Internet Mental Health

ALCOHOL-INDUCED NEUROCOGNITIVE DISORDER


WARNING:



President Trump is about to start a nuclear war with North Korea. New UN sanctions have cut North Korea's oil and money supply - hence its regime would soon fall without war. Both China and Russia have promised to defend North Korea if America attacks first. So America attacking North Korea could start a nuclear WW III. Nevertheless, Trump will attack North Korea as a distraction from his possible impeachment. US pro-war propaganda is becoming hysterical. This propaganda lies in stating that "food supplies would be decimated by radiation and up to 90% of the population would die within a year" after a nuclear bomb was exploded high in the atmosphere over America. The truth is that an electromagnetic pulse from such a high atmospheric nuclear explosion could destroy electronic devices for hundreds of miles beneath the blast. But the resulting electromagnetc pulse from such a blast is not lethal to humans. In the 1950s and 1960s, thousands of American soldiers were experimentally placed in trenches just a few miles from ground nuclear explosions, and the resulting electromagnetic pulse did not kill one of these American soldier "guinea pigs". However, this high radiation exposure decades later caused a dramatic increase in cancer in these human guinea pigs. The high radiation exposure from the Chernobyl Disaster did not kill the surrounding vegetation or animals.

By 2020 Climate Change Will Be Irreversible

By 2030 60% Of Tropical Rainforest Will Be Destroyed

Climate Change This Century Will Destroy India and Pakistan

Why Is This Warning On A Mental Health Website?

No such warning has ever been published on this website since its creation in 1995. However, the very high probability of a nuclear WW III, and the certainty of irreversible climate change in the next few years requires that this warning be posted. If Trump starts WW III, or does nothing to stop climate change, mental illness will be the least of our worries.





Expanded Quality of Life Scale For Alcohol-Induced Neurocognitive Disorder

Internet Mental Health Quality of Life Scale

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.

    Critical, Quarrelsome (Antagonism):

    • May become violent.

    Impulsive, Disorderly (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.

    Distressed, Easily Upset (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


Explanation Of Terms And Symbols

Internet Mental Health Quality of Life Scale

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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.

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

    Which Behavioral Dimensions Are Involved?

    Research has shown that there are 5 major dimensions (the "Big 5 Factors") of personality disorders and other mental disorders. There are two free online personality tests that assess your personality in terms of the "Big 5 dimensions of personality.

    This website uses these 5 major dimensions of human behavior to describe all mental disorders. (This website adds one more dimension, "Physical Health", but our discussion will focus on the first 5 major dimensions.)

    These 5 major dimensions of human behavior seem to represent 5 major dimensions whereby our early ancestors chose their hunting companions or spouse. To maximize their chance for survival, our ancestors wanted companions who were agreeable, conscientious, intelligent, enthusiastic, and calm.

      Which Dimensions of Human Behavior are Impaired in Alcohol-Induced Neurocognitive Disorder?

      THE POSITIVE SIDE OF THE "BIG 5" PERSONALITY DIMENSIONS THE NEGATIVE SIDE OF THE "BIG 5" PERSONALITY DIMENSIONS DESCRIPTION (Where red = this disorder)
      Agreeableness Antagonism       Sympathetic, Kind vs. Critical, Quarrelsome
      Conscientiousness Disinhibition       Industrious, Orderly vs. Impulsive, Disorderly
      Openness To Experience Impaired Intellect       Open-Minded, Creative vs. Cognitive Impairment
      Sociability (Extraversion) Detachment       Enthusiastic, Assertive vs. Reserved, Quiet
      Emotional Stability Negative Emotion       Calm, Emotionally Stable vs. Distressed, Easily Upset

    The 5 Major Dimensions of Mental Illness

    Our website uses the "Big 5 Factors" of personality as major dimensions of mental illness. Each of these 5 dimensions has a healthy side and an unhealthy side. The Big 5 Factors are: Agreeableness, Conscientiousness, Openness to Experience, Sociability (Extraversion), and Emotional Stability. Our website adds an additional factor, Physical Health. However, our discussion will primarily focus on the traditional "Big 5 Factors".



    The Following Pictures Are of The International Space Station

    AGREEABLENESS VS. ANTAGONISM
    .
    Agreeableness (Sympathetic, Kind)
    .
    Description: Agreeableness is synonymous with compassion and politeness; whereas Antagonism is synonymous with competition and aggression. Compassion reflects empathy, sympathy, and caring for others. Politeness reflects respect for others’ needs and desires and a tendency to refrain from aggression. The Agreeableness dimension measures the behaviors that are central to the concept of LOVE and JUSTICE.
    Descriptors: Compassionate, polite, kind, sympathetic, appreciative, affectionate, soft-hearted, warm, generous, trusting, helpful, forgiving, pleasant, good-natured, friendly, cooperative, gentle, unselfish, praising, sensitive.
    MRI Research*: Agreeableness was associated with increased volume in regions that process information about the intentions and mental states of other individuals.
    "I am helpful and unselfish with others."
    "I have a forgiving nature."
    "I am generally trusting."
    "I am considerate and kind to almost everyone."
    "I like to cooperate with others."
    "I don't find fault with others."
    "I don't start quarrels with others."
    "I am not cold and aloof."
    "I am not rude to others."
    "I feel other's emotions."
    "I inquire about others' well-being."
    "I sympathize with others' feelings."
    "I take an interest in other people's lives."
    "I like to do things for others."
    "I respect authority."
    "I hate to seem pushy."
    "I avoid imposing my will on others."
    "I rarely put people under pressure."
    .
    Antagonism (Critical, Quarrelsome)
    .
    * Callousness:
    "It's no big deal if I hurt other people's feelings."
    "Being rude and unfriendly is just a part of who I am."
    "I often get into physical fights."
    "I enjoy making people in control look stupid."
    "I am not interested in other people's problems."
    "I can't be bothered with other's needs."
    "I am indifferent to the feelings of others."
    "I don't have a soft side."
    "I take no time for others."
    .
    * Deceitfulness:
    "I don't hesitate to cheat if it gets me ahead."
    "Lying comes easily to me."
    "I use people to get what I want."
    "People don't realize that I'm flattering them to get something."
    .
    * Manipulativeness:
    "I use people to get what I want."
    "It is easy for me to take advantage of others."
    "I'm good at conning people."
    "I am out for my own personal gain."
    .
    * Grandiosity:
    "I'm better than almost everyone else."
    "I often have to deal with people who are less important than me."
    "To be honest, I'm just more important than other people."
    "I deserve special treatment."
    .
    * Suspiciousness:
    "It seems like I'm always getting a “raw deal” from others."
    "I suspect that even my so-called 'friends' betray me a lot."
    "Others would take advantage of me if they could."
    "Plenty of people are out to get me."
    "I'm always on my guard for someone trying to trick or harm me."
    .
    * Hostility:
    "I am easily angered."
    "I get irritated easily by all sorts of things."
    "I am usually pretty hostile."
    "I always make sure I get back at people who wrong me."
    "I resent being told what to do, even by people in charge."
    "I insult people."
    "I seek conflict."
    "I love a good fight."
    .
    ("Agreeableness vs. Antagonism" modified from "PID-5" by Kreuger RF, Derringer J, Markon KE, Watson D, Skodol AE and Between facets and domains: 10 aspects of the Big Five)
    *MRI Research: Testing predictions from personality neuroscience. Brain structure and the big five.




    CONSCIENTIOUSNESS VS. DISINHIBITION
    .
    Conscientiousness (Industrious, Orderly)
    .
    Description: Conscientiousness is synonymous with being industrious and orderly; whereas Disinhibition is synonymous with being impulsive and disorderly. The Conscientiousness dimension measures the behaviors that are central to the concept of SELF-CONTROL.
    Descriptors: Self-disciplined, achievement-oriented, industrious, competent, reliable, responsible, orderly, deliberate, decisive
    MRI Research*: Conscientiousness was associated with increased volume in the lateral prefrontal cortex, a region involved in planning and the voluntary control of behavior.
    "I do a thorough job. I want everything to be 'just right'. I want every detail taken care of."
    "I am careful."
    "I am a reliable hard-worker."
    "I am organized. I follow a schedule and always know what I am doing."
    "I like order. I keep things tidy."
    "I see that rules are observed."
    "I do things efficiently. I get things done quickly."
    "I carry out my plans and finish what I start."
    "I am not easily distracted."
    .
    Rigid Perfectionism (Excessive Conscientiousness)
    .
    "Even though it drives other people crazy, I insist on absolute perfection in everything I do."
    "I simply won't put up with things being out of their proper places."
    "People complain about my need to have everything all arranged."
    "People tell me that I focus too much on minor details."
    "I have a strict way of doing things."
    "I postpone decisions."
    .
    Disinhibition (Impulsive, Disorderly)
    .
    * Irresponsibility:
    "I've skipped town to avoid responsibilities."
    "I just skip appointments or meetings if I'm not in the mood."
    "I'm often pretty careless with my own and others' things."
    "Others see me as irresponsible."
    "I make promises that I don't really intend to keep."
    "I often forget to pay my bills."
    .
    * Impulsivity:
    "I usually do things on impulse without thinking about what might happen as a result."
    "Even though I know better, I can't stop making rash decisions."
    "I feel like I act totally on impulse."
    "I'm not good at planning ahead."
    .
    * Distractibility:
    "I can't focus on things for very long."
    "I am easily distracted."
    "I have trouble pursuing specific goals even for short periods of time."
    "I can't achieve goals because other things capture my attention."
    "I often make mistakes because I don't pay close attention."
    "I waste my time ."
    "I find it difficult to get down to work."
    "I mess things up."
    "I don't put my mind on the task at hand."
    .
    * Reckless Risk Taking:
    "I like to take risks."
    "I have no limits when it comes to doing dangerous things."
    "People would describe me as reckless."
    "I don't think about getting hurt when I'm doing things that might be dangerous."
    .
    * Hyperactivity:
    "I move excessively (e.g., can't sit still; restless; always on the go)."
    "I'm starting lots more projects than usual or doing more risky things than usual."
    .
    * Over-Talkativeness:
    "I talk excessively (e.g., I butt into conversations; I complete people's sentences)."
    "Often I talk constantly and cannot be interrupted."
    .
    * Elation:
    "I feel much more happy, cheerful, or self-confident than usual."
    "I'm sleeping a lot less than usual, but I still have a lot of energy."
    .
    ("Conscientiousness vs. Disinhibition" modified from "PID-5" by Kreuger RF, Derringer J, Markon KE, Watson D, Skodol AE and Between facets and domains: 10 aspects of the Big Five)
    *MRI Research: Testing predictions from personality neuroscience. Brain structure and the big five.




    OPENNESS TO EXPERIENCE vs. IMPAIRED INTELLECT
    .
    Open To Experience (Open-Minded, Creative)
    .
    Description: Open to Experience is synonymous with being open-minded and creative; whereas Closed to Experience is synonymous with being closed-minded and uncreative. The Openness to Experience dimension measures the behaviors that are central to the concept of WISDOM. Open-minded people ask "why?", are willing to challenge something that doesn't seem right, to listen to other people's opinions, and to be ever-ready to accept new truths, if the evidence is there. They are creative, flexible, and holistic in their thinking. They never stop questioning.
    Descriptors: Wide interests, imaginative, intelligent, original, insightful, curious, sophisticated, artistic, clever, inventive, sharp-witted, wise
    MRI Research*: Openness To Experience did not have any significant correlation with the volume of any brain structures. (This could suggest that "Openness To Experience", as defined here, is more a function of culture rather than of brain neurobiology.)
    Example: This video shows how we see what we want to see. What we pay attention to (or what we believe about the world) blinds us to reality. (Exit YouTube after first video.)
    "I am original, and come up with new ideas."
    "I am curious about many different things."
    "I am quick to understand things."
    "I can handle a lot of information."
    "I like to solve complex problems."
    "I have a rich vocabulary."
    "I think quickly and formulate ideas clearly."
    "I enjoy the beauty of nature."
    "I believe in the importance of art."
    "I love to reflect on things."
    "I get deeply immersed in music."
    "I see beauty in things that others might not notice."
    "I need a creative outlet."
    .
    Closed To Experience (Closed-Minded, Uncreative)
    .
    "I prefer work that is routine."
    "I have difficulty understanding abstract ideas."
    "I avoid philosophical discussions."
    "I avoid difficult reading material."
    "I learn things slowly."
    "I have few artistic interests."
    "I seldom notice the emotional aspects of paintings and pictures."
    "I do not like poetry."
    "I seldom get lost in thought."
    "I seldom daydream."
    .
    Cognitive Impairment
    .
    * Memory Impairment:
    "I have difficulty learning new things, or remembering things that happened a few days ago."
    "I often forget a conversation I had the day before."
    "I often forget to take my medications, or to keep my appointments."
    .
    .
    * Impaired Reasoning or Problem-Solving:
    "My judgment, planning, or problem-solving isn't good."
    "I lack creativity or curiosity."
    .
    Psychoticism
    .
    * Eccentricity:
    "I often have thoughts that make sense to me but that other people say are strange."
    "Others seem to think I'm quite odd or unusual."
    "My thoughts are strange and unpredictable."
    "My thoughts often don’t make sense to others."
    "Other people seem to think my behavior is weird."
    "I have several habits that others find eccentric or strange."
    "My thoughts often go off in odd or unusual directions."
    .
    * Unusual Beliefs and Experiences:
    "I often have unusual experiences, such as sensing the presence of someone who isn't actually there."
    "I've had some really weird experiences that are very difficult to explain."
    "I have seen things that weren’t really there."
    "I have some unusual abilities, like sometimes knowing exactly what someone is thinking."
    "I sometimes have heard things that others couldn’t hear."
    "Sometimes I can influence other people just by sending my thoughts to them."
    "I often see unusual connections between things that most people miss."
    .
    * Perceptual Dysregulation:
    "Things around me often feel unreal, or more real than usual."
    "Sometimes I get this weird feeling that parts of my body feel like they're dead or not really me."
    "It's weird, but sometimes ordinary objects seem to be a different shape than usual."
    "Sometimes I feel 'controlled' by thoughts that belong to someone else."
    "Sometimes I think someone else is removing thoughts from my head."
    "I have periods in which I feel disconnected from the world or from myself."
    "I can have trouble telling the difference between dreams and waking life."
    "I often 'zone out' and then suddenly come to and realize that a lot of time has passed."
    "Sometimes when I look at a familiar object, it's somehow like I'm seeing it for the first time."
    "People often talk about me doing things I don't remember at all."
    "I often can't control what I think about."
    "I often see vivid dream-like images when I’m falling asleep or waking up."
    .
    ("OPENNESS TO EXPERIENCE vs. BEING CLOSED TO EXPERIENCE" modified from "PID-5" by Kreuger RF, Derringer J, Markon KE, Watson D, Skodol AE and Between facets and domains: 10 aspects of the Big Five)
    *MRI Research: Testing predictions from personality neuroscience. Brain structure and the big five.




    SOCIABILITY (EXTRAVERSION) vs. DETACHMENT
    .
    Sociability (Enthusiastic, Assertive)
    .
    Description: Sociability is synonymous with being enthusiastic and assertive; whereas Detachment is synonymous with being reserved and quiet. Assertiveness encompasses traits relating to leadership, dominance, and drive. Enthusiasm encompasses both outgoing friendliness or sociability and the tendency to experience and express positive emotion. The Sociability (Extraversion) dimension measures the behaviors that are central to the concept of SOCIABILITY and LEADERSHIP.
    Descriptors: Enthusiastic, assertive, sociable, outgoing, talkative, active, energetic, outspoken, dominant, forceful, show-off, spunky, adventurous, noisy, bossy.
    MRI Research*: Sociability (extraversion) was associated with increased volume of medial orbitofrontal cortex, a region involved in processing reward information.
    "I'm talkative"
    "I'm not reserved."
    "I'm full of energy."
    "I generate a lot of enthusiasm."
    "I'm not quiet."
    "I have an assertive personality."
    "I'm not shy or inhibited."
    "I am outgoing and sociable."
    "I make friends easily."
    "I warm up quickly to others."
    "I show my feelings when I'm happy."
    "I have a lot of fun."
    "I laugh a lot."
    "I take charge."
    "I have a strong personality."
    "I know how to captivate people."
    "I see myself as a good leader."
    "I can talk others into doing things."
    "I am the first to act."
    .
    Attention Seeking (Excessive Sociability)
    .
    "I like to draw attention to myself."
    "I crave attention."
    "I do things to make sure people notice me."
    "I do things so that people just have to admire me."
    "My behavior is often bold and grabs peoples' attention."
    .
    Detachment (Reserved, Quiet)
    .
    * Social Withdrawal:
    "I don’t like to get too close to people."
    "I don't deal with people unless I have to."
    "I'm not interested in making friends."
    "I don’t like spending time with others."
    "I say as little as possible when dealing with people."
    "I keep to myself."
    "I am hard to get to know."
    "I reveal little about myself."
    "I do not have an assertive personality."
    "I lack the talent for influencing people."
    "I wait for others to lead the way."
    "I hold back my opinions."
    .
    * Intimacy Avoidance:
    "I steer clear of romantic relationships."
    "I prefer to keep romance out of my life."
    "I prefer being alone to having a close romantic partner."
    "I'm just not very interested in having sexual relationships."
    "II break off relationships if they start to get close."
    .
    * Anhedonia (Lack of Pleasure):
    "I often feel like nothing I do really matters."
    "I almost never enjoy life."
    "Nothing seems to make me feel good."
    "Nothing seems to interest me very much."
    "I almost never feel happy about my day-to-day activities."
    "I rarely get enthusiastic about anything."
    "I don't get as much pleasure out of things as others seem to."
    .
    * Restricted Affectivity:
    "I don't show emotions strongly."
    "I don't get emotional."
    "I never show emotions to others."
    "I don't have very long-lasting emotional reactions to things."
    "People tell me it's difficult to know what I'm feeling."
    "I am not a very enthusiastic person."
    .
    ("Sociability vs. Detachment" modified from "PID-5" by Kreuger RF, Derringer J, Markon KE, Watson D, Skodol AE and Between facets and domains: 10 aspects of the Big Five)
    *MRI Research: Testing predictions from personality neuroscience. Brain structure and the big five.




    EMOTIONAL STABILITY VS. NEGATIVE EMOTION
    .
    Emotional Stability (Calm, Emotionally Stable)
    .
    Description: Emotional Stability is synonymous with being calm and emotionally stable; whereas Negative Emotion is synonymous with being distressed and easily upset. The Emotional Stability dimension measures the "safety vs. danger" behaviors that are central to the concept of COURAGE.
    Descriptors: Stable, calm, relaxed, contented
    "I am relaxed, and I handle stress well."
    "I am emotionally stable, and not easily upset."
    "I remain calm in tense situations."
    "I rarely get irritated."
    "I keep my emotions under control."
    "I rarely lose my composure."
    "I am not easily annoyed."
    "I seldom feel blue."
    "I feel comfortable with myself."
    "I rarely feel depressed."
    "I am not embarrassed easily."
    .
    Negative Emotion (Distressed, Easily Upset)
    .
    Description: Degree to which people experience persistent negative emotions (anxiety, anger, or depression) and are easily upset. (This could be thought of as high threat sensitivity or low stress tolerance.)
    Descriptors: Emotional instability, anxiety, irritability, depression, rumination-compulsiveness, self-consciousness, vulnerability
    MRI Research*: Negative Emotion was associated with increased volume of brain regions associated with threat, punishment, and negative emotions.
    .
    * Emotional Instability:
    "I get emotional easily, often for very little reason."
    "I get emotional over every little thing."
    "My emotions are unpredictable."
    "I never know where my emotions will go from moment to moment."
    "I am a highly emotional person."
    "I have much stronger emotional reactions than almost everyone else."
    "My emotions sometimes change for no good reason."
    "I get angry easily."
    "I get upset easily."
    "I change my mood a lot."
    "I am a person whose moods go up and down easily."
    "I get easily agitated."
    "I can be stirred up easily."
    .
    * Anxiousness:
    "I worry about almost everything."
    "I'm always fearful or on edge about bad things that might happen."
    "I always expect the worst to happen."
    "I am a very anxious person."
    "I get very nervous when I think about the future."
    "I often worry that something bad will happen due to mistakes I made in the past."
    "I am filled with doubts about things."
    "I feel threatened easily."
    "I am afraid of many things."
    .
    * Separation Insecurity:
    "I fear being alone in life more than anything else."
    "I can't stand being left alone, even for a few hours."
    "I’d rather be in a bad relationship than be alone."
    "I'll do just about anything to keep someone from abandoning me."
    "I dread being without someone to love me."
    .
    * Submissiveness:
    "I usually do what others think I should do."
    "I do what other people tell me to do."
    "I change what I do depending on what others want."
    .
    * Perseveration:
    "I get stuck on one way of doing things, even when it's clear it won't work."
    "I get stuck on things a lot."
    "It is hard for me to shift from one activity to another."
    "I get fixated on certain things and can’t stop."
    "I feel compelled to go on with things even when it makes little sense to do so."
    "I keep approaching things the same way, even when it isn’t working."
    .
    * Depression:
    "I have no worth as a person."
    "Everything seems pointless to me."
    "I often feel like a failure."
    "The world would be better off if I were dead."
    "The future looks really hopeless to me."
    "I often feel just miserable."
    "I'm very dissatisfied with myself."
    "I often feel like nothing I do really matters."
    "I know I'll commit suicide sooner or later."
    "I talk about suicide a lot."
    "I feel guilty much of the time."
    "I'm so ashamed by how I've let people down in lots of little ways."
    "I am easily discouraged."
    "I become overwhelmed by events."
    .
    ("Emotional Stability vs. Negative Emotion" modified from "PID-5" by Kreuger RF, Derringer J, Markon KE, Watson D, Skodol AE and Between facets and domains: 10 aspects of the Big Five)
    *MRI Research: Testing predictions from personality neuroscience. Brain structure and the big five.


    The "Big 5 Factors" of Personality as Shown In Dogs

    The same "Big 5 Factors" of personality found in humans can be found in dogs. This makes sense because dogs, like humans, are a social species.



    AGREEABLENESS VS. ANTAGONISM
    .
    Agreeableness ("Friend")
    .
    Dog is friendly towards unfamiliar people.
    Dog is friendly towards other dogs.
    When off leash, dog comes immediately when called.
    Dog willingly shares toys with other dogs.
    Dog leaves food or objects alone when told to do so.
    .
    Antagonism ("Foe")
    .
    Dog is dominant over other dogs.
    Dog is assertive with other dogs (e.g., if in a home with other dogs, when greeting).
    Dog behaves aggressively towards unfamiliar people.
    Dog shows aggression when nervous or fearful.
    Dog aggressively guards coveted items (e.g., stolen item, treats, food bowl).
    Dog is quick to sneak out through open doors, gates.

    CONSCIENTIOUSNESS VS. DISINHIBITION
    .
    Conscientiousness ("Self-Controlled")
    .
    Dog works at tasks (e.g., getting treats out of a dispenser, shredding toys) until entirely finished.
    Dog works hard all day herding or pulling a sleigh (if a "working dog" on the farm or in the snow).*
    Dog is curious.
    .
    Disinhibition ("Disinhibited")
    .
    Dog is boisterous.
    Dog seeks constant activity.
    Dog is very excitable around other dogs.

    OPENNESS TO EXPERIENCE vs. IMPAIRED INTELLECT
    .
    Open To Experience ("Open-Minded")
    .
    Dog is able to focus on a task in a distracting situation (e.g., loud or busy places, around other dogs).
    .
    Closed To Experience ("Closed-Minded")
    .
    Dog is slow to respond to corrections.
    Dog ignores commands.
    Dog is slow to learn new tricks or tasks.

    SOCIABILITY (EXTRAVERSION) vs. DETACHMENT
    .
    Sociability ("Approach")
    .
    Dog is attention seeking (e.g., nuzzling, pawing or jumping up on family members looking for attention and physical contact).*
    Dog seeks companionship from people.
    Dog is affectionate.
    .
    Detachment ("Avoidance")
    .
    Dog is aloof.
    Dog gets bored in play quickly.
    Dog is lethargic.

    EMOTIONAL STABILITY VS. NEGATIVE EMOTION
    .
    Emotional Stability ("Safety")
    .
    Dog tends to be calm.
    Dog is relaxed when greeting people.
    Dog is confident.
    Dog adapts easily to new situations and environments.
    .
    Negative Emotion ("Danger")
    .
    Dog is anxious.
    Dog is shy.
    Dog behaves fearfully towards unfamiliar people.
    Dog exhibits fearful behaviors when restrained.
    Dog avoids other dogs.
    Dog behaves fearfully towards other dogs.
    Dog behaves submissively (e.g., rolls over, avoids eye contact, licks lips) when greeting other dogs.
    .
    Modified from Jones, A. C. (2009). Development and validation of a dog personality questionnaire. Ph.D. Thesis. University of Texas, Austin.

    * New items added by Phillip W. Long MD

    Notice the Personality Differences Between Dogs and Humans

    Dogs and humans are strikingly similar on 4 of the "Big 5 Factors" of personality. However, dogs and humans are quite different on the "Conscientiousness" factor - because the canine brain isn't designed to organize work projects. That's why dogs don't build dog houses.

    Two of the "Big 5 Factors" of dog personality are clearly a function of dogs being a social species that forms social hierarchies: (1) the "Agreeableness" factor describes "friend vs. foe" behaviors, and (2) the "Sociability" factor describes "approach vs. avoidance" behaviors.

    The "Openness to Experience" describes the ability to learn from experience. The "Emotional Stability" factor describes "safety vs. danger" behaviors.

    The Brain and the "Big-5 Factors" of Human and Dog Personality

    It could be that the "Big-5 Factors" of personality represent some extremely basic brain functions. For example, when a young man approaches a young woman, she must: (1) decide whether he is friend or foe ["Agreeableness"], (2) decide if this represents safety or danger ["Emotional Stability"], (3) decide whether to approach or avoid him ["Sociability"], (4) decide whether to be self-controlled or disinhibited ["Conscientiousness"], and (5) learn from this experience ["Openness to Experience"].


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    World Health Organization Delirium and Dementia Treatment Guidelines

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    Treatment



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    • 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!

    • Criteria For High Quality Research Studies

    • It is imperative that medical researchers conduct high quality research studies, otherwise the US Food and Drug Administration (FDA) refuses to licence their new drug or therapy. In 2009, the cost of successfully licensing one new drug or therapy under the FDA scheme was estimated to be US$1,000 million. Thus psychiatric research which leads to FDA approval of a new drug or therapy has to be of the highest quality; however the majority of psychological research studies on new therapies fail to reach these high standards for research. This could explain why two-thirds of psychological research studies can'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 for a (normally distributed) strictly positive variable (because the "cooked" M and SD would mathematically require the strictly positive variable's range of data to include negative numbers). For a normally distributed sample of size of 25-70, this occurs when the SD is greater than one-half of the M; for a sample size of 70+, this occurs when the SD is greater than one-third of the M [using these formulas].

        • 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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