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Alcohol dementia is a form of dementia caused by long-term, excessive drinking, resulting in neurological damage and impaired mental processing. In general, dementia occurs in people older than 65, and is a common cause of mental dysfunction. Dementia begins gradually, and progresses slowly.
Alcohol-Related Dementia (ARD) is currently the preferred medical term, and it covers the two main forms of alcohol induced dementia:
ARD patients often have symptoms of both forms, i.e. impaired ability to plan, apathy, and memory loss.
ARD may occur with other forms of dementia (mixed dementia). The diagnosis of ARD is widely recognized but rarely applied, due to a lack of specific diagnostic criteria.
Treatment is similar for both forms of ARD:
Alcohol-related dementia is a broad term currently preferred among medical professionals. Many experts use the terms alcohol (or alcoholic) dementia to describe a specific form of ARD, characterized by impaired executive function (planning, thinking, and judgment). Another form of ARD is known as wet brain (see Wet Brain below), characterized by short term memory loss and thiamine (vitamin B1) deficiency.
On many non-medical websites, the terms are often used interchangeably, creating significant confusion. Additionally, the term Alcohol Induced Persistent Dementia is another non-specific name that is sometimes used.
Epidemiological studies show an association between long term alcohol intoxication and dementia. Alcohol can damage the brain directly as a neurotoxin, or it can damage it indirectly by causing malnutrition, primarily a loss of thiamine (vitamin B1). Alcohol abuse is common in older persons, and alcohol related dementia is under-diagnosed. While moderate alcohol consumption (up to four glasses of wine per day) has been shown to protect against dementia, higher rates of consumption increase the chances of getting it.
Alcohol dementia presents as a global deterioration in intellectual function with memory not being specifically affected, but it may occur with other forms of dementia, resulting in a wide range of symptoms. Alcohol damages neurons, i.e., brain cells, throughout the brain. The lack of specific brain pathology has caused alcohol-related dementia to be under-recognized as a cause of intellectual loss.
Some alcohol dementia patients present with damage to the frontal lobes of their brain causing disinhibition, loss of planning and executive functions, and a disregard for the consequences of their behavior. Other types of alcohol-related dementia such as Korsakoff's Syndrome (see "Wet Brain" below) cause the destruction of certain areas of the brain, where changes in memory, primarily a loss of short term memory, are the main symptom. Most presentations of alcohol dementia are somewhere along the spectrum between a global dementia and Korsakoff's Psychosis, and may include symptoms of both.
Patients with alcoholic dementia may develop memory problems, language impairment, and an inability to perform complex motor tasks, like dressing. Patients may also develop apathy, irritability, and resistiveness. However, people who have alcohol-related dementia can have good verbal intelligence and their language skills may be preserved.
Heavy alcohol abuse damages the nerves in arms and legs, i.e. peripheral neuropathy, as well as the cerebellum that controls coordination, i.e. cerebellar ataxia. These patients frequently have problems with sensation in their extremities and may demonstrate unsteadiness on their feet.
Alcohol related dementia can produce a variety of psychiatric problems including psychosis (disconnection from reality), depression, anxiety, and personality changes. Patients with alcoholic dementia often develop apathy, related to frontal lobe damage, that may mimic depression. Alcoholics are more likely to become depressed than people who are not alcoholics, and it may be difficult to differentiate between depression and alcohol dementia.
The symptoms of alcohol dementia are essentially the same as the symptoms present in other types of dementia, making alcohol dementia difficult to diagnose. There are very few qualitative differences between alcohol dementia and Alzheimer's disease and it is therefore difficult to distinguish between the two. Some of these warning signs may include memory loss, difficulty performing familiar tasks, poor or impaired judgment and problems with language. However the biggest indicator is friends or family members reporting changes in personality.
Anyone who drinks excessive amounts of alcohol over a long period of time is at risk of succumbing to alcohol-related dementia. A male who drinks six or more alcoholic drinks a day is placing himself at a greater risk; the same goes for females who have four or more alcoholic drinks daily. However, this type of drinking would have to be sustained for a substantial amount of time.
The onset of alcohol dementia can occur as early as age thirty, although it is far more common that the dementia will reveal itself anywhere from age fifty to age seventy. The onset and the severity of this type of dementia is directly correlated to the amount of alcohol that a person consumes over his or her lifetime.
Alcohol has a direct effect on brain cells in the front part of the brain, resulting in poor judgment, difficulty making decisions, and lack of insight. Long-time alcohol abuse can often lead to poor nutrition problems causing parts of the brain to be damaged by vitamin deficiencies. These problems could also cause personality changes in some people.
The existence of alcohol-related dementia is widely acknowledged but not often used as a diagnosis, due to a lack of widely accepted, non-subjective diagnostic criteria; more research is needed.
Ideally, the person suspected of having any form of dementia should have a complete medical and mental health work-up done. A simple test for intellectual function, like the Folstein Mini-Mental Status Examination, is the minimum screen for dementia. The test requires 15 – 20 minutes to administer and is available in mental health centers.
Diagnosing alcohol related dementia can be difficult, due to the wide range of symptoms, and a lack of specific brain pathology. The Diagnostic and Statistical Manual of Mental Disorders, (DSM-IV), is a guide to aid doctors in diagnosing a range of psychiatric disorders, and may be helpful in diagnosing dementia.
Criteria for alcohol-induced persistent dementia in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV)
There are problems with DSM diagnostic criteria, however. Firstly, they are vague and subjective. Furthermore, the criteria for diagnosis of dementia were inspired by the clinical presentation of Alzheimer's disease and are poorly adapted to the diagnosis of other dementias. This has led to efforts to develop better diagnostic models.
Oslin (Int J Geriatr Psychiatry 1998) proposed alternative clinical diagnostic criteria which were validated. The criteria include a clinical diagnosis of dementia at least 60 days after last exposure to alcohol, significant alcohol use (i.e. minimum 35 standard drinks/week for males and 28 for women) for more than 5 years, and significant alcohol use occurring within 3 years of the initial onset of cognitive deficits. Oslin proposed the new and refined diagnostic criteria for Alcohol Related Dementia because he hoped that the redefined classification system would bring more awareness and clarity to the relationship between alcohol use and dementia.
Oslin's proposed classification of ARD:
At the current time there are no acceptable criteria to definitively define Alcohol Related Dementia.
If the symptoms of alcohol dementia are caught early enough, the effects may be reversed. The person must stop drinking and start on a healthy diet, replacing the lost vitamins, including, but not limited to, thiamine. Recovery is more easily achievable for women than men, but in all cases it is necessary that they have the support of family and friends and abstain from alcohol.
There is a case study of a patient who was treated with memantine; the patient was a 71 year old female who was treated with memantine for five weeks, at a dosage of 30 mg/daily to help improve memory and cognitive functioning. After the five week treatment the patient had shown improvement on the Mini-Mental State Examination from 18 to 22 points and her tests on the CERAD (Consortium to Establish a Registry for Alzheimer’s Disease) improved from zero to five on the Wordlist Recall and six to eight on the Drawing test. This is the only study of its kind but has promising outcomes for further research.
Another study, performed by Djokic and Zivkovic, provides evidence that treatment with Rivastigmine can improve symptoms of alcohol dementia. The patients were treated with a range of 3–12 mg every 24 hours, and the improvement in symptoms was seen around two and three months after the start of treatment.
Wet Brain, also called Wernicke–Korsakoff syndrome, is a form of alcohol related dementia that results from severe thiamine (vitamin B1) deficiency usually caused by alcoholism, poor nutrition, or poor absorption. The disease starts with Wernicke's Encephalopathy, and often progresses, if not treated, to Korsakoff's Psychosis.
The Korsakoff's Psychosis patient has severely impaired short-term recall, but this patient has excellent long-term memory and other intellectual functions.
Alcohol dementia is sometimes considered as synonymous with wet brain, however, dementia expert Richard E. Powers, MD considers alcohol dementia and wet brain as two separate forms of ARD. Primary treatment is similar for both forms, namely cessation of drinking and vitamin B replacement. A broader definition, such as "alcohol related dementia" has been introduced to encompass both forms of alcohol related cognitive disorders.
According to her family, the socialite Leonore Lemmon spent the last few years of her life with alcohol dementia, before dying in 1989.