An estimated half of alcoholics in the US have neurological deficits of varying severity, resulting from the neurotoxicity of ethanol, the nutritional deficiencies that often accompany alcoholism, and even repeated detoxifications. However, with early intervention, abstinence, and nutritional supplementation, these impairments can often be reversed or reduced.
- Autopsies reveal that 78% of people diagnosed with alcohol use disorder have brain pathology. This includes loss of white matter and neurons and structural abnormalities.
- There’s evidence that long-term alcohol exposure can cause neuronal loss and structural damage to the brain even in the presence of adequate thiamine.
- 80 to 90% of patients with Wernicke encephalopathy develop Korsakoff syndrome, with the symptoms often taking hold as those of WE abate
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What is alcoholic dementia?
Alcoholic dementia is an alcohol-related health condition characterized by a cognitive deterioration caused by long-term drinking. Several types are diagnosed, and there’s controversy over how related they may be.
- Wernicke encephalopathy (WE): an acute neurological syndrome that requires emergency treatment. WE is caused by thiamine deficiency and is characterized by mental confusion, ataxia (lack of muscle coordination), vision problems, low blood pressure, and hypothermia. If untreated it can lead to coma and death in around 20% of cases.Â
- Korsakoff syndrome (KS): a chronic memory condition that develops from thiamine deficiency, usually when Wernicke encephalopathy is left untreated or isn’t treated quickly enough. It’s therefore often diagnosed alongside WE. The concurrence of the two is known as Wernicke–Korsakoff syndrome or, colloquially, wet brain. Korsakoff syndrome causes confusion, memory loss, and difficulty taking in new information and learning new skills.[1]
- Alcohol-related dementia (ARD): a global deterioration in intellect; impairment in visuospatial skills, executive function, verbal abstract reasoning, working memory, IQ, attention, and speed of processing.[2]Â
Some scientists argue that all of these conditions should be grouped under the term alcohol-related brain damage (ARBD).
Other brain disorders associated with alcohol
Heavy alcohol use is also associated with a four times higher risk of developing other types of dementia.[3] Some of the elevated risks may be partly explained by a higher prevalence of traumatic brain injuries, as a result of falls, among drinkers.
Additionally, liver cirrhosis—in the US most commonly caused by excessive alcohol use—can also cause hepatic encephalopathy, a serious brain disorder resulting from the accumulation of toxins in the blood. Symptoms include forgetfulness, confusion, disorientation, and slurred speech.
What causes alcoholic dementia?
Autopsies reveal that 78% of people diagnosed with alcohol use disorder have brain pathology. This includes loss of white matter and neurons and structural abnormalities.[2]Â
Alcohol-related brain damage has been found in many parts of the brain, including:
- cerebral cortex: responsible for higher-level processes, including language, memory, thought, decision-making, emotions, intelligence, and personality
- limbic system: important in feeling and expressing emotions
- thalamus: central in communication within the brain
- hypothalamus: releases hormones and is involved in basic behavioral and physiological functions
- basal forebrain: involved in learning and memory
- cerebellum: important in posture and coordination and in learning basic tasks[4]
There are two theories about the cause of this damage. One theory holds that all brain damage and alcohol-related cognitive deficits are caused by thiamine deficiency and are all manifestations of Wernicke–Korsakoff syndrome (WKS), while another holds that alcohol itself causes damage.
Thiamine deficiency
Thiamine, also known as vitamin B1, is necessary for the extraction of energy from carbohydrates. Without thiamine, some neurons in the brain don’t receive enough energy and die. This atrophy is particularly concentrated in the thalamus, the hypothalamus, and mammillary bodies, resulting in amnesia.[4]
Thiamine is widely available in food, especially in whole grains, meat, and fish. In the US, many breads, cereals, noodles, and rice are enriched with thiamine. Chronic alcoholics often don’t take in enough thiamine because they don’t eat enough, getting most of their calories through alcoholic beverages. Thiamine deficiency and Wernicke's encephalopathy are also occasionally found in people who’ve had gastric bypass surgery, anorexia, prolonged vomiting, chemotherapy, and other causes of malnutrition.Â
However, alcoholics are particularly vulnerable because chronic alcohol use also decreases the absorption of thiamine in the gastrointestinal tract and impairs the use of thiamine in cells.[5]
Neurotoxicity from alcohol
There’s also evidence that long-term alcohol exposure can cause neuronal loss and structural damage to the brain even in the presence of adequate thiamine. Animal studies have shown dose-related ethanol-induced damage to the brain, especially the hippocampus, hypothalamus, and cerebellum, structures associated with memory and learning. In neuroimaging studies, alcoholics with no history of nutritional deficiency showed structure abnormalities, including changes to the corpus callous, pons, and cerebellum.
Therefore, some scientists argue that alcohol itself is neurotoxic, causing damage to the brain through glutamate excitotoxicity, oxidative stress, and the disruption of neurogenesis (the creation of new neurons).[2]
Detox
Detoxification from alcohol may also be damaging to the brain. Alcoholics and binge drinkers who go through repeated detoxification often exhibit symptoms of prefrontal cortex damage, including difficulty with executive function (problems with self-control, organization, working memory, and time management). They also have an impaired ability to learn new information.[6a]
During detox from alcohol, neurotransmission systems that are suppressed by alcohol show hyperexcitability. In acute withdrawal, this rebound can cause anxiety and seizures. In the long run, this hyperexcitability can cause brain damage.Â
What are the symptoms of alcoholic dementia?
Alcohol abuse can lead to a variety of neuropathic impairment conditions, each with its own specific symptoms.
Wernicke encephalopathy
Wernicke encephalopathy was traditionally identified by three symptoms
- change in mental state, usually confusion
- eye movement disorders, usually lateral nystagmus (involuntary eye movements)
- ataxia, usually presenting as gait disturbances and lack of balance
However, it’s now recognized that WE can cause other symptoms:
- other eye abnormalities, including changes to the pupils, impaired vision or vision loss, double vision, eyelid drooping
- hearing loss
- disorientation, apathy, irritability, lethargy, drowsiness
- difficulty swallowing
- amnesia
- depression
- hypothermia
- low blood pressure
- peripheral neuropathy
- coma[7]
Korsakoff syndrome
80 to 90% of patients with Wernicke encephalopathy develop Korsakoff syndrome, with the symptoms often taking hold as those of WE abate.[8]Â
Korsakoff syndrome is primarily a memory disorder. It causes:
- short-term memory loss, with an inability to form new memories or learn new information
- sporadic loss of long-term memory
- loss of memory after the onset of KS (anteretrograde amnesia)
- confabulation, or invented memories to fill in the gaps
- behavioral changes, often agitation or anger
- lack of focus or attention
- delirium or disorientation
- lack of content in speech[9]
Alcohol-related dementia
Alcohol-related dementia can encompass a wide range of symptoms, depending on which areas of the brain are affected. There are no specific diagnostic criteria, but symptoms may include:
- difficulty solving problems
- reduced ability to learn new things
- memory issues
- problems with balance
- personality changes
- reduced initiative and spontaneity
- inappropriate behavior
- impulsivity
- disregard for consequences
- poor judgment
- lack of goal-directed behaviors
- lack of motivation
- poor planning
- depression
- flat affect
- impaired emotional processing, eg. difficulty interpreting nonverbal emotional cues and reading facial expressions[4][10]
How to prevent alcoholic dementia
The best way to prevent alcoholic dementia is to drink only in moderation and, if you have a history of alcoholism, to stop entirely.
If you’re struggling with alcoholism, eat nutritious and well-balanced meals and take thiamine supplements while you seek treatment.
How is alcoholic dementia treated?
The cognitive impairments associated with alcohol use are often partly reversible with abstinence, although it may take months to years for the brain to heal. Brain scans show increased cerebral metabolism, especially in the frontal lobe, after less than a month of abstinence and, with continued abstinence, a partial reversal of brain tissue loss.[4]Â
Wernicke encephalopathy is a medical emergency and is treated with thiamine supplementation. Rapid treatment can prevent Korsakoff syndrome from developing.Â
The outlook for alcoholics who develop Korsakoff syndrome is poorer: around 75% are left with permanent brain damage and 25% are impaired enough to require long-term residential care or supported accommodation.[11]
Once the person has stopped drinking and their health has stabilized, they may need rehabilitation. This will usually include occupational therapy, as they learn to compensate for their cognitive deficits and live as independently as they can, and physiotherapy to address any gait and balance issues. This might be delivered through a dementia service or rehabilitation service for people with a brain injury.
Alcohol addiction treatment
Overcoming alcohol addiction is possible with the right help. This might be detox, in-patient rehab, medication, therapy, self-help groups, and nutritional support. For treatment options near you, visit our rehab directory.
