Tag Archive | parietal lobe

The Layperson’s Guide to 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, and 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:

Inappropriate behavior, including words and actions
Loss of executive function, including organizing and planning
Slowed thinking, reactions, and speaking
Garbled speech
Trouble executing basic skills functions like adding, subtracting, multiplying, and dividing
Decreased ability to concentrate
Decreased ability to complete tasks
Trouble with balance
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:

Severe 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 relapsed (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

Oct3

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.

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.

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.

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.

Other signs of alcohol-related dementia emerge as:

Inappropriate behavior, including words and actions
Loss of executive function, including organizing and planning
Slowed thinking, reactions, and speaking
Garbled speech
Trouble executing basic skills functions like adding, subtracting, multiplying, and dividing
Decreased ability to concentrate
Decreased ability to complete tasks
Trouble with balance
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.

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

Severe 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).

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.

And no one can change that but you.

The Rare Dementias: Corticobasal Degeneration (CBD)

Apr23

Corticobasal degeneration (CBD) – also known as corticobasal ganglionic degeneration (CBGD) – is a rare (occurs in less than 1% of the population) and progressive form of dementia.

The onset of symptoms typically occurs after the age of 60 and the average duration of the disease from onset of symptoms to death is six years.

Although the underlying cause of CBD is unknown, what is known is that CBD is the result of extensive and severe damage in multiple areas of the brain.

Research into this form of dementia is relatively new (it was discovered in 1968), but the most current research has found that there are similar, but not identical, changes in the brain protein tau to the changes observed in progressive supranuclear palsy and Pick’s Disease.

These areas of the brain where damage is extensive include the cortex (especially in the frontal lobe and parietal lobes) and the deep-brain basal ganglia region of the brain, with the hallmark feature in that area being significant neuron degeneration and the loss of pigment in dopaminergic neurons (signifying a decrease in dopamine production) in the substantia nigra, which controls movement.

Dopamine is a chemical produced by the brain (a neurotransmitter) that plays a leading role in movement, memory, pleasure, cognition, behavior, attention, sleep, and mood.

When dopamine production decreases in the substantia nigra, movement is severely affected.

Often this is the first visible symptom of CBD. It presents as stiff movement, shaky movement, jerky movement, slow movement, and increased lack of balance, increased lack of coordination, and clumsiness. Generally, movement problems affect one side of the body almost exclusively, but as CBD progresses, both sides of the body are affected.

Since these movement disorders can mimic both Parkinson’s Disease and the effects of a deep-brain stroke – one of the classic movement disorders associated with these is ideomotor apraxia (a common example is the inability to initiate walking where the foot seems to be stuck to the floor and can’t be lifted spontaneously to take a step forward) – those must be ruled out as the causes of the movement disorders.

Other early symptoms of CBD can include difficulty controlling the mouth muscles, cognition problems, and behavioral problems. Language and speech difficulties – dysphasia (an impaired ability to understand or use the spoken word) and dysarithia (an impaired ability to clearly articulate the spoken word) – are also early CBD symptoms.

(In my latest book, You Oughta Know: Recognizing, Acknowledging, and Responding to the Steps in the Journey Through Dementias and Alzheimer’s Disease, I devote a whole chapter to a comprehensive and in-depth discussion of the communication problems, including the different types of dysphasia, that occur with dementias and Alzheimer’s Disease, and ways to work with our loved ones to keep the lines of communication open for as long as possible.)

It is not unusual for CBD to be initially diagnosed, if the first symptoms are cognitive impairment and/or behavioral issues, as Alzheimer’s Disease or frontotemporal dementia. Similarly, if movement disorders are the first symptoms, CBD is often initially diagnosed as Parkinson’s Disease.

However, a clear diagnosis of CBD is usually made when both movement disorders and cognitive impairment and/or behavior problems appear simultaneously.

There is no known treatment for CBD. Unlike Parkinson’s Disease where dopamine-enhancing or dopamine-mimicking medications prove to be effective for some of the duration of the disease, these drugs have proven to be ineffective for treating CBD (this is likely because of the very different pathologies in the development and progression of the two diseases).

In the early stages of CBD, speech therapy and physical therapy may help with communication and stiffness and movement. However, as the disease progresses, these will become less effective and, in the end stage, they will be completely ineffective.

As CBD progresses, other symptoms appear and worsen, including:

Rigidity
Tremors
Involuntary muscle contractions
Involuntary eyelid spasms
Loss of sensory functions
“Alien hand/limb” syndrome (hand or limb movement that the person isn’t aware of nor has control over)

Because of the increased rigidity and lack of muscle coordination and use as CBD progresses, usually within five years of onset, sufferers will be unable to swallow and will be completely immobile. Even before this, though, one of the potentially-fatal risks associated with CDB is aspiration of food into the lungs because of impaired swallowing and the high likelihood of pneumonia as a result.

While a feeding tube may be considered as an alternative when CBD has progressed to the point where swallowing is significantly affected, it is, in my opinion, inhumane because it only prolongs the suffering from a disease that is ultimately fatal.

This is a quality-of-life choice. I can’t imagine for myself a life prolonged where I am completely immobile and completely dependent on everyone else for everything and I can do nothing for myself.

A feeding tube would be my worst nightmare. And for me, it would be the most cruel thing those in charge of making medical decisions for me could do to me.

Fortunately, I already have all my documents in place to make sure this can’t and won’t happen to me when and if the time comes that the choice needs to be made, because I’ve already made the choices.

So, as an aside, I would strongly urge everyone who reads this to get your wishes formalized and signed and communicated so that you have control over the end game of your life in this area.

Not only is the wise and prudent thing to do, but it eliminates the agony of wondering what to do so often seen in families where the person affected never talked about what he or she wanted and never took the time to answer these questions when he or she could.

The Layperson’s Guide to Alzheimer’s Disease

Jun19

Today’s post will provide an overview look at Alzheimer’s Disease. As I’ve stated before, Alzheimer’s Disease is a specific type of brain deterioration disease (dementia) that differs from other dementias.

While Alzheimer’s Disease is a type of dementia, not all dementias are Alzheimer’s Disease. “Alzheimer’s Disease” has become the catch-phrase for all neurological degeneration among the general population and that imprecision leads to a lack of understanding of the complexities of these diseases, especially when several types of dementia are present concurrently.

Dementias affect specific areas of the internal structure of the brain and are caused by specific abnormal occurrences within those areas. We’ve looked at vascular (multi-infarct) dementia, which is a result of small vessel ischemia within the blood vessels in the brain, and Lewy Body dementia, which occurs when abnormal proteins are deposited in the cortex of the brain.

Alzheimer’s Disease affects the whole brain, essentially eroding and diminishing, through the resulting atrophy, the whole structure of the brain. The two crucial components in Alzheimer’s Disease are the overabundant presence of plaques (beta-amyloid protein deposit fragments that accumulate in the spaces between neurons) and tangles (twisted fibers of disintegrating tau proteins that accumulate within neurons). Watch this short video to see how these plaques and tangles form and how they lead to neuron death.

While plaques and tangles, which lead to neuron death (the nerve cells get deprived of what they need to survive and be healthy), are part of the aging process, in our loved ones with Alzheimer’s Disease, there are so many of them that the brain slowly dies from the inside out.

It is clear from the picture above exactly why Alzheimer’s Disease is a systemic disease, because all areas of the brain are eventually impacted.

However, as Alzheimer’s Disease begins, the first area of the brain affected is the temporal lobe, which is, in part, responsible for long and short-term memory, and persistent short-term memory loss is usually one of the first symptoms of Alzheimer’s Disease to appear.

The second area of the brain to be affected is generally the frontal lobe, which handles information processing and decision-making. The last part of the brain to be affected is usually the parietal lobe, which is the area of the brain responsible for language and speech.

Alzheimer’s Disease has distinct stages in which symptoms materialize. The stages are (this lists the three main stages, but there is also a more comprehensive seven-stage breakdown, known as the Global Deterioration Scale or the Reisberg Scale):

Stage 1 – Mild – Recurring short-term memory loss, especially of recent conversations and events. Repetitive questions and some trouble with expressing and understanding language. Possible mild coordination problems with writing and using objects. May have mood swings. Need reminders for some daily activities, and may begin have difficulty driving.
Stage 2 – Moderate/Middle – Problems are evident. Continual memory loss, which may include forgetting personal history and the inability to recognize friends and family. Rambling speech. Unusual reasoning. More confusion about current events, time, and place. Tends to get lost in familiar settings. Experiences sleep issues (including sundowning). More pervasive changes in mood and behavior, especially when experiencing stress and change. May experience delusions, aggression, and uninhibited behavior. Mobility and coordination may be affected. Need set structure, reminders, and assistance with daily living.
Stage 3 – Severe/Late – Confused about past and present. Loses all ability to remember, communicate, or process information. Generally incapacitated with severe to total loss of verbal skills. Unable to care for self. Often features urinary and bowel incontinence. Can exhibit extreme mood disturbances, extreme behavior, and delirium. Problems with swallowing occur in this stage as well.

It’s important to remember that not all our loved ones with Alzheimer’s Disease – especially if there are other dementias present – will go through every aspect of each stage nor through all the stages before they die. That’s one of the real difficulties with “mixed-dementia” diagnoses, as these are called, because it’s difficult to tell which brain disease is causing which problems and that makes them more difficult to manage symptom-wise.

The medications generally prescribed for Alzheimer’s Disease are Aricept (mild to moderate stages), Namenda (moderate stage), and Excelon (mild to moderate). All three of these medications are cognitive enhancers. It’s not unusual to have more than one of these medications prescribed at a time.

I will talk specifically about sleep disturbances in dementias and Alzheimer’s Disease, including sundowning, in another post, but I will caution all caregivers to stay away from both non-prescription sleep medications like Tylenol PM, Advil PM, and ZZZQuil and prescription sleep medications like Lunesta and Ambien (all of these can actually make the symptoms worse and definitely make injury and/or death from a fall more likely).

Melatonin is naturally-occurring sleep hormone in humans. As people age, there is less melatonin produced. That’s why, in general, most older people who have never had sleep disorders eventually and gradually sleep less than their younger counterparts. However, the brain damage that dementias and Alzheimer’s Disease cause exacerbates this lack of melatonin.

So, it’s worth it to try a therapeutic dose (up to 20 mg per night is considered to be safe) of Melatonin. It is available over-the-counter at both brick-and-mortar and online drug stores.

Start with a 3 mg dose and add slowly. With my mom, a 5 mg dose provided enough for her to sleep as best as she could through the night. Do not overdose because this will disrupt the circadian rhythm further by producing late sleeping and grogginess during the day.

Usually our loved ones with dementia and/or Alzheimer’s Disease, even though these diseases are fatal (when the brain’s dead, you’re dead), don’t die from them specifically.

They die either from a concurrent health problem (in my mom’s case, it was congestive heart failure which lead to a major heart attack, a minimal recovery, and then her death twelve days later) or from complications that arise from the brain degeneration caused by the dementias and/or Alzheimer’s Disease.

The two most common causes of death in Alzheimer’s Disease are pneumonia (the brain controls swallowing, and once that becomes compromised, aspiration of food into the lungs is likely and leads to an infection) and fatal trauma to the head from falls.

Going Gentle Into That Good Night

Practical, applicable information for caregiving for our loved ones with dementias and Alzheimer's Disease

Tag Archive | parietal lobe

The Rare Dementias: Corticobasal Degeneration (CBD)

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