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Welcome back to The Deep Dive.
Today we're tackling a really significant area, neurocognitive disorders.
That's right.
We've drawn from a major psychiatry textbook to sort of unpack this whole spectrum.
It's quite broad, isn't it?
It goes from these really sudden crises to, well, much slower decline.
Exactly.
Our goal today is, you know, to bring some clarity.
We're looking at how these disorders are diagnosed, what separates the acute from the chronic conditions, and importantly, what the science tells us now about risks and treatments.
And when we talk about the scope, it's huge.
The DSM -5 lists these cognitive domains, attention, memory, language,
motor skills, executive function, social awareness.
It really covers the core of how we think and function.
Right.
It attacks the very basics of how we interact with the world.
And, you know, something that stood out was that it's not just an older adult issue.
Not at all.
The sources clearly state that things like TBI, traumatic brain injury, or infections mean younger adults can definitely be affected.
That's a crucial point.
And these cognitive issues rarely show up alone.
They often come bundled with significant psychiatric symptoms, things like depression, anxiety, even psychosis.
The diagnosis is really challenging.
Okay.
So let's start with the really acute side, the emergency.
Delirium.
This is the one with the sudden onset hours or days.
And that key feature is the fluctuation, right?
The disturbance in attention and awareness just waxes and wanes.
Yes.
And here's a striking thing, what we might call the prevalence paradox.
Delirium is incredibly common in hospitals.
How common?
Well, figures suggest maybe 14 to 24 percent of patients have it on admission.
And during the hospital stay, it can jump up to 56 percent.
Wow.
But here's the paradox.
Estimates are that 40, maybe even 60 percent of these cases are missed or misdiagnosed.
That seems incredibly high for something so serious, especially since it's not new.
You mentioned Hippocrates described a case.
Over 2 ,400 years ago.
Orosinus, the case was called.
Yeah.
He noted the agitation, the coherence and that key thing, the fluctuation.
So yeah, it's an ancient problem we're still struggling with.
Why is it missed so often then?
Often it boils down to not getting a good history.
You absolutely need input from a caretaker or family member because the patient themselves is confused.
Right.
You can't rely on their account.
Exactly.
And clinically, the tool we lean on is the confusion assessment method or CAM.
CAM.
Okay.
So it looks at four main things.
The acute onset, the inattention and fluctuation, disorganized thinking and altered consciousness.
In a busy ward, which of those is the absolute must catch sign?
The fluctuation combined with inattention.
That variability is the hallmark.
If someone's mental state is bouncing around over hours or even minutes, maybe clear now, confused later, you have to suspect delirium.
And there are different types, right?
One's easier to overlook.
Definitely.
Hypoactive delirium.
This is the quiet, sluggish, lethargic patient.
It often gets mistaken for depression, especially in older folks.
They don't cause trouble, so they slip by.
The hyperactive or mixed types are more obvious agitation, maybe hallucinations.
They're thought to carry the highest risk of, well, bad outcomes, morbidity, mortality.
And this is where sundowning fits in.
Yeah.
That's the term for symptoms worsening in the evening.
Likely due to fatigue, maybe less sensory input, fewer orientation cues as the day ends.
Okay.
So let's say the underlying cause is being treated, the infection, the medication issue, whatever it is, but the patient is still agitated, maybe unsafe.
What about using medications then?
The textbook really stresses caution here.
First line is always non -pharmacological.
Like what?
The DICE method is often mentioned.
Describe, investigate, create, evaluate.
It means tackling the environment first.
Make sure they have their glasses, their hearing aids, open the blinds, let them see daylight, simple orientation cues.
But what if that's not enough?
If safety is a real concern?
Then and only then do we consider medications, but strictly off -label.
There are no FDA approved drugs specifically for delirium.
So things like anti -psychotics.
Yes, like Haloperidol.
But it's used basically as a chemical restraint for hazard mitigation, not as a treatment for the delirium itself, just enough to manage dangerous agitation or psychosis.
Minimum dose, shortest time possible.
Got it.
Hazard mitigation, not treatment.
And there's one class of drugs you really need to be careful with.
Absolute critical point.
Benzodiazepines, like lorazepam, they are essential if the delirium is from alcohol or sedative withdrawal, like in DT's delirium tremens.
Right.
But give them to a typical older patient with delirium from, say, a UTI.
You risk making the confusion much, much worse, prolonging the whole crisis, knowing that distinction is vital.
Okay, that's the acute picture.
Let's shift gears to the other side of this.
The slow, progressive decline,
major neurocognitive disorder, which we often call dementia.
Right.
The key here, according to DSM -5, is a significant cognitive decline from where the person was before.
And this is crucial.
It has to interfere with their independence in daily life.
Like managing money or taking their meds correctly.
Exactly.
Paying bills, driving complex tasks.
That loss of independence is what separates major NCD from mild neurocognitive disorder, or MCI.
MCI has cognitive decline, but the person can still function independently.
The sheer numbers here are staggering.
Globally, something like 50 million people living with dementia now.
Around that, yes.
And projected to hit 152 million by 2050.
It's a massive global health challenge.
And the source mentioned a slightly higher prevalence in women.
Yes, about 1 .17 times the age standardized rate for men.
The reasons for that are still being explored.
In terms of causes, most dementia is neurodegenerative.
Alzheimer's diseases, the big one accounts for maybe 70, 80 percent, often mixed with other things like vascular damage or Lewy bodies.
Okay, let's focus on something actionable for the listener.
Monifiable risk factors.
If someone wants to protect their brain health, what does the evidence suggest helps most.
Vascular health is huge.
Keep that blood pressure in check.
Especially in midlife, the target mentioned is below 130 systolic.
Manage cholesterol, manage diabetes.
Lifestyle stuff too.
Definitely.
Don't smoke.
Stay physically active.
Watch the alcohol the threshold mentioned was more than 21 units a week being risky.
And education seems protective too.
Building that cognitive reserve early on helps.
Oh, and be mindful of chronic use of certain meds with anti -cholinergic effects.
Like some antidepressants or bladder medications.
Yeah, those kinds of things.
Worth discussing with a doctor if used long term.
Beyond memory loss, which everyone knows about, what other clinical signs really define dementia?
Some fascinating ones.
Apraxia, for instance.
That's where you lose the ability to do learned and motor tasks.
You know what a key is?
You understand unlock the door, but you can't quite coordinate the movements to actually do it.
So the understanding is there, but the execution fails.
Precisely.
And then there's agnosia, failing to recognize objects or even yourself in the mirror eventually.
These contribute hugely to the neuropsychiatric symptoms.
Which you said affect almost everyone with AD, like 90%.
Pretty much.
Mood changes,
anxiety, personality shifts,
especially prominent in frontotemporal dementia, psychosis, agitation.
These are often what cause the most distress for caregivers.
And paranoia often shows up in a specific way.
Yes, often related to the memory loss itself.
They can't find their glasses, so the brain fills the gap with someone must have stolen them.
It's a cognitive deficit driving the paranoid thought.
With Alzheimer's specifically, what about treatments for the cognitive symptoms themselves?
We have two mainstays.
Colinesterase inhibitors like Dunpezel, rifostigmine, galantamine.
They boost acylcholine, which is depleted in AD.
They can slow the decline a bit, temporarily, mostly in mild to moderate stages.
Dunpezel is approved for severe too.
And the other class?
Memmentine.
Works on the NMDA receptor system, approved for moderate to severe AD.
But it's important to stress, none of these stop the disease.
They just might ease the slope of decline for a while.
What about those newer anti -amyloid drugs we hear about, educanumab, lacanumab, they sound like a bigger deal.
They target the underlying amyloid plaques, which is a different approach.
They got accelerated FDA approval for mild AD or MCI.
But, and this is a big but, they carry a significant risk of ARI.
Amyloid -related imaging abnormalities, basically brain swelling or micro hemorrhages that show up on MRI scans.
It requires careful monitoring, so it's a potential step forward targeting the pathology, but with real risks that need managing.
It's not a simple fix.
Right.
Let's circle back quickly to mild cognitive impairment, MCI.
You mentioned it's kind of a transitional state, but not everyone progresses.
That's right.
It's very heterogeneous.
About 10 -15 % might progress to Alzheimer's each year, but a good number stay stable, and some even revert to normal cognition.
We talk about amnestic MCI memory focused, often linked to AD and non -amnestic MCI, affecting other domains, maybe pointing towards Lewy body or FTD later.
This variability highlights why diagnosis is moving towards biology, not just symptoms.
Tell us about that ATN system.
It's primarily a research framework right now, trying to define Alzheimer's based on biomarkers.
A is for amyloid, T for tau pathology, and N for neurodegeneration or neuronal injury.
So how is this used clinically?
Amyloid PET scans are becoming more common, especially when the diagnosis isn't clear.
Their biggest value might actually be in ruling out Alzheimer's.
If there's absolutely no amyloid plaque buildup, the dementia is very unlikely to be AD.
Okay, before we wrap up the different types, let's just crystallize the difference again.
Delirium versus dementia.
The quick takeaway.
Delirium.
Acute onset.
Fluctuating course.
Altered level of consciousness.
Think clouded.
Dementia.
Gradual onset.
Progressive course.
Generally clear consciousness until late stages.
Think loss of function.
But crucially, it can happen together.
Yes.
Having dementia is a major risk factor for developing delirium on top of it.
Makes things even more complicated.
Quickly then, what about causes that aren't neurodegenerative?
These seem important because some might be fixable.
Absolutely.
There's NCD due to another medical condition.
This is why baseline labs are essential checking things like vitamin B12, thyroid function, TSH, electrolytes.
You might find hypothyroidism or lupus causing cognitive symptoms that could improve with treatment.
And substance -related causes.
Yes.
Substance medication -induced NCD.
The key here is the impairment has to last beyond the period of intoxication or withdrawal.
Like Korsakoff syndrome.
That's the classic, severe example.
Caused by thiamine deficiency,
usually from chronic heavy alcohol use.
It leads to profound amnesia, often with confabulation making things up to fill memory gaps due to permanent damage in specific brain areas like the mammillary bodies.
So whether it's fast or slow, the underlying message seems to be about thorough assessment.
Definitely.
Rule out the reversible stuff with labs.
Use imaging like CT or MRI to check for structural problems like tumors or normal pressure hydrocephalus.
Treat what you can treat.
Manage risk factors for what you can't.
Of course, the ultimate confirmation for neurodegenerative types is still neuropathology, looking at the brain tissue itself usually after death.
So we've traced this spectrum from the sudden crisis of delirium to the slow decline of major neurocognitive disorder.
It really underscores the need to differentiate the urgent from the chronic.
And to appreciate the power we do have, especially regarding those modifiable risks, managing vascular health, staying active mentally and physically, diet.
These things matter.
And that point about early detection for delirium really stuck with me.
It's critical.
That study finding a three times lower mortality rate for delirious patients identified and treated early in the ER compared to those myths.
It really drives home that being vigilant, recognizing confusion early isn't just academic.
It can literally save lives across the whole spectrum of cognitive health.
Early awareness and intervention are key.
A powerful takeaway.
Thank you for guiding us through this incredibly complex but vital topic today.