Internet Mental Health

ALCOHOL-INDUCED NEUROCOGNITIVE DISORDER





Internet Mental Health Quality of Life Scale (Client Version)

Internet Mental Health Quality of Life Scale (Therapist Version)

Big 5 Factors Of Mental Illness And Code For This Disorder
(The "6th Big Factor" of Mental Health, "Physical Health", Is Coded Normal or Green)

ALCOHOL-INDUCED NEUROCOGNITIVE DISORDER

  • Insidious onset and gradual decline in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition):

    • When mild: One or more cognitive domains may be impaired (usually learning and memory), but this does not interfere with independence in everyday activities (e.g., paying bills or managing medications). When mild, it may be difficult to distinguish this dementia from that of another medical condition (e.g., thyroid disorders, vitamin B12 deficiency).

    • When major: At least two cognitive domains are impaired (usually learning and memory, executive functioning, perceptual-motor, language), and this interferes with independence in everyday activities.

Prediction

    Chronic and progressive: If the heavy alcohol use persists; there is progressive cognitive decline. Alcohol abstinence in combination with adequate diet usually prevents the worsening of this cognitive decline.

Problems

    Occupational-Economic Problems:

    • Impairment in social and occupational functioning ranges from none (at the start) to severe (at the end).

    • If Alcohol Use Disorder continues; eventually needs total nursing home care.

    Antagonistic (Antagonism):

    • May become violent.

    Disinhibited (Disinhibition):

    • May become impulsive, reckless, disrespectful and/or irresponsible.

    Cognitive Decline (Impaired Intellect):

    • Has significant cognitive decline in one (or more) of:

      • Complex attention: e.g., is unable to pay attention unless input is restricted and simplified; all thinking takes longer than usual; has difficulty holding new information in mind, such as reporting what was just said.

      • Executive function: loss of the ability to plan, make decisions, hold information briefly in memory to manipulate it (e.g., mental arithmetic), respond to feedback/error correction, override/inhibit old habits to learn new behaviors, or to have mental flexibility (ability to shift between two concepts, tasks, or response rules).

      • Learning and memory: repeats self in conversation, can't keep track of a short list of items when shopping or of plans for the day; requires frequent reminders to orient to the task at hand; can't repeat a list of words or digits.

        • Recent memory (memory for recent events) is impaired long before remote memory (memory acquired long ago).

        • Thus the last memories to be lost are: semantic memory (memory for facts), autobiographical memory (memory for personal events or people), and implicit (procedural) learning (unconscious learning of skills - like how to ride a bicycle).

      • Language: loss of the ability to speak or understand spoken or written language (aphasia).

      • Perceptual-motor: impaired ability to integrate perception with purposeful movement despite intact motor function; e.g., has significant difficulties with previously familiar activities (using tools, driving), or navigating in familiar environments; is often more confused at dusk, when shadows and lowering levels of light change perceptions.

        • Agnosia (failure to recognize or identify objects despite intact sensory function).

        • Apraxia (impaired ability to carry out motor activities despite intact motor function).

      • Social cognition: loss of the ability to recognize other's emotions or what they are thinking:

        • Mild: e.g., has a change in personality, such as less abillity to recognize social cues or read facial expressions, decreased empathy, increased extraversion or introversion, decreased inhibition, or subtle or episodic apathy or restlessness.

        • Major: e.g., behavior clearly out of acceptable social range; shows insensitivity to social standards of modesty in dress or of political, religious, or sexual topics of conversation; inappropriate clothing for weather or social setting.

    • When severe, may have delusions, hallucinations, and/or confusion.

    Anormally Inhibited or Disinhibited (Low or High Extraversion):

    • Social withdrawal (due to confusion).

    • May be hyperactive, hypoactive, or a mixture of both.

    Negative Emotions (Negative Emotion):

    • Mood may be anxious, depressed or highly changable.

    Medical:

    • Denial of illness; alcohol related hepatic, pancreatic, gastrointestinal, cardiovascular, or renal disease; cerebellar ataxia; peripheral neuropathy; cerebellar atrophy


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Alcohol-Induced Neurocognitive Disorder - Diagnostic Criteria, American Psychiatric Association

An individual diagnosed with alcohol-induced neurocognitive disorder needs to meet all of the following criteria:

  • The criteria are met for major or mild neurocognitive disorder:

    • Major Neurocognitive Disorder

    • Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on:

      • Concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function; and

      • A substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment.

    • The cognitive deficits interfere with independence in everyday activities (i.e., at a minimum, requiring assistance with complex instrumental activities of daily living such as paying bills or managing medications).

    • The cognitive deficits do not occur exclusively in the context of a delirium.

    • The cognitive deficits are not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia).

    • Mild Neurocognitive Disorder

    • Evidence of modest cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on:

      • Concern of the individual, a knowledgeable informant, or the clinician that there has been a mild decline in cognitive function; and

      • A modest impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment.

    • The cognitive deficits do not interfere with capacity for independence in everyday activities (i.e., complex instrumental activities of daily living such as paying bills or managing medications are preserved, but greater effort, compensatory strategies, or accommodation may be required).

    • The cognitive deficits do not occur exclusively in the context of a delirium.

    • The cognitive deficits are not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia).

  • The neurocognitive impairments do not occur exclusively during the course of a delirium and persist beyond the usual duration of alcohol intoxication and acute withdrawal.

  • The alcohol duration and extent of use are capable of producing the neurocognitive impairment.

  • The temporal course of the neurocognitive deficits is consistent with the timing of the alcohol use and abstinence (e.g., the deficits remain stable or improve after a period of abstinence).

  • The neurocognitive disorder is not attributable to another medical condition or is not better explained by another mental disorder.


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Diagnostic Features

Alcohol-Induced Neurocognitive Disorder shows cognitive decline from a previous level of performance in one or more cognitive domains of higher cortical functioning:

  • Complex attention: e.g., is unable to pay attention unless input is restricted and simplified; all thinking takes longer than usual; has difficulty holding new information in mind, such as reporting what was just said.

  • Executive function: loss of the ability to plan, make decisions, hold information briefly in memory to manipulate it (e.g., mental arithmetic), respond to feedback/error correction, override/inhibit old habits to learn new behaviors, or to have mental flexibility (ability to shift between two concepts, tasks, or response rules).

  • Learning and memory: repeats self in conversation, can't keep track of a short list of items when shopping or of plans for the day; requires frequent reminders to orient to the task at hand; can't repeat a list of words or digits.

  • Language: loss of the ability to speak or understand spoken or written language (aphasia).

  • Perceptual-motor: impaired ability to integrate perception with purposeful movement despite intact motor function; e.g., has significant difficulties with previously familiar activities (using tools, driving), or navigating in familiar environments; is often more confused at dusk, when shadows and lowering levels of light change perceptions.

  • Social cognition: loss of the ability to recognize other's emotions or what they are thinking:

These cognitive deficits are the result of chronic Alcohol Use Disorder, and persist beyond resolution of alcohol intoxication, withdrawal or delirium. These cognitive deficits eventually cause significant impairment in social or occupational functioning.

Heavy Drinking Increases The Risk For All Dementias

Heavy drinking is the strongest potentially modifiable risk factor for all dementias - particularly early-onset dementia. A retrospective analysis involving 30 million people in France showed that those with a history of alcohol use disorders had a threefold increased risk for dementia and that over half those with early-onset dementia had a history of alcohol problems.

Since consuming more than a couple of alcoholic drinks a day increases the risk for all dementias; the best thing you can do for your brain health is to cut down your alcohol intake.

Effective Therapies

There are no established treatment options for alcohol-induced cognitive impairment. Alcohol abstinence in combination with adequate diet usually prevents the worsening of this cognitive decline. It is essential that individuals with severe chronic alcoholism receive 200 mg/day of thiamine to prevent the irreversible neurological damage from Wernicke-Korsakoff syndrome (which presents with short-term memory loss, loss of muscle coordination, abnormal eye movements [nystagmus], confusion, and in severe cases coma and death).


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  • Alcohol Dementia - Wikipedia
  • UK Chief Medical Officers' Low Risk Drinking Guidelines - Summary, Gov. UK
  • UK Chief Medical Officers' Low Risk Drinking Guidelines - Full Report, Gov. UK
  • Thiamine for prevention and treatment of Wernicke-Korsakoff syndrome in people who abuse alcohol - Cochrane Library (Wernicke-Korsakoff syndrome [WKS] is a disorder of the brain caused by a deficiency of vitamin B1 [thiamine]. It is characterised by an acute onset of some or all of an eye movement disorder, lack of voluntary coordination of muscle movement [ataxia] and confusion. Patients may die in the acute phase, and many survivors go on to develop permanent memory impairment. Alcohol abuse is an important cause of WKS, although it is not the only consideration. Heavy drinking may lead to particular problems with uptake of thiamine from the diet. When recognised, WKS is treated with thiamine, but it is not clear how effective this is, particularly in managing the mental features.)
  • Alcohol dementia and alcohol delirium in aged alcoholics.In the present study, 126 alcoholics aged 60 years or older were compared with 104 alcoholics aged 35-45 years. No dementia was found in the younger group, whereas 62.7% of the aged patients had dementia; the dementia being irreversible in 32.9% of such patients. Cases of so-called alcohol dementia excluding organic brain diseases accounted for 42.1%. The percentage of aged alcoholics having dementia increased with age, being far beyond the frequency of senile dementia in the general aged. Among various physical complications, hepatic injury and myocardiopathy were more frequent in the aged alcoholics than in general aged people, suggesting that hypertension, myocardiopathy and hepatic injury underlie the manifestation of dementia. There was no case of dementia attributable to the direct effect of alcohol distinctly exceeding the effects of various physical factors.
  • Stories

    Rating Scales


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    Treatment Guidelines



    World Health Organization Delirium and Dementia Treatment Guidelines

    Download Printable Version


    Treatment



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      "In physical science a first essential step in the direction of learning any subject is to find principles of numerical reckoning and practicable methods for measuring some quality connected with it. I often say that when you can measure what you are speaking about and express it in numbers you know something about it; but when you cannot measure it, when you cannot express it in numbers, your knowledge is of a meagre and unsatisfactory kind: it may be the beginning of knowledge, but you have scarcely, in your thoughts, advanced to the stage of science, whatever the matter may be."

      Lord Kelvin (1824 – 1907)


    • The best summary on bad research is given by Laura Arnold in this TEDx lecture. If you read nothing else about research, you owe it to yourself to watch this short video - it is excellent!

    • Canadian researchers who commit scientific fraud are protected by privacy laws: There are criminals in every community - even in the scientific research community (especially if a lot of money is at stake). Criminal researchers can hide their fraud behind outdated privacy laws.

    • The power of asking "what if?"

    • The active placebo effect: 2300 years ago, the Greek Stoic philosophers taught that it is not the objective event, but our subjective judgment about the event, that determines our behavior. The active placebo effect bears witness to this ancient wisdom.

    • Criteria For High Quality Research Studies

    • It is troubling that a recent study found that two-thirds of important psychological research studies couldn't be replicated. High quality research must meet the following criteria:

      • Randomized Controlled Trial:
        Ask: Was the trial randomized? Was the randomization procedure described and was it appropriate? The best research design is to have research subjects randomly assigned to an experimental or control group. It is essential that confounding factors be controlled for by having a control group or comparator condition (no intervention, placebo, care as usual etc.).

      • Representative Sample:
        Ask: Do the research subjects represent a normal cross-section of the population being studied? Many psychological research studies using university students are flawed because their subjects are not representative of the normal population since they are all W.E.I.R.D. (White, Educated, Intelligent, Rich, and living in a Democracy).

      • Single Blind Trial:
        Ask: Was the treatment allocation concealed? It is essential that the research subjects are kept "blind" as to whether they are in the experimental or control group (in order to control for any placebo effects).

      • Double Blind Trial (Better Than Single Blind Trial):
        Ask: Were blind outcome assessments conducted? In a double blind study, neither the research subjects nor the outcome assessors know if the research subject is in the experimental or control group. This controls for both the placebo effect and assessor bias.

      • Baseline Comparability:
        Ask: Were groups similar at baseline on prognostic indicators? The experimental and control groups must be shown to be comparable at the beginning of the study.

      • Confounding Factors:
        Ask: Were there factors, that weren't controlled for, that could have seriously distorted the study's results? For example, research studies on the effectiveness of mindfulness cognitive therapy in preventing depressive relapse forgot to control for whether the research subjects were also simultaneously receiving antidepressant medication or other psychological treatments for depression.

      • Intervention Integrity:
        Ask: Was the research study protocal strictly followed? The research subjects must be shown to be compliant (e.g., taking their pills, attending therapy) and the therapists must be shown to be reliably delivering the intervention (e.g., staying on the research protocol).

      • Statistical analysis:
        Ask: Was a statistical power calculation described? The study should discuss its statistical power analysis; that is whether the study size is large enough to statistically detect a difference between the experimental and control group (should it occur) and usually this requires at least 50 research subjects in the study.

        Ask: Are the results both statistically significant and clinically significant? The results should be both statistically significant (with a p-value <0.05) and clinically significant using some measure of Effect Size such as Standardized Mean Difference (e.g., Cohen's d >= 0.33). The summary statistics should report what percentage of the total variance of the dependent variable (e.g., outcome) can be explained by the independent variable (e.g., intervention). In clinical studies, the study should report the number needed to treat for an additional beneficial outcome (NNTB), and the number needed to treat for an additional harmful outcome (NNTH).

          Number Needed To Benefit (NNTB): This is defined as the number of patients that need to be treated for one of them to benefit compared with a control in a clinical trial. (It is defined as the inverse of the absolute risk reduction.) Note: Statistically, the NNTB depends on which control group is used for comparison - e.g., active treatment vs. placebo treatment, or active treatment vs. no treatment.

          Number Needed To Harm (NNTH): This is defined as the number of patients that need to be treated for one of them to be harmed compared with a control in a clinical trial. (It is defined as the inverse of the absolute increase in risk of harm.)

          Tomlinson found “an NNTB of 5 or less was probably associated with a meaningful health benefit,” while “an NNTB of 15 or more was quite certain to be associated with at most a small net health benefit.”

        Ask: Does the researcher accept full responsibility for the study's statistical analysis? The researcher should not just hand over the study's raw data to a corporation (that may have $1,000 million invested in the study) to do the statistical analysis.

      • Completeness of follow-up data:
        Ask: Was the number of withdrawals or dropouts in each group mentioned, and were reasons given for these withdrawals or dropouts? Less than 20% of the research subjects should drop out of the study. The intervention effect should persist over an adequate length of time.

      • Handling of missing data:
        Ask: Was the statistical analysis conducted on the intention-to-treat sample? There must be use of intention-to-treat analysis (as opposed to a completers-only analysis). In this way, all of the research subjects that started the study are included in the final statistical analysis. A completers-only analysis would disregard those research subjects that dropped out.

      • Replication of Findings:
        Ask: Can other researchers replicate this study's results? The research study's methodology should be clearly described so that the study can be easily replicated. The researcher's raw data should be available to other researchers to review (in order to detect errors or fraud).

      • Fraud:
        Ask: Is there a suspicion of fraud? In a research study, examine the independent and dependent variables that are always measured as a positive whole number (e.g., a variable measured on a 5-point Likert-type scale ranging from "1 = definitely false to 5 = definitely true" etc.). For each of these variables, look at their sample size (n), mean (M) and standard deviation (SD) before they undergo statistical analysis. There is a high suspicion of fraud in a study's statistics:

        • If the M is mathematically impossible (online calculator): This is one of the easiest ways to mathematically detect fraud. The mean (M) is defined as "the sum (Sum) of the values of each observation divided by the total number (n) of observations". So: M = Sum/n. Thus: (Sum) = (M) multiplied by (n). We know that, if a variable is always measured as a positive whole number, the sum of these observations always has to be a whole number. For these variables to test for fraud: calculate (M) multiplied by (n). This calculates the Sum which MUST be a positive whole number. If the calculated Sum isn't a positive whole number; the reported mean (M) is mathematically impossible - thus the researcher either cooked the data or made a mistake. A recent study of 260 research papers published in highly reputable psychological journals found that 1 in 2 of these research papers reported at least one impossible value, and 1 in 5 of these research papers reported multiple impossible values. When the authors of the 21 worst offending research papers were asked for their raw data (so that its reliability could be checked) - 57% angrily refused. Yet such release of raw data to other researchers is required by most scientific journals. (Here is an example of a research paper filled with mathematically impossible means.)

        • If the SD is mathematically impossible (online calculator): When researchers fraudulently "cook" their data, they may accidently give their data a mean and standard deviation that is mathematically impossible.

        • If the SD/M is very small (i.e., the variable's standard deviation is very small compared to the mean suggesting data smoothing).

        • If the SD's are almost identical (i.e., the variables have different means but almost identical standard deviations).

        • If the 4th digit of the values of the variables aren't uniformly distributed - since each should occur 10% of the time (Benford's Law).

        • If the researcher is legally prevented from publishing negative findings about a drug or therapy because that would violate the "nondisclosure of trade secrets" clause in the research contract (i.e., it is a "trade secret" that the drug or therapy is ineffective - hence this can not be "disclosed"). Approximately half of all registered clinical trials fail to publish their results.

        • If the researcher refuses to release his raw data to fellow researchers (so that they can check its validity). In order to be published in most scientific journals, a researcher must promise to share his raw data with fellow researchers. Thus a researcher's refusal to do so is almost a sure indicator of fraud.

        • If the research study's data contradicts the study's own conclusions - surprisingly, this often occurs.

    • Calling Bullshit In The Age of Big Data - "Bullshit is language, statistical figures, data graphics, and other forms of presentation intended to persuade by impressing and overwhelming a reader or listener, with a blatant disregard for truth and logical coherence." Reading the syllabus of this university course should be required reading for every student of mental health. This syllabus is absolutely fantastic!

    • Statistical Methods in Psychology Journals: Guidelines and Explanations - American Psychologist 1999

    • Not All Scientific Studies Are Created Equal - video

    • The efficacy of psychological, educational, and behavioral treatment

    • Estimating the reproducibility of psychological science

    • Psychologists grapple with validity of research

    • Industry sponsorship and research outcome (Review) - Cochrane Library

    • 'We've been deceived': Many clinical trial results are never published - (text and video)

    • Junk science misleading doctors and researchers

    • Junk science under spotlight after controversial firm buys Canadian journals

    • Medicine with a side of mysticism: Top hospitals promote unproven therapies - Are some doctors becoming modern witchdoctors?

    • When Evidence Says No, But Doctors Say Yes


    • Cochrane Reviews (the best evidence-based, standardized reviews available)

    Research Topics

    Research Articles

    • Alcoholic organic brain disease: nosology and pathophysiologic mechanisms. (1986) - Study of alcoholic chronic organic brain syndrome may have applicability to the large population of alcoholics with less severe cerebral dysfunction. Brain impairment in alcoholics may be conceptualized as two clinically and neuropathologically distinguishable organic brain syndromes: alcohol amnestic disorder or Korsakoff's psychosis (KP) and alcoholic dementia. Alcoholic organic brain disease may result from two interacting pathophysiological processes: nutritional (thiamine) deficiency and ethanol neurotoxicity. Subcortical periventricular lesions associated with KP result primarily from thiamine deficiency, whereas ethanol neurotoxicity and various secondary effects of alcoholism may contribute to the cortical neuropathological changes associated with alcoholic dementia. These two patterns of brain damage may be differentiable in individual alcoholics using cognitive tests and other measures of CNS function and, therefore, allow selection of a treatment strategy based on pathophysiological considerations. Studies in animals and humans suggest that a genetic predisposition to thiamine deficiency may contribute to alcoholism-associated dysfunction of brain and other organ systems and possibly have a causative role in the development of alcoholism.

    • Cerebral dysfunction in chronic alcoholism: role of alcoholic liver disease. (1994) - Evidence suggests that liver disease per se may contribute to the cognitive and motor impairments encountered in chronic alcoholics. Neuropathologic studies reveal astrocytic changes (Alzheimer type II astrocytosis) in the brains of alcoholic cirrhotic patients who died in hepatic coma. Pathophysiologic mechanisms responsible for hepatic (portal-systemic) encephalopathy in alcoholics include the loss of neuron-astrocytic metabolic trafficking as well as selective alterations of serotoninergic and dopaminergic function. In addition, there is evidence to suggest that endogenous ligands for both central-type (GABA-related) and "peripheral-type" (astrocytic) benzodiazepine receptors are implicated in the pathogenesis of hepatic encephalopathy in these patients. Chronic liver disease may also interfere with brain thiamine homeostasis and thus contribute to the pathogenesis of the Wernicke-Korsakoff syndrome in chronic alcoholism.

    • Aetiology of alcoholic brain damage: alcoholic neurotoxicity or thiamine malnutrition? (1994) - The clinical presentation of brain damaged alcoholics is heterogenous and includes minimal cognitive impairment, amnesia and dementia. Whichever neurobiological technique is used, eg neuropathology, structural and functional neuroimaging, the clinico-pathological evidence suggests that thiamine malnutrition, affecting the diencephalon, can account for all clinical forms. Alcohol neurotoxicity can cause neuronal damage in cerebral cortex and can contribute to cognitive impairment but there is little direct evidence to support the need for a distinct clinical category of alcoholic dementia. Most organic brain syndromes in alcoholics therefore can be considered as variants of the Wernicke-Korsakoff syndrome and rigorous attention should be paid to the nutritional status of all alcoholics.

    • Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease. (1995) - Chronic alcoholism results in brain damage and dysfunction leading to a constellation of neuropsychiatric symptoms including cognitive dysfunction, the Wernicke-Korsakoff Syndrome, alcoholic cerebellar degeneration and alcoholic dementia. That these clinically-defined entities result from independent pathophysiologic mechanisms is unlikely. Alcohol and its metabolite acetaldehyde are directly neurotoxic. Alcoholics are thiamine deficient as a result of poor diet, gastrointestinal disorders and liver disease. In addition, both alcohol and acetaldehyde have direct toxic effects on thiamine-related enzymes in liver and brain. Alcoholics frequently develop severe liver disease and liver disease per se results in altered thiamine homeostasis, in cognitive dysfunction and in neuropathologic damage to astrocytes. The latter may result in the loss of neuron-astrocytic trafficking of neuroactive amino acids and thiamine esters, essential to CNS function. The present review article proposes mechanisms whereby the effects of alcohol, thiamine deficiency and liver disease combine synergistically to contribute to the phenomena of cognitive dysfunction and "alcoholic brain damage".

    • Alcoholism and dementia. (1995) - This article reviews epidemiological, neurological, cognitive, and imaging data on alcohol-induced dementia. Recent studies indicate that "heavy alcohol use" (variously defined) is a contributing factor in 21-24% of cases of dementia. Research difficulties include lack of positive diagnostic criteria, few post-mortem studies, and no accepted pathological mechanism. Sulcal widening and ventricular enlargement (occasionally reversible) are the strongest findings in patients with alcohol-induced dementia. There is evidence for peripheral neuropathy, ataxia, sparing of language, and improved prognosis when patients with alcohol-induced dementia are compared to other dements. Case examples, etiologic theories, and recommendations for research, training, and clinical practice are included.

    • The neuropathology of alcohol-specific brain damage, or does alcohol damage the brain? (1998) - The aim of this review is to identify neuropathological changes that are directly related to the long-term use of excessive amounts of alcohol (ethanol). There is still debate as to whether alcohol per se causes brain damage. The main problem has been to identify those lesions caused by alcohol itself and those caused by other common alcohol-related factors, principally thiamin deficiency. Careful selection and classification of alcoholic cases into those with and without these complications, together with detailed quantitative neuropathological analyses, has provided us with useful data. There is brain shrinkage in uncomplicated alcoholics which can largely be accounted for by loss of white matter. Some of this damage appears to be reversible. However, alcohol-related neuronal loss has been documented in specific regions of the cerebral cortex (superior frontal association cortex), hypothalamus (supraoptic and paraventricular nuclei), and cerebellum. The data is conflicting for several regions: the hippocampus, amygdala and locus ceruleus. No change is found in the basal ganglia, nucleus basalis, or serotonergic raphe nuclei. Many of the regions that are normal in uncomplicated alcoholics are damaged in those with the Wernicke-Korsakoff syndrome. Dendritic and synaptic changes have been documented in uncomplicated alcoholics and these, together with receptor and transmitter changes, may explain functional changes and cognitive deficits that precede the more severe structural neuronal changes. The pattern of damage appears to be somewhat different and species-specific in animal models of alcohol toxicity. Pathological changes that have been found to correlate with alcohol intake include white matter loss and neuronal loss in the hypothalamus and cerebellum.

    • The neuropsychological consequences of abstinence among older alcoholics: a cross-sectional study. (2000) - BACKGROUND: The older alcoholic has been distinguished from the younger alcoholic with regard to both the acute effects of alcohol and also the recovery of functioning with abstinence. Few studies, however, have included samples of exclusively older subjects. In this investigation we examined the recovery of functioning in an older cohort of recovering alcoholics (age range 55-83) to determine which neuropsychological functions improve and which remain impaired with abstinence. METHODS: We used a cross-sectional design, comparing three demographically matched groups on a battery of neuropsychological tests: (a) older alcoholics who had been abstinent for greater than 6 months, (b) older alcoholics who had been abstinent for less than 6 months, and (c) a control group of older subjects without alcohol abuse histories. RESULTS: In almost all tasks, the alcoholics who were abstinent for less than 6 months performed worse than the control group. In contrast, the alcoholics who had been abstinent for more than 6 months differed from the control group on learning and recall of a word list, immediate and delayed recall of a complex figure, initial letter fluency, and clock drawing. CONCLUSIONS: Memory and executive skills appear to be resistant to recovery or at least slower to recover with abstinence in the older alcoholic. The impairment with visuospatial skills reported in prior investigations of alcoholics may be related to compromised executive functions, which interfere with the encoding of more complex visuospatial information and thus affect recall of such information. Studies that involve larger samples of older alcoholics are needed to understand their ability to recover cognitive functioning with abstinence.

    • Alcohol-induced cognitive disorder: alcohol dementia (2002) - Cognitive impairment is frequently observed in patients with alcohol misuse or alcohol addiction. Multiple cognitive functions are reduced in these patients. Frontal lobe functions, as planning, abstract thinking, set shifting or continuous performance are most frequently affected. Alcohol amnestic syndrome, alcohol dementia and the Wernicke-Korsakow-Syndrome constitute distinct entities. Alcohol dementia follows the diagnostic criteria of dementia with clear evidence for alcohol abuse or alcohol addiction. The diagnostic procedure of alcohol-induced cognitive impairment includes medical history, physical and neuropsychiatric examinations; laboratory examinations, neuropsychological assessment, brain imaging and electroencephalographic recordings. At the moment, there are no established treatment options for alcohol-induced cognitive impairment. Some evidence is provided that nootropics might be of benefit. Alcohol abstinence is a most important step. Psychosocial interventions are essential to support the patients in their daily activities.

    • The role of thiamine deficiency in alcoholic brain disease. (2003) - A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol-induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke-Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.

    • Comparisons of Korsakoff and non-Korsakoff alcoholics on neuropsychological tests of prefrontal brain functioning. (2004) - BACKGROUND: Evidence suggests that alcoholics exhibit particular deficits in brain systems involving the prefrontal cortex, but few studies have directly compared patients with and without Korsakoff's syndrome on measures of prefrontal integrity. METHODS: Neuropsychological tasks sensitive to dysfunction of frontal brain systems were administered, along with standard tests of memory, intelligence, and visuospatial abilities, to 50 healthy, abstinent, nonamnesic alcoholics, 6 patients with alcohol-induced persisting amnestic disorder (Korsakoff's syndrome), 6 brain-damaged controls with right hemisphere lesions, and 82 healthy nonalcoholic controls. RESULTS: Korsakoff patients were impaired on tests of memory, fluency, cognitive flexibility, and perseveration. Non-Korsakoff alcoholics showed some frontal system deficits as well, but these were mild. Cognitive deficits in non-Korsakoff alcoholics were related to age, duration of abstinence (less than 5 years), duration of abuse (more than 20 years), and amount of alcohol intake. CONCLUSIONS: Abnormalities of frontal system functioning are most apparent in alcoholics with Korsakoff's syndrome. In non-Korsakoff alcoholics, factors contributing to cognitive performance are age, duration of abstinence, duration of alcoholism, and amount of alcohol consumed.

    • The alcoholism generator. (2006) - Alcohol exposure largely affects 3 populations: fetuses, adolescents, and adults. These 3 developmental stages are inextricably intertwined such that elevated alcohol exposure at any time increases the probability of exposure at the others. This circular interdependency is called the alcoholism generator. Furthermore, exposure to large amounts of alcohol at these 3 times can cause cognitive dysfunction, largely through mechanisms of alcohol-induced perturbations in neurogenesis and synaptogenesis. Breaking this cycle is key to reducing problem alcohol drinking and the associated sequelae.

    • Supporting the long-term residential care needs of older homeless people with severe alcohol-related brain injury in Australia: the Wicking Project. (2007) - For years, community service providers have been frustrated with the lack in availability of long-term, specialized supported accommodation for older people, particularly older homeless people, with severe acquired brain injury (ABI) and challenging behaviors. Although the incidence of ABI (particularly alcohol-related brain injury) is far wider than being confined to the homeless population, it is frequently misdiagnosed and very often misunderstood Wintringham is an independent welfare company in Melbourne, Australia, that provides secure, affordable, long-term accommodation and high quality services to older homeless people. The high incidence of alcohol abuse among the resident population has led us to adapt our model ofcare to accommodate a complexity of need. However, there are some individuals with severely affected behaviors that continue to challenge Wintringham's capacity to provide adequate support. The deficiency in highly specialized, long-term supported accommodation for older people with severe alcohol-related brain injury (ARBI) is the driving force behind this project. We aim to further develop and improve the current Wintringham model of residential care to better support people with these complex care needs. We will report on the synthesis of this project which aims to test a specialized model that can be reproduced or adapted by other service providers to improve the life circumstances of these frequently forgotten people.

    • Cognitive impairment in Aboriginal people with heavy episodic patterns of alcohol use. (2007) - BACKGROUND: With chronic alcohol abuse, cognitive studies suggest that progressive cognitive decline may precede more serious and irreversible neurological syndromes. The early detection of cognitive impairment may therefore aid in the prevention of permanent brain damage. Despite the devastating consequences of alcohol abuse among Aboriginal Australians, the effects on brain function have never been studied in this population and a lack of appropriate assessment tools has prevented the development of such research. AIMS: To determine the impact of long-term and heavy episodic alcohol use on cognitive function in Aboriginal people. DESIGN: Cross-sectional comparing heavy episodic alcohol users with non-alcohol users. SETTING: Two remote Aboriginal communities in north-east Arnhem Land, northern Australia. SUBJECTS: The control group consisted of 24 non-drinkers (15 males, nine female) and the heavy episodic group consisted of 20 people (19 males, one female) who had been drinking alcohol in a heavy episodic style (median 14 drinks per occasion) for a mean of 8.9 years (SD = 5.0). MEASUREMENTS: Interview to obtain demographic information, substance abuse history and symptoms of mental health and wellbeing, together with a computerized cognitive assessment battery (CogState Ltd). FINDINGS: Compared with non-drinkers, heavy episodic drinkers showed reduced psychomotor speed (P = 0.04) and reduced accuracy when performing tasks of attention (P = 0.045), working memory (P = 0.04), implicit memory (P = 0.03) and associate learning and memory (P = 0.001). CONCLUSIONS: Specific cognitive abnormalities that suggest frontostriatal abnormalities and have been observed in association with chronic alcoholism in other populations were observed among Aboriginal Australians who were heavy episodic alcoholic users.

    • The neuropathology of alcohol-related brain damage. (2009) - Excessive alcohol use can cause structural and functional abnormalities of the brain and this has significant health, social and economic implications for most countries in the world. Even heavy social drinkers who have no specific neurological or hepatic problems show signs of regional brain damage and cognitive dysfunction. Changes are more severe and other brain regions are damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke-Korsakoff syndrome). Quantitative studies and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the damage are not understood. A human brain bank targeting alcohol cases has been established in Sydney, Australia, and tissues can be used for structural and molecular studies and to test hypotheses developed from animal models and in vivo studies. The recognition of potentially reversible changes and preventative medical approaches are important public health issues.

    • Clinical and pathological features of alcohol-related brain damage. (2011) - One of the sequelae of chronic alcohol abuse is malnutrition. Importantly, a deficiency in thiamine (vitamin B(1)) can result in the acute, potentially reversible neurological disorder Wernicke encephalopathy (WE). When WE is recognized, thiamine treatment can elicit a rapid clinical recovery. If WE is left untreated, however, patients can develop Korsakoff syndrome (KS), a severe neurological disorder characterized by anterograde amnesia. Alcohol-related brain damage (ARBD) describes the effects of chronic alcohol consumption on human brain structure and function in the absence of more discrete and well-characterized neurological concomitants of alcoholism such as WE and KS. Through knowledge of both the well-described changes in brain structure and function that are evident in alcohol-related disorders such as WE and KS and the clinical outcomes associated with these changes, researchers have begun to gain a better understanding of ARBD. This Review examines ARBD from the perspective of WE and KS, exploring the clinical presentations, postmortem brain pathology, in vivo MRI findings and potential molecular mechanisms associated with these conditions. An awareness of the consequences of chronic alcohol consumption on human behavior and brain structure can enable clinicians to improve detection and treatment of ARBD.

    • Neuroanatomy and neuropathology associated with Korsakoff's syndrome. (2012) - Although the neuropathology of Korsakoff's syndrome (KS) was first described well over a century ago and the characteristic brain pathology does not pose a diagnostic challenge to pathologists, there is still controversy over the neuroanatomical substrate of the distinctive memory impairment in these patients. Cohort studies of KS suggest a central role for the mammillary bodies and mediodorsal thalamus, and quantitative studies suggest additional damage to the anterior thalamus is required. Rare cases of KS caused by pathologies other than those of nutritional origin provide support for the role of the anterior thalamus and mammillary bodies. Taken together the evidence to date shows that damage to the thalamus and hypothalamus is required, in particular the anterior thalamic nucleus and the medial mammillary nucleus of the hypothalamus. As these nuclei form part of wider memory circuits, damage to the inter-connecting white matter tracts can also result in a similar deficit as direct damage to the nuclei. Although these nuclei and their connections appear to be the primary site of damage, input from other brain regions within the circuits, such as the frontal cortex and hippocampus, or more distant regions, including the cerebellum and amygdala, may have a modulatory role on memory function. Further studies to confirm the precise site(s) and extend of brain damage necessary for the memory impairment of KS are required.

    • Function and dysfunction of prefrontal brain circuitry in alcoholic Korsakoff's syndrome. (2012) - The signature symptom of alcohol-induced persisting amnestic disorder, more commonly referred to as alcoholic Korsakoff's syndrome (KS), is anterograde amnesia, or memory loss for recent events, and until the mid 20th Century, the putative brain damage was considered to be in diencephalic and medial temporal lobe structures. Overall intelligence, as measured by standardized IQ tests, usually remains intact. Preservation of IQ occurs because memories formed before the onset of prolonged heavy drinking--the types of information and abilities tapped by intelligence tests--remain relatively well preserved compared with memories recently acquired. However, clinical and experimental evidence has shown that neurobehavioral dysfunction in alcoholic patients with KS does include nonmnemonic abilities, and further brain damage involves extensive frontal and limbic circuitries. Among the abnormalities are confabulation, disruption of elements of executive functioning and cognitive control, and emotional impairments. Here, we discuss the relationship between neurobehavioral impairments in KS and alcoholism-related brain damage. More specifically, we examine the role of damage to prefrontal brain systems in the neuropsychological profile of alcoholic KS.

    • Alcohol-induced blackout as a criminal defense or mitigating factor: an evidence-based review and admissibility as scientific evidence. (2013) - Alcohol-related amnesia--alcohol blackout--is a common claim of criminal defendants. The generally held belief is that during an alcohol blackout, other cognitive functioning is severely impaired or absent. The presentation of alcohol blackout as scientific evidence in court requires that the science meets legal reliability standards (Frye, FRE702/Daubert). To determine whether "alcohol blackout" meets these standards, an evidence-based analysis of published scientific studies was conducted. A total of 26 empirical studies were identified including nine in which an alcohol blackout was induced and directly observed. No objective or scientific method to verify the presence of an alcoholic blackout while it is occurring or to confirm its presence retrospectively was identified. Only short-term memory is impaired and other cognitive functions--planning, attention, and social skills--are not impaired. Alcoholic blackouts would not appear to meet standards for scientific evidence and should not be admissible.

    • Alcohol induced cognitive deficits. (2014) - Previous studies could show a complex relationship between alcohol consumption and cognition but also with processes of ageing both social and biological. Acute effects of alcohol during intoxication include clinical signs such as excitation and reduced inhibition, slurred speech, and increased reaction time but also cognitive dysfunction, especially deficits in memory functions. However, these cognitive deficits during alcohol intoxication are reversible while patients with alcohol addiction and chronic alcohol intake show severe impairments of cognitive functions especially deficits in executive functions. Frontal executive impairments in these patients include deficits in problem solving, abstraction, planning, organizing, and working memory.Additionally, gender specific deficits are relevant for the course of the disease and its concomitant health problems with female alcoholics showing a higher vulnerability for cognitive dysfunction and brain atrophy at earlier stages of alcoholism history.

    • Alcohol-induced psychotic disorder: a systematic literature review. (2015) - BACKGROUND: From the second half of the 19th century eminent psychiatrists began referring to alcohol-induced psychotic disorder (AIPD) as a specific alcoholic psychosis. Over the last decades interest in AIPD seems to have declined: the last review dates form 1989. AIM: To review the recent literature on AIPD, revive interest in the disorder, evaluate the current scientific evidence and assess its clinical value. METHOD: We performed a Medline search based on the following terms: 'Psychoses, Alcoholic' [Mesh] OR 'alcohol induced psychotic disorder' OR 'alcoholic hallucinosis' OR 'alcohol hallucinosis'. Our search was restricted to articles written in English or Dutch and published between 1-1-1988 and 31-1-2013. RESULTS: We found 164 papers, from which we selected 21 for further discussion. The quality of the papers selected was variable, most of the papers being the result of clinical research. The most important findings referred to epidemiology: 0.4% lifetime prevalence in the general population, 4.0% in patients with alcohol dependence. We found only limited evidence of psychopathological differentiation between delirium and primary psychotic disorder. Correct diagnosis of AIPD is important because of the implications regarding the length and nature of the treatment: short or long course of antipsychotics, referral to a substance-abuse unit. CONCLUSION: AIPD has survived as a clinical entity. However, scientific evidence of this is limited. Further research is needed because it is vitally important that the patient receives the most appropriate treatment.

    • Self-awareness of cognitive dysfunction: Self-reported complaints and cognitive performance in patients with alcohol-induced mild or major neurocognitive disorder. (2016) - Patients with Korsakoff's syndrome (KS) typically have difficulties in recognizing the impact of their alcohol-related cognitive deficits on daily-life functioning. In this study, mean scores on self-reported complaints (measured with Minnesota Multiphasic Personality Inventory-2-Restructured Form; MMPI-2-RF) and cognitive performance (measured with the Wechsler Adult Intelligence Scale-Third edition; WAIS-III; and the California Verbal Learning Test; CVLT) are compared between two matched patient groups with severe (KS) and mild alcohol-related cognitive disorders or non KS (NKS). ... Despite their alcohol-related cognitive impairments, both groups report no cognitive complaints at all indicating self-awareness impairment. In addition to KS patients, also NKS patients are at risk that their apparently "without cognitive complaints" appearance on self-report questionnaires can be easily overlooked. These findings may have important clinical implications for diagnostic and treatment purposes.



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