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