Tag Archive | alcohol-related dementia

Profiles in Dementia: David Cassidy (1950 – 2017)

David CassidyDavid Cassidy was a singer, songwriter, and guitarist, who catapulted to fame as Keith Partridge in the 1970’s television show The Partridge Family.

Although Cassidy aspired to have the musical chops and freedom of Mick Jagger (The Rolling Stones) and John Lennon and Paul McCartney (The Beatles), his long-running stint on The Partridge Family relegated him to performing “bubblegum” music. It was something he hated, but depended on after the TV series ended to continue to make a living. Continue reading

Profiles in Dementia: Malcolm Young (1953 – 2017)

Malcolm Young suffered from alcohol-related dementiaMalcolm Young, along with his younger brother Angus, founded AC/DC, one of the first metal rock groups, in 1973.

AC/DC quickly gained traction with its driving rhythm and shouted vocals and moved into the spotlight of the music scene after just a couple of years in the recording studio.
Continue reading

Confabulation, Alcohol Abuse, and Alcohol-Related Dementia

Confabulation breaks trustOne of the lifelong struggles we, as human beings, do – or should be doing – battle with is being consistently honest both with ourselves (I submit this may be the hardest part of this battle because our capacity for self-deception seems to have no limits) and with others.

I have written here before about the interconnected relationship between honesty and trust. When we are dishonest with someone, we break their trust. Continue reading

Profiles in Dementia: Rita Hayworth (1918 – 1987)

Rita Hayworth Alzheimer's Disease Alcohol-Related DementiaRita Hayworth was an American actress whose career peaked in the 1940’s as Columbia Pictures’ most lucrative female lead, with a career that included 61 movies over a 37-year span.

One of Hayworth’s most acclaimed performances was in 1946’s Gilda, starring opposite leading man Glenn Ford. Hayworth also starred in two movies with Fred Astaire, who said she was his favorite dancing partner on screen.

However, fame and fortune could not stave off Hayworth’s personal demons, one of which was alcoholism.

By the late 1950’s, Hayworth’s chronic abuse of alcohol had ravaged the beauty of her younger years and had aged her considerably, making her no longer as attractive to Columbia as a leading lady even though she wasn’t 40 years old yet.

Alcoholism also created havoc in Hayworth’s personal life – she married and divorced five times (to men who in their own rights were not good choices).

By the 1970’s, when Hayworth was in her mid-50’s, the ravages of years of alcohol abuse began to also affect her brain. From 1972 until her death 1987, Hayworth’s cognitive impairment, memory loss, and repetitive outrageous behavior were what kept her name in the news headlines.

Rita Hayworth as an older womanHayworth died in February 1987 at the age of 68. Although she was the first public face of Alzheimer’s Disease (then a relatively-unheard-of form of dementia), there is absolutely no doubt that Hayworth also had alcohol-related dementia (also in 1987, mixed dementias and the many types of dementia were relatively unheard of as well), which probably hastened both her neurological decline and her death.

The Layperson’s Guide to Neural Disorders That Often Lead to Neurodegeneration and Dementia

Normal brain cellMost dementias – Lewy Body dementia, vascular dementia, early-onset dementias, alcohol-related dementia, and Alzheimer’s Disease among them – appear seemingly suddenly as primary and distinct neurodegenerative processes without definitive causes (except in the case of genetic inheritance, which primarily occurs in rare dementias like Corticobasal Degeneration, Progressive Supranuclear Palsy, and Fatal Familial Insomnia and some of the early-onset dementias).

However, there are a group of neural disorders, which are caused by the same genetic mutation that affects lipid storage in the body, that often have dementia as a secondary symptom as the diseases progress.  

Structure of cell membraneThese neural disorders (all these have sphingolipid metabolism dysfunction in common) – which include Niemann-Pick disease, Tay Sachs disease, and Gaucher disease – are characterized by by increased levels of a particular type of sphingolipid.

There is no cure for these neural disorders and they are all fatal (in many cases, during childhood).

Anatomy of a sphingolipidSpingolipids are the biological product of a chemical process that creates a protective layer on nerve cell membranes and ensures proper – and protective – cell signaling and are critical to optimal brain function.

The genesis of sphingolipids are long-chain – also known as sphingoid – bases that normally have a length of 18 carbons, although they can also have lengths of 16 or 20 carbons. The length of long-chain bases is determined by serine palmitoyltransferase (STP), a multiprotein enzyme.

Chemistry of sphingolipidIn neural disorders like Niemann-Pick disease, Tay Sachs disease, and Gaucher disease, a mutation (known as Stellar) in one of the proteins that makes up STP creates an abnormally high number of 20 carbon long-chain bases, which dramatically interferes with sphingolipid metabolism.

This causes neurodegeneration to occur. In all these neural disorders, much of the neurodegeneration begins soon after birth.

In Tay Sachs disease, neurodegeneration of the brain and spinal cord begins at about six months of age. The average lifespan is four years.

Gaucher disease has three subtypes.

In Type 1 Gaucher disease, symptoms, which include anemia, bone deterioration, and liver and spleen impairment, are non-neurological and do not materialize until middle age. The average life expectancy for Type 1 is 68 years.

Type 2 and Type 3 Gaucher disease are both neuropathic forms of the disease.  Neurodegenerative symptoms include abnormal eye movements, seizures, and systemic brain damage.

In Type 2 Gaucher disease, the onset of symptoms is within three to six months of age. Deterioration is rapid; the average life expectancy is about two years of age.

 Type 3 Gaucher disease is a slower onset and involving version of Type 2. The average onset of neurological involvement is late childhood into adolescence. Life expectancy ranges from the mid-twenties to, in extremely rare cases, the early forties.

Niemann-Pick disease has four types: Type A, Type B, Type C1 and Type C2.

Niemann-Pick disease Type A occurs in infants. Symptoms include enlargement of the liver and spleen (around three months of age) and a failure to thrive during the first year of life. At one year, widespread damage to the lungs occurs, and there is a progressive loss of neurological and motor function.

A cherry red spot on the macula is a common denominator in Tay Sachs Disease and Niemann Pick disease Type 1Along with Tay Sachs disease, Niemann-Pick disease Type A also has a common eye deformity consistent with neurometabolic disease, known as a cherry spot, that occurs within the macula and is often what initially identifies the two neural disorders.

While most children born with Niemann-Pick disease Type A die in infancy, a few may live as long as four years.

Niemann-Pick disease Type B includes most of the same symptoms as Type A (motor skills are not usually affected), but the onset of symptoms is during adolescence. Most people with Niemann-Pick disease Type B survive into adulthood, but mortality rates climb dramatically between twenty and thirty years of age.

Niemann-Pick disease Type C (C1 and C2 are caused by different gene mutations, but the symptoms are the same) is characterized by severe liver disease, severe pulmonary infections, progressive neurodegeneration, and increasing difficulty with speech and swallowing that deteriorates completely over time.

The onset of Niemann-Pick disease Type C can be at any age, but it is most commonly seen by the age of five. The life expectancy with this type is under twenty years of age when symptoms appear in childhood. When symptoms appear later, the life expectancy is ten to twenty years after symptoms begin.

 

 

The Layperson’s Guide to Alcohol-Related Dementia

pouring-shots-alcohol-related-dementia

In “Lifestyle Dementia: Underdiscussed, Overlooked, But a Very Real and Present Danger,” and “Is the Precipitous Rise in Dementias and Alzheimer’s Disease Over the Last Twenty to Thirty Years Linked to Lifestyle?,” we see that certain lifestyle factors and choices can make the likelihood of developing dementias and Alzheimer’s Disease more probable.

Two lifestyle factors that can contribute to the development of dementias and Alzheimer’s Disease – and the onset of these is usually before age 65 – are chronic, long-term alcohol abuse and alcoholism. This type of dementia is called alcohol-related dementia and can manifest itself in various forms.

This post will take a look at how chronic, long-term alcohol abuse and alcoholism affects the brain and what the behaviors and symptoms of the dementia looks like.

We all know that drinking enough alcohol at one time impairs the brain. Common symptoms include slurring words, exhibiting general motor impairment, including stumbling and walking off-balance, making poor decisions (like driving, for example), being less able to hear sound at a normal volume, experiencing vision problems, and being unable to think clearly. 

These behaviors occur because alcohol depresses the central nervous system , causing it to slow down its responses and reactions. The brain stem (made up of the Pons, Medulla, and Midbrain), which regulates breathing, heart rate, lifestyle dementia alcohol related going gentle into that good nightand consciousness, as well all other areas of the brain are affected by alcohol:

  • Frontal – involved in movement, problem-solving, concentrating, thinking, mood, behavior, and personality
  • Temporal – involved in hearing, language, and memory
  • Parietal – involved in sensation awareness, language, perception, attention, and body awareness 
  • Occipital – involved in vision and perception
  • Cerebellum – involved in posture, balance, and coordination of movement

Chronic, long-term alcohol abuse and alcoholism have even more devastating – and permanent – effects on the brain, eventually leading to alcohol-related dementia.

Usually the first noticeable symptoms of chronic, long-term alcohol abuse and alcoholism are cognitive. Memory loss is common, but a unique feature of memory loss with people who are chronic, long-term alcohol abusers or alcoholics is confabulation.

Confabulation occurs when, instead of recalling accurate memories because of the damage to the brain, the person distorts, makes up, and misinterprets memories about themselves, others, and the world around them.

As difficult as it is to believe for those on the receiving end of confabulation, there is no conscious intent to be dishonest. It is simply the result of extensive neurological damage.

One of the most challenging aspects of people who confabulate is that although they are giving blatantly false information, the information can appear to be coherent, internally consistent, and relatively normal.

People who confabulate have incorrect memories that run the gambit from slight, almost imperceptible changes to the most outlandish made-up stories you can imagine.

The maddening thing about this is that they generally very confident – to the point of arguing down anyone (because they know the memory is fabricated) who tries to correct or challenge them – about their recollections, despite overwhelming concrete evidence that contradicts them.

Other signs of alcohol-related dementia emerge as:

  1. Inappropriate behavior, including words and actions
  2. Loss of executive function, including organizing and planning
  3. Slowed thinking, reactions, and speaking
  4. Garbled speech
  5. Trouble executing basic skills functions like adding, subtracting, multiplying, and dividing
  6. Decreased ability to concentrate
  7. Decreased ability to complete tasks
  8. Trouble with balance
  9. Diminished hearing

With alcohol-related dementia, as with all other dementias, the person who has alcohol-related dementia loses the self-awareness that anything is wrong, both neurologically and behaviorally.

Most cases of alcohol-related dementia involve global neurological deterioration. Everything is affected.

However, two very specific types of alcohol-related dementia, Wernicke encephalopathy and Korsakoff syndrome (known together as Wernicke-Korsakoff Syndrome), which are the result of a vitamin B1 (thiamine) deficiency, have key features specific to them. There can be some reversal of symptoms with B1 (thiamine) therapy, but there is still permanent neurological damage and concurrent alcohol-related dementia.

Wernicke encephalopathy (commonly known as “wet brain”) causes damage in the thalamus and hypothalamus. Its symptoms include:

  • alcohol-related dementia Wernicke encephalopathy going gentle into that good nightSevere confusion and decreased mental activity that can lead to comas and death
  • Loss of muscle coordination (ataxia) that can cause tremors in the legs
  • Vision deterioration including abnormal eye movements, drooping eyelids, and persistent double vision

As symptoms of Wernicke encephalopathy disappear, Korsakoff syndrome symptoms appear. These include:

  • Loss of ability to form new memories
  • Moderate to severe loss of all memories
  • Confabulation
  • Visual and auditory hallucinations  

Malcolm Young, the 61-year-old co-founder and guitarist for the band AC/DC, has been moved to a nursing home and his family has confirmed that he has dementia (he’s unable to remember any of the band’s songs).

Young’s addiction to alcohol is well-known. Although he sought rehabilitation treatment for alcoholism during the band’s tour in 1988, it appears that he malcolm young ac/dc dementia going gentle into that good nightrelapsed (the statistics on the efficacy of alcohol rehab are grim: from 50 to 90% of people who’ve been through treatment relapse, often, over a period of time, habitually consuming even more alcohol than they did before entering treatment) and never sought treatment again.

In April of this year, Young was hospitalized with what was described to the media as a stroke (chronic alcohol abuse has very detrimental effects on blood, including causing the platelets to clump together and form clots, and these clots, when they travel to the brain are responsible for strokes), so this would be entirely consistent with what we know about Young’s lifestyle. 

There are systemic physiological effects of chronic, long-term alcohol abuse and alcoholism, including nerve damage in the arms and legs (peripheral neuropathy), liver damage (cirrhosis), heart damage, and kidney damage.

Concurrent with all of that is the irreversible neurological damage to the brain that results in alcohol-related dementia, which can emerge as early as 30 years of age, but more commonly begins emerging after the age of 50 in chronic, long-term alcohol abusers and alcoholics.

Drinking alcohol in moderation is fine. But I urge you to take an honest look at your drinking patterns and behavior. If you find that you are a chronic, long-term alcohol abuser or an alcoholic, then it’s time today to find a way to stop drinking alcohol for good.

But no one else can do that for you. Only you can make the choice to stop drinking alcohol and then follow through with actually doing it for the rest of your life. 

And here’s the key: until the rest of your life becomes more important than alcohol, you will be unsuccessful at choosing and taking action to stop drinking alcohol.

Because you are the only one who can take the action, every time you drink alcohol, as a chronic, long-term alcohol abuser or an alcoholic, you show yourself and the rest of the world the choice you’re making and you show yourself and the rest of the world what the most important thing in your life is.

And no one can change that but you.

Alcohol-Related Dementia: A Lifestyle Dementia

pouring-shots-alcohol-related-dementia

In “Lifestyle Dementia: Underdiscussed, Overlooked, But a Very Real and Present Danger,” and “Is the Precipitous Rise in Dementias and Alzheimer’s Disease Over the Last Twenty to Thirty Years Linked to Lifestyle?,” we see that certain lifestyle factors and choices can make the likelihood of developing dementias and Alzheimer’s Disease more probable.

Two lifestyle factors that can contribute to the development of dementias and Alzheimer’s Disease – and the onset of these is usually before age 65 – are chronic, long-term alcohol abuse and alcoholism. This type of dementia is called alcohol-related dementia and can manifest itself in various forms.

This post will take a look at how chronic, long-term alcohol abuse and alcoholism affects the brain and what the behaviors and symptoms of the dementia looks like.

We all know that drinking enough alcohol at one time impairs the brain. Common symptoms include slurring words, exhibiting general motor impairment, including stumbling and walking off-balance, making poor decisions (like driving, for example), being less able to hear sound at a normal volume, experiencing vision problems, and being unable to think clearly. 

These behaviors occur because alcohol depresses the central nervous system , causing it to slow down its responses and reactions. The brain stem (made up of the Pons, Medulla, and Midbrain), which regulates breathing, heart rate, lifestyle dementia alcohol related going gentle into that good nightand consciousness, as well all other areas of the brain are affected by alcohol:

  • Frontal – involved in movement, problem-solving, concentrating, thinking, mood, behavior, and personality
  • Temporal – involved in hearing, language, and memory
  • Parietal – involved in sensation awareness, language, perception, attention, and body awareness 
  • Occipital – involved in vision and perception
  • Cerebellum – involved in posture, balance, and coordination of movement

Chronic, long-term alcohol abuse and alcoholism have even more devastating – and permanent – effects on the brain, eventually leading to alcohol-related dementia.

Usually the first noticeable symptoms of chronic, long-term alcohol abuse and alcoholism are cognitive. Memory loss is common, but a unique feature of memory loss with people who are chronic, long-term alcohol abusers or alcoholics is confabulation.

Confabulation occurs when, instead of recalling accurate memories because of the damage to the brain, the person distorts, makes up, and misinterprets memories about themselves, others, and the world around them.

As difficult as it is to believe for those on the receiving end of confabulation, there is no conscious intent to be dishonest. It is simply the result of extensive neurological damage.

One of the most challenging aspects of people who confabulate is that although they are giving blatantly false information, the information can appear to be coherent, internally consistent, and relatively normal.

People who confabulate have incorrect memories that run the gambit from slight, almost imperceptible changes to the most outlandish made-up stories you can imagine.

The maddening thing about this is that they generally very confident – to the point of arguing down anyone (because they know the memory is fabricated) who tries to correct or challenge them – about their recollections, despite overwhelming concrete evidence that contradicts them.

Other signs of alcohol-related dementia emerge as:

  1. Inappropriate behavior, including words and actions
  2. Loss of executive function, including organizing and planning
  3. Slowed thinking, reactions, and speaking
  4. Garbled speech
  5. Trouble executing basic skills functions like adding, subtracting, multiplying, and dividing
  6. Decreased ability to concentrate
  7. Decreased ability to complete tasks
  8. Trouble with balance
  9. Diminished hearing

With alcohol-related dementia, as with all other dementias, the person who has alcohol-related dementia loses the self-awareness that anything is wrong, both neurologically and behaviorally.

Most cases of alcohol-related dementia involve global neurological deterioration. Everything is affected.

However, two very specific types of alcohol-related dementia, Wernicke encephalopathy and Korsakoff syndrome (known together as Wernicke-Korsakoff Syndrome), which are the result of a vitamin B1 (thiamine) deficiency, have key features specific to them. There can be some reversal of symptoms with B1 (thiamine) therapy, but there is still permanent neurological damage and concurrent alcohol-related dementia.

Wernicke encephalopathy (commonly known as “wet brain”) causes damage in the thalamus and hypothalamus. Its symptoms include:

  • alcohol-related dementia Wernicke encephalopathy going gentle into that good nightSevere confusion and decreased mental activity that can lead to comas and death
  • Loss of muscle coordination (ataxia) that can cause tremors in the legs
  • Vision deterioration including abnormal eye movements, drooping eyelids, and persistent double vision

As symptoms of Wernicke encephalopathy disappear, Korsakoff syndrome symptoms appear. These include:

  • Loss of ability to form new memories
  • Moderate to severe loss of all memories
  • Confabulation
  • Visual and auditory hallucinations  

Malcolm Young, the 61-year-old co-founder and guitarist for the band AC/DC, has been moved to a nursing home and his family has confirmed this week that he has dementia (he’s unable to remember any of the band’s songs).

Young’s addiction to alcohol is well-known. Although he sought rehabilitation treatment for alcoholism during the band’s tour in 1988, it appears that he malcolm young ac/dc dementia going gentle into that good nightrelapsed (the statistics on the efficacy of alcohol rehab are grim: from 50 to 90% of people who’ve been through treatment relapse, often, over a period of time, habitually consuming even more alcohol than they did before entering treatment) and never sought treatment again.

In April of this year, Young was hospitalized with what was described to the media as a stroke (chronic alcohol abuse has very detrimental effects on blood, including causing the platelets to clump together and form clots, and these clots, when they travel to the brain are responsible for strokes), so this would be entirely consistent with what we know about Young’s lifestyle. 

There are systemic physiological effects of chronic, long-term alcohol abuse and alcoholism, including nerve damage in the arms and legs (peripheral neuropathy), liver damage (cirrhosis), heart damage, and kidney damage.

Concurrent with all of that is the irreversible neurological damage to the brain that results in alcohol-related dementia, which can emerge as early as 30 years of age, but more commonly begins emerging after the age of 50 in chronic, long-term alcohol abusers and alcoholics.

Drinking alcohol in moderation is fine. But I urge you to take an honest look at your drinking patterns and behavior. If you find that you are a chronic, long-term alcohol abuser or an alcoholic, then it’s time today to find a way to stop drinking alcohol for good.

But no one else can do that for you. Only you can make the choice to stop drinking alcohol and then follow through with actually doing it for the rest of your life. 

And here’s the key: until the rest of your life becomes more important than alcohol, you will be unsuccessful at choosing and taking action to stop drinking alcohol.

Because you are the only one who can take the action, every time you drink alcohol, as a chronic, long-term alcohol abuser or an alcoholic, you show yourself and the rest of the world the choice you’re making and you show yourself and the rest of the world what the most important thing in your life is.

And no one can change that but you.