All right. Thank you, everyone, for

having me here and thank you,

everyone, for coming.

So my name is Karen Bardwell

and I'm one of the geriatric fellows

and I'm presenting on Pakistan ISM

features as a result of aging.

The reason why I picked this topic

is because as our older population

continues to age and as more baby

boomers enter the elderly age,

we're beginning to see a lot more

Parkinson features, especially among

older adults.

And a lot of times we see these

patients in clinic and we wonder,

is this someone who should I

be suspicious for Parkinson's?

They're awfully they're walking

awfully slow right now.

I think they may have a shuffling

gait. Is this something that I

should be concerned enough that I

need to refer to a

neurologist for establishing a

diagnosis of Parkinson's?

So I want to shed light that

Pakistan has some features can occur

as a result of aging as well.

So first thing I want to say is I

have no financial disclosures or

conflicts of interest with the

materials in the presentation.

And so our objective today is we're

going to be describing the nature

and the prevalence of Parkinsonism

features as a result of aging.

And I also want to help with

distinguishing Parkinson's disease

from other causes of Parkinsonism.

So let's delve into a case here.

And this was actually a case that I

saw while I was working in the

Movement Disorders Clinic.

And we have an 80 year old gentleman

who presented with the chief

complaint of generalized slowing of

gait in the last twelve months

with reduced arm swing bilaterally.

He's also complaining of multiple

falls in the last six months.

Patient also complains that he has

had dreams that can behavior

which he has controlled melatonin,

50 milligrams at bedtime as well as

clonazepam, one milligram at

bedtime.

He complains that he has both a

diminished sense of taste and smell.

Also, he complains that

he's had multiple episodes of

Precint happy in the last two months

out of. He was recently Star Alphas

and Alpha Zosyn for

BPH. In addition to already being

on hydrochlorothiazide and

lisinopril for hypertension,

pertinent negatives in this case.

So he does not have a resting

tremor.

He denies any constipation,

denies any bowel movement changes,

and General denies any behavior

changes and has no hallucinations

or delusions.

When reviewing his medications, you

don't see that he's on any dopamine

blocking agents.

He is noted to have some mild

cognitive impairment.

So dropping a little bit further

into this case

before the patient came to the

Movement Disorders Clinic, they

already saw a neurologist and

there was a suspicion for

Parkinson's plus syndrome.

The reason for this is that the

patient possessed multiple

Parkinsonism features, but also

had frequent falling and orthostatic

symptoms. And there was a concern

for this autonomic.

And therefore, diagnostic

testing was performed prior to the

patient coming into the clinic,

including an MRI brain which didn't

show any structural lesions or askey

make changes.

A DOT scan, which I'm gonna go into,

but basically a scan,

as you can see, in the top right

corner.

It basically received

injection of eye open flooring and

basically is taken up by the

dopamine pathways.

And as you could see at the top over

here on the image,

the left side shows a normal

scan where it's a comma shaped

appearance denoting that the

dopamine pathways are intact

and that that's, again, on the right

side shows decreased uptake.

Showing that probably something

that's consistent with Parkinson's

disease.

Furthermore, the patient already had

table till testing.

And this is a test that's done to

assess for multiple system

atrophy, which is one of the

Parkinson's plus syndrome, which was

our deposit for Ortho Stacie's.

In fact, his blood pressure dropped

from a systolic of 162 to 97.

He was ultimately referred to the

Movement Disorders Clinic because it

was the concern for Parkinson's plus

syndrome.

And to establish his final

diagnosis.

So let's

so question what is the most

plausible diagnosis at this time?

So we have a Parkinson's plus

syndrome, B, Parkinson's disease, or

C, age related Parkinsonism.

All right. I'll see. Yes.

Everyone got it. Just like the title

of my presentation.

So age related, Parkinsonism,

is the diagnosis here.

And I'm going to delve into this a

little bit more as to why.

But.

Let's go over the differential

diagnosis. Let's just say you don't

know. And what are some

diagnoses that you would consider at

this time? Well, one Parkinson's

disease, he possesses a lot of

features with that Parkinson's

plus syndrome.

Perhaps he's demonstrating some

orthostatic symptoms.

Could this be a sign of.

Could this be a sign of multiple

system atrophy,

dementia with Lewy bodies?

Drug induced Parkinsonism.

Although we already noted that he

wasn't on any dopamine blocking

agents as well as age related

Parkinsonism.

So Parkinson's disease is a neuro

degenerative process.

Right. We lose our dopaminergic

neurons specifically in our nitrous

tritle pathway.

As a result, we see a lot of the

symptoms as we have,

including Braddick.

Brady.

Brady. Conesa, rigidity,

postural changes, etc..

Parkinson's Plus Syndrome is a group

of disorders with defining

features are similar to Parkinson's,

but also have faster progression.

And the U.S. have an impaired

responsiveness to leave a dopa

carbon dopa, including the three

that we talked about multi-system

atrophy, which is characterized by

disordered Naamua, progressive

supranuclear palsy, which is

characterized with

ocular paresis, as well as axial

rigidity and frequent falling and

cortical Basle syndrome, which is

characterized by prominent apraxia.

So what I want to discuss here

is that we see a lot of signs of

Parkinsonism in our clinic as well.

They're frequently found in the

older adults who don't actually have

Parkinson's disease.

We see a lot of patients who have

braided Kornelia.

We do see a lot of patients who are

partial and instabilities

specifically with hyper kyphosis.

We do see some patients that just

look like they're pretty rigid

at baseline and sometimes they have

resting tremor or sometimes they

could have kinetic tremors.

But Parkinsonism, signs are

seen in our population.

So looking at it, there was a study

that was done in East Boston,

Massachusetts, that was published in

1996, which actually investigated

the prevalence of Parkinsonism signs

in the elderly population.

They looked at patients over the age

of 65 and did a structural

neurological examination among

community dwelling adults.

And out of 467

attitude individuals.

Hundred and fifty nine had a

partisanism.

And for sure, we don't have one

hundred fifty nine out of foreign or

67 individuals with Parkinson's

disease.

They also noted that the prevalence

was markedly increased with age.

Over the over eighty.

So this is their results from the

study. And this is a busy slide.

But I just wanted everyone to pay

attention to the red boxes here.

They stratified.

They stratified according to age.

And as we could see here,

as the age goes up specifically

above 85, we start to see a lot

more, a more more prevalence

of a lot of these symptoms or

Greater Conesa. We've seen as much

as 37 percent of individuals

gave disturbance, was seen quite

prominently in 52 percent of

individuals.

Rigidity and tremor were also noted

as well. And then generalized

Parkinsonism ism was seen in about

50 percent of patients.

So it is quite common.

There was another study published by

Dr. Buchmann and colleagues

in 2016 which actually looked at

2001 elderly individuals

that were aged about 77 years old

and median age initially without

Parkinsonism, and followed them over

five years to investigate the

development of Parkinsonism in

five years, nine hundred sixty

four out of 2001, individuals do

up Parkinsonism, which was defined

as having two out of the four

cardinal features of

the symptoms Parkinsonia.

Parkinsonism gate was the most

common and they found that

Parkinsonism was associate with

H, but not with sex or education.

And there may be some other symptoms

that may be involved that might be

causing us, such as sleep disorders,

neuroticism,

etc. But

basically there might be some other

conditions that might be associated

with it, but couldn't infer

causality from this.

So what actually happens

or what actually happens in older

adults? Well.

As we know, the.

That's in the in Parkinson's

disease, we have the Negress radio

pathway, right.

Which is regulated by dopamine,

but in older adults.

Out of all the systems, that extra

pyramidal system actually gets quite

affected just secondary to age.

And a lot of these individuals may

have slowing up their movement.

As a result, they may have a gait

disorder as a result, postural

instability.

And as a result, they'll have

difficulty with balance, resulting

in false.

The extra pyramidal system that's

affected in older adults constitutes

a lot more than the Negroes.

Frido, Padthaway.

There's other pathways involved as

well, including the cerebellum,

including the cortical spinal track.

But one thing to note about extra

pyramid's system is that it

modulates the movement so

as elderly individuals start losing

this function. You can start seeing

a lot of common signs that are

related to Parkinsonism.

So slowing of movement

and in fact, about 15

to 30 percent of individuals, older

adults have.

Or at least its movement

slows down by 50 to 30 percent

in older adults compared to younger

adults.

And they have.

Has been demonstrated in literature

that they have decreased peak

velocity and prolonged deceleration,

which may serve a evolutionary

purpose because accuracy is for

favored over speed.

Especially important for elderly

individuals to prevent injuries and

prevent falls. So this is

so slowing a movement is definitely

something that we see.

Now, postural instability, hyper

kyphosis, we see a lot of

individuals in our clinic who have

hyper kyphosis doesn't mean they

have Parkinson's disease.

This could be multifactorial.

So bone changes, low betrayal of

bone mineral density, having any

compression fractures or

osteoarthritis.

Muscle changes, cells.

A lot of patients may have poor

spinal extensor weakness.

And then finally, CNS changes, as we

talked about with the extra pair

metal system.

The brain's adjustment of the Paris

spinal musculature can lead to hyper

kyphosis as well.

So.

Moving on. So which one of these

features is not a common early sign

of Parkinson's disease?

Yep. So the answer is B.

So as we know, Parkinson's

disease, especially early

Parkinson's disease, you can

definitely have an impairment of

smell.

Constipation is one of the changes

that we see. And in REM sleep

behavior disorder.

So I just want to go a little bit

into this as well and discuss how

this could be a result of aging as

well.

So olfaction, as we know,

we have multiple olfactory receptors

in our nose which are able to detect

the detect the smell

and then transmit it to our brain.

There was actually a study that

reported that about 62 percent

of individuals have olfactory

impairment.

This is most prominent over the age

of 80.

And not really so prominent between

the age of 60 and 80.

And this is due to the fact that we

just lose a lot of our olfactory

bulbs.

And as well as our CNS processing

also decreases with age as well.

And finally, REM sleep behavior

disorder, as we know, this

is an early finding of Parkinson's

disease where people

begin to act up their dreams

secondary to not being

secondary to not having the

paralysis effect of being in REM

sleep.

It is usually one of the earliest

manifestations.

However, there is a good proportion

of patients who don't have who just

have isolated REM sleep behavior

disorder.

Add up to 60 percent are idiopathic.

It is important to note that they

are associate with alpha synuclein

diseases as well as narcolepsy.

And therefore a lot of these

individuals will achey

progressed to having one of these

diseases in the end.

But it's important to know that REM

sleep behavior disorder can occur

as an isolated phenomenon.

So back to our patient.

So our table tilt testing was

positive, and I guess one of the

pearls about this is that when

anyone is to perform table till

testing, we should probably

take them off all their

antihypertensive.

This can really affect the test.

And this is definitely a pearled

that a lot of the movement disorder

specialists have tried to

up, have tried to preach as well.

The scan,

at least in this individual.

So this is a unique case in that

we already had a desk and done was

show normal radio tracer uptake in

the tribal areas, demonstrating

that the dopamine pathways were

completely intact because we

already had the scan.

We therefore did not try at

therapeutic dose of leave a dopa

carbon dopa because we had a normal

death scan and we were already

concerned for Ortho Stacie's and

therefore we did not place this

person on these on this medications.

And instead recommendations were

placed for a formal exercise

program.

Now, how does this relate to

clinical practice?

Well.

Parkinson's disease is the clinical

diagnosis and has

always been I guess we

just had the benefit of having a CAT

scan here. So what happens if we see

this patient in our clinic

who we are concerned for Parkinson's

disease, and

we are also aware that Parkinson's

signs can also occur as a result

of aging?

Well, one thing we could do

is we could either refer to

neurology to make a diagnosis

or we could actually trialled them

on Sinemet ourselves.

And the purpose behind this is that

sentiment is a pretty cheap

medication.

It is a safe medication as well,

provided it don't have orthostatic

symptoms or ortho Stacie's in

general.

And if titrated correctly, you

can determine your answer in about

six weeks as to whether or not they

respond.

And another important note to make

is that Levodopa caba dopa

should not help with age related

Parkinsonism because age related

Parkinsonism is related to the

tire extra pyramidal

system.

And therefore just replenishing

dopamine is not enough

to have these patients all of a

sudden and fix their entire system,

because as we talked about, the

experimental system makes up much

more than Legris radial pathway.

So that is something that we can

definitely do in our clinical

practice whenever we see these

patients.

So.

Going to my final take home points

Parkinsonism features as a result of

aging are quite common

in the older population.

This is especially true for patients

over the age of 80.

And a lot of these patients we see

us do posture some

British Canisius lowness shuffling

gait. And because of this, they are

at increased risk of fall.

It is difficult to distinguish age

related Parkinsonism from

Parkinson's disease and the primary

care setting and therefore a

therapeutic caba don't believe a

DOPA trial may be warranted.

And if only that that scan is

useful, if diagnosis is uncertain,

or if you're concerned for a

Parkinson's plus syndrome.

And that's the end of my presentation.