Alcohol-related dementia
Alcohol-related dementia (ARD) is a form of dementia caused by long-term, excessive consumption of alcoholic beverages, resulting in neurological damage and impaired cognitive function. Terminology. 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 (Wernicke–Korsakoff syndrome), characterized by short term memory loss and thiamine (vitamin B1) deficiency. 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. On many non-medical websites, the terms wet brain and alcohol-related dementia are often used interchangeably, creating significant confusion. Additionally, the term alcohol-induced persistent dementia is another nonspecific name that is sometimes used. Signs and symptoms. Alcohol-related 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. Certain individuals with alcohol-related dementia 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 Wernicke encephalopathy 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. Individuals affected by  alcohol-related dementia may develop memory problems, language impairment, and an inability to perform complex motor tasks such as getting dressed. Heavy alcohol consumption also damages the nerves in arms and legs, i.e. peripheral neuropathy, as well as the cerebellum that controls coordination thereby leading to the development of 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. People with an alcohol use disorder are more likely to become depressed than people without alcohol use disorder, and it may be difficult to differentiate between depression and alcohol dementia. Pathophysiology. 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 use disorder is common in older persons, and alcohol-related dementia is under-diagnosed. Diagnosis. The signs and symptoms of alcohol-related dementia are essentially the same  as the symptoms present in other types of dementia, making alcohol-related 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. 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. Diagnostic criteria. 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. Criteria for alcohol-induced persistent dementia in the Diagnostic and  Statistical Manual of Mental Disorders (DSM-IV) include the following: There are problems with DSM diagnostic criteria. First, 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 five years, and significant alcohol use occurring within three 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. Treatment. ARD is treated with abstinence from further alcohol consumption. Prognosis. Multiple withdrawals and binge drinking may significantly exacerbate  cognitive deficits. Older individuals are at greater risk of cognitive changes. Recovery. Following abstinence, many deficits often resolve rapidly (in as little as a week). Further gradual recovery of cognitive abilities may take place over several years. Executive function, working memory, perceptual impairment, and motor impairments often persist after short-term abstinence. Recovery of cognitive skills appears correlated to recent intake levels and duration of abstinence, rather than to lifetime cumulative alcohol intake. Older individuals are less likely to recover completely following cessation of alcohol intake. Epidemiology. The onset of alcohol dementia can occur as early as age 30, although  it is far more common that the dementia will reveal itself anywhere from age 50 to 70. The onset and the severity of this type of dementia is directly correlated to the amount of alcohol that a person consumes over their lifetime. Sex appears to be a risk factor for cognitive impairment, with females being more susceptible despite lower alcohol intake. A French study, looking at other studies of thousands of subjects, found that moderate alcohol consumption (up to four glasses of wine per week) was associated with lower levels of dementia, and vice versa. There is insufficient evidence to  assume that alcohol is protective against dementia at any level of intake; some studies found the opposite effect, and the quality of evidence from current epidemiological studies is poor overall (since observational studies assessing health effects of alcohol intake cannot adequately control for confounding factors). Notable cases. According to her family, the socialite Leonore Lemmon (fiancée of George Reeves) spent the last few years of her life with alcohol dementia, before dying in 1989. The Australian entertainer and "King of Comedy" Graham Kennedy was suffering from alcohol-related dementia at time of his death in 2005. Alcohol-related dementia