limbic system. This may lead to troubles recognizing emotional facial expressions and “interpreting nonverbal emotional cues".<ref name=":0" /> |
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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]].<ref name="Ward-">{{Cite journal | last1 = Ward | first1 = RJ. | last2 = Lallemand | first2 = F. | last3 = de Witte | first3 = P. | title = Biochemical and neurotransmitter changes implicated in alcohol-induced brain damage in chronic or 'binge drinking' alcohol abuse. | url = http://alcalc.oxfordjournals.org/cgi/content/full/44/2/128?view=long&pmid=19155229 | journal = [[Alcohol Alcohol]] | volume = 44 | issue = 2 | pages = 128–35 |date=March–April 2009 | doi = 10.1093/alcalc/agn100 | pmid = 19155229 }}</ref> |
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[[Binge drinking]], or heavy episodic drinking, can lead to damage in the limbic system that occurs after a relatively short period of time. This brain damage increases the risk of [[dementia]] and abnormalities in mood and cognitive abilities. Binge drinkers also have an increased risk of developing chronic alcoholism.[[File:Alcohol_drinking_icon.svg|link=https://en.wikipedia.org/wiki/File:Alcohol_drinking_icon.svg|right|thumb]][[Alcoholism]] is also associated with many other health problems including [[memory disorders]], [[Hypertension|high blood pressure]], muscle weakness, heart problems, [[Anemia|anaemia]], low immune function, [[Alcoholic liver disease|liver disease]], disorders of the digestive system, and pancreatic problems. It has also been correlated with [[Depression (mood)|depression]], unemployment and family problems with an increased risk of domestic abuse. |
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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.<ref name="pmid19410598">{{cite journal |vauthors=Crews FT, Boettiger CA |title=Impulsivity, frontal lobes and risk for addiction |journal=[[Pharmacol. Biochem. Behav.]] |volume=93 |issue=3 |pages=237–47 |date=September 2009 |pmid=19410598 |pmc=2730661 |doi=10.1016/j.pbb.2009.04.018 |url=}}</ref> |
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Parental history of alcoholism and/or binge drinking and gender has an influence on susceptibility to alcohol dependence as higher levels are typically seen in males and in those with a family history.<ref name=":5">{{Cite journal|last=Courtney|first=Kelly E.|last2=Polich|first2=John|date=2009-1|title=Binge Drinking in Young Adults: Data, Definitions, and Determinants|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748736/|journal=Psychological bulletin|volume=135|issue=1|pages=142–156|doi=10.1037/a0014414|issn=0033-2909|pmc=PMC2748736|pmid=19210057}}</ref> |
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==Signs and symptoms== |
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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.<ref name="pmid19410598"/> |
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== Prevalence == |
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There are nearly 20 million alcoholics in the United States. In about half, “neuropsychological disabilities can range from mild to severe”<ref name=":0" /> with approximately 2 million requiring lifelong care after developing permanent and debilitating conditions. Prolonged alcohol abstinence can lead to an improvement in these disabilities. For those with mild impairments, some improvement has been seen within a year, but this can take much longer in those with higher severity damage.<ref name=":0" /> |
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[[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.<ref name="pmid19410598"/> |
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Excessive drinking costs the US approximately $250 billion in 2010.<ref name=":1">{{Cite journal|last=Sacks|first=Jeffrey J.|last2=Gonzales|first2=Katherine R.|last3=Bouchery|first3=Ellen E.|last4=Tomedi|first4=Laura E.|last5=Brewer|first5=Robert D.|date=2015-11-01|title=2010 National and State Costs of Excessive Alcohol Consumption|url=http://www.ajpmonline.org/article/S0749-3797(15)00354-2/pdf|journal=American Journal of Preventive Medicine|language=English|volume=49|issue=5|pages=e73–e79|doi=10.1016/j.amepre.2015.05.031|issn=0749-3797}}</ref> These costs broadly included health care, loss productivity, property damage, criminal justice, and motor vehicle crashes. A very large portion of these costs are due to binge drinking. These costs fall on the taxpayers, including non-drinkers.<ref name=":1" /> |
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Excessive alcohol consumption is responsible for approximately 1,500,000 deaths and 51,898,400 [[Potential years of life lost|potential years of life]] lost globally<ref>{{Cite journal|last=Rehm|first=Jürgen|last2=Shield|first2=Kevin D.|date=2014|title=Alcohol and Mortality|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908708/|journal=Alcohol Research : Current Reviews|volume=35|issue=2|pages=174–183|issn=2168-3492|pmc=PMC3908708|pmid=24881325}}</ref> in 2010. |
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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 (sedative-hypnotic withdrawal)|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.<ref name="Stephens-2008">{{Cite journal | last1 = Stephens | first1 = DN. | last2 = Duka | first2 = T. | title = Review. Cognitive and emotional consequences of binge drinking: role of amygdala and prefrontal cortex. | journal = Philos Trans R Soc Lond B Biol Sci | volume = 363 | issue = 1507 | pages = 3169–79 |date=Oct 2008 | doi = 10.1098/rstb.2008.0097 | pmid = 18640918 | pmc = 2607328 }}</ref> |
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== Populations at Risk == |
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Alcoholics often present with smaller brain volumes which is probably due to alcohol induced [[neurotoxicity]].<ref name="pmid19410598"/><ref>{{cite journal|last1=Monnig|first1=M. A.|last2=Tonigan|first2=J. S.|last3=Yeo|first3=R. A.|last4=Thoma|first4=R. J.|last5=McCrady|first5=B. S.|title=White matter volume in alcohol use disorders: a meta-analysis|journal=Addiction Biology|date=2013|volume=18|issue=3|pages=581–92|doi=10.1111/j.1369-1600.2012.00441.x|pmid=22458455|pmc=3390447}}</ref> 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.<ref name="Courtney-2009">{{Cite journal | last1 = Courtney | first1 = KE. | last2 = Polich | first2 = J. | title = Binge drinking in young adults: Data, definitions, and determinants. | journal = Psychol Bull | volume = 135 | issue = 1 | pages = 142–56 |date=Jan 2009 | doi = 10.1037/a0014414 | pmid = 19210057 | pmc = 2748736 }}</ref> |
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=== Adolescents and Genetic Factors === |
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The impulsivity and sensation seeking seen in adolescence may lead to increased alcohol intake and more frequent binge drinking episodes, leaving adolescents particularly at risk for alcoholism. The still developing brain of adolescents is more vulnerable to the damaging neurotoxic and neurodegenerative effects of alcohol.<ref name=":4">{{Cite journal|last=Crews|first=Fulton Timm|last2=Boettiger|first2=Charlotte Ann|date=2009-9|title=Impulsivity, Frontal Lobes and Risk for Addiction|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730661/|journal=Pharmacology, biochemistry, and behavior|volume=93|issue=3|pages=237–247|doi=10.1016/j.pbb.2009.04.018|issn=0091-3057|pmc=PMC2730661|pmid=19410598}}</ref> “High impulsivity has [also] been found in families with alcoholism, suggestive of a genetic link. Thus, the genetics of impulsivity overlaps with genetic risks for alcohol use disorder and possibly alcohol neurodegeneration".<ref name=":4" /> |
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* [[Health effects of alcohol (disambiguation)]] |
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** [[Alcohol and health]] |
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** [[Alcohol intoxication]] |
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** [[Short-term effects of alcohol consumption]] |
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** [[Long-term effects of alcohol consumption]] |
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** [[Health effects of wine]] |
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| ⚫ | There is also 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. All three of these genetic traits contribute heavily to an alcohol use disorder.<ref name=":4" /> |
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==References== |
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{{reflist}} |
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== Neurological Deficits == |
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[[File:Brain_Anatomy_Striatum.png|link=https://en.wikipedia.org/wiki/File:Brain_Anatomy_Striatum.png|thumb|Brain Anatomy]]Alcoholics can typically be divided into two categories, uncomplicated and complicated.<ref name=":2" /> Uncomplicated alcoholics do not have nutritional deficiency states or liver disease, but have a reduction in overall brain volume due to [[white matter]] cerebral atrophy. The severity of atrophy sustained from alcohol consumption is proportional to the rate and amount of alcohol consumed during a person’s life.<ref name=":6">{{Cite journal|last=Harper|first=Clive|date=March 2009|title=The Neuropathology of Alcohol-Related Brain Damage|url=https://0-academic-oup-com.libus.csd.mu.edu/alcalc/article/44/2/136/184817|journal=Alcohol and Alcoholism|volume=4 (2)|pages=136–140|via=}}</ref> Complicated alcoholics may have liver damage that impacts brain structure and function, and/or nutritional deficiencies “that can cause severe brain damage and dysfunction”.<ref name=":2" /> |
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Alcoholics often present with decreased brain volume, or cerebral atrophy, due to alcohol induced [[Neurotoxicity|neurotoxicity.]]<ref name=":4" /><ref>{{Cite journal|last=Monnig|first=Mollie A.|last2=Tonigan|first2=J. Scott|last3=Yeo|first3=Ronald A.|last4=Thoma|first4=Robert J.|last5=McCrady|first5=Barbara S.|date=2013-5|title=White Matter Volume in Alcohol Use Disorders: A Meta-Analysis|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3390447/|journal=Addiction biology|volume=18|issue=3|pages=581–592|doi=10.1111/j.1369-1600.2012.00441.x|issn=1355-6215|pmc=PMC3390447|pmid=22458455}}</ref> Increased [[microglia]] density and expression of proinflammatory cytokines also occur showing evidence of neurodegeneration.<sup>[1]</sup> Animal studies find that heavy and regular binge drinking causes neurodegeneration in corticolimbic brain regions areas which are involved in learning and spatial memory. Corticolimbic brain regions affected include 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.<ref name=":5" /> |
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brain damage from binge drinking is known to occur, it is unclear how the frequency and length of these drinking sessions impacts 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.<ref name=":5" /> In the same study, an [[MRI brain scan]] found that levels of [[N-Acetylaspartic acid|N-acetylaspartate]] (NAA), a metabolite biomarker for neural integrity, was lower in binge drinkers. Additionally, abnormal brain metabolism, a loss of white brain matter in the [[frontal lobe]], and higher parietal gray matter NAA levels were found. This shows a correlation between binge drinking, poor executive functioning, and working memory. A decrease in frontal lobe NAA levels is associated with impaired executive functioning and processing speed in neuro-performance tests.<ref name=":5" /><p>The volume of the [[corpus callosum]], a large white matter tract that connects the two hemispheres, is shown to decrease with alcohol abuse due to a loss of myelination. This affects the integration between the two cerebral hemispheres and cognitive function. A limited amount of myelin can be restored with alcohol abstinence, leading to transient neurological deficits.<ref name=":6" /></p>The neurons affected by alcohol abuse in the frontal cortex typically have a large [[Soma (biology)|soma]], or cell body. This type of neuron is more susceptible to Alzheimer’s Disease and normal aging. Research is still being conducted to determine whether there is a direct link between excessive alcohol consumption and Alzheimer’s Disease.<ref name=":6" /> |
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Alcoholism is frequently associated with cerebellum atrophy in complicated alcoholics. [[Purkinje cell|Purkinje cells]], the cerebellar output cells, in the [[Cerebellar vermis|vermis]] are reduced in number by 43%.<ref name=":6" /> One of the cerebellum’s functions is to organize higher order functioning of the cerebral cortex. This does not occur with the reduced cerebellar output caused by alcohol abuse. The cerebellum is also responsible for refining crude motor output from the [[primary motor cortex]]. When this refinement is missing, symptoms such as unsteadiness and [[ataxia]]<ref name=":6" /> will occur. A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of [[GABAA receptor|GABA-A receptor]]. This causes an increase in the neurotransmitter [[Gamma-Aminobutyric acid|GABA]] in cerebellar purkinje cells, [[Granule cell|granule cells]], and [[Interneuron|interneurons.]]<ref name=":6" /> |
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Binge drinkers and alcoholics who go through multiple detoxifications show impairments in executive control tasks, showing prefrontal cortex dysfunction. Animal studies show that repeated alcohol withdrawals are associated with an inability to learn new information.<ref name=":8">{{Cite journal|last=Stephens|first=David N|last2=Duka|first2=Theodora|date=2008-10-12|title=Cognitive and emotional consequences of binge drinking: role of amygdala and prefrontal cortex|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2607328/|journal=Philosophical Transactions of the Royal Society B: Biological Sciences|volume=363|issue=1507|pages=3169–3179|doi=10.1098/rstb.2008.0097|issn=0962-8436|pmc=PMC2607328|pmid=18640918}}</ref> Alcohols acute effects on GABAergic enhancement and NMDA suppression causes alcohol induced neurotoxicity and [[Kindling (sedative-hypnotic withdrawal)|kindling]], or worsening of alcohol withdrawal symptoms with each subsequent withdrawal period. This may cause CNS depression leading to a partial acute tolerance to these withdrawal effects. This tolerance is followed by a damaging [[rebound effect]] during withdrawal. This rebound causes hyperexcitability of neurotransmission systems. If this hyper-excitability state occurs multiple times, kindling and neurotoxicity can occur leading to increased alcohol-related brain damage. Damaging [[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 due to these damaging effects.<ref name=":8" /> |
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=== Thiamine Deficiency === |
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<p>A nutritional deficiency in thiamine can exacerbate alcohol-related brain damage. There is a genetic component to [[thiamine deficiency]] causing [[malabsorption]]. More frequently however, thiamine deficiency is caused by excessive alcohol consumption leading to [[Wernicke's encephalopathy|Wernicke’s encephalopathy]] and [[Korsakoff's syndrome|Korsakoff’s Syndrome]] which frequently occur simultaneously, known as [[Wernicke–Korsakoff syndrome|Wernicke-Korsakoff syndrome.]]<ref name=":3">{{Cite journal|last=Arts|first=Nicolaas JM|last2=Walvoort|first2=Serge JW|last3=Kessels|first3=Roy PC|date=2017-11-27|title=Korsakoff’s syndrome: a critical review|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708199/|journal=Neuropsychiatric Disease and Treatment|volume=13|pages=2875–2890|doi=10.2147/NDT.S130078|issn=1176-6328|pmc=PMC5708199|pmid=29225466}}</ref> [[Brain lesion|Lesions]], or brain abnormalities, are typically located in the [[diencephalon]] which result in [[Anterograde amnesia|anterograde]] and [[retrograde amnesia]], or memory loss.<ref name=":3" /></p> |
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== Neuroimaging == |
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One method that is used to study the effect alcohol has on the brain and its components is through [[neuroimaging]]. There are two main subsections of methods in this field, hemo-dynamic and electromagnetic, each is discussed below. These techniques have allowed scientists to study functional, biochemical, and anatomical changes of the brain due to prolonged alcohol abuse.<ref name=":0" /> The precision and ability to repeatedly scan an individual has a variety of benefits for both clinicians and researchers. Neuroimaging can also provide valuable information regarding the risk an individual has for developing alcohol dependence and the efficacy of treatment.<ref name=":0" /> |
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=== Hemo-dynamic Methods === |
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<p>This type of neuroimaging creates images by observing and recording changes in blood volume, blood flow, blood oxygenation and energy metabolism.<ref name=":0" /> [[Positron emission tomography]] (PET) and [[Single-photon emission computed tomography]] (SPECT) are common hemo-dynamic techniques used. These methods require the injection of a radioactive labeled molecule, such as glucose. The injection of these radioactive materials, albeit minimal still exposes the body to harmful radiation. The patient is then observed while performing a memory task. PET and SPECT studies have confirmed and expanded previous findings that stated the prefrontal regions of the cortex are particularly susceptible to decreased metabolism in alcohol abusing patients.<ref name=":0" /></p>Other hemo-dynamic methods that are commonly used are [[Magnetic Resonance Imaging]] (MRI) and [[functional Magnetic Resonance Imaging]] (fMRI). These methods are noninvasive, and has no radioactive risk involved. The fMRI method records the metabolic changes in a particular brain structure or region that is under question. Although the MRI method can clearly distinguish grey matter from white matter, it is unable to detect individual damage to nerve fibers that form the white matter. For this scientists use a MRI derivative technique known as [[Diffusion Tensor Imaging]] (DTI) which is able to determine the orientation and integrity of specific nerve pathways.<ref name=":0" /> Using this method has confirmed previous studies which concluded that heavy drinking disrupts the microstructure of nerve fibers.<ref name=":0" /> Yet another MRI derivative technique, Magnetic Resonance Spectroscopy Imaging (MRSI), can provide further information about the neurochemistry of our brains, and can even detect the distribution of certain metabolites, neurotransmitters, and as it so happens, alcohol.[[File:MRI_brain.jpg|link=https://en.wikipedia.org/wiki/File:MRI_brain.jpg|right|thumb|Parasagittal render of human brain with MRI]] |
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=== Electromagnetic Methods === |
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While the hemo-dynamic methods are effective for observing the spatial and chemical changes in an individual, they are limited when trying to demonstrate the time sequence of these changes. Electromagnetic methods are capable of real time detection of electrical currents in the brain. [[Electroencephalography]] (EEG) utilizes small electrodes that are attached to a patient’s scalp, and then the recordings are averaged by a technique known as [[Event-Related Potentials]] (ERP) in order to determine the time sequences after a presented stimulus such as a word or image.<ref name=":0" /> Another electromagnetic method that is used called [[Magnetoencephalography]] (MEG) utilizes sensors in a machine to the measure magnetic field created by the brain’s electrical activity. These techniques are noninvasive and harmless, providing exquisite detail about the order and timing of electrical activity, however, the spatial resolution is poor. |
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These methods of neuroimaging have provided information that is congruent with previous finding that alcohol has altering effects on multiple levels of one’s nervous system.<ref name=":0" /> These effects include impairment of both lower order brain stem functions and higher order functioning such as problem solving. These methods of study have also shown differences in electrical brain activity and responsiveness of healthy individuals compared to alcohol-dependent and different yet from those with a family history of alcoholism.<ref name=":0" /> The topic of genetic markers for the predisposition for alcoholism is highly debated in the scientific community.[[File:EEG_recording.jpg|link=https://en.wikipedia.org/wiki/File:EEG_recording.jpg|right|thumb|Man ready for EEG recording]] |
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=== Clinical Applications === |
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<p>Cognitive and functional symptoms from excessive alcohol consumption are caused by decreased volume in the cerebral cortex and cerebellum.<ref name=":7">{{Cite journal|date=2005-02-01|title=Ethanol and brain damage|url=https://www.sciencedirect.com/science/article/pii/S1471489204001924|journal=Current Opinion in Pharmacology|language=en|volume=5|issue=1|pages=73–78|doi=10.1016/j.coph.2004.06.011|issn=1471-4892}}</ref> Atrophy of these brain regions leads to altered neuronal circuits and therefore functional deficits. In Korsakoff patients, magnetic resonance imaging (MRI) shows atrophy of the thalamus and mamillary bodies. Positron Emission Tomography (PET) showed decreased metabolism, and therefore decreased activity in the thalamus and other diencephalon structures.<ref name=":7" /> Uncomplicated alcoholics, Chronic Wernicke’s Encephalopathy (WE) and Korsakoff psychosis patients had significant loss in frontal cortical neurons, white matter, hippocampus and the basal forebrain.<ref name=":7" /> Additionally uncomplicated alcoholics have shrinkage in raphe neurons, the mamillary bodies, and the thalamus. However, WE and Korsakoff patients had overall more brain volume loss. The degree of atrophy is correlated with the amount of alcohol.<ref name=":7" /></p> |
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== Treatment and Prevention == |
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The effects of alcoholism and Wernicke-Korsakoff syndrome can have drastic effects for the individuals afflicted and their loved ones, however, the treatment options are very limited compared to other ailments. Most patients with alcohol-related cognitive defects experienced improvement of their symptoms over the first two to three months of treatment.<ref name=":6" /> Others have said to seen increase in cerebral metabolism as soon as one month after treatment.<ref name=":0" /><p>Education is the best supported alcoholism prevention method.<ref name=":6" /> This consists of providing information about risk factors and mechanisms of actions conducted from studies on alcohol-related brain damage to the public. This would assist patients in rehabilitation, increase treatment efforts, and reduce mortality by influencencing doctors to pay closer attention to the warning signs.<ref name=":6" /></p> |
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<references /> |
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[[Category:Alcohol abuse]] |
[[Category:Alcohol abuse]] |
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[[Category:Neurology]] |
[[Category:Neurology]] |
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Revision as of 22:58, 9 April 2018
Alcohol-related brain damage alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe,[1] limbic system, and cerebellum,[2] with widespread cerebral atrophy, or brain shrinkage caused by neuron degeneration.
Frontal lobe damage becomes the most prominent as alcoholics age and can lead to impaired neuropsychological performance in areas such as problem solving, good judgement, and goal-directed behaviors.[1] Impaired emotional processing results from damage to the limbic system. This may lead to troubles recognizing emotional facial expressions and “interpreting nonverbal emotional cues".[1]
Binge drinking, or heavy episodic drinking, can lead to damage in the limbic system that occurs after a relatively short period of time. This brain damage increases the risk of dementia and abnormalities in mood and cognitive abilities. Binge drinkers also have an increased risk of developing chronic alcoholism.
Alcoholism is also associated with many other health problems including memory disorders, high blood pressure, muscle weakness, heart problems, anaemia, low immune function, liver disease, disorders of the digestive system, and pancreatic problems. It has also been correlated with depression, unemployment and family problems with an increased risk of domestic abuse.
Parental history of alcoholism and/or binge drinking and gender has an influence on susceptibility to alcohol dependence as higher levels are typically seen in males and in those with a family history.[3]
Prevalence
There are nearly 20 million alcoholics in the United States. In about half, “neuropsychological disabilities can range from mild to severe”[1] with approximately 2 million requiring lifelong care after developing permanent and debilitating conditions. Prolonged alcohol abstinence can lead to an improvement in these disabilities. For those with mild impairments, some improvement has been seen within a year, but this can take much longer in those with higher severity damage.[1]
Impact
Excessive drinking costs the US approximately $250 billion in 2010.[4] These costs broadly included health care, loss productivity, property damage, criminal justice, and motor vehicle crashes. A very large portion of these costs are due to binge drinking. These costs fall on the taxpayers, including non-drinkers.[4]
Excessive alcohol consumption is responsible for approximately 1,500,000 deaths and 51,898,400 potential years of life lost globally[5] in 2010.
Populations at Risk
Adolescents and Genetic Factors
The impulsivity and sensation seeking seen in adolescence may lead to increased alcohol intake and more frequent binge drinking episodes, leaving adolescents particularly at risk for alcoholism. The still developing brain of adolescents is more vulnerable to the damaging neurotoxic and neurodegenerative effects of alcohol.[6] “High impulsivity has [also] been found in families with alcoholism, suggestive of a genetic link. Thus, the genetics of impulsivity overlaps with genetic risks for alcohol use disorder and possibly alcohol neurodegeneration".[6]
There is also 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. All three of these genetic traits contribute heavily to an alcohol use disorder.[6]
Neurological Deficits
Alcoholics can typically be divided into two categories, uncomplicated and complicated.[2] Uncomplicated alcoholics do not have nutritional deficiency states or liver disease, but have a reduction in overall brain volume due to white matter cerebral atrophy. The severity of atrophy sustained from alcohol consumption is proportional to the rate and amount of alcohol consumed during a person’s life.[7] Complicated alcoholics may have liver damage that impacts brain structure and function, and/or nutritional deficiencies “that can cause severe brain damage and dysfunction”.[2]
Pathophysiology
Alcoholics often present with decreased brain volume, or cerebral atrophy, due to alcohol induced neurotoxicity.[6][8] Increased microglia density and expression of proinflammatory cytokines also occur showing evidence of neurodegeneration.[1] Animal studies find that heavy and regular binge drinking causes neurodegeneration in corticolimbic brain regions areas which are involved in learning and spatial memory. Corticolimbic brain regions affected include 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.[3]
brain damage from binge drinking is known to occur, it is unclear how the frequency and length of these drinking sessions impacts 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.[3] In the same study, an MRI brain scan found that levels of N-acetylaspartate (NAA), a metabolite biomarker for neural integrity, was lower in binge drinkers. Additionally, abnormal brain metabolism, a loss of white brain matter in the frontal lobe, and higher parietal gray matter NAA levels were found. This shows a correlation between binge drinking, poor executive functioning, and working memory. A decrease in frontal lobe NAA levels is associated with impaired executive functioning and processing speed in neuro-performance tests.[3]
The volume of the corpus callosum, a large white matter tract that connects the two hemispheres, is shown to decrease with alcohol abuse due to a loss of myelination. This affects the integration between the two cerebral hemispheres and cognitive function. A limited amount of myelin can be restored with alcohol abstinence, leading to transient neurological deficits.[7]
The neurons affected by alcohol abuse in the frontal cortex typically have a large soma, or cell body. This type of neuron is more susceptible to Alzheimer’s Disease and normal aging. Research is still being conducted to determine whether there is a direct link between excessive alcohol consumption and Alzheimer’s Disease.[7]
Alcoholism is frequently associated with cerebellum atrophy in complicated alcoholics. Purkinje cells, the cerebellar output cells, in the vermis are reduced in number by 43%.[7] One of the cerebellum’s functions is to organize higher order functioning of the cerebral cortex. This does not occur with the reduced cerebellar output caused by alcohol abuse. The cerebellum is also responsible for refining crude motor output from the primary motor cortex. When this refinement is missing, symptoms such as unsteadiness and ataxia[7] will occur. A potential cause of chronic alcoholic cerebellar dysfunction is an alteration of GABA-A receptor. This causes an increase in the neurotransmitter GABA in cerebellar purkinje cells, granule cells, and interneurons.[7]
Excitotoxicity and Kindling
Binge drinkers and alcoholics who go through multiple detoxifications show impairments in executive control tasks, showing prefrontal cortex dysfunction. Animal studies show that repeated alcohol withdrawals are associated with an inability to learn new information.[9] Alcohols acute effects on GABAergic enhancement and NMDA suppression causes alcohol induced neurotoxicity and kindling, or worsening of alcohol withdrawal symptoms with each subsequent withdrawal period. This may cause CNS depression leading to a partial acute tolerance to these withdrawal effects. This tolerance is followed by a damaging rebound effect during withdrawal. This rebound causes hyperexcitability of neurotransmission systems. If this hyper-excitability state occurs multiple times, kindling and neurotoxicity can occur leading to increased alcohol-related brain damage. Damaging 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 due to these damaging effects.[9]
Thiamine Deficiency
A nutritional deficiency in thiamine can exacerbate alcohol-related brain damage. There is a genetic component to thiamine deficiency causing malabsorption. More frequently however, thiamine deficiency is caused by excessive alcohol consumption leading to Wernicke’s encephalopathy and Korsakoff’s Syndrome which frequently occur simultaneously, known as Wernicke-Korsakoff syndrome.[10] Lesions, or brain abnormalities, are typically located in the diencephalon which result in anterograde and retrograde amnesia, or memory loss.[10]
Neuroimaging
One method that is used to study the effect alcohol has on the brain and its components is through neuroimaging. There are two main subsections of methods in this field, hemo-dynamic and electromagnetic, each is discussed below. These techniques have allowed scientists to study functional, biochemical, and anatomical changes of the brain due to prolonged alcohol abuse.[1] The precision and ability to repeatedly scan an individual has a variety of benefits for both clinicians and researchers. Neuroimaging can also provide valuable information regarding the risk an individual has for developing alcohol dependence and the efficacy of treatment.[1]
Hemo-dynamic Methods
This type of neuroimaging creates images by observing and recording changes in blood volume, blood flow, blood oxygenation and energy metabolism.[1] Positron emission tomography (PET) and Single-photon emission computed tomography (SPECT) are common hemo-dynamic techniques used. These methods require the injection of a radioactive labeled molecule, such as glucose. The injection of these radioactive materials, albeit minimal still exposes the body to harmful radiation. The patient is then observed while performing a memory task. PET and SPECT studies have confirmed and expanded previous findings that stated the prefrontal regions of the cortex are particularly susceptible to decreased metabolism in alcohol abusing patients.[1]
Other hemo-dynamic methods that are commonly used are Magnetic Resonance Imaging (MRI) and functional Magnetic Resonance Imaging (fMRI). These methods are noninvasive, and has no radioactive risk involved. The fMRI method records the metabolic changes in a particular brain structure or region that is under question. Although the MRI method can clearly distinguish grey matter from white matter, it is unable to detect individual damage to nerve fibers that form the white matter. For this scientists use a MRI derivative technique known as Diffusion Tensor Imaging (DTI) which is able to determine the orientation and integrity of specific nerve pathways.[1] Using this method has confirmed previous studies which concluded that heavy drinking disrupts the microstructure of nerve fibers.[1] Yet another MRI derivative technique, Magnetic Resonance Spectroscopy Imaging (MRSI), can provide further information about the neurochemistry of our brains, and can even detect the distribution of certain metabolites, neurotransmitters, and as it so happens, alcohol.
Electromagnetic Methods
While the hemo-dynamic methods are effective for observing the spatial and chemical changes in an individual, they are limited when trying to demonstrate the time sequence of these changes. Electromagnetic methods are capable of real time detection of electrical currents in the brain. Electroencephalography (EEG) utilizes small electrodes that are attached to a patient’s scalp, and then the recordings are averaged by a technique known as Event-Related Potentials (ERP) in order to determine the time sequences after a presented stimulus such as a word or image.[1] Another electromagnetic method that is used called Magnetoencephalography (MEG) utilizes sensors in a machine to the measure magnetic field created by the brain’s electrical activity. These techniques are noninvasive and harmless, providing exquisite detail about the order and timing of electrical activity, however, the spatial resolution is poor.
These methods of neuroimaging have provided information that is congruent with previous finding that alcohol has altering effects on multiple levels of one’s nervous system.[1] These effects include impairment of both lower order brain stem functions and higher order functioning such as problem solving. These methods of study have also shown differences in electrical brain activity and responsiveness of healthy individuals compared to alcohol-dependent and different yet from those with a family history of alcoholism.[1] The topic of genetic markers for the predisposition for alcoholism is highly debated in the scientific community.
Clinical Applications
Cognitive and functional symptoms from excessive alcohol consumption are caused by decreased volume in the cerebral cortex and cerebellum.[11] Atrophy of these brain regions leads to altered neuronal circuits and therefore functional deficits. In Korsakoff patients, magnetic resonance imaging (MRI) shows atrophy of the thalamus and mamillary bodies. Positron Emission Tomography (PET) showed decreased metabolism, and therefore decreased activity in the thalamus and other diencephalon structures.[11] Uncomplicated alcoholics, Chronic Wernicke’s Encephalopathy (WE) and Korsakoff psychosis patients had significant loss in frontal cortical neurons, white matter, hippocampus and the basal forebrain.[11] Additionally uncomplicated alcoholics have shrinkage in raphe neurons, the mamillary bodies, and the thalamus. However, WE and Korsakoff patients had overall more brain volume loss. The degree of atrophy is correlated with the amount of alcohol.[11]
Treatment and Prevention
The effects of alcoholism and Wernicke-Korsakoff syndrome can have drastic effects for the individuals afflicted and their loved ones, however, the treatment options are very limited compared to other ailments. Most patients with alcohol-related cognitive defects experienced improvement of their symptoms over the first two to three months of treatment.[7] Others have said to seen increase in cerebral metabolism as soon as one month after treatment.[1]
Education is the best supported alcoholism prevention method.[7] This consists of providing information about risk factors and mechanisms of actions conducted from studies on alcohol-related brain damage to the public. This would assist patients in rehabilitation, increase treatment efforts, and reduce mortality by influencencing doctors to pay closer attention to the warning signs.[7]
- ^ a b c d e f g h i j k l m n o Oscar-Berman, Marlene (June 2003). "Alcoholism and the Brain". Alcohol Research & Health. 27(2): 125–133.
- ^ a b c "Neuropathology of alcoholism". Handbook of Clinical Neurology. 125: 603–615. 2014-01-01. doi:10.1016/B978-0-444-62619-6.00035-5. ISSN 0072-9752.
- ^ a b c d Courtney, Kelly E.; Polich, John (2009-1). "Binge Drinking in Young Adults: Data, Definitions, and Determinants". Psychological bulletin. 135 (1): 142–156. doi:10.1037/a0014414. ISSN 0033-2909. PMC 2748736. PMID 19210057.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link) - ^ a b Sacks, Jeffrey J.; Gonzales, Katherine R.; Bouchery, Ellen E.; Tomedi, Laura E.; Brewer, Robert D. (2015-11-01). "2010 National and State Costs of Excessive Alcohol Consumption". American Journal of Preventive Medicine. 49 (5): e73–e79. doi:10.1016/j.amepre.2015.05.031. ISSN 0749-3797.
- ^ Rehm, Jürgen; Shield, Kevin D. (2014). "Alcohol and Mortality". Alcohol Research : Current Reviews. 35 (2): 174–183. ISSN 2168-3492. PMC 3908708. PMID 24881325.
{{cite journal}}: CS1 maint: PMC format (link) - ^ a b c d Crews, Fulton Timm; Boettiger, Charlotte Ann (2009-9). "Impulsivity, Frontal Lobes and Risk for Addiction". Pharmacology, biochemistry, and behavior. 93 (3): 237–247. doi:10.1016/j.pbb.2009.04.018. ISSN 0091-3057. PMC 2730661. PMID 19410598.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link) - ^ a b c d e f g h i Harper, Clive (March 2009). "The Neuropathology of Alcohol-Related Brain Damage". Alcohol and Alcoholism. 4 (2): 136–140.
- ^ Monnig, Mollie A.; Tonigan, J. Scott; Yeo, Ronald A.; Thoma, Robert J.; McCrady, Barbara S. (2013-5). "White Matter Volume in Alcohol Use Disorders: A Meta-Analysis". Addiction biology. 18 (3): 581–592. doi:10.1111/j.1369-1600.2012.00441.x. ISSN 1355-6215. PMC 3390447. PMID 22458455.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link) - ^ a b Stephens, David N; Duka, Theodora (2008-10-12). "Cognitive and emotional consequences of binge drinking: role of amygdala and prefrontal cortex". Philosophical Transactions of the Royal Society B: Biological Sciences. 363 (1507): 3169–3179. doi:10.1098/rstb.2008.0097. ISSN 0962-8436. PMC 2607328. PMID 18640918.
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