Cognitive Impairment Pt 1 Flashcards
define conition
delirium
dementia
neurocognitive disorder
pseudodementia
Terminology with the root ‘cog’
- Cognition: That operation of the mind by which we become aware of objects of
thought or perception; it includes all aspects of perceiving, thinking, and
remembering. - Delirium: A clinical state characterized by fluctuating disturbances in cognition,
mood, attention, arousal, and self-awareness, which arises acutely either without
prior intellectual impairment or superimposed on chronic intellectual impairment. - Dementia: A deterioration of intellectual function and other cognitive skills, leading
to a decline in the ability to perform activities of daily living (ADL). - Neurocognitive Disorder: Term used in DSM-V for cognitive impairment, including
dementia and amnestic disorder. - Pseudodementia: Dementia is mimicked by functional psychiatric illness.
- Terminology with the root ‘cog’ - recognize, incognito, precognition, cognizant
Dementia - Terminology
alzhemier’s disease
vascular dementias
lewy body dementia
fronto temporal dementias
other dementias
- Not one specific disease
- Impacts memory, behaviour, thinking, social ability
- A deterioration of intellectual function and other cognitive skills
- Interferes with function
- The public’s assumption:
- cognition = memory
Epidemiology - Sex
Epidemiology - SES
Absolute 10-year risk
of Alzheimer disease,
vascular dementia
and all dementia for
APOE genotypes
stratified by sex and
age groups.
women are usually affected more than men. And that’s true for all the age groups, and it’s true for all the different risks. And even here we have some genetic breakdown. Even based on the same genetics, women are at higher risk.
Second, it’s also associated with age.
So when people are in their 60s, yes, there are a few people that will develop dementia that’s still considered relatively young for dementia, we see this normally in the late seventies and eighties
It’s something that is onset in later life. So the longer we extend our life expectancy, the more we anticipate seeing dementia increase.
read WHO
G20
Canada’s Dementia Strategy
- Prioritize quality of life for people living with
dementia and caregivers - Respect and value diversity to ensure an
inclusive approach, with a focus on those
most at risk or with distinct needs - Respect the human rights of people living
with dementia to support their autonomy and
dignity - Engage in evidence-informed decision
making, taking a broad approach to gathering
and sharing best available knowledge and
data - Maintain a results-focused approach to
tracking progress, including evaluating and
adjusting actions as needed.
none of these statements particularly talk about medications. They’re a little bit more realistic, such as supporting people. I’m respecting their rights, engaging them
Cognitive Impairment
Medical Conditions
Examples
- Neuro/Psych
- Depression
- Seizure
- Trauma
- Endocrine
- hypothyroidism
- Nutritional
- B12 deficiency
- Infection
- Pneumonia
- COVID
- Sensory decline
- Vision impairment
- Hearing loss
- Pulmonary
- Hypoxia (COPD)
Cognitive Impairment
Medications
- Direct action
- Anticholinergics
- Psychotropic
- Benzodiazepines
- Neuroleptics
- Ethanol
- Opioids
- Indirect action
- Diuretics
- e.g. electrolyte abnormality
- Withdrawal of medications
Anticholingecis: acetylcholine is essential for cognitive function. And when we block acetylcholine, we impair cognitive function. So most of you have enough reserve. You could take a single dose of diphenhydramine or dimenhydrinate and you might be a bit sleepy.If we give an anti-cholinergic like that to say an older person, particularly who is frail, they could look like they get zero out of 30 on a cognitive test. It can be so impairing.
- evidence now that long-term use of anticholinergics. Might lead predispose people to develop dementia.
psychotropic medications, many of them also have anti-cholinergic effects
Indirectly acting. So these are medications where the side effect is something that will disrupt cognition. So the most common is actually diuretics leading to an electrolyte abnormality and then people get confused. Then withdrawal of medications. So something like a benzo or someone is changing seizure medications that can also lead to patients being confused
Assessment
?
Cognitive Changes and Domains Affected
* The A’s
- Aphasia – word finding, incomplete sentences,
conversation - Apraxia – purposeful movement (e.g. dressing)
- Agnosia – recognition (e.g. people, place)
- Abstraction (executive function)
- ADLs
Brief Screening Tools
- MMSE (Folstein)
- Used since 1970’s
- Required by FDA in drug trials
- Must pay licensing fees to use
- MoCA (Montreal Cognitive Assessment)
- Assesses executive function
- Developed to diagnose MCI
- Others introduced in Alberta
- SLUMS (St Louis University Mental Status Examination)
- RUDAS (Rowland Universal Dementia Assessment Scale)
- Administered by trained healthcare professionals
- Inform diagnosis but not definitive on their own
using SLUMS now
moca is a bit, has a few more questions that had that test executive function. So usually the scores are a little bit lower because that’s our highest level of cognitive function. It’s a harder test.
Further Investigation
moca is a bit, has a few more questions that had that test executive function. So usually the scores are a little bit lower because that’s our highest level of cognitive function. It’s a harder test.
how many seeds are in a watermelon? And some of you look a bit puzzled in this moment. So it’s not like there’s a correct answer. Or the whole point is we’re seeing how patients respond. So what might be inappropriate response there It’s more to see how they think through the problem of answering the question that’s executive function.
a trail making test. So you can see on part a, so on the left-hand side, it’s just 1234. So we ask patients to take a pen, just connect these numbers. On the second one trail be, you’ll notice there’s numbers and letters. That’s cognitively more demanding. So they have to do one a to b3c and connect those in sequence. So this is testing if patients can sequence and prioritize things, can they follow the instructions? Can they handle two tasks, cognitive tasks at the same time?
Biomarkers
* Emerging technology
* Used in research studies
* Not routine in clinical practice
- Examples
- Some sampling from blood and CSF
- Amyloid beta (1-42)
- Glial fibrillary acidic protein (GFAP) (only blood)
- Phosphorylated tau (pTau)
- Neurofilament light (NFL)
\You’ll see blood tests are done, but that’s more to rule out other things that they don’t have hypothyroidism, that their diabetes is managed. There is no B12 deficiency.
- Imaging
- CT head or MRI may be ordered\
imaging is something that is a little bit controversial. But if you’re looking up a patient on net care under diagnostic imaging, it might taste CT head or MRI of the head. And so that helps us see if there’s atrophy, if there’s loss of volume, if there is vascular damage. So it’s helpful. It’s not required by expected according to guidelines, but sometimes it is helpful
Alzheimer Disease
etiology
A progressive
degenerative disease of
the brain of unknown
etiology characterized by
diffuse atrophy
throughout the cerebral
cortex with distinctive
histopathologic changes
termed senile plaques
and neurofilbrillary
tangles
.
these are autopsy samples, photos, left, you should see a normal brain. And on the right, this is a brain with Alzheimer’s disease. So there is dramatic amount of atrophy that occurs. Some patients lose about one-third of the cortex.
We’ve had some patients that have even had brain tumors that were not detected.
there’s so much space in the cranium that actually a tumor can grow and it won’t be detected because they won’t have seizures.
- Genetics – Chromosomes 1, 14, 21
- ApoE
- Deposition of foreign bodies
- Dysregulation of neurotransmitters
- Inflammation
- Environmental agents
- Vascular risk factors
Tauopathy
beta amyloid is a large protein outside the cell. It’s called amyloid precursor protein or APP.
as protein is needed, there’s little snips of amino acids taken off. The amino acids in this simplistic diagram represented by scissors cutting the protein. And so you should have little segments of useable protein for rebuilding cell walls or whatever.
But what happens over time is the enzymes are not cutting the protein appropriately. So instead of being a creating usable proteins that help cell function, these become unusable proteins and they start to accumulate.
instead of useful protein now you have short strands, you have fibrils forming. They start to accumulate with each other. So you end up with huge pieces, huge plaques like this of unusable protein. And now enzymes cannot break it down. And it just interferes with cell function. So it’s interfering between cells. So this is extracellular.
\At the same time, you have an internal problem within the cells. Instead of just being a clap? structure, cells have three-dimensional shape because of tubules, microtubules. So it gives us cell shape, but it also helps with moving enzymes,different materials throughout the cell. So it’s a bit of a transport mechanism within the cell. So in Alzheimer disease we have these plaques happening outside the cell and within the cell, these microtubules are collapsing. So instead of being nice tubes, they end up just being here what they call tangled clumps of tau protein. So essentially we have a protein processing disorder.
what we end up with is a brain that has plaques, intracellular and collapsed structure, intracellular. And in the end, the cells cannot communicate with each other and they can’t function with this collapse structure and they die.
Pathophysiology
- Extracellular beta-amyloid
- Intracellular NFT
* These changes result in:
* Abnormalities in cell metabolism
* Cell death
Risk Factors
- Numerous methods of categorizing
- Modifiable, non-modifiable
- Social, physical
- Brain, external to the brain
- Etc.\
- 40% of cases are potentially
preventable based on 12
modifiable risk factors
it’s showing at the top. They even have early life in the top. And how important formal education is. Of course, children learn things whether they’re in school or not. But that kind of structured demand on cognitive function. Where students have to learn, they have to study math and languages and geography, et cetera. Those types of things are really important, really early on in terms of brain development. So the trajectory is that someone is less likely to develop dementia later on
in later life, we start to see a quite a big role for smoking. I already mentioned depression. Depression might mimic dementia, but also over a long period of time. It does affect the brain and people are at higher risk.
all of the risks really are things that start much earlier in life.
in midlife, you might be surprised that hearing loss is so large. Hearing loss has a few different roles there. It’s actually a neurodegenerative condition as well. But it’s also because when you don’t hear things, you are not as engaged. You’re not have as much cognitive demand. So you kinda live, we say in a little bubble or your world is a bit smaller.
traumatic brain injury, of course, damaging the brain, but hypertension contributes 2%\
Alcohol, 21 units per week, that’s a fair bit, contributes about as much as obesity. So this is midlife.
their bottom line is about 60% of the risks aren’t really known
Risk Factors – Non-Modifiable
- Age
- Female sex
- Especially after age 80y
- Head circumference
- Related to Down Syndrome
- Family history
- Genetics
- Carrying at least one APOE4 allele
