0:00

We're gonna move on to our next case three provide a

0:03

history is possible stroke.

0:05

On further digging you learn. This is a 63 year

0:08

old who is a smoker their last known

0:11

well was unconfirmed out of at the

0:14

facility that they're coming from perhaps it was two

0:17

days ago is the best guess so they're not

0:20

really a candidate for hyper acute intervention. In this

0:23

case. The chief complaint was altered mental status in on, you

0:26

know, further examination. Neurologists figure that this is mainly in

0:29

Aphasia. They also had a right arm weakness. So we do

0:32

have a focal neurologic deficit. So we're going to be looking for

0:35

abnormalities on the contralateral cerebral hemisphere that

0:38

can explain this weakness their NIH

0:41

Stroke Scale was nine and so once

0:45

again from the vignette or not,

0:48

really a TPA thrombectomy candidate and have this back in mind

0:51

when we're interpreting the Imaging, so

0:54

we're going to start off by looking at

0:57

are CT.

1:03

They're non contrast CT. I'm going to throw it

1:06

on to stroke windows.

1:09

So we can see an area of hypodensity and gray white differentiation laws indicating

1:12

a recent infarct involving

1:15

the left caught eight head interior limit

1:18

internal capsule larger region of the

1:21

superior frontal gyrus on the left and

1:24

middle frontal gyrus a little bit as well and some

1:27

spots in the center of Samoa Valley

1:30

which, you know could potentially hit the quirical spinal tract

1:33

and account for the right-sided motor

1:36

deficits seen on exam. Okay. So

1:39

our impression here is some

1:42

infarction in the less purple hemisphere, but

1:45

vascular territory is this going to be well this Superior

1:48

frontal gyrus is going to be ac/a territory. The head

1:51

of the cloud is AC territory, but this

1:54

is starting to go a little bit at the margins that

1:57

they see territory towards the AC to MCA Watershed. So

2:00

we're going to keep that in mind here.

2:05

So I measured out the hypodensity volume

2:08

just based on you know, kind of measuring length

2:11

times with times height divide by

2:14

2 about 40 milliliters and next.

2:17

We're going to look at our CTA that

2:20

followed this study.

2:25

to look for any abnormalities of the ACA or MCA

2:28

and

2:33

Well, wait for it to load here.

2:40

So it's going to be quite difficult to

2:43

tell about I'll tell you there is no large vessel occlusion. There

2:46

is

2:49

some loss of the arborization of distal ACA branches

2:52

supplying that infarctic region. So maybe there's a distal

2:55

AC occlusion, but there's

2:58

no large vessel occlusion that we could see

3:01

on the CT of the

3:04

head. You see the mca's are intact the aca's at

3:07

least proximately are patent and

3:10

the intracranial icas are pain as well.

3:13

But there is an abnormality in the neck which is the abramality

3:16

you want to focus on here. And when is zoom

3:19

in here for everyone's benefit and so

3:22

we can look at the left internal credit artery.

3:25

It's very small, right?

3:27

So here's the left internal carotid artery.

3:30

We see a bunch of plaque here. We see the the Luminous small

3:33

then we lose the contrast of pacification altogether and then

3:36

we get to the crowded bifurcation as Peyton again. So the

3:39

question for the audience is if we

3:43

can launch the poll, you know, how do we best describe

3:46

this left ICA lesion? Okay.

3:49

So again, we have contrast the

3:52

pacification here at the bifurcation. Then we have some plaque. We

3:55

don't see the contrast going

3:58

quite so well, but then we see immediate reconstitution

4:01

here at the level of the crowded ball to a

4:04

small narrowed artery.

4:07

And looks like the whole artery is smaller

4:10

much smaller than the ipsilateral external

4:14

crater artery and also smaller than the contralateral internal

4:17

provided artery all the way up into the

4:20

intracranial portion of it. But the intrapreneurial

4:23

screw bar arteries are normal in caliber.

4:31

This patient does have an anterior communicating artery. So

4:34

they have some Supply from

4:37

the contralateral side potentially.

4:42

across the Acom

4:45

supplying their ACA

4:48

But because there's this ipsilateral carotid abnormality on

4:51

a patient who has infarct and symptoms. This

4:54

is considered symptomatic carotid disease the question is how

4:57

would you describe this carotid abnormality on your

5:00

report?

5:05

okay, and a plurality shows

5:08

occlusion with retrograde filling, but I

5:11

think the best answer here is going to be near occlusion

5:14

so near occlusion is

5:18

A concept in kratosenosis where you have

5:21

such a tight stenosis that you may

5:24

not even see the Lumen very well, but it's only

5:27

for a short segment that you don't see that contrast and

5:30

may well be that the Lumen is so small. It's below the

5:33

resolution of your CTA and we know

5:36

it's not retrograde feeling because retrograde if

5:39

this were completely occluded a much longer segment of

5:42

the cervical ICA would be Nona pacified

5:45

with contrast either with thrombus or with, you know,

5:49

static column of blood because the

5:52

retrograde, you know, pushing of that contrast not gonna

5:55

come all the way down into the neck because there's no

5:58

outflow to the ICA in the neck because there

6:01

are no branches of the IC in the neck. So retrograde feeling really never

6:04

calms down all the way into the next retrograde feeling might come

6:07

down to the pair of thalamic segment to the Future segment where there

6:10

is an outflow there are branches to it, but it

6:13

is not going to calm down all the way to the neck

6:16

and instead. We have a concept called.

6:18

Near occlusion where we see the distal

6:21

vessel is opacity. It's a smaller caliber than

6:24

the contralateral side. And this is a separate entity from

6:27

conventional stenosis. So conventional stenosis are

6:30

defined by the minimal Lumen diameter divided

6:33

by the distal normal vessel

6:36

diameter. Unfortunately the distal the distal

6:39

vessel here is smaller because the stenosis

6:42

is so tight and hemodynamically significant. They're just

6:45

not enough pressure to pop that distal vessel

6:48

open.

6:50

So what we're going to look at here. So this

6:53

is a case of IC in your occlusion with distal

6:56

full collapse and no intracranial lvo is

6:59

now we're going to just take

7:02

a look at the CT perfusion and and kind of see what

7:05

that tells us about the

7:08

status of the Q problem.

7:11

But also The Chronic problem in this case. So the cube

7:14

problem we know were the acute infarcs of the kadi and

7:17

that distal ACA territory note here

7:20

that the cpf map did not

7:23

segment the anterior caudate and fart and that's probably an

7:26

artifact of the fact that the infarct

7:29

is so well established and hypoense that the algorithm has

7:32

chosen to exclude it from its CBF

7:35

segmentation because it's things it's a well-establishing for

7:38

it could be a chronic infarct or something like that. We know from the

7:41

clinical scenario that's going to be more recent to that. It is

7:44

including this ACA territory infarct and then

7:47

and so that's incl

7:50

the CBF less than 30% segmentations the

7:53

TMax.

7:55

Or the area that is hypoperfused is

7:58

essentially the the left MCA territory.

8:01

It's a little bit patchy but the

8:04

corresponds to essentially the MCA territory a

8:07

little bit of the infarctic ACA

8:10

territory, but you know really it's mostly the the

8:13

MCA territory here. So the large

8:16

mismatched volume.

8:18

But we're gonna interpret this knowing that this

8:21

is not an acute intracranial large vessel occlusion. This

8:24

is a symptomatic cervical carotid

8:27

disease. They probably had emboli that went

8:30

into the ACA and caused the infarctica

8:33

the caudi and then migrated distally to

8:36

cause the kind of a distal ACA infarct at

8:39

the superior frontal gyrus. And so when

8:42

reporting these perfusion abnormalities, we're

8:45

going to have to kind of understand. What is the

8:48

underlying vascular abnormality that we saw on the CTA?

8:51

And not you know describe this in the same way

8:54

we would as if this were due to an M1 occlusion because

8:57

that's not exactly the case here.

9:00

So the there is

9:03

a mismatch volume there is an area of hypoperfusion as

9:06

defined by teamector and six seconds that's relatively

9:09

large corresponding MCA territory. And and now

9:12

we're going to take a look at the MRI just to

9:15

Define. You know, what is the extent of infarct the

9:18

DWI Trace images

9:21

really show? Well what we saw on CT at

9:24

the Cod 8 and the superior frontal Charis, but

9:27

we also see the string of multiple dots of

9:30

infarcts and this is going to be along the

9:33

ACA to MC Watershed territory in this further supports

9:36

that there's a hyperfusion phenomenon going on in the

9:39

neck. And so there's a

9:43

symptomatic crotis stenosis a neuroclusion causing

9:46

hypoperation hypopervision left

9:49

cerebral hemisphere

9:51

in the distal watersheds that can

9:54

account for these DWI abnormalities, so

10:00

These show these Watershed infarcts as well

10:03

as the territorial infarcts. So it's a complicated picture. But just

10:06

to convince you that this is a near occlusion and

10:09

not a complete occlusion, which is important for therapy management.

10:13

I'm going to show you the digital subtraction in geography.

10:16

So an often these cases where there's any doubt that there's

10:19

a conclusion versus neuroclusion. You want to do a DSA

10:22

to define whether that vessel

10:25

is actually paying so we have a common karate artery injection

10:28

and we see anter grade filling of that

10:31

cervical internal priority, but it's slow and

10:34

that's what we expect to see with a near

10:37

occlusion contrast is getting past this very tightenosis, but

10:40

it's slowly Peters this way up the neck.

10:43

And so this confirms our suspicion on Imaging

10:46

of near occlusion. There is Trace anter

10:49

grade flow and I

10:52

didn't show you this but they also found on the DSA that

10:55

there is collateral flow through the external carotid artery through the autonomic

10:58

artery. So that provides some collateral flow and they were able

11:01

to treat this because it was near occlusion and not occlusion there can they

11:04

could pass this notice. They did a balloon angioplasty. They

11:07

place a stent there and they placed patient on Dual antiplately

11:10

therapy.

11:12

So in summary, what is this case about this is a case of

11:15

a symptomatic carotid neurocclusion these cases

11:18

of near occlusion, but not so much

11:21

occlusion our candidates for revascularization.

11:25

It remains controversial what the optimal management should

11:28

be. Is it revascularization or just best medical therapy that

11:31

remains an open question the research literature.

11:34

The role of CT perfusion is unclear. But

11:37

I think is that there is emerging uses more

11:40

common be more commonplace. We're

11:43

seeing CT profusions and cases of people who have chronic

11:46

carotid Sano exclusive

11:49

disease or in this case acute on chronic Center who's

11:52

disease and what it what the

11:55

information that the CD profusion provides is that there is

11:58

some human Dynamic compromise. There is

12:01

Transit delay into that left cerebral

12:04

hemisphere left MCA territory what the

12:07

MRI confirm is that there are water in Parks indicating

12:10

that you know at some point there is a perfusion compromise

12:13

in that territory in the

12:16

water sheds suffered as a result.

12:19

So on a pause here and take any questions that people

12:22

may have

12:24

And near occlusion be called tight stenosis.

12:29

You can call it a lot of things.

12:32

And has been called many things in the past.

12:35

But there's a good review paper many years

12:38

ago in ajnr is actually

12:41

a series of two review papers on the concept of crot

12:44

in your occlusion. That's really the terminology that

12:47

I think people should try to coalesce upon because it

12:50

has this clearly defined definition. I

12:58

might describe it as there's a tight stenosis,

13:01

but

13:03

you should not measure it in the same

13:06

way that you would measure a conventional stenosis on CTA by

13:09

using the distal vessel diameter

13:12

as your denominator. So, you know, that's the main thing

13:15

I would avoid bonus points. If you use the

13:18

term near occlusion and bonus points, if you're referring clinicians

13:21

understand what in your occlusion is but that is

13:24

the terminology of

13:27

choice in my mind. Although it. I understand it's not

13:30

universally understood fundamentally what it means

13:33

is that it's just so tight that the distal vessel

13:36

has partially or completely collapsed.

13:41

Got another question for you. Do we do DSA for

13:44

future prevention? Because after two days that may

13:47

not help the patient.

13:49

After two days, it may not what help the patient.

13:54

Yes, so in this case, it's not a

13:57

hyperacute intervention. It's really for secondary

14:00

prevention of future Strokes. So we have situation where

14:03

he have a symptomatic carotid disease,

14:06

but it's not to you

14:09

know.

14:13

Prevent the development of or you know

14:16

reverse to stroke or anything. The stroke has happened that the

14:19

immediate intervention is make sure they're you know, blood pressure

14:22

is good enough to support flow through that

14:25

carotid artery. And then on more Subacute time

14:29

scale, you know during the same admission or within a

14:32

couple weeks or something to do either decide

14:36

about best medical therapy versus revascularization

14:39

to prevent

14:42

another stroke in the same territory.

14:46

because there is you know, hyper-profused kind of

14:49

tissue at risk your brain may be able to Auto regulate and

14:52

compensate for the time being but

14:55

You know that might not always be the case. You might go home and you know,

14:58

you get sick and get dehydrated suffer another

15:01

hypo perfusion episode and have another infarct.