Chapter 28: Cognitive Disorders in Psychiatric Nursing

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Welcome back to the Deep Dive.

I have to be honest with you.

I usually look forward to recording these.

We get to talk about history or cool new tech or, you know, space.

But today, I've been dreading this one a little bit.

It feels heavy.

I can guess why.

We are tackling Chapter 28 today, Cognitive Disorder.

Yeah, it's the brain failure chapter.

And I think the reason that it hangs so heavy is that we all have this low -level background anxiety about it.

You know, you lose your keys or you walk into a room and completely forget why you walked in there and that little voice in the back of your head whispers, is this it?

Is this the start?

It is universal fear.

And actually, the source text, which is this dense psychiatric nursing textbook, it tackles that philosophical weight right out of the gate.

There's a section called Norm's Notes.

Norm is the author offering these sort of sidebar insights.

And he puts his finger right on the wound.

He talks about the fear of losing the real you.

That part really stopped me in my tracks because when we're kids, we play that, you know, that morbid game, right?

We'd rather lose an arm or a leg.

And you sit there and you debate the physics of it.

Can I still play soccer?

Can I play video games?

It's all physical.

It's about mechanics.

Right.

It's a functional question.

But Norm argues that as you age, as you mature, you realize the physical stuff is, well, it's manageable.

You can live without a leg.

We have prosthetics.

We have wheelchairs.

Life goes on.

But there's no prosthetic for your personality.

Exactly.

There's no replacement for your memories for your sense of self.

Norm says, and this is a direct quote, when you can no longer reason clearly and rationally, the real you has been taken.

That is the nightmare scenario.

Yeah.

It's the idea that the vessel is still there, the body is breathing, the heart is beating, but the pilot has ejected.

The lights are on, but nobody's home.

That's it.

Precisely.

And Norm also notes, with a bit of dark humor, I think, that fortunately the government is run by older people, so they're terrified of this too.

Oh, that's a good point.

Consequently, they spend a lot of money studying how to stop or reverse these conditions.

He just says he wants the researchers to hurry up.

Don't we all?

So here's our mission statement for today.

We are going to take this massive scary topic and we're going to break it down.

We're targeting nursing students who need to know how to spot this on the ward, but also really anyone who is insanely curious about how the brain breaks down.

We want to demystify brain failure.

And a big part of that is separating the, I forgot my keys, moments from actual pathology.

We're going to talk about the difference between a slow decline and a sudden medical emergency, which is a distinction that literally saves lives.

And we'll cover the reversible dementias.

I was shocked to learn that some are reversible, and then of course the big irreversible ones like Alzheimer's.

And since this is based on a psychiatric nursing text, we are going to look at the how.

How do you care for a human being who is drifting away from reality?

The pharmacology, the environment, what we call milieu management, and most importantly, the human connection.

It's going to be a journey.

Where do we start?

Let's start at the beginning, the fundamentals.

All right, let's unpack this.

Section one, the warning signs in the emergency.

We have to start with definitions.

When we say cognition in a medical context, what exactly are we measuring?

What does that word even mean?

In the context of this chapter, cognition really revolves around two central pillars, learning and memory.

Cognitive disorders are essentially assaults on the human brain that disrupt these fundamental abilities to acquire new information and recall old information.

So what are the red flags?

Is it just forgetting a name here and there?

I do that all the time.

It's broader than that.

Forgetting a name can be normal, you know, brain overload.

The text list common changes like disorientation, so not knowing the date, the season, or where you are.

Decreased concentration is a big one.

But one that really stands out to me, and I think is tragic, is the loss of abstract thinking.

What does that mean in practice?

Well, the text mentions that a patient might lose the ability to understand a joke.

Wow.

That's profound.

A life without humor because you can't make the abstract connection between the setup and the punchline.

Exactly.

Jokes rely on double meanings or unexpected twists, right?

If your brain can only process the literal concrete world, humor just evaporates.

Language disturbances are also really common.

But here's a key concept to hold onto as we go through this.

Often, motor skills remain intact even when memory fails.

So the body works, but the driver is missing.

Precisely.

The text puts it this way.

The body can walk, reach, grab, and even drive a car.

But the directive intelligence, the map, the purpose, the why is gone.

That disconnect is what makes these disorders so dangerous, not just emotionally, but physically.

Now before we get to the really severe stuff, we have to talk about this gray area.

The text calls it mild cognitive impairment or MCI.

This is one that worries me.

Is this just getting old?

Where's the line?

That is the million dollar question, isn't it?

MCI is defined as a regression in cognition that is not a result of normal aging.

It's a noticeable decline, but it's not severe enough to be called dementia.

Before the DSM -5, we didn't really have clear criteria for this.

It was just this fuzzy concept.

But now we do.

Now we do.

The criteria focus on modest decline that does not prevent independence.

That's the key difference.

Okay.

Give me an example.

What does that look like in real life?

Because modest decline still sounds pretty vague.

The text gives us a great clinical example of a Mrs.

Peacock.

She's a 72 -year -old retired head librarian.

Now just think about that profile for a second.

A librarian.

Organized, sharp, deals with catalogs and systems.

She's someone who has spent her entire life knowing exactly where everything is.

Right.

She used to coordinate conferences, manage budgets, all of that.

But now her daughter has to remind her to take her medication.

She recognizes that she's having memory problems, which is key.

She still has insight into her condition.

But here's the distinction.

She still lives independently.

She volunteers at the library.

Her peers, the other volunteers, haven't reported any problems.

So she's not helpless.

She's not burning the house down or getting lost.

No, not at all.

She can feed herself.

She can dress herself.

She can handle basic activities of daily living.

But the complex tasks, the instrumental activities, things like balancing a checkbook, managing a complex schedule, that's becoming really hard for her.

The high -level executive function is slipping.

And why does this matter?

Why do we need a label for,

I'm having trouble with my checkbook?

Is it just to pathologize aging?

No, it's because it's a major risk factor.

The source material states very clearly that individuals with symptoms of MCI who also possess a genetic predisposition are highly likely to progress to Alzheimer's disease.

It's a warning flare.

It tells us we need to watch this person closely.

Is there anything we can do at that stage?

Yeah.

Or is it just a waiting game for the inevitable?

There are interventions.

The text mentions that while no specific drug is approved to cure or reverse MCI, healthy habits matter immensely.

Things like improving sleep hygiene, treating any underlying depression, because depression can look a lot like cognitive decline.

We'll get to that exercising and engaging in mentally stimulating activities, puzzles, games, like crosswords, Sudoku, crosswords, board games.

Absolutely.

The text also suggests a really interesting one.

Comparing a movie to the book it was based on.

Oh, I like that.

It requires holding two different complex narratives in your head at the same time and actively analyzing the differences.

It's a real workout for the brain.

It forces it to make new connections.

Okay.

So that's the slow the warning flare.

Now I want to pivot to something that sounds much, much more intense.

Delirium.

The text calls this a medical emergency.

That's strong language.

It absolutely is, and it deserves it.

The etymology here is fascinating.

The word delirium comes from Latin delira.

It literally means out of one's furrow.

Out of one's furrow, like a plaid going off the track in a field.

Exactly.

Imagine you are plowing a field, you're in the groove, everything is straight and orderly, and then suddenly, wham, the plow jumps the track and you are tearing up the crops going in a completely different direction.

Some clinicians call it brain failure, and that's a good analogy.

It's as serious as heart failure or kidney failure.

So how do we tell the difference between this and dementia?

If you see an older person who is confused, how do you know if it's a slow decline or this, this thunderstorm?

The key is the onset.

Dementia is a slow creeping fog.

It happens over months and years.

Delirium is a thunderstorm.

It is acute and rapid.

We are talking about development over hours to days.

So you're fine on Tuesday, and on Wednesday, you're seeing things.

Yes.

And the consciousness fluctuates wildly.

One moment, they might be alert and oriented.

The next, they're completely confused and agitated.

Their sleep cycle gets destroyed, often experiencing what we call day -night reversal, where they sleep all day and are wide awake and agitated all night, and the hallucinations can be incredibly vivid.

The text had a specific detail about the hallucinations that really creeped me out, seeing multicolored rats.

It's very common to have visual hallucinations or tactile ones, like feeling bugs crawling under the skin.

You might see a patient picking at the air, trying to open an invisible bottle or button an invisible shirt.

It's very distinctive behavior.

It's called carphologia.

And you said this is usually secondary to a physical problem.

Yes.

And this is why it's a medical emergency.

The brain isn't the primary problem.

It's reacting to something else in the body going terribly wrong.

It could be an infection like pneumonia or a urinary tract infection, especially in the elderly.

It could be what they call ICU psychosis from the sensory overload and sleep deprivation of being in the hospital.

But a huge, huge culprit is medication toxicity.

We need to pause on this because the text specifically calls out And this is a story that I think everyone listening needs to hear.

This is so important.

This is the case of Mrs.

Edwards, and it is a dramatic, almost unbelievable illustration of polypharmacy, taking too many drugs at once, even if they seem harmless.

Set the scene for us.

What happened?

Mrs.

Edwards is 64, not terribly old.

She was found by her family crawling on her bedroom floor.

She had found her husband's pistol and was waiting to shoot him because she was convinced, absolutely certain, that he was plotting to kill her.

Oh my goodness.

So she's having a total psychotic break.

Paranoia, delusions, the whole nine yards.

That's what it looked like.

A brand new acute psychosis.

But when the medical team dug into what she was taking, they found the culprit.

She had a simple head cold, so she was taking a cough syrup.

She was also taking an allergy capsule for her sinuses.

And because she couldn't sleep, she was taking a sleeping pill to get some rest.

That sounds like a standard flu season cocktail.

I mean, I've probably done that myself.

Many, many people have.

But chemically, it was a bomb.

All three of those medications contained the active ingredient diphenhydramine.

You know it as the brand name Benadryl.

The pink allergy pill?

The very same.

Diphenhydramine is a potent anticholinergic.

It blocks the neurotransmitter acetylcholine in the brain.

Acetylcholine is critical for memory and clear thinking.

So when you take three doses of it at once, effectively, you dry up the brain's ability to process reality.

So she wasn't mentally ill.

She was toxic.

She was poisoned by cold medicine.

She was delirious due to toxicity.

The cure wasn't a psychiatric drug.

It was simply stopping the cold medicine.

Her cognition returned to completely normal within a few days.

That is terrifying and also a huge relief that it was reversible.

That is the hallmark of delirium.

It is usually reversible if you find and treat the underlying cause.

The text provides a really useful table, table 28 -1, that breaks this down cleanly for students.

Delirium.

Rapid onset.

A reversible cause is likely.

And consciousness fluctuates.

Dementia.

Slow onset.

Progressive deterioration.

And consciousness is usually consistent until the very late stages.

There was one other term mentioned in this section.

Pseudo -dementia.

Is that like fake dementia?

It's a term that is kind of fading from use, but it's important to know.

It describes severe depression that mimics the symptoms of dementia.

If you are profoundly depressed, you might have memory deficits, apathy, loss of interest, and psychomotor slowing that look a lot like Alzheimer's.

So you treat the depression and the dementia gets better.

That was the old thinking.

The text notes that we now understand depression might actually be a prodrome, an early sign or risk factor of a future dementia, rather than just a mimic.

The two are very closely linked.

Okay, so we've established the warning signs with MCI and the medical emergency of delirium.

Now let's talk about the dementias themselves.

And the text splits these into potentially reversible and irreversible.

I feel like as a nurse or a family member, you pray for the reversible ones.

You absolutely do.

The text emphasizes that a nurse must rule out the reversible ones first.

You don't want to sentence someone to an Alzheimer's diagnosis if they have something that's actually fixable.

Let's talk about the first one.

Normal pressure hydrocephalus, or NPH.

This one seems really tricky to diagnose.

It is, and it's often misdiagnosed as Alzheimer's or Parkinson's.

NPH happens when there is an impaired return of cerebrospinal fluid.

That's the fluid that bathes and Christians the brain and spinal cord.

It builds up in the ventricles, the chambers of the brain.

But the normal pressure part is confusing.

If fluid is building up, shouldn't the pressure be high?

You'd think so, but that's the paradox.

The pressure reading from a spinal tap stays normal, or only slightly high, but that excess fluid still takes up space.

Pressing on and damaging the surrounding brain tissue.

And there's a classic triad of symptoms to look for.

I've heard the mnemonic, wet,

wobbly, and wacky.

That is the classic medical school mnemonic, yes.

It's a good way to remember it.

The text lists them in the order they usually appear.

Number one, unsteady gait, or apraxia.

That's the wobbly.

The wobbly.

Number two, urinary urgency, or incontinence.

The wit.

And number three, dementia.

The wacky.

Exactly.

And the text notes that the gait issues usually happen first.

It's a very specific kind of walk.

It describes it as walking like the floor is sticky, they have trouble initiating movement, and their feet seem glued to the floor.

It's a magnetic gait.

That's a great visual.

I can picture that perfectly.

And if you catch it, it's treatable.

The treatment is neurosurgery.

They put in a ventricular peritoneal shunt.

It's basically a thin tube with a one -way valve that drains the excess fluid from the brain down into the abdominal cavity, the peritoneum, where it's just safely absorbed by the body.

Wow.

Does it work?

Does it reverse the symptoms?

The outcomes are actually very good.

70 to 90 percent of patients show improvement if it's caught early enough.

The text introduces us to Mrs.

Burkhalter.

She was misdiagnosed with Alzheimer's.

But looking back at her history, her family realized she had gait issues first, then the bladder problems, and only then did the memory decline start.

The classic triad.

In order.

In perfect order.

They put in a shunt, and her walking and bladder control came back almost immediately.

Her memory improved slightly, but the quality of life difference was just massive.

She could walk again.

That is incredible.

A surgery that can essentially reverse dementia symptoms.

Yeah.

What about the other reversible one?

Vitamin B12 deficiency.

This seems so simple.

It is.

And it's more common than people realize, especially in the elderly population.

It's usually due to pernicious anemia, which is an autoimmune issue, or just general malabsorption from age or GI problems.

You're eating B12, but your body just isn't absorbing it.

And this damages the brain.

It causes demyelination of the cerebrum and spinal cord.

Think of your nerves like electrical wires.

Myelin is the rubber insulation around the wire.

B12 deficiency strips that insulation off.

So the wire's short out.

The signals get scrambled.

Exactly.

The symptoms often start as peripheral neuropathy numbness or tingling in the hands and feet, but it can absolutely progress to full blown delirium, psychosis, and dementia like symptoms.

The example here is Mrs.

Washington.

Yes.

A very sad case.

An elderly woman found living in squalor.

She was profoundly malnourished and very weak in her extremities.

Everyone assumed it was just old age and neglect, but her blood work showed a severe B12 deficiency.

And the treatment is just B12.

The treatment is simple.

B12 replacement.

Usually by injections because the gut isn't absorbing it anyway.

You have to take them for life, but it stops the damage and can reverse many of the symptoms.

So moral of the story.

Check the B12 levels and check the gate before you jump to the conclusion that it's Alzheimer's.

Always.

Fix the body first.

Rule out the reversible causes.

But sadly, we have to move on to the irreversible ones.

And we have to start with the big one.

The one that accounts for 50 to 80 % of all dementias.

Alzheimer's disease.

The fifth leading cause of death for those over 64.

It's not just memory loss.

It is a terminal illness.

It is a massive progressive structural change in the brain.

The text goes into the path of physiology.

What is actually happening inside the skull?

And I want to spend a minute here because the imagery is so intense.

We have tangles and plaques.

Let's break those down.

What is a tangle?

Okay.

So imagine the internal transport system inside a single neuron, a single brain cell.

You have these long tracks like railroad tracks called microtubules.

They carry nutrients and other essential molecules from one end of the cell to the other.

Okay.

So the track is the cell's lifeline.

It is.

And these tracks are held together and stabilized by a specific protein called tau.

You can think of tau as the railroad ties that keep the rails parallel and stable.

Got it.

Tracks and ties.

In Alzheimer's, for reasons we don't fully understand,

that tau protein detaches from the tracks and collapses.

It gets chemically altered and then twists up with other tau proteins into these thick insoluble threads.

So the railroad ties just come loose and get all tangled up.

Yes.

And without the ties, the tracks fall apart.

The text says the microtubules collapse and the tau twists into what we call neurofibrillary tangles.

The cell's transport system is destroyed.

The cell essentially starves and dies from the inside out.

Okay.

So that's inside the cell.

The cell collapses from within.

What about the plaques?

Where do they come in?

The plaques are outside the cell, in the space between the neurons.

They are made of a different protein called beta amyloid.

The text uses an analogy here that I really like.

Imagine a larger protein called APP, or amyloid precursor protein.

It's stuck in the cell membrane like a toothpick stuck through the skin of an orange.

Okay.

I'm picturing a toothpick sticking out of an orange peel.

Right.

Normally, enzymes come along and act like scissors.

They snip that toothpick cleanly at the surface.

And the little piece that's snipped off is harmless and gets recycled by the body.

But in Alzheimer's, different enzymes do the snipping and they cut in the wrong places.

They create these longer misshapen pieces of beta amyloid that are chemically sticky.

And those sticky pieces clump together.

They clump together into these dense, hard plaques in the space between the cells.

So the tracks inside the cells are broken and the space between the cells is gummed up with this protein gunk.

Correct.

And that gunk directly interferes with synapses, the communication signals between neurons.

It blocks the signal and it also triggers a massive inflammatory response that causes even more damage.

And on top of all that, there's a massive loss of a specific neurotransmitter, acetylcholine, which is absolutely essential for forming memories.

Right.

The cells that produce acetylcholine are some of the first to die.

And the result of all this cell death, all these tangles and plaques is brain atrophy.

The brain literally shrinks.

I've seen pictures of this.

It's horrifying.

It is.

The ridges of the brain get narrow and thin.

The sulci, the grooves between them get wide and deep.

The ventricles, the fluid -filled spaces in the middle get huge because the brain tissue around them is just disappearing.

The text describes a normal brain weighing about three pounds.

An advanced Alzheimer's brain might weigh less than half that.

It effectively withers away.

That's a terrifying thought.

Is it genetic?

It can be.

The text distinguishes between early onset and late onset.

Early onset is the rare familial type.

It happens fast, striking people in their 30s, 40s, or 50s.

It's autosomal dominant, linked to mutations on chromosomes 1, 14, and 21.

Autosomal dominant means if you have that gene, you get the disease.

There's no escaping it.

For familial early onset, yes.

If a parent has it, the offspring has a 50 % chance of inheriting the gene.

And if they do, they will develop the disease.

It's a certainty.

Late onset, the much more common form, is different.

It's linked to a gene on chromosome 19 that codes for apolipoprotein E4, or APOE4.

So if you have the APOE4 gene, you're also guaranteed to get it.

No, and that's a crucial distinction.

Having the APOE4 gene significantly increases your risk, but it is not a guarantee.

Some people with the gene never develop Alzheimer's, and many people with Alzheimer's don't have the gene.

It's a risk factor, not a cause.

The text also mentions some older theories that have been mostly debunked.

I feel like everyone heard the aluminum pots and pans rumor back in the 90s.

Right.

Aluminum and antacids, or cookware, or mercury and dental fillings.

The text is clear.

The FDA has reviewed the data and says dental amalgams are safe.

There isn't definitive proof linking aluminum cookware to Alzheimer's.

Those theories have largely fallen out of favor.

But there's one study the text highlights that I absolutely loved.

It's fascinating.

The NUNS study.

This is where we get a little glimmer of hope.

Oh, this is one of the most important longitudinal studies in dementia research.

It's a group of several hundred Catholic NUNS who agreed to undergo yearly cognitive testing and then donate their brains to science upon their death.

And it's a perfect study group, isn't it?

It's an incredible study group because they're so homogenous.

They have very similar lifestyles, diets, and environments.

They don't smoke.

They don't drink heavily.

It controls for a lot of outside variables.

And what was the shocking finding?

They found that some of these NUNS had brains that upon autopsy were just full of plaques

Physically, pathologically,

they had severe Alzheimer's disease.

Their brains were riddled with it.

But when they were alive, they were fine.

They were fine.

They had no symptoms.

Their cognitive test scores were normal right up until the end.

How is that possible?

Their brains were full of the disease, but they weren't acting sick.

It doesn't make any sense.

The leading theory is something called cognitive reserve.

The researchers went back and looked at the autobiographies these NUNS wrote when they entered the convent in their early 20s.

They found that the NUNS who showed high idea density and linguistic complexity in their early writing were the ones who were protected from the symptoms later in life.

So having a more complex active brain early in life built some kind of buffer.

That's the idea.

These NUNS were constantly learning, teaching, and engaging their minds.

They essentially had so much backup connectivity in their brains, so many redundant pathways that they could bypass the damage caused by the plaques and tangles.

That is incredible.

It's like having extra roads on a map.

If the main highway gets blocked by a plaque, your brain just says, no problem, I'll take these side streets I built 50 years ago.

That's a perfect analogy.

It doesn't stop the underlying disease process, but it can mask the symptoms, allowing you to function at a high level for much longer.

It's a powerful argument for lifelong learning.

So when the symptoms do eventually show up, the text groups them into the forays.

I think this is a really helpful framework for remembering what to look for clinically.

The first A is amnesia.

Right.

Memory loss.

But it's a specific pattern.

Short -term memory goes first.

They can't remember what they had for breakfast, but they can tell you a detailed story from their wedding 60 years ago.

Long -term memory is the last to go.

And this leads to that regression we hear about.

Exactly.

The text mentions a woman confusing her 50 -year -old son for her deceased husband, because in her mind, she's living in a time when her husband was that age.

She's living in 1980, not 2024.

That's just heartbreaking.

The second A is aphasia.

Language disturbance.

This can be expressive aphasia.

They know what they want to say, but they can't find the words.

They might describe a watch as the thing you tell time with on your arm.

Or it can be receptive aphasia, not being able to understand what is said to you.

It's a fundamental communication breakdown.

The third A is apraxia.

This one is the inability to perform purposeful modi tasks despite having intact motor function.

So you have the muscles to put on a shirt.

You have the flexibility.

Your arm works fine.

But your brain has lost the blueprint, the sequence of steps for how to do it.

You might stare at the shirt and not know which hole your head goes in or try to put both legs through one sleeve.

The knowledge of the action is gone.

And the fourth A, agnosia.

This is the failure to recognize familiar objects or people.

The text gives the classic example of using a fork to comb your hair.

You see the fork.

Your eyes work perfectly.

But the concept of fork is gone.

It's just an object with tines that looks like it could work on hair.

Or, more painfully, not recognizing your own spouse or child.

Beyond the four As, there are these other behaviors that make caregiving so incredibly hard.

Sundowning is a famous one.

Yes, sundowning syndrome.

It's a marked increase in agitation, restlessness, and confusion that hits in the late afternoon and early evening after about 4 .30 p .m.

As the sun goes down, the confusion goes up.

It's very common and very, very exhausting for caregivers.

And confabulation.

This one is so tricky because it just sounds like lying.

It does, but it's unconscious.

It's not malicious.

The patient has a memory gap.

Someone asks, what did you do today?

They don't know.

To save face or just to make sense of a confusing world, their brain fills in that gap with a made -up but often plausible story.

I went to lunch with the president.

They aren't trying to deceive you.

In that moment, they believe it.

It's a defense mechanism against the void.

And then there are delusions.

How are these different from, say, the delusions in schizophrenia?

It's a great question.

Schizophrenic delusions are often bizarre.

Aliens have implanted a chip in my brain.

The CIA is beaming thoughts at me.

Alzheimer's delusions are usually much more reality -based, but false.

Someone stole my mortgage papers.

My spouse is having an affair.

They are rooted in the mundane world of family and finances, which almost makes them harder to fact check sometimes because they sound plausible.

OK, we have covered the giant that is Alzheimer's, but the text lists several other irreversible dementias.

We need to distinguish these because the presentation and the care can be really different.

Let's start with vascular dementia.

This is the second most common type of dementia.

It's not caused by plaques and tangles, but by multiple small strokes or other vascular lesions that cut off blood flow to parts of the brain.

How is the progression different from Alzheimer's?

You said Alzheimer's is a smooth downward slope.

Vascular dementia is described as stepwise.

It's a different pattern of decline.

The person is stable on a plateau of functioning.

Then they have a small stroke, maybe a silent one they don't even notice physically, and their cognitive ability suddenly drops a level.

Then they plateau at that new lower level for a while.

Then another stroke, another drop.

It's a series of steps down, not a smooth slide.

And the text says speech is often preserved longer than in Alzheimer's.

Yes, that's a common finding.

Unlike Alzheimer's, where word finding goes relatively early, vascular patients can often keep their language skills longer.

But the risk factors are the same ones as for stroke.

Hypertension, diabetes, high cholesterol.

The clinical example is Mr.

Babb.

He had a history of TIAs and a car accident.

He was confused about dates, but could still do complex math.

Certain parts of his brain were working perfectly, while others were offline due to lack of blood flow.

Then there is frontotemporal lobe dementia, also known as Pick's disease.

This one seems particularly cool for the family.

It is, in a unique way.

This one involves atrophy, or shrinking, of the frontal and anterior temporal lobes first.

And remember, from basic neuroanatomy, the frontal lobes are our breaks.

They control personality, impulse control, judgment, and social appropriateness.

The text uses the word disinhibition.

That is the key symptom, the core feature.

The example in the book is Mrs.

Brewer.

She was found nude in the foyer of her assisted living facility, cursing at the staff.

Her memory was relatively good.

She knew where she was, she knew who the staff were.

But her judgment, her filter, her sense of what is socially acceptable, was completely gone.

So if you see drastic personality changes, and social inappropriateness before the major memory loss kicks in, you should think frontotemporal.

Exactly.

With Alzheimer's, memory goes first.

With FTD, the personality goes first.

What about Parkinson's -related dementia?

About 10 % of people with Parkinson's disease develop dementia annually.

But here is the drug dilemma that the text highlights.

It's a real clinical catch -22.

Right.

Parkinson's is caused by a lack of dopamine.

So you give drugs to increase dopamine to help with the movement symptoms, the stiffness, the tremors.

Correct.

But a side effect of high dopamine levels in the brain can be hallucinations and psychosis.

So if you then give antipsychotic drugs to stop the hallucinations, and most of those drugs work by blocking dopamine,

you make the Parkinson's stiffness and tremors much, much worse.

You're stuck between a rock and a hard place.

Yeah.

You can either help them move or help them not see things.

But it's very hard to do both.

The example was Mr.

McGreevey, who had to balance his ability to walk against seeing visual hallucinations.

It's a very difficult clinical balance.

You often have to explain to the family that we may have to tolerate some mild, non -threatening hallucinations in order to keep their loved one mobile and prevent falls.

Which brings us to a related condition.

Dementia with Lewy bodies or DLB?

This is similar to Parkinson's in some ways, but distinct.

In DLB, the Lewy bodies, which are abnormal protein deposits, are found throughout the cortex, not just in the substantia nigra like in Parkinson's.

The key feature here, the one you have to know for your exams, is fluctuation.

Wild swings in their condition.

Wild swings.

They can be lucid and completely themselves one day and then profoundly confused and psychotic the next.

And they have extreme dangerous sensitivity to anti -psychotic medications.

The text mentions a black box warning on these drugs for this population.

Yes.

Giving a patient with Lewy body dementia a standard anti -psychotic, especially an older one, can be very dangerous.

Even fatal.

It can cause a severe reaction called neuroleptic malignant syndrome.

You have to be incredibly careful.

Let's move through the last few quickly.

Quadesfeld -Jacob disease or CJD.

This is the scary one, the really scary one.

It is.

It's a prion disease.

Prions are misfolded proteins that cause other proteins to misfold in a chain reaction.

This leads to what's called spongiform encephalopathy.

The brain tissue literally develops holes in it until it looks like a sponge.

Like mad cow disease.

It's the human variant.

It is incredibly rapid and universally fatal.

90 % of people diagnosed die within one year.

It's contagious via neural tissue or bodily fluids, so there are specific precautions for health care workers.

The example, Mrs.

Mercer, went from hostility to blindness to myoclonic jerks and death in a matter of months.

It is just devastatingly fast.

Then there's AIDS dementia complex.

This occurs in the late stages of HIV, as the virus directly affects the brain, causing cortical atrophy.

It often happens in younger patients, like the example of Mrs.

Halston, who is only 36.

It causes agitation, apathy, and memory loss.

An alcohol -related dementia.

We have two terms here that students always mix up.

Wernicke's and Korsakoff's.

Can you distinguish them for us?

Absolutely.

Wernicke's encephalopathy is the acute phase.

It's a medical emergency.

You see a classic triad of confusion, ataxia, which is an unsteady, staggering walk, and specific eye movement issues.

It's caused by a severe thiamine or vitamin B1 deficiency.

If you treat it with high -dose intravenous thiamine immediately, it can be reversed.

And if you don't, if you miss it.

It progresses to Korsakoff's syndrome.

This is the chronic, irreversible phase.

The hallmark is profound.

Antigrade amnesia.

You cannot make new memories.

You are effectively stuck in the past.

And you see major, major confabulation.

They will tell you elaborate, detailed stories to mask the fact that they can't remember what happened five minutes ago.

And finally, Huntington's disease.

This is a purely genetic disorder.

It's autosomal dominant, caused by a mutation on chromosome 4.

It involves what are called CAG repeats in the DNA.

This is the gene sequencing part that's so predictive.

Right.

If you have a normal number of these CAG repeats, you're fine.

If you have more than 40 repeats of that sequence, you will get the disease.

There is no maybe.

It causes a triad of symptoms.

Correa, which are these involuntary, jerky, dance -like movements, personality changes, and eventually a severe dementia.

And the ethical dilemma is massive here, because it usually hits in the prime of life, the 30s or 40s.

If your parent has it, you have a 50 % chance of having the gene.

Do you get tested?

That is the agonizing question.

To test or not to test?

If you test positive, you know your fate.

Does that knowledge ruin the good years you have left?

Or does it allow you to plan your life, to make decisions about career and family?

And if you have kids, you know you might have passed it on.

It is an incredibly heavy burden.

We've covered a lot of devastating diseases.

Now let's talk about what the nurse actually does.

Section five, psychotherapeutic management.

This is the practical toolkit.

What can we do?

The nurse's role is absolutely critical.

Let's start with communication.

The golden rule from the text is live in the moment.

Because they can't access the past or the future reliably.

Correct.

So you join them in their reality, in the now.

And nonverbal communication is key.

A smile, gentle touch, making eye contact.

They might not understand your words, but they can read your tone and your body language.

If you are stressed and anxious, they will become agitated.

Your calm is contagious.

The text also says to avoid things like sarcasm and metaphors.

Yes.

Their thinking is concrete.

If you say, it's raining cats and dogs, they might get anxious and look out the window for the animals.

Keep your sentences short and simple.

And most importantly, do not argue.

Do not try to reorient them to reality if they are distressed.

Can you give an example of that?

Sure.

If a patient is watching a TV drama and thinks it's a real argument happening in the room, do not say, that's not real.

It's just a TV show.

You can't debate someone whose brain isn't processing reality correctly.

You'll just escalate their agitation.

Instead, you validate the emotion.

Sounds like those people are very angry.

And then you redirect, that looks upsetting.

Let's go over here and get a snack.

Validate, then redirect.

What about care strategies for daily life?

Routine is everything.

The text emphasizes this.

Do the same thing at the same time every day.

It provides a scaffold for them when their internal clock is broken.

For nutrition, finger foods are great for patients who wander.

They can eat while they walk.

And they often develop a preference for sweet foods, so you can use that to keep their calorie count up.

And of course, assess their swallowing constantly to prevent aspiration.

And the wandering.

This is such a huge safety risk.

How do we manage that without using restraints?

We want to avoid restraints at all costs.

So you manage the environment,

create continuous walking paths, like circular hallways, so they don't hit dead ends and get frustrated.

But my favorite tip from the text is camouflaging the exits.

Like painting the door to look like the wall?

Yes.

Or paint it to look like a bookshelf.

Put a beautiful mural on it.

If it doesn't look like a door, they often won't even try to open it.

It just blends into the background.

That's brilliant.

But there was a very specific warning about floor mats that I found fascinating.

Ah, yes.

The black mat phenomenon.

This is a critical safety tip.

Do not paint a black hole on the floor.

And do not put a solid black mat in front of a door.

Why not?

Because of changes in depth perception and contrast sensitivity in the aging brain.

To a dementia patient, a dark black mat on a light -colored floor doesn't look like a mat.

It looks like a bottomless pit.

A hole.

A hole in the floor so they'll be terrified to cross it.

Exactly.

They might stop dead in their tracks, refusing to move and getting very agitated.

Or, even worse, they might try to jump over it.

You have an 85 -year -old trying to broad jump a welcome mat.

That is a recipe for a broken hip.

A catastrophic fall.

It's a very specific, practical detail that shows you have to learn to see the world through their eyes, not your own.

What about meds?

We talk about benadryl being bad.

What is good?

What can we use?

For Alzheimer's, the main class of drugs is the cholinesterase inhibitors.

These are drugs like Dunpecel, Aricept, Ribostigmine, Exelon, and Galantamine.

How do they work?

What's cholinesterase?

OK, so remember how Alzheimer's destroys the cells that make acetylcholine?

These drugs can't stop that.

But what they can do is make the most of the acetylcholine that's left.

There's an enzyme in the brain called acetylcholinesterase that acts like a little janitor, sweeping up and breaking down acetylcholine after it's used in the synapse.

So these drugs, they fire the janitor.

That's a great way to put it.

They inhibit that enzyme.

By blocking the janitor, they leave more acetylcholine in the synapse for a longer period of time, which boosts the signal and helps with memory and thinking.

But the text gives a pretty stark reality check about what these drugs can and can't do.

They do.

It's so important to understand they do not cure the disease.

They do not stop the progression.

They mask the deterioration for a time.

They can buy, on average, six months to a year of better functioning.

But if you stop the drug, the patient doesn't just go back to where they were.

They crash down to where they would have been without the drug all along.

It can be a very precipitous drop.

And there was one other main drug, Mementine, which is sold as Namenda.

Right.

And it works completely differently.

It blocks a neurotransmitter called glutamate.

In Alzheimer's, damaged cells can leak too much glutamate, which causes something called excitotoxicity.

It literally excites the neighboring neurons to death.

Mementine helps to calm that process down.

It's used for moderate to severe AD, often in combination with a drug like Aricept.

OK, let's bring all of this to life with the case study of Roberta Evans.

This story really helped me see the whole progression.

It's a great case study.

Roberta is an 81 -year -old retired teacher.

She was fiercely independent, lived alone.

But the first sign wasn't her forgetting things.

It was her judgment.

She got scammed out of $1 ,000 by con artists who called her on the phone.

That was the red flag.

The executive function, the scam detector, and the frontal lobe failed first.

Exactly.

Then when her son disabled her car to keep her safe, she started wandering the streets.

She was eventually found by social services, living in filth, forgetting to eat or bathe.

She was diagnosed with Alzheimer's.

Her score on the mini mental state exam, the MMSE, was 23 out of 30.

Which is in the mild to moderate range.

But her reaction to the diagnosis was classic.

I'm not crazy.

She had total denial and a complete lack of insight into her deficits, which is also a symptom of the disease.

The care plan was so interesting because they didn't just throw a prescription at her.

No.

The first thing they did was address her other health problems.

They found she had untreated diabetes.

She had literally forgotten she had it, so her blood sugar was out of control, which makes cognition much worse.

They got that under control.

Then they moved her to an assisted living facility for safety and structure.

And she responded to the cholinesterase inhibitors, to the Aricept.

She did.

The medication and the new structured environment helped stabilize her.

She lived for three more years in that assisted living facility before her decline required a full nursing home.

It's a bittersweet success story.

The drugs and the care didn't cure her, but they bought her three years of safety, dignity and relative independence.

And that really defines the nurse's role, doesn't it?

You aren't fixing the brain.

You are preserving the person for as long as you possibly can.

Exactly.

The transition from independence to needing care is a fall, a long, slow fall.

The nurse is there to catch them gently and make the landing as soft as possible.

So we have reached the end of our deep dive.

This was a lot.

It's a heavy topic.

To recap,

cognitive disorders are a spectrum.

Delirium is a medical emergency.

You have to fix the body to save the brain.

And Alzheimer's is the big one.

The irreversible structural change.

And the golden rule from the text, promote maximum functioning and have patience.

Patience is everything.

You have to have an endless supply of it.

I want to leave everyone with a provocative thought, something to chew on going back to that genetic section.

We know we can test for Huntington's with almost 100 % certainty.

And we're getting closer to predictive tests for Alzheimer's.

So the question is, if you could get a blood test right now that told you with certainty that in 20 years you would lose your mind,

would you want to know?

It's the ultimate question, isn't it?

Is that knowledge a power that lets you live your remaining good years to the fullest?

Or is it a crushing burden that ruins the time you have left?

Something to mull over.

Thank you so much for joining us on this deep dive into the mind.

Thank you.

It was a pleasure.

This is the last minute lecture team signing off.