Understanding Alcohol Dependent Dementia & Ways to Cope

Alcohol-related dementia (ARD) is a disease that exists in many forms. As a result, diagnosing this illness may present some challenges. The hardest part of dealing with this diagnosis is not only how life changes. It is knowing that drinking was a choice that led to the emotional turmoil caretakers experience caring for someone with this condition. However, it is more important to be compassionate and equally supportive. For those with ARD, drinking may be the only way to cope with pain, disappointment, and failure. As a relative of someone with dementia, learning about the etiology of this condition will help to formulate a proper treatment plan.



ARD may be considered a silent epidemic because this condition does not discriminate. ARD can target anyone with a history of chronic alcohol consumption concurrent with other factors such as prior head trauma, age, and sex. Susceptibility may increase proportionally to changes in frequency, duration, and dose of alcohol consumption over time (Gupta & Warner, 2008). In fact, Harper (1998) reported that chronic alcoholics demonstrate significant loss of brain tissue compared to controls. Overall white brain matter is affected, with reduction of the number of cortical neurons in the superior frontal cortex, hypothalamus and cerebellum. ARD has widespread effects targeting many brain regions, which becomes further complicated by other comorbidities. The purpose herein is to explore the causes of ARD and propose useful treatment options.

Alcohol Related Neurotoxicity and Excitotoxicity  Long-term alcohol use increases ammonia and manganese toxins which contributes to encephalopathy (Gupta & Warner, 2008). Because of liver cirrhosis, toxins that would be metabolized normally cannot be degraded. Dahlberg and Colleagues (2011) provided a more detailed account of how these toxins reach the brain. Their research demonstrated that ammonia toxins traveled through the cerebrospinal fluid (CSF) causing swelling in the lateral ventricles and cortical matter shrinkage due to fluid accumulation. Results displayed that ammonia toxins formed abscesses surrounded by capsules that contained reactive astrocytes and fibrous tissue. However, these capsules did not serve as a diffusion barrier and distributed to cortical, cerebellar, parietal, and occipital regions altering neurotransmission and astrocytic potassium handling. Patients suffered from disorentiation, expressive aphasia, seizures, or fevers depending on the brain region affected. Dahlberg postulated that in addition to liver failure, abscesses remained problematic when toxins breached the capsule and penetrated cell membranes. They also suggested that DNA, RNA proteins, and other nitrogen-containing compounds may serve as catalysts for ammonia regeneration.

 Another outcome of chronic alcohol intake is inhibition of N-methyl-D-aspartate (NMDA) and up-regulation of the NMDA receptor subtype, resulting in glutamatergic excitotoxicity and high levels of intracellular calcium (Ridley et al., 2013). Support for the neurotoxicity hypothesis emerged from animal studies, which demonstrated that dose related ethanol-induced damage to the hippocampus, hypothalamus, and cerebellum that correspond with impairments in memory and learning (Brust et al., 2010; Crews et al., 2004). Although neurotoxicity is one consequence of chronic alcohol use, there are other manifestations of ARD compared to other forms of dementia.

Neuropsychological Comparisons Between Forms of Dementia

Obtaining an ARD diagnosis may lead to some setbacks. The primary concern is distinguishing alcohol induced pathology from brain damage due to the alcoholic lifestyle (i.e.vitamin deficiency, malnutrition, head trauma, liver disease, diabetes) (Vetreno et al., 2011). ARD becomes progressive when alcohol use persists exacerbating memory loss, neurotoxicity, and hepatic encephalopathy (Harper, 1998). Because these deficits are widespread, ARD can be difficult to identify. 


Calderon and colleagues (2001) characterized the most common forms of Dementia. Alzheimer’s Dementia (AD) may be diagnosed by overall deficits in attentional function, memory, and difficulty with visuospatial tasks. As the disease progresses, patients become incontinent, are often found wandering, and experience difficulty accessing long-term memories. Dementia with the presence of Lewy Bodies (DLB) and Beta-Amyloid 42 plaques may cause tissue necrosis within the cerebral cortex, brainstem nuclei, substantia nigra (SN), locus coeruleus (LC), and components of the basal forebrain cholinergic system (BFCS). These plaques are easily identifiable through brain scans. The clinical features of DLB include a cortical dementia with fluctuating confusion, spontaneous parkinsonism, great difficulty with visuospatial, visuoperceptual, and praxic ability. By this time, cognitive and memory impairments may be irreparable. Compared to AD, patients with ARD perform better on semantic tasks and on verbal memory recognition tasks. However, some patients with ARD are unlikely to demonstrate symptoms of language impairment (Oslin et.al., 1997).

Hepatic Encephalopathy Hepatic Encephalopathy (HE) is a form of ARD recognized by progression of liver cirrhosis. High levels of serum ammonia become mediated by reduced hepatic clearance which becomes a correlate with the severity of acute HE (Butterworth, 1993;1987). Other toxins such as short and medium length amino acids, phenols, and mercaptans derived from the gut contribute to this disease process (Butterworth, 2003; Van Theil et al.,1985; Zaki et al., 1983). Diagnostics for HE may be challenging because neuroimaging can produce results that occur independently, namely abnormalities in gray or white brain matter (De la Monte & Kril, 2015). As summarized in the above section, persistence of liver failure leads to the development of hyperammonia and neurotoxic injury to the brain, which results in metabolic encephalopathy. As a consequence of these metabolic changes, astrocytosis, brain acidosis, and RNA degradation occurs (Butterworth, 1987; Hazell & Butterworth, 1999; Sheedy et al., 2012).


The neuropathology of acute HE is characterized by the abundance of astrocytes in gray matter structures in deep cerebral nuclei and the cerebral cortex. These astrocytes exist as large pale nuclei with peripheral distributed chromatin and scant cytoplasm (Butterworth, 1994). Chronic HE, on the other hand, causes pseudolaminar spongy degeneration deep in the cerebral cortex (Victor et al., 1965). These authors also warn that molecular and biochemical studies of brain disease must be carefully evaluated in order to avoid any mistattributions. Factors such as tissue pH, intactness of RNA and changes in gene expression should be examined in order to make accurate distinctions between different forms of alcohol induced impairments versus illnesses unrelated to substance use.

Wernicke’s Encephalopathy & Korsakoff’s Syndrome Wernicke’s encephalopathy (WE) occurs as a result of Thiamine B1 deficiency. This is due to inadequate nutritional intake in addition to the inhibitory effects on thiamine absorption through the gastrointestinal tract and T1 activation via phosphorylation. The symptoms of this kind of deficiency are associated with altered mental status, ataxia, and opthalmoplegia (Todd et al., 1999). WE can be caused by nutritional deficiency alone in the absence of dependence and abuse. In the presence of alcohol however, thiamine transport is compromised across the blood-brain barrier, and damages apoenzymes (a protein that forms an active enzyme by combination with a coenzyme), increasing the T1 levels needed for metabolism (Thomson et al., 2012). WE has an acute onset with the presence of occular abnormalities, gait incoordination, and motor problems (Sechi & Serra, 2007). As WE worsens, it is possible to develop Korsakoff’s syndrome (KS). KS is a disorder that is principally characterized by severe memory defects, in particular a striking loss of working memory that accompanies relatively little loss of reference memory (Victor et al., 1971; Sechi & Serra, 2007). Patients with KS are likely to demonstrate symptoms of anterograde amnesia and are unable to recall recent occurences, despite retaining information that is implicit. As a result of this, KS patients are able to acquire motor skills and develop conditioned responses to environmental stimuli (Fama et al., 2006). 


For those who experience an ongoing battle with alcohol use, it may be difficult to quit. Acute withdrawal in long-term alcoholics results in tremors, hallucinations, seizures, agitation, and fluctuating levels of alertness (Ridley et. al., 2013). Over 75% of autopsied chronic alcoholics have significant brain damage and over 50% of detoxified alcoholics display some degree of learning and memory impairment (Vetreno et. al., 2011). If ARD exists prior to withdrawal, it is probable that the these symptoms will persist after maintained sobriety. Although current research provides little inspiration for patient recovery, there are ways to combat the causes of ARD.

 With all disorders that affect the brain, there is a spectrum of severity. If impairments are moderate, there still may be a chance for improvement. In order to help patients with ARD, we must first face the stigma against alcoholics head-on. More often than not, doctors and clinicians assume that the choice to drink alcohol should be punished by lack of support and proper treatment. Whether or not the person diagnosed with ARD decides to get clean, we as a society should stand behind them one hundred percent. We are all part of the problem. By calling someone a “drunk” we are making them feel unworthy of help, compassion, and empathy. If we can take a moment to understand life through the eyes of an alcoholic, perhaps we can acquire the ability to be sympathetic. Whether or not a chronic alcoholic requests treatment, they do need it. It is our duty as a society to provide that assistance with no judgment and the utmost support.

Steps towards recovery:

  • Stop drinking. Attend a rehab facility that is geared towards needs of the patient by using an individualized treatment plan. Depending on prior mental health history, the patient may require intense psychotherapy with psychotropic medicines as an adjunct to counseling. It is important that addiction and mental health issues are being adequately managed.

  • Consult a general medical physician for evaluation of overall health status. If there are pre-existing conditions, it would be useful to obtain a referral for a specialist, (i.e. cardiologist if a heart condition surfaces). If ARD is still moderate, consult another physician experienced with alcohol related conditions.

  • Visit a Neurologist for an accurate assessment and diagnosis regarding memory loss. A Neuropsychologist can further evaluate cognitive impairment and formulate specific treatment plans to improve deficits.

  • As a family member, it is critical to remain SUPPORTIVE and compassionate with unconditional love. Most importantly, be by their side every step of the way no matter what obstacles you may endure as a family. This is how genuine recovery begins and is maintained. Do not allow your feelings of anger and bitterness to interfere with the recovery process. If there are issues that need to be addressed, it is best to do that within family counseling where you have a proper platform to work through your issues without causing more damage and resentment.


References

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Sheedy D, Say M, Stevens J, Harper CG, Kril JJ. Influence of liver pathology on markers of postmortem brain tissue quality. Alcohol Clin Exp Res. 2012; 36(1):55–60.10.1111/j. 1530-0277.2011.01580.x

Butterworth RF. Cerebral dysfunction in chronic alcoholism: role of alcoholic liver disease. Alcohol Suppl. 1994; 2:259–265

Victor M, Adams RD, Cole M. The acquired (non-Wilsonian) type of chronic hepatocerebral degeneration. Medicine. 1965; 44(5):345–396

Hazell AS, Butterworth RF. Hepatic encephalopathy: an update of pathophysiologic mechanisms. Proc Soc Exp Biol Med. 1999; 222(2):99–112

Zaki AE, Wardle EN, Canalese J, Ede RJ, Williams R. Potential toxins of acute liver failure and their effects on blood-brain barrier permeability. Experientia. 1983; 39(9):988–991

Van Thiel DH, Gavaler JS, Tarter R, Schade RR, Stone BG. Hepatic encephalopathy and the neural regulation of hypothalamic pituitary function. Semin Liver Dis. 1985; 5(1):70– 83.10.1055/s-2008-1041759

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Butterworth RF. Portal-systemic encephalopathy: a disorder of neuron-astrocytic metabolic trafficking. Dev Neurosci. 1993; 15(3–5):313–319.

Harper C. The Neuropathology of alcohol-specific brain damage, or does alcohol damage the brain? J Neuropathol Exp Neurol 1998; 57:101-10.

Gupta S, Warner J. Alcohol-Related Dementia: a 21st-century silent epidemic? British Journal of Psychiatry 2008;193: 351-353.

Ridley, NJ., Draper B, Withall A. Alcohol-related Dementia: and update of the evidence. Alzheimer’s Research & Therapy 2013; 5:3.

Oslin DW, Streim JE, Parmelee P, Boyce AA, Katz IR: Alcohol abuse: a source of functional disability among residents of a VA nursing home. Int J Geriatr Psychiatry 1997, 12:825-832.

J Calderon, R J Perry, S W Erzinclioglu, G E Berrios, T R Dening, J R Hodges. Perception, attention, and working memory are disproportionately impaired in dementia with Lewy bodies compared with Alzheimer’s disease. J Neurol Neurosurg Psychiatry, 2001;70:157–164.

Vetreno RP, Hall JM, Savage LM. Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment. Neurobio Learn Mem, 2011; 96(4): 596-608.

Dahlberg D, Ivanovic J, Hassel B. Toxic levels of ammonia in human brain abscess. J Neurosurg, 2016; 124: 854-860.

Brust JC: Ethanol and cognition: indirect effects, neurotoxicity, and neuroprotection: a review. Int J Environ Res Public Health, 2010; 7:1540-1557. 

Crews FT, Collins MA, Dlugos C, Littleton J, Wilksons L, Neafsey EJ, Pentney R, Snell LD, Tabakoff B, Zou J, Noronha A: Alcohol-induced neurodegeneration: when, where and why? Alcohol Clin Exp Res, 2004; 28:350-364.

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