Alcohol-mediated brain damage is associated with changes in personality and behavior, cognitive impairment and dementia.

Patients suffering from AD are easily irritable, often jealous, frustrated and angered. Due to an overall loss of inhibitions, these emotions are expressed explicitly. Family members and friends may furthermore report emotional lability, mood swings and insensitivity to others. At the same time, the patient suffers from fear of being alone.

Cognitive impairment manifests in form of the inability to master everyday life. The patient is unable to make decisions, to connect events and to resolve problems. Patients may experience problems in finding words, following conversations and they may be unable to recognize people. Temporal and spatial orientation may be limited, too.

Dementia may be present in form of anterograde and retrograde amnesia. The former refers to the patient's inability to form new memories, i.e. to learn. In contrast, retrograde amnesia will aggravate disorientation in time, space and among other people. This leaves affected individuals confused and frustrated and thus enhances the abovementioned behavioral problems.

• Falling

  About a year and a half ago, she began falling and dropping things. Suspecting a neurological condition, I begged her to go to the doctor but she refused. [agingcare.com]

  If he has suffered falls, you might request a brain scan to check for subdural hematomas or other issues. You can also raise your questions about alcohol cravings and muscle twitches. [helpforalzheimersfamilies.com]

  Cassidy seemed intoxicated at the concert outside L.A., falling off the stage, forgetting words and unsteady on his feet. The singer now says he was diagnosed with early-stage dementia ... first reported by People. [tmz.com]

  While Australians overall are drinking less, it is the under 30’s which are driving the fall while Baby Boomers aged between 60 and 69 have increased their alcohol intake by six per cent. [oxleyhomecare.com.au]

• Weakness

  Muscles may be weak and may show atrophy (loss of tissue mass). Examination of the eyes shows abnormalities of eye movement. Blood pressure and body temperature measurement may be low; pulse (heart rate) may be rapid. [zarcrom.com]

  Tests that may be used to diagnose alcoholic dementia include: nervous/muscular system testing, such as looking for abnormal eye movement, increased pulse, muscle weakness, and low blood pressure blood testing to detect vitamin B1 levels and transketolase [addictioncampuses.com]

  Testing In alcohol related dementia, examination of the nervous system can reveal various types of damage, including: Abnormal eye movement Decreased or abnormal reflexes Fast pulse (heart rate) Low blood pressure Low body temperature Muscle weakness [verywellmind.com]

  A Word From Verywell Wernicke-Korsakoff syndrome is a set of conditions that can cause symptoms of confusion, memory loss, and disorientation, as well as physical signs such as muscle weakness and eye movement problems. [verywellhealth.com]

  Weak evidence without control group Radboudumc researchers Machteld van Egmond, Maroeska Rovers, and Niels van Heerbeek are the first to compare the outcomes of two groups of patients following different treatment strategies: septoplasty and non-surgical [radboudumc.nl]

• Inflammation

  But too much alcohol overwhelms the cells, leading to inflammation and cell death. [eurekalert.org]

  (esophagitis) Stomach Cancer Inflammation ( gastritis ) Ulcers Liver A bleeding tendency (coagulopathy) Cancer Fatty liver Inflammation ( hepatitis ) Severe scarring ( cirrhosis ) Pancreas Inflammation ( pancreatitis ) Low blood sugar levels ( hypoglycemia [merckmanuals.com]

  "There's a lot of feeling that brain inflammation is involved in Alzeimer's disease," he said. "If alcohol is increasing molecules that are suppressing inflammation in other tissues, then it probably also does that in the brain." [articles.latimes.com]

  Experts aren’t sure why moderate alcohol consumption helps the brain, though it may reduce inflammation. Inflammation has been tied to heart disease, strokes and other ills, and may also raise the risk of Alzheimer’s and other forms of dementia. [alzinfo.org]

  Prof Anstey, who heads the Ageing Research Unit at the CMHR, said that it wasn’t clear why light to moderate drinkers were less likely to develop dementia, but suggested that it could be to do with a protective effect of alcohol in reducing inflammation [sciencealert.com]

• Fatigue

  Excessive alcohol consumption can also cause: High blood pressure Heart disease Cancer, including breast, throat and liver cancer Liver cirrhosis (irreversible scarring of the liver) Poor sleep Fatigue or depression Weight gain or loss Smoking harms practically [dementiacare.org.uk]

  How Dementia Caregivers Can Cope With Compassion Fatigue Every caregiver faces challenges in the daily routine of providing ongoing care for a parent or senior loved one. This includes experiencing burnout, exhaustion and... [aplaceformom.com]

  This is an autoimmune disease (unrelated to alcohol consumption) that causes a range of problems in such as fatigue, low blood pressure, rapid heart rate, muscle weakness and shortness of breath. [newenglandnightingales.com]

  Many experts also recommend that anyone with a history of heavy alcohol use who experiences symptoms associated with Wernicke encephalopathy, including acute confusion, prolonged nausea and vomiting, unusual fatigue or weakness, or low body temperature [alz.org]

• Fishing

  Further studies are needed to confirm whether fish oil protects against alcohol-related dementia. "Fish oil has the potential of helping preserve brain integrity in abusers," Collins said. "At the very least, it wouldn't hurt them." [eurekalert.org]

  […] person and the family should be assisted to: devise an individualised plan focusing on strengths and interests follow guidance to remain alcohol free attend a self-help group eat a healthy balanced diet high in thiamine (leafy green vegetables, oily fish [dementiauk.org]

  The traditional Mediterranean diet, which includes foods like fish, fruits and vegetables, whole grains and red wine, has also been linked to a lower risk for Alzheimer’s. [alzinfo.org]

  Some fat in our diet is important, particularly unsaturated fat found in oily fish, nuts, seeds and avocados. Oily fish, like salmon and sardines, contains omega-3 fatty acids. [alzheimersresearchuk.org]

  Like all fish and seafood, shrimp is a source of omega-3 fatty acids, which help temper inflammation and may reduce risk for heart disease, Type 2 diabetes and much more. [livestrong.com]

• Pneumonia

  Subsequently, he developed aspiration pneumonia with associated fever reaction and expired. [ncbi.nlm.nih.gov]

  Death is usually a result of another illness, such as pneumonia or an infection. The average lifespan after the onset of symptoms is about seven years. Is there treatment available? At present there is no cure for Lewy body disease. [dementia.org.au]

  He was rushed to the local hospital where pneumonia in one lung was treated effectively and efficiently, a fracture near his hip was repaired and he was diagnosed with brain damage. [web.archive.org]

  Because people may be very drowsy, vomited material may enter the lungs (be aspirated), sometimes leading to pneumonia and death. [merckmanuals.com]

• Diarrhea

  […] effects you might notice while drinking alcohol (or shortly after) can include: feelings of relaxation or drowsiness a sense of euphoria or giddiness changes in mood lowered inhibitions impulsive behavior slowed or slurred speech nausea and vomiting diarrhea [healthline.com]

  […] levels Anemia (fatigue, weakness, and light-headedness) Birth defects Low thiamin levels Neurologic damage, dementia, difficulty walking and controlling eye movements Low iron levels Anemia Low niacin levels ( niacin deficiency ) Pellagra (skin damage, diarrhea [merckmanuals.com]

• Delusion

  Hallucinations and delusions may be a symptom of the Alzheimer's dementia or they could represent delirium. [everydayhealth.com]

  You will not know you are making up stories or repeating questions or information, and you may attribute your emotional changes to other events in your life, misinterpreting other peoples’ actions based on alcoholic delusions. [cleanandsoberlive.com]

  Hallucinations Delusions Impaired memory Personality changes – ranging from depressed and withdrawn to excited and irritable. [healthhype.com]

• Confusion

  Testing for thiamine disorders when acute confusion and disorientation is present is critical to identification and appropriate treatment. [verywellhealth.com]

  These memory and brain problems have similar symptoms such as memory issues, mood issues, or confusion. Our center for alcohol detox in Boca Raton explores how these conditions are connected to alcoholism and binge drinking. [banyanboca.com]

  Additionally, thiamine may be administered to improve eye movement and vision problems, confusion, and muscle coordination. [addictioncampuses.com]

  These include extreme confusion, vomiting, disorientation and muscle spasms Long-term effects of ARD may vary but may include confusion, difficulty learning or processing information or memory loss Short-term treatment for ARD involves thiamine and vitamin [therecoveryvillage.com]

  Signs and Symptoms Confusion may be the most obvious early symptom of dementia, but this confusion is also accompanied by obvious memory problems. [alcoholism.about.com]

• Cognitive Impairment

  Completely abstaining from alcohol among those without mild cognitive impairment, and consuming more than 14 alcoholic drinks each week among those with mild cognitive impairment, were associated with lower scores on a dementia screening test, the researchers [healio.com]

  […] that 10-20% of those diagnosed with mild cognitive impairment tend to progress to a form of dementia within 5 to 10 years. [sciencemediacentre.org]

  Prolonged alcohol use can have direct neurotoxic effects resulting in cognitive impairment and dementia. [floridarehab.com]

  It may involve personality changes, cognitive impairment and communication problems. Alcohol-mediated brain damage is associated with changes in personality and behavior, cognitive impairment and dementia. [symptoma.com]

  impaired immediate recall or generalized cognitive impairment. [doi.org]

• Stroke

  […] mortality rate (a special type, most strokes are clot related) and stubbonly remained alive despite my dire predicament on the liver front. [patient.info]

  For example, statistically, alcohol consumption has a J-shaped effect on the relative risk for heart disease, stroke, and diabetes. Moderate consumption reduces risk, and excess use markedly increases risk. [medscape.com]

  Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011 Feb;42(2):517-84. PubMed. [alzforum.org]

  Nine Risk Factors for Early Dementia The nine risk factors that accounted for 68 percent of YOD cases in the study population, in order of importance, are: alcohol use history of stroke use of antipsychotic medication depression a father with dementia [healthline.com]

• Confabulation

  Memory loss is common, but a unique feature of memory loss with people who are chronic, long-term alcohol abusers or alcoholics is confabulation. [goinggentleintothatgoodnight.com]

  Confabulation is the most distinct symptom which occurs with this disorder. With confabulation, a patient tells “honest lies.” [cleanandsoberlive.com]

  Alcoholics often develop personality and behavioural changes, social and personal neglect, confabulation, lack of insight, empathy and emotional control. [ncbi.nlm.nih.gov]

  Confabulation – This is the medical term for chronic lying and it is one of the key signs of alcohol dementia. [caregiverrelief.com]

• Forgetful

  It’s absolutely normal to forget things once in a while. Memory loss by itself does not mean you have dementia. There is a difference between occasional forgetfulness and forgetfulness that is cause for serious concern. [healthline.com]

  So if mrs / mister used to forget where she / he had put stuff and still forgets, she / he has not changed on that point. In that case, leave the “not changed” answer checked. [dementiatest.org]

The diagnosis of AD is based on the patient's medical history and the results of their clinical examination. Usually, these will indicate prolonged alcohol abuse and physical as well as mental consequences of their addiction. These findings are particularly important since symptoms manifested by AD patients resemble those observed in individuals suffering from other types of dementia. Cognitive impairment, memory loss and the inability to resolve problems or to realize day-to-day tasks are not pathognomonic for AD.

Besides, symptoms observed during withdrawal or while suffering from other detrimental consequences of alcohol abuse, e.g., liver failure, should not be taken into account when diagnosing AD. It has been proposed to diagnose AD not before 60 days of absolute abstinence and thus when withdrawal and associated symptoms have passed.

The Mini Mental Status Examination is a short and easily available test used to evaluate the mental health of the patient. Its result may support the tentative diagnosis of dementia.

In order to confirm the diagnosis of AD and according to the criteria established in the Diagnostic and Statistical Manual of Mental Disorders (DSM), the following conditions need to be fulfilled in cases of AD:

• Cognitive deficits consisting in anterograde or retrograde amnesia as well as aphasia, apraxia, agnosia or limitations in abstract thinking and planning. Both memory and cognition problems are required for diagnosis of AD.
• The aforementioned memory and cognition problems affect the patient's social life and/or career. A significant decline in cognitive functioning needs to be detected when compared to their previous life.
• The detected symptoms are permanent and do not diminish after delirium. They are also not associated with withdrawal.
• Clinical history, physical examination or laboratory results support the relation between those symptoms and substance abuse.

Diagnoses of cognitive deficits, such as memory loss and cognition problems that can hardly be objective and precise definitions of the aforementioned symptoms, have not yet been established. It should be noted that the DSM criteria are based on ample experiences with patients suffering from Alzheimer’s disease. They may not be transferable to AD without modifications.

Suggestions have been mode to complement the DSM criteria. According to these suggestions, AD may only be diagnosed if the patient has a history of at least five years of alcohol abuse. The onset of symptoms pointing at dementia should occur within a maximum of three years after this period of excessive alcohol consumption. Such a prolonged period of alcohol abuse presumably damages other organ systems, too, and an AD patient should therefore also present hepatic, cardiovascular, gastrointestinal or other alcohol-related diseases. Alterations detected with neuroimaging methods may further support the diagnosis of AD. Such methods may also be used to monitor potential recovery processes taking place during abstinence. White matter shrinking is associated with sulcal and ventricular dilation and may improve with abstinence.

While ataxia and peripheral sensory neuropathy may be observed in AD patients, other focal neurological signs as well as symptoms commonly attributed to cerebral infarction, subdural hematoma or other brain pathologies are not characteristic for AD. They require an adequate workup.

Alcohol cessation is mandatory. Supportive care may be provided during withdrawal and subsequent recovery, but no therapy is available to revoke permanent brain damage.

Because the cerebral metabolism depends on thiamine and since alcohol impairs thiamine absorption, this vitamin should be supplemented in order to avoid further tissue damage and even to stimulate recovery processes.

AD patients may suffer from severe damage to different organ systems that probably require medical attention.

Complete abstinence from alcohol allows for a certain degree of recovery. Nevertheless, brain damage caused by prolonged alcohol abuse seems to be only partially reversible. In this context, it is rather unsurprising that a significant share of patients are unable to completely recover from AD and thus require personal care.

AD results from long-term alcohol abuse. It is not yet clear whether dementia results form direct neurotoxic effects mediated by ethanol (this would render AD a primary alcoholic dementia) or if alcoholism interferes with other metabolic processes that, in turn, affect cognitive function and memory (and AD would be regarded a secondary alcoholic dementia). Such may be the case for thiamine absorption.

Alcoholism is known to affect the absorption of thiamine, a vitamin that acts as a cofactor for several essential enzymes. In the setting of thiamine deficiency, thiamine-dependent cellular systems begin to fail, resulting eventually in cell death. Because thiamine-dependent enzymes play an essential role in cerebral energy utilization, thiamine deficiency may propagate brain tissue injury by inhibiting metabolism in brain regions with higher metabolic demands and high thiamine
turnover.

The mechanism described above is also the etiology behind the Wernicke encephalopathy. Unsurprisingly, this disease is also related to alcoholism. Patients may present symptoms of Wernicke encephalopathy and Korsakoff syndrome, and are then diagnosed with Wernicke-Korsakoff syndrome. Due to similar pathophysiological causes, no consensus has been reached regarding clear definitions and distinctions of these diseases from AD [2] [3].

Reliable data regarding the exact prevalence of AD are not available. The majority of AD patients is older than 50 years. It has been estimated that AD accounts for approximately 10% of all cases of dementia. Since dementia is not necessarily a unifactorial disease, alcoholism may contribute to as much as 25% of all cases of dementia.

Recently, it has been reported that alcohol consumption is increasing among women and older people [4]. These results yielded additional research efforts, so more recent data can be expected soon.

Ethanol directly affects the central nervous system, the liver, the heart and the thyroid gland.

Pathological and histopathological examinations of nervous tissue from alcoholics reveal severe loss of neurons and white matter [1] [5]. This kind of damage mainly affects the frontal lobe, corpus callosum and cerebellum. Here, perfusion and metabolism are altered, neuronal density is reduced and the overall volume of these parts of the brain is diminished [6]. In animal studies regarding ethanol-induced brain damage, hippocampus and hypothalamus were also found to be affected. These results may explain impaired learning and memory dysfunctions [7] [8].

Certain degrees of brain damage have been detected in four out of five autopsies of people that had suffered from alcoholism [9]. However, these lesion seem to be partially reversible and there are studies reporting white matter and volume restoration as well as cognitive and memory improvements [10] [11]. Prolonged periods of abstinence are necessary for clinical improvement and recurrent alcohol consumption delays recovery processes [10]. In contrast, neuronal loss seems to be a permanent, irreversible consequence of alcoholism [1].

The molecular mechanisms behind AD remain poorly understood. It is known that ethanol binds to γ-aminobutyric acid (GABA) receptors, but this is most probably not the only effect mediated by alcohol in the brain. It has been suggested that alcohol causes neuronal death due to oxidative stress and glutamate excitotoxicity [12]. The latter may be further potentiated by overexpression of N-methyl-D- aspartate (NMDA) receptors during alcoholism. Cholinergic neurotransmission may also be altered by excessive alcohol consumption. Additionally, ethanol seems to inhibit neurogenesis.

Prolonged alcohol abuse is the cause of AD. Individuals maintaining an excess consumption of alcohol over longer periods of time suffer from addiction and need professional help to overcome it. The best preventive measure for AD is therefore to avoid excess alcohol intake, development of an addiction and ethanol-mediated brain damage.

Any patient diagnosed with dementia should avoid alcohol irrespective of the cause of the primary disease.

Prolonged alcohol abuse causes severe brain damage, mainly neuronal and white matter loss and finally alcohol dementia (AD) [1]. Such damage results in memory loss and cognitive impairment, whereby the latter may be observed as communication problems, limited motor functions, difficulties to recognize persons and objects and the inability to organize and plan day-to-day life. Changes in personality and behavior may also be noted. These symptoms generally manifest after years of alcohol abuse and may even appear after alcohol intake has been stopped. Nevertheless, they may partially be reversible and certain symptoms may improve during abstinence.

Treatment consists in cessation of alcohol consumption and supportive care. The prognosis depends on the degree of brain damage and some recovery may be achieved over time. There are, however, no treatment options for irreversible brain damage and neuronal loss.

Impaired cognitive functions, i.e., problems regarding speech, motor skills, abstract thinking and planning, as well as memory loss characterize distinct forms of dementia. Memory problems may arise when trying to remember something that happened in the past, but they may also occur when trying to form new memories. This renders the demented individual unable to learn. Another very frequent and commonly known symptom of dementia is the inability to recognize persons or objects the patient should be able to identify. People suffering from dementia often have difficulties to orient themselves in time and space.

Now all these symptoms are caused by alterations affecting the central nervous system. These alterations differ between distinct forms of dementia and strongly depend on their cause. In case of alcohol dementia (AD), the prolonged abuse of alcohol causes severe brain damage. Furthermore, excessive alcohol consumption compromises other organ systems such as liver, heart and gastrointestinal tract, and patients suffering from AD generally present various comorbidities that may even potentiate each other. With regards to the gastrointestinal tract for instance, alcohol reduces the absorption of thiamine, a vitamin essential for cerebral metabolism. Brain cells are thus not only directly damaged by ethanol, but also suffer from thiamine deficiency and are therefore unable to sustain their energy supply.

AD is diagnosed based upon the patient's medical history and clinical examination. Psychological tests are used to assess their cognitive functions. Certain imaging techniques may be applied to evaluate possible brain damage.

While moderate alcohol consumption should be self-evident for everyone, individuals diagnosed with any form of dementia should totally avoid alcohol. Cessation of alcohol consumption is also mandatory for AD patients. Professionals may help people to overcome their addiction. The aforementioned brain damage may be partially reversible and although recovery will take some time, memory and cognition may be improved to a certain degree. Supportive care will be given to alleviate symptoms and enhance recovery.

1. Harper C. The neuropathology of alcohol-related brain damage. Alcohol Alcohol. 2009; 44(2):136-140.
2. Bowden SC. Alcohol-related dementia and Wernicke-Korsakoff syndrome. In: Ames D, Burns A, O'Brien J, eds. Dementia. Vol 4. London: Edward Arnold; 2010:730–737.
3. Moriyama Y, Mimura M, Kato M, Kashima H. Primary alcoholic dementia and alcohol-related dementia. Psychogeriatrics. 2006; 6:114–118.
4. Blazer DG, Wu LT. The epidemiology of alcohol use disorders and subthreshold dependence in a middle-aged and elderly community sample. Am J Geriatr Psychiatry. 2011; 19(8):685-694.
5. Harper C, Matsumoto I. Ethanol and brain damage. Curr Opin Pharmacol. 2005; 5(1):73-78.
6. Sullivan EV, Harding AJ, Pentney R, et al. Disruption of frontocerebellar circuitry and function in alcoholism. Alcohol Clin Exp Res. 2003; 27(2):301-309.
7. Brust JC. Ethanol and cognition: indirect effects, neurotoxicity and neuroprotection: a review. Int J Environ Res Public Health. 2010; 7(4):1540-1557.
8. Crews FT, Collins MA, Dlugos C, et al. Alcohol-induced neurodegeneration: when, where and why? Alcohol Clin Exp Res. 2004; 28(2):350-364.
9. Goldstein G, Shelly C. Neuropsychological investigation of brain lesion localization in alcoholism. Adv Exp Med Biol. 1980; 126:731-743.
10. Bartsch AJ, Homola G, Biller A, et al. Manifestations of early brain recovery associated with abstinence from alcoholism. Brain. 2007; 130(Pt 1):36-47.
11. Sullivan EV, Pfefferbaum A. Neurocircuitry in alcoholism: a substrate of disruption and repair. Psychopharmacology (Berl). 2005; 180(4):583-594.
12. Bates ME, Bowden SC, Barry D. Neurocognitive impairment associated with alcohol use disorders: implications for treatment. Exp Clin Psychopharmacol. 2002; 10(3):193-212.