Dementia is a syndrome or a group of symptoms characterized by a decline in cognitive (intellectual) abilities resulting in the impairment of social and occupational functioning. Excessive use of alcohol over a prolonged duration can lead to brain damage. The impact of chronic alcohol on cognitive function can be variable and can range from mild cognitive impairment to alcohol-induced dementia that may be irreversible. 

What is Alcohol-Induced Dementia?

Prolonged alcohol use, especially in large quantities, can impact the brain in many ways and can lead to the development of dementia. Alcohol-related dementia or alcohol-induced dementia may be caused either due to the direct effects of alcohol on the brain or due to the indirect effects of alcohol, such as by causing vitamin B1 deficiency. Alcohol and its metabolite acetaldehyde can directly cause permanent structural and functional damage to the brain leading to impaired cognitive function. 

Excessive alcohol intake can result in the loss of neurons (gray matter) due to hyper-excitation, oxidative stress and impaired generation of new neurons. Chronic alcohol intake is associated with the loss of neurons in the hippocampus, hypothalamus and cerebellum. Prolonged alcohol intake can also damage white matter, which is mostly comprised of the axons of neurons that are responsible for carrying impulses from the cell body of one neuron to another. Damage to white matter changes the connectivity between different brain regions. Chronic alcohol intake can result in damage to white matter in the prefrontal cortex, corpus callosum (the white matter tract that connects the two cortical hemispheres) and cerebellum. 

Alcohol-related dementia may also be caused by thiamine deficiency. Alcohol directly interferes with the absorption and utilization of vitamin B1 or thiamine. Thiamine plays an important part in the metabolism or breakdown of sugars into other molecules in the brain among other tissues. Thiamine is also necessary for the production of various neurotransmitters in the brain. Thiamine deficiency can disrupt the functioning of neurons and cause brain damage. Thiamine deficiency also has a severe impact on the cardiovascular system and can cause damage to blood vessels in the brain. The human body is not capable of producing thiamine, making it necessary to acquire this vitamin from food sources. Besides interfering with the absorption and utilization of thiamine, chronic alcohol users often have a poor diet resulting in thiamine deficiency. Thiamine deficiency can lead to Wernicke-Korsakoff syndrome that involves cognitive impairment. 

Wernicke-Korsakoff Syndrome

Wernicke-Korsakoff syndrome is caused by thiamine deficiency that may be either due to poor diet or due to impaired thiamine metabolism caused by chronic alcohol intake. 

Wernicke-Korsakoff syndrome involves cognitive impairment and in many cases, represents a form of alcohol-related dementia or alcohol-induced dementia. Wernicke-Korsakoff syndrome consists of two different conditions: Wernicke’s encephalopathy and Korsakoff’s psychosis. Thiamine deficiency leads to Wernicke’s encephalopathy which is generally short-lived and severe. The symptoms of Wernicke’s encephalopathy include paralysis of the nerves that move the eyes (resulting in abnormal eye movements and eyelid drooping), loss of muscle coordination (particularly of the legs leading to tremors), and mental confusion. Wernicke’s encephalopathy is characterized by neuronal loss in the hypothalamus (paraventricular nucleus) and the midbrain (periaqueductal gray). Wernicke’s encephalopathy is often followed by Korsakoff syndrome and the two conditions are referred together as the Wernicke-Korsakoff syndrome. Korsafoff’s psychosis tends to be a chronic and debilitating condition. Korsakoff syndrome is characterized by memory loss, disorientation and confabulation. Confabulation involves making up information without the intention to do so.

Treatment of Wernicke’s encephalopathy by the administration of thiamine can prevent the progression of the condition and the development of Korsakoff syndrome. Improvement in mental state can be observed after two to three weeks of administration of thiamine. If untreated, Korsakoff syndrome may develop, with the symptoms of Wernicke-Korsakoff syndrome often being persistent and potentially irreversible. About 80% to 90% of individuals with Wernicke’s encephalopathy caused by chronic alcoholic intake tend to develop Korsakoff’s psychosis. Many individuals (25%) with Wernicke-Korsakoff syndrome require long-term institutionalization. Individuals with Wernicke-Korsakoff syndrome may show gradual improvement, often over a period of many years. Abstinence from alcohol is also necessary for maximal recovery. About 20% of the individuals with Wernicke-Korsakoff syndrome may show irreversible cognitive deficits involving learning and memory, whereas about half of the patients tend to show irreversible gait abnormalities. The mortality rate due to Wernicke-Korsakoff syndrome is around 10% to 15%. Wernicke Korsakoff syndrome occurs in 1% to 2% of the general population in the United States and is observed in individuals between the ages of 30 and 70 years.

How Can Alcohol Cause Dementia?

Alcohol can have direct neurotoxic effects resulting in dementia. Alcohol can also cause dementia indirectly, such as due to vitamin B1 deficiency. Whether brain damage is caused directly by alcohol or indirectly through a nutritional deficiency or a combination of both remains a matter of debate within the scientific community. 

Excessive use of alcohol is also associated with an increased risk of head injuries that may contribute to brain damage along with the aforementioned causes. Chronic alcohol use is also associated with a higher risk for a range of cardiovascular diseases or conditions such as high blood pressure, stroke, cardiomyopathy, and ischemic heart disease. Chronic alcohol intake can thus lead to vascular dementia. Hepatic failure due to chronic alcohol intake impairs the ability of the liver to get rid of toxins. This danger can expose the brain to toxins and cause damage to neurons.

Alcoholic Dementia Symptoms

One of the distinguishing signs of alcohol-induced dementia from other types of dementia is the lack of impairment of language-related skills in most cases. Unlike some of the other types of dementia, there is considerable variability in the types of symptoms presented by individuals with alcohol-induced dementia.

Some of the symptoms of alcohol-related dementia include:

  • Amnesia or memory loss
  • Impaired ability to form new memories
  • Impaired motor coordination or balance
  • Deficits in executive functioning (such as planning, thinking, reasoning and processing abstract information)
  • Difficulty in recognizing objects

Alcohol Dementia Treatment

Some of the cognitive deficits caused by alcohol-induced neurotoxic effects can be reversed by abstaining from alcohol use. Improvement of cognitive function may require a long period of time after stopping alcohol use. If alcohol-related dementia is caused by a thiamine deficiency, treatment with thiamine can reverse the effects of Wernicke Korsakoff syndrome. Thiamine treatment can improve the symptoms of mental confusion, deficits in muscle coordination and eye movements. Thiamine treatment does not improve symptoms of impaired memory and thinking in most cases. The possibility of reversing the deficits caused by alcohol use is the highest during the early stages of the disease. However, in more than half of the cases, such cognitive deficits are not reversible.

Other guidelines for the treatment of alcohol-induced dementia include the use of pharmacological treatments and psychosocial interventions. A few studies have shown that medications like memantine and rivastigmine that are used for the treatment of other types of dementia may also be useful in improving cognitive function in individuals with alcohol-induced dementia. For individuals who do not respond to abstention or other forms of therapy, psychosocial interventions such as cognitive behavioral therapy may be useful in slowing cognitive decline and possibly improving cognitive function.

If you or a loved one struggle with alcohol use, Orlando Recovery Center can help. You deserve a healthier future, contact Orlando Recovery Center today and take the first step toward long-term sobriety.

Sources:

Ridley, Nicole J.; Brian Draper; Adrienne Withall. “Alcohol-related dementia: an update of the evidence.” Alzheimer’s Research & Therapy, February 2013. Accessed August 23, 2019.

Martin, Peter R.; Charles K. Singleton; and Susanne Hiller-Sturmhöfel. “The role of thiamine deficiency in alcoholic brain disease.” Alcohol Research & Health, 2003. Accessed August 23, 2019.

Akhouri, Shweta; Newton, Edward J. Wernicke-Korsakoff Syndrome. NCBI Bookshelf: StatPearls Updated,  March 15, 2019. Accessed August 23, 2019.

National Organization for Rare Disorders.”Wernicke-Korsakoff Syndrome.” 2005. Accessed August 23, 2019.

Sachdeva, Ankur; Mina Chandra; Mona Choudhary; Prabhoo Dayal; Kuljeet Singh Anand. “Alcohol-related dementia and neurocognitive impairment: a review study.” International Journal of High Risk Behaviors & Addiction, September 2016. Accessed August 23, 2019.