Alcohol Dementia

Long-term, excessive consumption of alcohol may lead to neurological damage resulting in alcohol dementia. It may involve personality changes, cognitive impairment and communication problems.

  • Processes: Poison
  • Incidence: 406 / 100.000

Overview

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.

Etiology

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].

Epidemiology

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.

Pathophysiology

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.

Prognosis

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.

Presentation

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.

Workup

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.

Treatment

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.

Prevention

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.

Patient Information

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.

References

  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.

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