Alcohol-related dementia

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Alcohol-related dementia
Specialty Neurology

Alcohol-related dementia (ARD) is a form of dementia caused by long-term, excessive consumption of alcohol, resulting in neurological damage and impaired cognitive function. [1]

Contents

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. [2] 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, [3] 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. [2]

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. [3]

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. [3] People with an alcohol use disorder are more likely to become depressed than people without alcohol use disorder, [4] 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. [5] Alcohol can damage the brain directly as a neurotoxin, [5] or it can damage it indirectly by causing malnutrition, primarily a loss of thiamine (vitamin B1). [2] Alcohol use disorder is common in older persons, and alcohol-related dementia is under-diagnosed. [3]

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. [6] 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. [7]

A simple test for intellectual function, like the Folstein mini–mental state examination, is the minimum screen for dementia. The test requires 15–20 minutes to administer and is available in mental health centers. [8]

Diagnosing alcohol-related dementia can be difficult due to the wide range of symptoms and a lack of specific brain pathology. [3] The Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) is a guide to aid doctors in diagnosing a range of psychiatric disorders, and may be helpful in diagnosing dementia. [9]

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. [10] Criteria for alcohol-induced persistent dementia in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) include the following:

A. The development of multiple cognitive deficits manifested by both:
  1. Memory impairment (impaired ability to learn new information or to recall previously learned information)
  2. One (or more) of the following cognitive disturbances:
  • (a) Aphasia (language disturbance)
  • (b) Apraxia (impaired ability to carry out motor activities despite intact motor function)
  • (c) Agnosia (failure to recognize or identify objects despite intact sensory function)
  • (d) Disturbance in executive functioning (i.e. planning, organizing, sequencing, abstracting)
B. The cognitive deficits in criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.
C. The deficits do not occur exclusively during the course of a delirium and persist beyond the usual duration of substance intoxication or withdrawal.
D. There is evidence from the history, physical examination, or laboratory findings that deficits are etiologically related to the persisting effects of substance use. [7]

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. [5]

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. [10] 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. [11]

Oslin's proposed classification of ARD:

At the current time there are no acceptable criteria to definitively define alcohol-related dementia.

A. The criteria for the clinical diagnosis of probable alcohol-related dementia include the following:
  1. A clinical diagnosis of dementia at least 60 days after the last exposure to alcohol.
  2. Significant alcohol use as defined by a minimum average of 35 standard drinks per week for men (28 for women) for greater than a period of five years. The period of significant alcohol use must occur within three years of the initial onset of dementia.
B. The diagnosis of alcohol-related dementia is supported by the presence of any of the following:
  1. Alcohol related hepatic, pancreatic, gastrointestinal, cardiovascular, or renal disease i.e. other end-organ damage.
  2. Ataxia or peripheral sensory polyneuropathy (not attributed to other causes).
  3. Beyond 60 days of abstinence, the cognitive impairment stabilizes or improves.
  4. After 60 days of abstinence, any neuroimaging evidence of ventricular or sulcal dilatation improves.
  5. Neuroimaging evidence of cerebellar atrophy, especially in the vermis.
C. The following clinical features cast doubt on the diagnosis of alcohol-related dementia:
  1. The presence of language impairment, especially dysnomia or anomia.
  2. the presence of focal neurologic signs or symptoms (except ataxia or peripheral sensory polyneuropathy).
  3. Neuroimaging evidence for cortical or subcortical infarction, subdural hematoma, or other focal brain pathology.
  4. Elevated Hachinski Ischemia Scale score.
D. Clinical features that are neither supportive nor cast doubt on the diagnosis of alcohol-related dementia included:
  1. Neuroimaging evidence of cortical atrophy.
  2. The presence of periventricular or deep white matter lesions on neuroimaging in the absence of focal infarct(s).
  3. The presence of the Apolipoprotein c4 allele. [11]

Treatment

ARD is treated with abstinence from further alcohol consumption. [12]

Prognosis

Multiple withdrawals and binge drinking may significantly exacerbate cognitive deficits. Older individuals are at greater risk of cognitive changes. [12]

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. [12]

Older individuals are less likely to recover completely following cessation of alcohol intake. [12]

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. [13]

Sex appears to be a risk factor for cognitive impairment, with females being more susceptible despite lower alcohol intake. [12]

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. [5] 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). [14] [15]

Notable cases

The Australian entertainer and "King of Comedy" Graham Kennedy had alcohol-related dementia at time of his death in 2005. [16]

Terminology

Alcohol-related dementia is a broad term currently preferred among medical professionals. [10] If a person has alcohol-related 'dementia' they will struggle with day-to-day tasks. This is because of the damage to their brain, caused by regularly drinking too much alcohol over many years. [17] This affects memory, learning and other mental functions. Korsakoff's syndrome and Wernicke–Korsakoff syndrome are particular forms of alcohol related brain injury which may be related to alcohol related dementia. [18] 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). [5]

Related Research Articles

<span class="mw-page-title-main">Dementia</span> Long-term brain disorders causing impaired memory, thinking and behavior

Dementia is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person's ability to perform everyday activities. This typically involves problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms of dementia include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, their caregivers, and their social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than might be caused by the normal aging process.

<span class="mw-page-title-main">Dementia with Lewy bodies</span> Type of progressive dementia

Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and regulation of automatic bodily functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive impairment interferes with normal daily functioning. Together with Parkinson's disease dementia, DLB is one of the two Lewy body dementias. It is a common form of dementia, but the prevalence is not known accurately and many diagnoses are missed. The disease was first described on autopsy by Kenji Kosaka in 1976, and he named the condition several years later.

<span class="mw-page-title-main">Vascular dementia</span> Dementia resulting from stroke

Vascular dementia is dementia caused by a series of strokes. Restricted blood flow due to strokes reduces oxygen and glucose delivery to the brain, causing cell injury and neurological deficits in the affected region. Subtypes of vascular dementia include subcortical vascular dementia, multi-infarct dementia, stroke-related dementia, and mixed dementia.

<span class="mw-page-title-main">Wernicke–Korsakoff syndrome</span> Combined presence of Wernickes encephalopathy (WE) and Korsakoffs syndrome

Wernicke-Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and alcoholic Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome. It mainly causes vision changes, ataxia and impaired memory.

<span class="mw-page-title-main">Korsakoff syndrome</span> Mental illness caused by a lack of thiamine in the brain

Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.

<span class="mw-page-title-main">Frontotemporal dementia</span> Types of dementia involving the frontal or temporal lobes

Frontotemporal dementia (FTD), also called frontotemporal degeneration disease or frontotemporal neurocognitive disorder, encompasses several types of dementia involving the progressive degeneration of the brain's frontal and temporal lobes. Men and women appear to be equally affected. FTD generally presents as a behavioral or language disorder with gradual onset. Signs and symptoms tend to appear in late adulthood, typically between the ages of 45 and 65, although it can affect people younger or older than this. Currently, no cure or approved symptomatic treatment for FTD exists, although some off-label drugs and behavioral methods are prescribed.

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired, typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means a decrement in the size of the cell, which can be due to progressive loss of cytoplasmic proteins. In brain tissue, atrophy describes a loss of neurons and the connections between them. Brain atrophy can be classified into two main categories: generalized and focal atrophy. Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location. If the cerebral hemispheres are affected, conscious thought and voluntary processes may be impaired.

<span class="mw-page-title-main">Corticobasal degeneration</span> Rare neurodegenerative disease

Corticobasal degeneration (CBD) is a rare neurodegenerative disease involving the cerebral cortex and the basal ganglia. CBD symptoms typically begin in people from 50 to 70 years of age, and typical survival before death is eight years. It is characterized by marked disorders in movement and cognition, and is classified as one of the Parkinson plus syndromes. Diagnosis is difficult, as symptoms are often similar to those of other disorders, such as Parkinson's disease, progressive supranuclear palsy, and dementia with Lewy bodies, and a definitive diagnosis of CBD can only be made upon neuropathologic examination.

Psychoorganic syndrome (POS), also known as organic psychosyndrome, is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

<span class="mw-page-title-main">Organic brain syndrome</span> Disorder of mental function whose cause is alleged to be known as physiological

Organic brain syndrome, also known as organic brain disease, organic brain damage, organic brain disorder (OBD), organic mental syndrome, or organic mental disorder, refers to any syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders. Originally, the term was created to distinguish physical causes of mental impairment from psychiatric disorders, but during the era when this distinction was drawn, not enough was known about brain science for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine. While mental or behavioural abnormalities related to the dysfunction can be permanent, treating the disease early may prevent permanent damage in addition to fully restoring mental functions. An organic cause to brain dysfunction is suspected when there is no indication of a clearly defined psychiatric or "inorganic" cause, such as a mood disorder.

Mild cognitive impairment (MCI) is a diagnosis that reflects an intermediate stage of cognitive impairment that is often, but not always, a transitional phase from cognitive changes in normal aging to those typically found in dementia, especially dementia due to Alzheimer's disease. MCI may include both memory and non-memory neurocognitive impairments. About 50 percent of people diagnosed with MCI have Alzheimer's disease and go on to develop Alzheimer's dementia within five years. MCI can also serve as an early indicator for other types of dementia, although MCI may also remain stable or remit. Many definitions of MCI exist. A common feature of many of these is that MCI involves cognitive impairments that are measurable but that are not significant enough to interfere with instrumental activities of daily living.

Pseudodementia is a condition that leads to cognitive and functional impairment imitating dementia that is secondary to psychiatric disorders, especially depression. Pseudodementia can develop in a wide range of neuropsychiatric disease such as depression, schizophrenia and other psychosis, mania, dissociative disorders, and conversion disorders. The presentations of pseudodementia may mimic organic dementia, but are essentially reversible on treatment and doesn't lead to actual brain degeneration. However, it has been found that some of the cognitive symptoms associated with pseudodementia can persist as residual symptoms and even transform into true neurodegenerative dementia in some cases.

The NINCDS-ADRDA Alzheimer's Criteria were proposed in 1984 by the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association and are among the most used in the diagnosis of Alzheimer's disease (AD). These criteria require that the presence of cognitive impairment and a suspected dementia syndrome be confirmed by neuropsychological testing for a clinical diagnosis of possible or probable AD; while they need histopathologic confirmation for the definitive diagnosis. They specify as well eight cognitive domains that may be impaired in AD. These criteria have shown good reliability and validity.

<span class="mw-page-title-main">Posterior cortical atrophy</span> Medical condition

Posterior cortical atrophy (PCA), also called Benson's syndrome, is a rare form of dementia which is considered a visual variant or an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.

The diagnosis of schizophrenia, a psychotic disorder, is based on criteria in either the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, or the World Health Organization's International Classification of Diseases (ICD). Clinical assessment of schizophrenia is carried out by a mental health professional based on observed behavior, reported experiences, and reports of others familiar with the person. Diagnosis is usually made by a psychiatrist. Associated symptoms occur along a continuum in the population and must reach a certain severity and level of impairment before a diagnosis is made. Schizophrenia has a prevalence rate of 0.3-0.7% in the United States.

Alcohol-related brain damage alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe, limbic system, and cerebellum, with widespread cerebral atrophy, or brain shrinkage caused by neuron degeneration. This damage can be seen on neuroimaging scans.

Corticobasal syndrome (CBS) is a rare, progressive atypical Parkinsonism syndrome and is a tauopathy related to frontotemporal dementia. CBS is typically caused by the deposit of tau proteins forming in different areas of the brain.

References

  1. ↑ Ridley, Nicole J; Draper, Brian; Withall, Adrienne (25 January 2013). "Alcohol-related dementia: an update of the evidence". Alzheimer's Research & Therapy. 5 (1): 3. doi: 10.1186/alzrt157 . ISSN   1758-9193. PMC   3580328 . PMID   23347747.
  2. 1 2 3 "Alcohol-related dementia". Archived from the original on 8 March 2019. Retrieved 21 October 2015.
  3. 1 2 3 4 5 Alcohol Induced Dementia [usurped]
  4. ↑ "Alcohol - Special Subjects". Merck Manuals Consumer Version. Retrieved 21 October 2015.
  5. 1 2 3 4 5 Derouesné, Christian; Pierucci-Lagha, Amira (December 2003). "John Libbey Eurotext - Psychologie & NeuroPsychiatrie du vieillissement - Alcool et vieillissement". Psychologie & Neuropsychiatrie du Vieillissement. 1 (4): 237–249. Retrieved 21 October 2015.
  6. ↑ "What's Alcohol-Related Dementia?". health-cares.net. 18 July 2005. Archived from the original on 8 March 2019. Retrieved 5 March 2008.
  7. 1 2 Moriyama Y.; Mimura M.; Kato M.; Kashima H. (2006). "Primary alcoholic dementia and alcohol-related dementia". Psychogeriatrics. 6 (3): 114–118. doi:10.1111/j.1479-8301.2006.00168.x. S2CID   144119653.
  8. ↑ Fiodor, Kosova. "Dementia test". Dementia Test. Retrieved 7 June 2019.
  9. ↑ David Pingitore-Randy A. Sansone (1998-10-15). "Using DSM-IV Primary Care Version: A Guide to Psychiatric Diagnosis in Primary Care". American Family Physician. 58 (6): 1347–52. PMID   9803199 . Retrieved 21 October 2015.
  10. 1 2 3 Warner, James; Gupta, Susham (2008). "Alcohol-related dementia: a 21st-century silent epidemic? - The British Journal of Psychiatry". The British Journal of Psychiatry. 193 (5): 351–353. doi: 10.1192/bjp.bp.108.051425 . PMID   18978310.
  11. 1 2 Oslin, D. (1998). ALCOHOL RELATED DEMENTIA: PROPOSED CLINICAL CRITERIA. International Journal of Geriatric Psychiatry, 13(4), 203-212.
  12. 1 2 3 4 5 Ridley, Nicole J; Draper, Brian; Withall, Adrienne (2013-01-25). "Alcohol-related dementia: an update of the evidence". Alzheimer's Research & Therapy. 5 (1): 3. doi: 10.1186/alzrt157 . ISSN   1758-9193. PMC   3580328 . PMID   23347747.
  13. ↑ Hockley, Julie. "Alcohol Related Dementia (ARD)" (PDF). Archived (PDF) from the original on 2022-01-14.
  14. ↑ Wiegmann, Caspar; Mick, Inge; Brandl, Eva J; Heinz, Andreas; Gutwinski, Stefan (2020-01-09). "Alcohol and Dementia – What is the Link? A Systematic Review". Neuropsychiatric Disease and Treatment. 16: 87–99. doi: 10.2147/NDT.S198772 . ISSN   1176-6328. PMC   6957093 . PMID   32021202.
  15. ↑ Rehm, Jürgen; Hasan, Omer S. M.; Black, Sandra E.; Shield, Kevin D.; Schwarzinger, Michaël (2019-01-05). "Alcohol use and dementia: a systematic scoping review". Alzheimer's Research & Therapy. 11 (1): 1. doi: 10.1186/s13195-018-0453-0 . ISSN   1758-9193. PMC   6320619 . PMID   30611304.
  16. ↑ Mangos, John (7 June 2005). "The King and I". The Bulletin. NineMSN.com. p. 31. Archived from the original on 19 June 2005. Retrieved 4 February 2008.
  17. ↑ "Alcohol-related 'dementia' | Alzheimer's Society". www.alzheimers.org.uk. Retrieved 2022-10-04.
  18. ↑ "Alcohol related dementia". www.dementia.org.au. Retrieved 2022-10-04.
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