Case Review Live - Head CT Perfusion Cases, Dr. Francis Deng (4-13-23)
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Today we are honored to welcome Dr. Francis ding for
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an interactive case review of head CT profusion cases,
0:45
Dr. Francis Tang is a board-certified radiologist
0:48
who completed his Radiology residency and
0:51
neuroradiology fellowship at Massachusetts General Hospital.
0:54
He is on the neuro Radiology faculty at
0:57
Johns Hopkins University.
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Please remember to use the Q&A feature to submit any questions you have
1:02
so we can get to as many as we can before our time is up
1:05
with that. We're ready to begin. Today's case review Dr. Dang.
1:08
Please take it from here.
1:10
Thank you everyone for joining me. Today. We're going to take a look
1:13
at a handful of cases that utilize head CT perfusion. Now
1:16
this session is going to be intended for the
1:19
intermediate to Advanced learner somebody who already has some
1:22
fundamental understanding of the concept of CT perfusion
1:25
that we're not going to go through in detail. And really
1:28
this is more focus on a case-based review
1:31
of the possible indications and uses of
1:34
CT profusion both. Well establish and emerging indications
1:37
for CT perfusion and hopefully
1:40
it'll allow you to gain some more confidence with your
1:43
interpretations of brain CT perfusion. So
1:46
let's begin with our first case the provided
1:49
history is stroke like symptoms and I'm sure
1:52
if you're practicing radiologist, you'll understand that
1:55
the provided history is often inadequate in these cases that
1:58
and so we should take every opportunity we can to dig
2:01
a little into electronic medical record find any useful clinically
2:04
relevant information that we can to
2:07
help us with our interpretation and so in this
2:10
As we learned that this patient is 81 years old. They have
2:13
a history of atrial fibrillation. They're not on anticoagulation. So
2:17
that's a stroke risk factor their last known well 16 hours
2:20
ago. And now they're presenting with right-sided hemiplegia
2:23
and a left gaze deviation. So with that information
2:26
we're going to really scrutinize the left scribble hemisphere
2:29
for a causative lesion and their NIH stroke
2:32
scales 24, so it's quite high. It's likely this is
2:35
going to be a debilitating large vessel.
2:38
stroke if present
2:40
So the first thing we're going to do is examine our
2:43
non-contrast head CT the first step of any stroke Imaging
2:46
workup to distinguish hemorrhagic stroke
2:49
from ischemic stroke. And once we've excluded intracranial hemorrhage,
2:52
we're going to now focus on where is the
2:55
ischemic stroke?
2:57
How extensive are the early skin exchanges and
3:00
how do we best communicate the location
3:03
instant of that ischemic change.
3:06
So now is a good time to launch our first poll question,
3:09
which is about how extensive
3:12
is this infarct as expressed with
3:16
the aspect score. So I'm going to talk while you
3:20
guys answer the question by first pausing
3:23
at the level of the basal ganglia here
3:26
to tell you that the aspects score is the
3:29
Alberta Stroke Program early CT score for
3:34
expressing the extent of infarct in a middle super artery territory
3:37
stroke. Okay, so that is scored
3:40
on images of a non-conhead CT at level
3:43
the basal ganglia and at the level of above the
3:46
basal ganglia. So at the ganglionic level we score areas
3:49
of the cerebral cortex the basal
3:52
ganglia the insula and internal capsule and then above
3:55
the level of easy ganglia. We score multiple areas of
3:58
the cortex here.
4:01
So take a few seconds. Look at the area of high potency gray
4:04
white differentiation loss here and
4:07
come up with your expression on non-con
4:10
head CT. What is the aspects score?
4:28
All right, so it looks like the
4:31
Scores are all over the place. Yeah, a
4:34
plurality chose two and that
4:37
tied with five the correct answer
4:40
here is one and let me tell you why so
4:43
the maximum score you can have when giving
4:46
an aspect scores 10 and
4:49
that means a completely normal hit CT without any Railway
4:52
differentiation loss in the MCA territory and you
4:55
subtract that point for each of the following areas that
4:58
are involved at the ganglionic level. So
5:01
frontal curriculum is called the M1 territory. So that's
5:04
lost here and two territory is anterior part
5:07
of the temporal lobe that's affected here. And three
5:10
is the posterior part of the temporal lobe and like the
5:13
lateral occipital lobe. So that's affected here.
5:16
The caught it nucleus is another that's affected here.
5:19
Part of the putanium is affected here. The
5:22
insular cortex is affected here. The
5:25
internal capsules. The only part of the aspects score
5:28
that's not affected in this situation and then above the basal ganglia
5:31
level. We have the M3. Sorry the
5:34
M for M5 and M6 cerebral cortex.
5:37
That's roughly dividing to thirds this MCA territory
5:40
that are all affected by this ischemic
5:43
stroke in addition to the MCA territory,
5:46
which has an access for of
5:49
one in this case. There's also in Far involving
5:52
the ACA territory. We see this medial part
5:55
of the frontal lobe being involved with
5:58
this loss at where you are differentiation. So overall this
6:01
is a very large territory ink part involving nearly
6:04
the entire MCA territory sparing
6:07
some of the butane internal capsule and also
6:10
enviral involving a large portion of the ACA territory
6:13
as well.
6:15
So the next step
6:18
in imaging is a CTA and CTP,
6:21
but we can already make a lot of conclusions based on
6:24
non-con scte alone, which is why I wanted to emphasize that
6:27
evaluation and providing an
6:30
aspect score with that regard. So the next
6:34
part of our Imaging evaluation is that we're
6:37
going to look at is our CT perfusion and the
6:40
CT perfusion. We can see on this summary map
6:43
provided by the vendor rapid that the
6:46
cereal blood flow in that left for hemisphere
6:49
is very low the CB of less than 30% is
6:52
segmented out at a volume of 287 milliliters.
6:55
And once again, this includes the MCA territory
6:58
the ACA territory sparing some parts
7:01
of the deep kind of
7:04
lenticulous right region.
7:06
Now looking at the TMax greater than six seconds
7:09
math. This is essentially that entire territory
7:12
as well and it probably artifactually counts
7:15
some of the contralateral, you know,
7:18
ripe ride or region. So we're going to you know,
7:21
mentally take off a little bit of this volume when interpreting
7:24
these numbers so your cvf less than
7:27
30% is going to be your ischemic core your TMax
7:30
career then six seconds gonna be your critical hype
7:33
who perfusion volume and the
7:36
mismatch in between of these and between these they have
7:39
38 millimeters, but that's probably an overestimate is
7:42
what would you you would consider your penumbra or
7:45
tissue at risk that could be salvaged if
7:48
you were to intervene. Unfortunately what
7:51
we can see from these parameters summary Maps
7:54
is that the core is large. It's essentially most
7:57
of the lesserable hemisphere, you know, except the
8:00
PCA territory, and this is a matched defect
8:03
in terms of
8:06
The comparing the TMax the CBF less than
8:09
30 territories.
8:13
Some other things we can derive from these summary Maps we
8:16
can see that there's a hypoperfusion index which is the
8:19
ratio of TMax greater than 10 seconds to TMax
8:22
for then six seconds volume. And this is quite High meaning
8:25
that this tissue is severely ischemic greater
8:28
than 0.4 is considered
8:31
high and that indicates that there's poor collateral.
8:35
flow into this hypoperfused territory
8:43
Another thing we can observe on these summary images
8:46
is that there's a flattening of this
8:49
arterial input function on this time attenuation curve. We
8:52
see that it starts going up around 15 seconds and doesn't
8:55
come back down towards Baseline until after 45 seconds. So
8:58
with this curve is greater than 30 seconds, which is
9:01
strongly suspicious for cardiac output failure
9:04
cardiac dysfunction causing
9:07
a widening of this arterial input
9:10
function curve. So that's something that I think is
9:13
relevant to mention because sometimes you may be the first
9:16
to suggest that possibility because the patient doesn't come
9:19
with pre-existing diagnosis of cardiac disease.
9:24
So the
9:27
last thing that we're going to take a look at so in you
9:30
know in summary the CT perfusion shows large
9:33
core essentially matched
9:36
defect poor collaterals poor cardiac output and now
9:39
we're going to examine the CT angiogram just
9:42
to see what are the
9:46
Vessel deficits that are concomitant with this perfusion
9:49
deficit so as expected there is a cutoff of
9:52
this left MCA add the distal M1 segment. That's
9:55
after giving off an anterior temporal Branch.
9:58
But you know, most of the MCA territory is Downstream of
10:02
this large vessel occlusion. In
10:05
addition. There's a cutoff here of the ACA the
10:08
left ACA right at the a1a2 junction.
10:11
So that accounts for that ACA invark
10:14
we could have predicted all this just based on looking at our CT
10:17
perfusion parameter maps and using that to
10:20
inform our evaluation of the CT angiogram.
10:23
Okay distally, we
10:26
see their it's a relatively decreased density
10:29
of vessels and the distal territory indicating poor
10:32
collateralization. The rapid software
10:35
does highlight this area as suspicious for large
10:38
vessel occlusion. And you know, it has highlighted
10:41
that for us based on this decrease density of blood
10:44
vessels.
10:45
So back to our sides, we have A2 and
10:48
M1 occlusions on the left. We have believed in collaterals. This
10:51
patient was outside of the TPA window.
10:54
So they were not receiving from a license. The infarc
10:57
was too large to
11:00
Be a good candidate for mechanical thrombectomy because
11:03
the benefit would not be realized in this
11:06
situation. There's essentially no tissue left
11:09
to save if you were to take out that clot.
11:13
They were admitted to the neurological Intensive Care
11:16
Unit where they underwent intensive care for swell watch
11:20
they receive high porosmal or therapy. They
11:23
considered Hemi cranic to me if it was within the
11:26
goals of care, but unfortunately this patient progressed to
11:29
have cerebral swelling herniation. They
11:32
were put on comfort care and died within a few
11:35
days.
11:36
So what we learned from this case, so this is a case of
11:39
a completed stroke. They were within the so called
11:42
late window late hyperacute window. That's 6 to 24 hours after stroke
11:45
on set. But the CT perfusion imaging
11:48
basically showed no penumbra of salvageable
11:51
tissue at risk. They were not a
11:54
hyperacute intervention candidate based on the findings these, you
11:58
know, non eligibility for you know
12:02
mechanical term back to me could be made on a non contrast CT alone
12:05
because they were so obvious and that there
12:08
was a large territory in far however, not
12:11
all cases are as obvious and in
12:14
those cases CT perfusion can help I wanted to show you an
12:17
obvious case just so you can match up the non-con CT findings with
12:20
that of CT perfusion.
12:26
Does anyone have any questions on the first case? If
12:29
you have any questions, please drop them in the chat and we'll try
12:32
to address it after each case.
12:36
If not, we'll move on.
12:42
To our second case the provided history is concerned for
12:45
MCA stroke, of course, that's not adequate. So
12:48
we're gonna dig into the chart and find out a little bit more information. So
12:51
it turns out that they're a 28 year old intravenous drug
12:54
user. They've had a recent bout of
12:57
mitral valve under carditis and there's still on antimicrobial
13:00
therapy for this. They were last
13:03
known well two hours ago. They're in the hospital and the
13:06
nurse came in uncheck on them and notice new deficits. They had a
13:09
left sided hemiplegia and a right side of gaze
13:12
deviation as well as confusion their NIH Stroke
13:15
Scale was assessed at 12.
13:18
So the what we can learn from this vignette
13:21
so far. Is that even though
13:24
they're in the TPA window, you
13:27
know within three and a half four and a half hours that
13:30
because
13:33
they have this history of endocarditis. There's
13:36
a relative contraindication to giving TPA. However,
13:39
there's still potentially a candidate for mechanical thrombectomy.
13:42
There's still considered within the early window, you know
13:45
less than six hours in terms of candidate see
13:48
for mechanical Farm back to me. So now we're going to examine our
13:51
CT Imaging cases starting with
13:54
a non-con at CT as we do in
13:58
every stroke case
14:01
And what we can notice here, I'm going to turn it
14:04
on stroke Windows just to really accentuate that great white differentiation is
14:07
that we don't have gray white differentiation laws. We actually
14:10
see areas where there's accentuation of the gray white differentiation. That's
14:13
because of the subcore why matter hypodensity and
14:16
we might consider this phasergenic edema, which is because it
14:19
looks a little swollen and it's limited to the subcortical white
14:22
matter in these right parallelandic region
14:25
as well as this left posterior Temple region.
14:30
But actually if we look a
14:33
little closer we might notice that there is subtle right
14:36
differentiation loss at the right basal ganglia.
14:39
You see how the distinction between the sub-install Y
14:42
matter of attainment is maintaining on the left side, but not really the
14:45
white right side. There's a blurring of the gray white
14:48
Junction. And so there is this indicates
14:51
a hypodensity of the ptainment and
14:54
part of the codate as well.
14:57
So what aspects score would you get this? I would give
15:00
this an eight based on a loss of caught it if you came in this case.
15:04
So now let's move on to the CT perfusion. We
15:07
see that rapid has segmented a cvf lesson
15:10
30% volume of 21 milliliters. This corresponds
15:13
to mostly the white matter of the
15:16
right MCA territory in the right frontal and
15:19
parietal lobes and then there's a larger area
15:22
of T Max elevation greater than six seconds. They
15:25
have segmented 102 milliliters in this
15:28
corresponds to a large region of the right Mills
15:31
or artery territory.
15:33
And this kind of gets into the basal ganglia
15:36
that we saw the subtle hypodensity and non-continent CT
15:39
as well. So this is a case where there's a large mismatch 81
15:42
milliliters mismatch ratio 4.9.
15:48
Take a look at the other parameter Maps. The hypoperfusion index is
15:51
0.4. So borderline terms
15:54
of the adequacy of collaterals here.
16:00
And a relatively good looking aif curve. Now.
16:03
We're going to use that information to inform our
16:06
evaluation of the CT angiogram
16:09
and here we see as expected a
16:12
cutoff of the right MCA M1 segment
16:15
a large vessel occlusion.
16:18
And we're not going to stop at just looking at
16:21
the mips of the CTA. We're
16:24
also going to look at here the source
16:27
images of the CTA because we still
16:30
have unexplained those areas of azogenic Edema, right? That's we
16:33
see this like faint area of enhancement the right pair of
16:36
romantic region corresponding to the area that demon and
16:39
the left parietal region. We see a rim inhanding abnormality at
16:42
the left posterior temporal and
16:45
parietal region that in the
16:48
context of having endocarditis would
16:51
be suspicious for cerebral assess. So they have that going on
16:54
in addition to their large vessel occlusion stroke,
16:57
okay.
16:58
so
17:00
in summary, we have areas of
17:04
age edema aspects 8 we have
17:07
a mismatch. We have a right M1 occlusion.
17:10
And we also have as a kind of almost incidental
17:13
finding left temporal lobe brain abscess
17:16
and maybe another area in the right Carrier Landing region, so
17:21
What comments do I have to make about this study?
17:26
Number one in the early window CT perfusion
17:29
is not strictly required. Although we
17:32
do obtain it in many cases to look for a stroke mimics when
17:35
evaluating candidacy for mechanical thrombectomy.
17:40
The core that we saw in this case relatively small
17:43
is estimated around 21 milliliters, but
17:46
we're going to take a look at what the final chord look like
17:49
on MRI a little bit later. There was a Target mismatch profile
17:52
and remember to look at the CT's Source images
17:55
for any incidental lesions. So and this
17:58
patient was treated with aspiration
18:01
from back to me. They achieved good reperfusion and
18:04
Tiki great three floors restoration after a
18:07
single pass and they're neurologic deficits improved in
18:10
a stroke scale of one for minor facial policy.
18:13
So our next study that we're going
18:16
to take a look at is the MRI that's obtained as
18:19
a fall of afterthron bectomy. And at this time
18:23
I'm going to pull up the DWI.
18:26
And scroll to the b1000 images
18:29
and we can activate the poll in the situation. Now, I'm
18:32
going to tell you that this area of infarct delineated on the
18:35
DWI affecting the car date and the putamine and a little
18:38
bit of the Globus paladis here amounted to only about
18:41
10 milliliters by segmented out this area. That's hyperintense
18:44
on the DWI just 10 millimeters. And
18:47
remember this CT perfusion estimate of
18:50
the CBF left in 30%
18:53
volume was greater than
18:56
that 20 something milliliters and
18:59
that area that was segmented out on the CBF map
19:02
and the white matter is not really infarctica on
19:06
this post-thrombectomy MRI. So
19:09
the question for you is what is the term for when
19:12
you overestimate the infarct on the initial CTP
19:15
compared to follow up Imaging in the fall of gold standard
19:18
is going to be MRI after your intervention.
19:22
And while you're answering that I'm going to point out a couple other findings.
19:25
Here's the little brain abscess and
19:28
the left posterior temporal lobe region. Here's
19:31
that kind of developing brain abscess or you
19:34
know, sequela of septic emboli in the right period Landing
19:37
region and all multiple other small enhancing
19:40
post side that consequence of their,
19:43
you know, endocarditis and septic. Anboli
19:46
you just incidental to this process of the right
19:49
MCA in part, okay.
19:53
So take a take a gander at the
19:56
answer choices. We have Shadow penumbra ghost core
19:59
Phantom mismatch misery perfusion and CBF
20:02
shading.
20:08
Okay, and we have a florality
20:11
getting the right answer which is Ghost core the
20:14
other terms. I totally made up Shadow penumbra Phantom
20:17
mismatch misery perfusion CBS shading. So this concept
20:20
of ghost core is just
20:23
the term to mean that in that you've
20:26
overestimated what is
20:29
infarct on your CTP?
20:32
So what I mean by this when we look at
20:35
the CTF CTP parameter Maps based
20:38
on CDF lesson 30% We are
20:41
making an estimate on what will progress or
20:44
has already progressed to infarction. It
20:47
is not the gold standard for
20:50
determining what is infarction. That would be DWI, but
20:53
often we don't obtain DWI as
20:56
the first Imaging and that's where CT perfusion
20:59
comes in. Unfortunately CT perfusion. There is some
21:02
variability and a hot on how well it's able to estimate
21:05
what is in fact the infarctic core.
21:09
And we know that this phenomenon of
21:12
ghost core is more common in
21:15
the early hypercute window less than
21:18
six hours. It's relatively more common to see that there's
21:21
an overestimation of what turns out to be the
21:24
infarcore and we see this after the reperfusion therapy
21:27
on the fall of MRI a smaller core than
21:30
was predicted.
21:32
So that was the case here in summary.
21:35
This was a case of a small stroke with a significant penumbra.
21:38
There were a good candidate for reperfusion therapy
21:41
by mechanical thrombectomy. And
21:44
to remember that the the CDF segmentations can
21:47
overestimate infarctica in the
21:50
early window.
21:52
So do we have any questions for this kind
21:55
of chat doctor? Dang, do we consider mismatch between CBF
21:58
and TMax without cbv?
22:02
So that's a good question. So so far.
22:05
I haven't had the time to show you guys the cbv
22:08
map but it is good practice to look at
22:11
all of the parameter Maps CBF cbv
22:14
and MTT when looking at
22:17
your stroke cases, so
22:22
In this case, you know
22:25
we can see relatively.
22:31
Maintained areas of cpv and and most
22:34
of this territory but actually decrease cbv in
22:37
that area that we saw was in parked
22:40
in the basal ganglia that would confirm our suspicions the MTT.
22:44
We would expect to be elevating that territory and sometimes
22:47
this is more visually striking and even more sensitive than
22:50
the CBF and
22:53
CBB Maps. The MTT is often, you
22:56
know more visually striking. So on your qualitative analysis, it's good
23:00
to look at all the parameter Maps together this
23:03
the CBB the CBF and MTT, but
23:06
the parameters that
23:09
are
23:10
most commonly used to predict what
23:13
is core and what is critical hypoperfusion
23:17
are going to be your CBF and your TMax
23:20
there have been many studies on using
23:23
cbv to predict core but somehow the
23:26
stroke leadership just has coalesced on CBF less
23:30
than 30 as the primary predictor of your ischemic core.
23:35
Got another question in the Q&A box for this specific case. Could
23:38
The increased volume be because of vasogenic Edema
23:41
was included in the core.
23:46
In the increased volume because
23:49
of vasogenic Edema was
23:52
included in the court. Well not exactly because
23:55
this volume that is
23:58
being segmented on the CBF. Lesson. 30% Maps is really
24:01
in the white matter of the Corona radiata
24:05
and Central Valley and and some
24:08
of this corresponds to the vasogenic edema
24:11
and the parallelogic region. So yes, I think in part you're
24:14
correct, but also some of this was not, you know, really vasogenic edema
24:17
kind of in the more anterior parts of
24:20
the corona radiata I think is
24:25
Perhaps hypoperfused, but did not
24:28
turn out to be infarcted.
24:31
One more question for this case and then we'll move on.
24:34
How is the volume of infarct calculated on MRI?
24:38
So so there
24:41
are two ways to kind of
24:45
A practically speaking calculate the volume of infarct on
24:48
MRI.
24:51
Number one is you can kind of
24:54
use the kind of
24:57
a two diameter measuring approach. You measure
25:00
the
25:04
Diameter of the area that's hyperintense on DWI and
25:07
you estimate by the ellipsoid method, you know
25:10
ABC divided by two the approximate volume that is
25:13
affected here. Another way is
25:16
if your packs has a way to do a
25:19
thresholding based segmentation, you can ask it
25:22
to segment everything that looks hyperintense in this
25:25
region.
25:26
Another way is that if this is plugged into some
25:29
commercial software like
25:32
rapid it will take the ADC map and
25:35
segment everything that falls below a certain
25:38
ADC threshold like 620 and it'll give
25:41
you the volume for that. So there are multiple ways to estimate the
25:44
infarct volume on DWI. If
25:47
you're doing yourself, I would
25:50
either measure or use your
25:53
packs to segment the areas hyperintense on the DWI, or if
25:56
you can plug into commercial software or have
26:00
your technologist send it to Rapid or Vis
26:03
or for instance. They can calculate the regions that
26:06
have a ADC below a certain threshold.
26:15
Okay.
26:17
We're gonna move on to our next case three provide a history is
26:20
possible stroke.
26:22
On further digging you learn. This is a 63 year old who is
26:25
a smoker their last known well was unconfirmed
26:28
out of at the facility that
26:31
they're coming from perhaps it was two days ago is
26:34
the best guess so they're not really a candidate
26:37
for hyperacute intervention. In this case. The chief
26:40
complaint was altered mental status in on, you know, further examination
26:43
neurologist figure that this is mainly in Aphasia. They
26:46
also have a right arm waking it. So we do have a focal neurologic
26:49
deficit. So we're going to be looking for abnormalities on
26:52
the contralateral cerebral hemisphere that can
26:55
explain this weakness their NIH Stroke Scale
26:58
was nine and so once
27:01
again from the vignette or
27:04
not, really a TPA thrombectomy candidate and have this back in mind
27:07
when we're interpreting the Imaging, so
27:10
we're going to start off by looking at
27:13
are CT.
27:19
They're non contrast CT. I'm going to throw it
27:22
on to stroke windows.
27:25
So we can see an area of hypodensity and gray white differentiation laws
27:28
indicating a recent infarct involving
27:31
the left caudate head anterior limit
27:34
internal capsule larger region of
27:37
the superior frontal gyrus on the left
27:40
and visual frontal gyrus a little bit as well and
27:43
some spots in the center of Seminole Valley
27:46
which you know could potentially hit the quirical spinal tract
27:49
and account for the right-sided motor
27:52
deficits seen on exam. Okay. So
27:55
our impression here is some
27:58
infarction in the lesserable hemisphere.
28:01
What vascular territory is this going to be? Well, this Superior
28:04
frontal gyrus is going to be ac/a territory. The head
28:07
of the cloud is AC territory, but this
28:10
is starting to go a little bit at the margins that
28:13
they see territory towards the AC to MCA Watershed. So
28:16
we're going to keep that in mind here.
28:21
So I measured out the hypodensity
28:24
volume just based on you know, kind of
28:27
measuring length times with times height divide by
28:30
2 about 40 milliliters and next.
28:34
We're going to look at our CTA that followed
28:38
this study.
28:41
to look for any abnormalities of the ACA or
28:44
MCA and
28:49
Well, wait for it to load here.
28:56
So it's going to be quite difficult to
28:59
tell but I'll tell you there is no large vessel occlusion.
29:02
There is
29:05
some loss of the arborization of distal ACA branches
29:08
supplying that infarctic region. So maybe there's a distal
29:11
AC occlusion, but there's
29:14
no large vessel occlusion that we could
29:17
see on the CT of the
29:20
head. You see the mca's are intact the aca's at
29:23
least proximately are patent and
29:26
the intracranial icas are painting as
29:29
well. But there is an abnormality in the neck which is the abramality
29:32
you want to focus on here. And when I
29:35
zoom in here for everyone's benefit and so
29:38
we can look at the left internal credit artery.
29:41
It's very small, right?
29:43
So here's the left internal carotid artery.
29:46
We see a bunch of plaque here. We see the the Luminous small
29:49
then we lose the contrast to pacification altogether and
29:52
then we get to the crowded bifurcation as Peyton again. So the
29:55
question for the audience is if we
29:59
can launch the poll, you know, how do we best describe
30:02
this left ICA lesion? Okay.
30:05
So again, we have contrast the
30:08
pacification here at the bifurcation. Then we have some plaque. We
30:11
don't see the contrast going
30:14
quite so well, but then we see immediate reconstitution
30:17
here at the level of the crowded ball to
30:20
a small narrowed artery.
30:23
And looks like the whole artery is smaller
30:26
much smaller than the ipsilateral
30:29
external crater artery and also
30:32
smaller than the contralateral internal provider artery all the
30:35
way up into the intracranial portion of it.
30:38
But the intrapreneurial screw bar arteries are normal
30:41
in caliber.
30:47
This patient does have an anterior communicating artery, so
30:50
they have some.
30:53
Supply from the contralateral side potentially
30:58
across the Acom
31:01
supplying their ACA
31:04
But because there's this ipsilateral carotid abnormality on
31:07
a patient who has infarct and symptoms. This
31:10
is considered symptomatic carotid disease the question is how
31:13
would you describe this carotid abnormality on your
31:16
report?
31:21
okay, and a plurality shows
31:24
occlusion with retrograde filling, but I
31:27
think the best answer here is going to be near occlusion
31:30
so near occlusion is
31:34
A concept in kratosenosis where you
31:37
have such a tight stenosis that you may
31:40
not even see the Lumen very well, but it's only
31:43
for a short segment that you don't see that contrast and
31:46
may well be that the Lumen is so small. It's below the
31:49
resolution of your CTA and we
31:52
know it's not retrograde feeling because retrograde if
31:55
this were completely occluded a much longer segment
31:58
of the cervical ICA would be Nona pacified
32:01
with contrast either with thrombus or with, you
32:04
know, static column of blood because
32:07
the retrograde, you know, pushing of
32:10
that contrast not gonna come all the way down into the
32:13
neck because there's no outflow to the ICA in
32:16
the neck because there are no branches of the IC in the neck. So retrograde
32:19
feeling really never comes down all the way into the
32:22
next retrograde feeling might come down to the pair of thalamic segment
32:25
to the Future segment where there is an outflow there are branches to it,
32:28
but it is not going to calm down
32:31
all the way to the neck and instead. We have a concept called.
32:34
Near occlusion where we see the distal
32:37
vessel is opacity. It's a smaller caliber than
32:40
the contralateral side. And this is a separate entity from
32:43
conventional stenosis. So conventional stenosis are
32:46
defined by the minimal Lumen diameter divided
32:49
by the distal normal vessel
32:52
diameter. Unfortunately the distal the distal
32:55
vessel here is smaller because the stenosis
32:58
is so tight in hemodynamically significant. They're just
33:01
not enough pressure to pop that distal vessel
33:04
open.
33:06
So what we're going to look at here. So this
33:09
is a case of IC in your occlusion with
33:12
distal full collapse and no intracranial lvo is
33:15
now we're going to just take
33:18
a look at the CT perfusion and and kind of see what
33:22
that tells us about the status of the
33:25
Q problem. But also The Chronic
33:28
problem in this case. So the cube problem we know
33:31
were the acute infarcts of the kadi and that distal ACA
33:34
territory note here
33:37
that the CPA map did not segment the anterior codate
33:40
infarct and that's probably an artifact
33:43
of the fact that the infarct is so well
33:46
established and hypoense that the algorithm has chosen to exclude
33:49
it from its CBF segmentation
33:52
because it's things it's a well-establishing for it could be
33:55
a chronic infarct or something like that. We know from the clinical scenario that's
33:58
going to be more recent to that. It is including this ACA
34:01
territory infarct and then and so
34:05
that's including
34:06
the CBF less than 30% segmentations the
34:09
TMax.
34:11
Or the area that is hypoperfused is
34:14
essentially the the left MCA
34:17
territory. It's a little bit patchy but it
34:20
corresponds to essentially the MCA territory a
34:23
little bit of the infarctic ACA
34:26
territory, but you know really it's mostly the the
34:29
MCA territory here. So the large
34:32
mismatched volume.
34:34
But we're gonna interpret this knowing that
34:37
this is not an acute intracranial large vessel occlusion.
34:40
This is a symptomatic cervical carotid
34:43
disease. They probably had emboli that went
34:46
into the ACA and caused the infarctica
34:49
and then migrated distally to
34:52
cause the kind of a distal AC in fact
34:55
at the superior frontal gyrus. And so you
34:58
want to when reporting these perfusion abnormalities, we're
35:01
going to have to kind of understand what if the
35:04
underlying vascular abnormality that we saw on the CTA.
35:07
And not you know describe this in the same
35:10
way we would as if this were due to an M1 occlusion
35:13
because that's not exactly the case here.
35:16
So the there is
35:19
a mismatch volume there is an area of hypoperfusion as
35:22
defined by team actor and six seconds that's relatively
35:25
large corresponding MCA territory. And and now
35:28
we're going to take a look at the MRI just to
35:31
Define. You know, what is the extent of infarct
35:34
the DWI Trace
35:37
images really show? Well what we saw on CT at
35:40
the Cod 8 and the superior frontal Charis,
35:43
but we also see the string of multiple dots of
35:46
infarcts and this is going to be along the
35:49
ACA to MC Watershed territory and this further supports
35:52
that there's a hyperfusion phenomenon going on in the
35:55
neck. And so there's a
35:59
symptomatic crowd stenosis a neuroclusion causing
36:02
hypoperation hypopervision and
36:05
left cerebral hemisphere
36:07
in the distal watersheds that can
36:10
account for these DWI abnormalities, so
36:16
These show these Watershed infarcts as
36:19
well as the territorial infarcts. So it's a complicated picture. But just
36:22
to convince you that this is a near occlusion and
36:25
not a complete occlusion, which is important for therapy management.
36:29
I'm going to show you the digital subtraction in geography.
36:32
So in often these cases where there's any doubt that
36:35
there's occlusion versus neurocclusion you want to do a
36:38
DSA to define whether that
36:41
vessel is actually paying so we have a common karate artery injection
36:44
and we see anter grade filling of
36:47
that cervical internal priority, but it's slow and
36:50
that's what we expect to see with a near
36:53
occlusion contrast. It's getting past this very tight stenosis, but
36:56
it's slowly Peters this way up the neck.
36:59
And so this confirms our suspicion on Imaging
37:02
of near occlusion. There is Trace anter
37:05
grade flow and I
37:08
didn't show you this but they also found on the DSA that
37:11
there is collateral flow through the external product order through the
37:14
ophthalamic artery. So that provides some collateral flow and they were
37:17
able to treat this because it was near occlusion and not occlusion there can they
37:20
could pass this gnosis. They did a balloon angioplasty. They
37:23
place a stent there and they placed patient on Dual
37:26
antiplately therapy.
37:28
So in summary, what is this case about this is a case
37:31
of a symptomatic carotid neurocclusion these cases
37:34
of near occlusion, but not so
37:37
much occlusion our candidates for revascularization. It
37:40
remains controversial what the
37:43
optimal management should be. Is it revascularization or
37:46
just best medical therapy that remains an open question
37:49
the research literature
37:51
The role of CT perfusion is unclear. But I think is
37:54
that there is emerging uses more common be
37:57
more commonplace. We're seeing CT profusions and
38:00
cases of people who have chronic carotidocious
38:03
disease or in
38:06
this case acute on chronic Center who's disease and what
38:09
it what the information that the
38:12
CD profusion provides is that there is some human Dynamic
38:15
compromise. There is Transit delay
38:18
into that left cerebral hemisphere left
38:21
MCA territory what the MRI confirm
38:24
is that there are water in Parks indicating that you know
38:27
at some point there is a perfusion compromise in
38:30
that territory in the watersheds suffered
38:33
as a result.
38:35
So on a pause here and take any questions that people
38:38
may have
38:40
And near occlusion be called tight stenosis.
38:45
You can call it a lot of things.
38:48
It has been called many things in the past.
38:51
But there's a good review paper many years
38:54
ago in H&R. There's actually
38:57
a series of two review papers on the concept prod
39:00
in your occlusion. That's really the terminology that
39:03
I think people should try to coales upon because
39:06
it has this clearly defined definition. I
39:14
might describe it as there's a tight stenosis,
39:17
but
39:19
you should not measure it in the same
39:22
way that you would measure a conventional stenosis on CTA
39:25
by using the distal vessel
39:28
diameter as your denominator. So, you know, that's the main
39:31
thing I would avoid bonus points. If you
39:34
use the term near occlusion and bonus points, if you're referring clinicians
39:37
understand what in your occlusion is but that
39:40
is the terminology of
39:43
choice in my mind. Although it. I understand it's
39:46
not universally understood fundamentally what it means
39:49
is that it's just you know, that's so tight that the distal
39:52
vessel has partially or completely collapsed.
39:57
Another question for you. Do we do DSA for
40:00
future prevention? Because after two days that may
40:03
not help the patient.
40:06
After two days, it may not what help the patient.
40:10
Yes, so in this case, it's not a
40:13
hyperacute intervention. It's really for secondary
40:16
prevention of future Strokes. So we have situation where
40:19
you have a symptomatic carotid disease,
40:22
but it's not to you
40:25
know.
40:29
Prevent the development of or you know
40:32
reverse to stroke or anything. The stroke has happened. The immediate
40:35
intervention is make sure they're you know, blood pressure
40:38
is good enough to support flow through
40:41
that carotid artery. And then on more Subacute time
40:45
scale, you know during the same admission or within a
40:48
couple weeks or something to do either
40:51
decide about best medical therapy versus
40:54
revascularization to prevent
40:58
another stroke in the same territory.
41:02
because there is you know, hyper-profused kind of
41:05
tissue at risk your brain may be able to Auto regulate
41:08
and compensate for the time being but
41:11
You know that might not always be the case. You might go home and you know,
41:14
you get sick and get dehydrated suffer another
41:17
hypo perfusion episode and have another infarct.
41:22
Okay.
41:24
Our next Case Case for write a
41:27
history is post-op evaluation. We're gonna have a poll question
41:30
here in a little this is
41:33
actually, you know on further digging you find out it's
41:36
a 73 year old or three days after suffering aneurysmal silver
41:39
acting hemorage or modified Fisher grade one
41:42
hunt has great for
41:44
They are treated with a flow diverting device across
41:47
it right internal front artery aneurysm
41:50
that ruptured.
41:52
They're being monitored in the neurological ICU, which transcranial
41:55
dopplers and most recently that had
41:58
shown Peak elevated elevated Peak velocities in
42:02
the right middle server artery.
42:04
So what are they thinking here post that b valve? That's
42:07
not telling us what they're concerned about. What they're concerned about is we have
42:10
to read in between the lines. They're concerned about vasospasm and deletes
42:13
Frugal. Ischemia. So we can activate the poll here. The question
42:17
is how long after supper actor
42:20
Hemorrhage is the peak incidents and severity of vasospasm.
42:23
Is it one day three days
42:26
seven days 14 days or 21 days.
42:38
This is going to be a case about the use of CT perfusion in
42:41
visaspasm and delete cerebral.
42:44
Ischemia.
42:54
While you're working on that I'm going to load up the images for the
42:57
CT and CTP.
43:06
right
43:12
Okay, why don't we close the poll?
43:16
So the
43:18
plurality of answers was three days, but
43:21
that's not the correct answer. The correct answer was the second most common
43:24
Choice here was seven days. So 34% of
43:27
you chose seven days, so
43:30
Visa spasm as onset around three
43:33
days peaks in incidents and severity around seven
43:36
days and then returns back to normal after
43:39
about three weeks. In
43:42
this case. It's a just a few days
43:45
after hammerage. It's at the very Leading Edge
43:48
of when you can see videos spasm and
43:51
struggle. Ischemia. So on the non-con head
43:54
CT, we see the external ventricular train. We
43:57
see some scatter subarachnoid hemorrhage, but we don't really see
44:00
a great white differentiation laws. Let's
44:03
turn on our stroke windows. We don't see well establish
44:06
infarct here. And so we're gonna
44:09
now turn to our cerebral blood
44:12
flow segmentation masks.
44:15
We see nothing with segmented in terms
44:18
of CBF less than 30% and there
44:21
are some areas segmented as Team Max career than
44:24
six seconds of 28 milliliters. This is corresponding to
44:27
part of the watersheds.
44:30
That kind of ACA territories in the
44:33
middle parts of the cerebral hemispheres as well
44:36
as the kind of a posterior MCA and
44:40
PCA territory here in this like Perry atrial white
44:43
matter region.
44:46
In the face of bilateral perfusion
44:49
abnormalities, I would not rely on
44:52
the CBF map segmentation
44:55
analysis by itself
44:58
because it is a relative CBF. It is
45:01
comparing to the contralateral side that
45:04
is presumably normal. But if you have bilateral abnormalities
45:07
that kind of presumption goes out the window. So
45:10
let's take a look at our color maps for CDF
45:13
and if we
45:16
take this right MCA territory to be our
45:19
internal control for what is possibly normal
45:22
then relative to that. We have some
45:25
reduced areas of cvf corresponding
45:28
to the ACA territory
45:31
is bilaterally the PCA territories and
45:34
this part of the kind of
45:37
right MCA inferior division territory as well
45:40
and the kind of watersheds between the MCA and
45:43
the PCA.
45:44
And we're gonna use these abnormalities kind
45:48
of inform our view of the CTA.
45:51
Right? So the term Visa spazm as
45:54
detected on CTA indicates narrowing of
45:58
the large and medium vessel, uh arteries
46:01
in the head
46:04
and we can see that the MCS are relatively preserved
46:07
maybe some mild spasm and
46:10
the emcees in terms of their caliber, you know, the imagine your
46:13
mind what they would look like normally but the pca's are
46:16
very very small the PCS are diffusely small
46:19
so very severely vasospastic
46:22
and we look A sagittal myth
46:25
at the aces. The aces are diffusely
46:28
regular very small caliber.
46:30
It's our diffusely based as spastic and this
46:33
kind of confirms what the findings on
46:36
transcranial Doppler is but it's actually in a different territory than
46:39
was revealed by transcranial Doppler which is often unreliable.
46:42
If you're not able to get a good sonographic window into
46:45
the head and instead what we
46:48
can add in terms of value. Here are the territory
46:51
is a profusion abnormality concordant with
46:54
the territories of medium and large vessel bezospasm
46:57
that we see it really
47:00
indicates a kind of a widespread
47:03
abnormality in this case that could potentially
47:06
be symptomatic in this patient if
47:09
they had, you know, any worsening neurologic
47:12
exam.
47:13
but fortunately we did not
47:16
see well established infarct yet, but we're
47:19
concerned about it based on the areas of relatively qualitatively
47:22
speaking reduced group of blood flow
47:25
on our qualitative analysis of the CBF
47:28
Maps Okay, so
47:32
So in summary, you know with these CT images shows
47:35
there was phases spasm resulting in some hypo
47:38
perfusion in the ACA right MCA inferior
47:41
Division and related border zones.
47:45
So once again, I would I would say don't rely
47:48
too much on your CBF Maps because remembering it
47:51
is a relative comparison that they're
47:54
making the segmentation off of and we have bilateral perfusion
47:57
abnormalities. You have to fall back on your qualitative analysis
48:00
of where you think the perfusion abnormalities are
48:03
compared to relatively well preserve
48:06
vascular territories. I would also
48:09
caution you not to over read these parameter
48:12
maps that were designed for acute large
48:15
vessel occlusion Strokes. These parameters
48:18
are not well validate in the setting of vasospasm after
48:22
subarachnoid hemorage. It does what I mean is that, you
48:25
know, CBF less than 30 doesn't necessarily predict reliably
48:28
the development of an infarct in that
48:31
territory and team. Actually that's six seconds is you know,
48:34
not
48:35
Validated As the metric of
48:38
choice for predicting, you know, what is critical hypoperfusion.
48:41
And and so this
48:44
is still an emerging area of practice. And so I
48:47
would you know before we have good evidence about how to
48:50
interpret these findings, I would you know, say refrain from using
48:53
the same thresholds and terminology you would use
48:56
for a large vessel inclusion stroke like core in Fark
48:59
or penumbra and just state that there are these regions of
49:02
hypoperfusion. They correspond or not to areas
49:05
of Asia spas and that you can see on CTA in
49:08
this case the patient had a
49:11
follow-up CT exam several days
49:14
later three days later. So this is at Peak severity of
49:17
cerebral basis spasm.
49:20
And we can see the interval development of these small
49:23
moderate size infarcts where
49:26
we saw those areas
49:29
of relatively decreasing blood flow at the
49:32
right MCA PCA border Zone here.
49:35
And kind of a cortisone between the AC and
49:38
PCA territory here as well on the right cerebral hemisphere.
49:46
Okay, so acute infarctions involving distillation territory
49:49
and mcpca Watershed territories. This
49:52
patient was taken to digital subtraction
49:55
and geography that verified the
49:58
presence of bilateral ACA as well as PCA vasospasm
50:01
and they were treated with intra-arterior overapamil
50:04
in the base of spasm improved.
50:07
Okay.
50:08
So in summary, what was this case about this is the case of basis spasm
50:11
after subarachnoid hemorrhage and this starts. Typically
50:15
after three days at Peaks that
50:18
when we can it resolves after two or three weeks CTP has
50:22
an emerging role in helping diagnose. Ischemia. Ischemia. Meaning
50:25
it can be due to large vessel
50:28
medium vessel or even small vessel basis spasm rather
50:31
than just the macrobaster of Asia
50:34
spasm that we necessarily see on CTA and so can be considering
50:37
an adjunct at the time that you're concerned that a
50:40
subarachary hemorrhage patient is getting worse neurologically.
50:44
Okay any questions about this case?
50:47
There is a question.
50:51
How can we know this is vasospasm or
50:54
just chronic a sterile skoretic narrowing?
50:59
Yeah, how can we distinguish bezospasm from
51:03
chronic? Atheroscleric narrowing? That's
51:06
a good question. So primarily you would want
51:09
to compare to your initial presentation
51:12
CTA on your initial presentation CT. You
51:15
might have Sebring Hemorrhage, but you probably wouldn't have visual spasm
51:18
right away.
51:19
That initial CT is obtained to look for aneurysms after
51:22
you have a separate hammerage, right? And so
51:25
they the comparison would allow you
51:28
to confidently say this is a new abnormality and these abnormalities
51:31
are so diffuse in multiple vascular
51:34
territories and their news so
51:37
compatible with vazospasm.
51:40
What is the prognosis in Visa spasm?
51:46
Well, I think it highly depends on the degree of
51:49
business spasm and the leads
51:52
for bothchemia. So these patients with subarachary hammers can
51:55
have all kinds of neurologic sequelaeveloping the
51:58
weeks after the suburbage either due
52:01
to hydrocephalus or due to delay cerebral.
52:04
Ischemia. And I think
52:07
as with any other stroke highly depends on the territory involved
52:10
and the extent of that infarction.
52:15
Okay.
52:17
Our next case comes with the history of
52:20
stroke like symptoms. Okay digging further you
52:23
find that there are 63 year old patient. They have a history of hypertension
52:26
on presentation. They had a severely elevated
52:29
blood pressure at 162 over 72 their
52:32
last known well three hours ago. They presented
52:35
with left side of weakness and a left gaze deviation.
52:38
It's a little bit unusual pattern. They're NH Stroke
52:41
Scale was 16.
52:43
So first thing we're going to look at is the non-conhead CT.
52:47
And I'm going to describe the abnormalities without telling you the diagnosis.
52:53
So there are some subcortical why matter hypodensities in this
52:56
medial paralantic region and
52:59
continuing through the parietal lobes. It is
53:02
really bilateral, but worse on the right side and it
53:05
continues a little bit until occipital Loops as well.
53:08
I don't see definitely loss of great white differentiation.
53:17
So now we're going to move on to see that.
53:21
Okay. So again buy parietal occipital subcortical
53:24
edema now, we're going to look at the
53:27
CT perfusion.
53:29
So CBF less than 30 map. There's
53:32
nothing segmented the TMax greater than six
53:35
seconds. There's nothing segmented but wait, you know,
53:38
we wouldn't stop just looking at the summary Maps. We want to look at the color
53:41
parameter
53:44
Maps as well. So here is a
53:48
The cbv map we see an asymmetry here, right?
53:53
So there's relatively high cbv
53:56
in this right parietal region.
53:59
Take a look at what the TMax shows.
54:02
The team actually is a deeper shade of blue meaning decreased TMax
54:05
in that region.
54:09
The MTT is relatively unremarkable the CBF
54:12
again shows High CBF in
54:15
that region. So so it kind of extended the right
54:18
frontal as well the right frontal and parietal region show
54:21
hyper perfusion.
54:27
Okay.
54:30
So at this point we can launch the poll while I
54:33
pull up just the next part of
54:36
the study.
54:39
Question is what is almost likely diagnosis? Is it acute MCA
54:42
infarct Subacute MCA infarctica science thrombosis
54:45
Todd paresis to account
54:48
for their left-sided hemiplegia or hemiplegic
54:51
migraine.
54:55
And I'll tell you the CTA was on remarkable. There's no
54:58
large vessel occlusion.
55:02
There was I suppose some greater
55:05
prominence of vessels in that hyper perfused
55:08
area. So this just corresponds to the macrovascular manifestation.
55:11
You can see the vessels a little bit better or that CBB is
55:14
elevated.
55:30
Okay.
55:34
and the poll
55:39
So kind of a plurality people chose Venus
55:42
sinus thrombosis followed by hemiplegic migraine originally. The
55:45
right answer here is Todd Paris is so this is
55:48
where putting together clinical information is important to arriving at
55:51
the correct diagnosis. So they had a left-sided hemiplegia and
55:54
also left gazed
55:57
deviation and the Imaging findings.
56:00
I'll tell you the subcortical edema was
56:03
really suggested posterior reversible encephalopathy
56:06
syndrome, and we know that as part of that syndrome you
56:09
can have seizures as part of seizures. You can
56:12
have a post ictal period where you have paralysis of
56:15
if that
56:19
area of seizure activity involved, you know
56:22
motor cortex and what have you so this is a case of Todd paralysis
56:25
following a seizure complicating p****
56:28
reversible encephalopathy syndrome.
56:31
The patient went on to get brain MRI that
56:34
shows the classic findings of press right
56:37
we have isogenic edema in this distribution
56:40
that is under the superior frontal sulci continuing
56:43
into the parietal and occipital lobes
56:46
a little bit until lateral temporal lobes
56:49
as well involving both cerebellar hemispheres. This is
56:52
flare hyperintense. In this case, you know,
56:55
we do see some areas of restricted diffusion. That's okay
56:58
as long as it's not the dominant finding that can be still compatible
57:01
with press.
57:03
There are also some findings of microhemorages and
57:07
some of those areas that were severely involved
57:10
and that can be a minor finding
57:13
in press it's not the dominant abnormality is
57:16
really this classic distribution of vasogenic Edema. That would be
57:19
most compatible with press.
57:25
Okay, so we showed major Gengar edema in
57:28
pattern compatible with press this was
57:31
treated with anti-epileptic drugs and anti-hypertensive drugs
57:35
right treatment for Price history in the underlying cause in this case of severe
57:38
hypertension.
57:40
So what is this case about?
57:42
This is a stroke mimic. Okay, stroke mimics
57:45
present like strokes, but
57:48
it's not due to acute. Ischemia.
57:51
When you see that the summary maps on your CTP for
57:54
core infarct or tissue at risk are negative
57:57
think again, think about
58:00
looking at the color maps to look for any
58:03
abnormal hyper perfusion. Okay, that could be
58:06
due to stroke and it's like seizure but also like hemiplegic migraine
58:09
and then also
58:12
use your non-conscious head CT to guide you towards
58:15
any specific diagnosis in the case of press. Sometimes you
58:18
can see subtle. Laserjanka Dima already evident on the
58:21
noncon has CTE, but of course MRI would be more sensitive.
58:24
So press and seizure, you know
58:27
Cedar due to other causes press
58:30
without seizure. And so and so on so forth. They
58:33
most often show increase CBF early
58:36
in the disease and then decrease CBF later on
58:39
so it can be a little variable but people presenting, you know,
58:42
hyperacutly they tend to have increased CBF
58:46
so if we have any questions about this case
58:52
We're going to go a little over the hour. I have two more cases.
58:59
Okay period next case has a history of
59:02
stroke. Okay digging further you find that there are 67
59:05
year old they have a history of atrial fibrillation. They were
59:08
found down their lasting one week ago their classical
59:11
Coma Scale is eight so we know from this vignette, they're not
59:14
really a candidate or hypercute interventions. But nonetheless the
59:17
what we call the brain attack team was activated. They
59:20
were started on the pathway that includes CT CT
59:23
perfusion and CT angiography.
59:26
So let's take a look at the first
59:29
Imaging study in our group.
59:32
So this is going to be a little bit complicated.
59:39
So we have our non-conhead CT.
59:41
That identifies bilateral abnormalities bilateral
59:44
hypodensities and strugal hemispheres
59:47
on the left side. We
59:50
see these gyrofoam hyper densities that may
59:53
represent emeractive transformation of this larger
59:56
area of infarct. What is this infarct territory
59:59
corresponds to corresponds to the MCA inferior
60:02
division as well as posterior super
60:05
artery Division and there's also
60:08
an area of hypodensity involving the right insula and
60:11
temporal cortex.
60:13
There are some areas of hypodensity that seem a
60:16
little older in the luxurable hemisphere and a
60:19
smaller one the right Servo Hemisphere. Okay. So that's what
60:22
the non-con had CT shows. There's already swelling there's midline shift.
60:25
There's sulfill effacement. So we know that some of
60:28
this is going to be somewhat established.
60:31
Look at our summary Maps the CBF less than 30 volume segmented
60:34
by rapid as zero milliliters.
60:38
The TMax greater than six seconds is segmented at 127 milliliters.
60:42
And what is it highlighting here? It's highlighting parts
60:45
of the superior divisions of both the middle
60:48
artery territories as well as part of the inferior division
60:51
of the left Middlebury territory
60:54
so we can load the pole now
60:57
while I pull up a couple more images
61:00
Asking what is the closest estimate that you have to the
61:03
volume of infarcture? That is either acute or
61:06
Subacute?
61:08
Is it zero is a 127 or
61:11
is it 120?
61:23
and full of these images side by side for the TMax and
61:26
the non-conhead CT as I
61:29
explained my rationale once we see the
61:32
answers and you guys have finished answering
61:51
Okay, so a plurality of you chose 127 milliliters.
61:56
But the correct answer is 270 milliliters
61:59
and here's my rationale why so
62:02
the 127 is coming from the summary map
62:05
of the TMax elevation. Unfortunately, what is
62:08
represented by the TMax elevation here is not
62:11
exactly corresponding to what is apparent as
62:14
infarct on a non-con head CT.
62:19
In this situation we want to use the
62:22
non-continhect to our advantage in defining
62:25
the areas of Subacute established infarct. Okay,
62:28
these are areas that are not being
62:31
caught on the CBF map because they have
62:34
reproduced already or there are so hypodents
62:37
that the rapid software is considering them chronic
62:40
infarct or something along those lines. And so
62:43
in order to do this analysis and you know,
62:46
I would break it down into vascular segments. Okay.
62:49
So if we look at the left middle sobriety territory, what we
62:52
know is in fact it is this inferior Division
62:55
and that is hypoperfused. What we know
62:58
is not in fact it is this Superior division involving the
63:01
frontal lobe and that is hypo perfused
63:04
as well.
63:06
In this posterior cerebral artery territory, we know that is infarctica
63:09
based on non-con head CT, but this is actually hyper perfused
63:12
based on the TMax map. We see a deep blue here. That's a
63:15
decrease in TMax.
63:17
But just because that is decreased doesn't mean it's not already irreversibly
63:20
infected we can tell that on the non-con
63:23
head CT.
63:24
On the right middle super artery inferior division
63:27
territory. We see similar picture of high per
63:31
profusion meaning decreased TMax here, but we
63:34
know that area is infarcted because it's hypodense and blurred
63:37
out on our non-con CT. Okay, and then
63:40
Superior division there is an elevation of TMax. So
63:43
it is hypoperfused but a non-con CT we do
63:46
not see establishing farther. Okay. So we kind
63:49
of repeat this analysis for all the different vascular territories to come
63:52
to our conclusion of what is infarcted and what is
63:55
not infarcted so we can make it two by two table using your team acts
63:58
estimating. What is hypo perfused and what
64:01
is hyper perfused.
64:03
And what is established infarct? What is
64:06
nine farting? Okay.
64:08
And so we're going to use these kind of perfusion abnormalities
64:11
to our advantage when we review the
64:14
CT angiogram. Okay, so we saw
64:17
hypo perfusion both Superior inferior divisions of the
64:20
left MCA. So we're going to look for approximal left MCA occlusion
64:25
indeed. We find an MCA M1 occlusion on
64:28
the left side that accounts for that hypo perfusion team acceleration
64:31
in both Superior and impure division territories.
64:35
On the right side. We don't see a large vessel occlusion in
64:38
the right MCA, but we know that there was hypoperfusion
64:41
in that right Superior division territory. So
64:44
if we kind of scroll in the sagittal myths to that area
64:47
we can see there's an area of severe stenosis of
64:50
one of the M2 branches here that
64:53
supply that frontal lobe where we saw that region of
64:56
high vote for Fusion. So this is like steno exclusive disease is
64:59
severe that may account for that area of
65:02
hyperperfusion. Okay, but we don't see persistent occlusion
65:06
that would account for the infer that we see so presumably
65:09
it infarcted and Rec analyzed and
65:12
you know, we don't see the persistent occlusion there anymore.
65:16
So those are the findings
65:19
of how we use the CT profusion
65:22
to our benefit when seeing these
65:25
multifocal infarction multiple of asset territories.
65:28
We're going to suggest an embolic etiology and
65:31
supporting that is actually looking at the arterial
65:34
input function on our time with attenuation curves.
65:37
We can see that it starts going up around like 12
65:40
seconds doesn't come back down to Baseline. Well after 40 seconds,
65:43
so the time it takes to go up and come back down
65:46
as greater than 30 seconds which again should suggest in your
65:49
mind the possibility of cardiac dysfunction underlying all
65:52
this and we know this patient has a history age for fibrillation. It's unclear
65:55
what their ejection fraction is,
65:58
but that was evaluated by bedside echocardiography and
66:01
that was found to be depressed supporting this conclusion.
66:07
So what are some teaching points to get
66:10
away from to take away from this CT case?
66:13
So when you have bilateral perfusion abnormalities or
66:16
Subacute infarcs, these are often not
66:19
picked up on the rcbf summary Maps when you
66:22
have reperfusion of embarks. You may
66:25
not meet the TMax thresholds that you typically use
66:28
to define hypoperfusion of infarctic or
66:31
potentially infarctic territory on your summary
66:34
Maps as well and these cases of Subacute infarc
66:37
really rely heavily on your non-con CT to
66:40
determine what it's matched versus mismatched non-con CT
66:43
determine what is infarct core and
66:46
your team active determine
66:49
what is
66:51
kind of hype with perfused tissue use the
66:54
CTP to your advantage to look for a medium vessel abnormalities
66:57
that are difficult detect on CTA by itself. We see a
67:00
large region of hypo perfusion. We're going to really scrutinize the medium vessels
67:03
that supply that area for standard occus
67:06
disease.
67:07
So the next part is really just
67:10
an MRI that confirms some
67:13
of the abnormalities that we saw in CT just to
67:16
convince you guys that you know, I'm not making this stuff up that
67:19
when we look on the DWI. We
67:22
see these areas of hyperintensity is not
67:25
really hyper intense like a hyper acute infarctica. It's
67:28
kind of a mild signal
67:31
intensity and that's because it's now a Subacute in
67:34
Far a lot of Asian godema in the area as well
67:37
in that left MCA Imperial Division and
67:40
then posterior cerebral artery territory as
67:43
well a more recent and far from the right temporal
67:46
insular region of that right MCA inferior Division.
67:49
And then we see that chronic infarct
67:52
in the left Superior server Hemisphere
67:55
and more recent infant right Superior server atmosphere
67:58
and the GRE confirms the
68:01
suspicion for particular hemorrhagic transformation in this
68:04
gyrofoam pattern in that area of subway.
68:07
Optical hemisphere
68:12
So MRI confirms our suspicion that we could
68:15
identify on close analysis of the CT including areas
68:19
of particular Hemorrhage and this Subacute infarct. This
68:22
patient was managed with anticoagulation for
68:25
their presumably cardioabolic
68:28
source of stroke in summary
68:31
was this case about this is a case of bilateral late
68:34
acute or sub acute infarcts. The pitfalls
68:37
to know about is at hyper perfusion can
68:40
exist in these cases because of luxury perfusion after
68:43
either treatment of clot or
68:46
spontaneous revastarization due to clot autolysis
68:49
or recruitment of collateral flow.
68:54
The rcbf summary Maps can be
68:57
falsely negative when the abnormalities are bilateral as
69:00
and in these
69:03
cases you got to rely heavily on your non-con CT
69:06
to delineate what is established infarct
69:09
or not?
69:10
So we have any questions on that.
69:13
Yes, we've got two.
69:15
Are you performing the perfusion before or after the CT
69:18
angio? Does it make a difference?
69:22
I don't know that it makes a difference. I think either can be done depends on
69:25
the protocol at your institution. We have
69:28
set up on your scanner.
69:32
This might be more General on stroke protocols. What do
69:35
you perform first CTP or CTA? Is there any difference performing one
69:38
or the other first?
69:42
Yeah, I I I'm not an expert on the technical
69:45
factors there. I think
69:48
both have been done and
69:51
I don't know which one is preferred.
69:56
That's it for the case. Yeah, and my old institution. We did CTA
69:59
followed by CTP.
70:05
You did have to wait a couple minutes after a
70:08
CTA to let that contrast equilibrate. So you
70:11
get back to Baseline before we start your CTP. And
70:14
so it does add a few minutes before you
70:17
have a reliable signal for CTP. But usually
70:20
you're doing your technologists
70:23
are doing stuff on the on the on the scanner trying to
70:26
gear out for the CTP. Anyway, so the time
70:30
passes pretty quickly, but that's how we did things
70:33
where I trained.
70:36
Got one more question for this one isn't anticoagulation contraindicated
70:39
given hemorrhagic transformation.
70:44
That's a good question. So I'm not a stroke neurologist
70:47
or neurontinence intensivists. I will
70:50
say that.
70:52
The degree of hemorrhagic transformation is informative
70:55
in determining how and
70:58
when to initiate anticoagulation. So
71:01
anticoagulation is indicated when people have
71:04
a cardiabolic source such as with atrial fibrillation and the
71:07
timing of the initiation of that anticoagulation.
71:13
Depends on how large the territory you're infarct
71:16
is and whether you've had symptomatic
71:19
hemorrhagic transformation or not, but
71:22
it's not a strict contraindication, but people
71:25
do vary about when they start anticoagulating for
71:28
this patient and atrial fibrillation some
71:31
might wait, you know two weeks after the stroke before
71:34
beginning into coagulation. So what I
71:37
indicate on the slide that the trim was anticoagulation, I don't think it was immediately begun
71:40
because they were suppressants of
71:43
of because there's a presence of hemorrhagic transformation.
71:46
That would be a relative contradictation to immediate initiation
71:49
of anticoagulation.
71:55
All right. Our last case comes with the history
71:58
of altered mental status.
72:00
You dig deeper into the chart and find out this is
72:03
a 61 year old patient. They've had a history of rectal
72:06
cancer. They had an episode of sudden confusion
72:09
that was characterized also by
72:12
diffuse weakness, but they couldn't really tell you it was going on.
72:15
They don't really remember that episode very well, but onlookers say
72:18
they were nonverbal or a little bit but then they
72:21
recovered their strength returned on examination. Now in
72:24
the emergency department their NHL scale is only
72:27
one. So we're gonna check out our non-con head
72:30
CT in this situation. I'm going to point out a
72:33
couple of abnormalities that I think are potentially relevant
72:36
potentially incidental also not point out
72:39
all the abnormalities. So take a close. Look at these images for
72:42
any findings that you may see. One thing
72:46
I will point out is that there are some scattered cortical calcifications.
72:49
These might be due to Chronic calcificus.
72:54
And then there's also a hypertensity here in the left civilian fissure.
72:57
That was thought to be small amount
73:00
of subarachnoid hemorrhage, okay.
73:04
But we did not see any loss of gray white differentiation to
73:07
indicate early ischemic change.
73:15
And there is one additional abnormality that is on
73:18
this image, but I'm not going to point it out because I will
73:21
give it give the case away. Okay?
73:26
So now we're going to move on to the CT perfusion.
73:32
So I'm gonna pull up the summary Maps. First of all, there's nothing
73:35
segmented as CBF less than 30% There
73:38
was a small finding that was highlighted as
73:41
team actor and then six seconds, but I think some of it is kind
73:44
of motion artifact or
73:47
calvarium some of the corresponds to Superior sagittal
73:50
sinus.
73:53
And so we're going to take a closer. Look at the color maps
73:56
to try to figure out what is exactly going
73:59
on here.
74:02
So I'm going to pull up the TMax and while
74:06
I'm doing this we can activate the poll
74:09
question. I'm going to pull up something else, which is the TTD which
74:13
is provided by single via not
74:16
rapid, but this stands for time to train.
74:20
it's kind of a complementary measure to TMax TMax
74:23
is a time to get the peak of the of the
74:28
time attenuation curve and time to train as the kind
74:31
of the down slope to that.
74:34
And so you notice that there is a asymmetry here. There's
74:37
a little bit higher T Mac little
74:40
bit higher time to train in the right right a little
74:43
bit in the left right A lobe as well as the right
74:46
occipital lobe and maybe even
74:49
posterior temporal lobe question is
74:52
what which were the following diagnosis is most likely
74:55
in this case. We also see an area the team
74:58
axis decrease, you know, it's like very deep blue. So
75:01
there's a suggestion this is hyper perfused.
75:04
If we examine the CVV Maps,
75:07
we can support that suspicion. There's elevated cbv in
75:10
this left parietal region. So kind
75:13
of have kind of complementary bilateral after
75:17
maladies going on this patient.
75:20
So is it transient ischemic attacks? Orbital Venous Thrombosis
75:23
posterior reversible encephalopathy syndrome
75:26
metastatic disease and so forth.
75:29
And it looks like now a great job everyone
75:32
66% of you chose the right
75:35
answer which is super Venous Thrombosis. Now, I want
75:38
to rewind a
75:41
little bit and take a look at our non-con SAT
75:44
to see in retrospect. Can we see the abnormality that
75:47
we're looking at it? So there is this hyper density in this
75:50
right transfer sinus extending into
75:53
the superior sagittal sinus at the hyperdense drove against
75:56
sinus is concerning for thrombosis.
76:01
I'm gonna pull up our CTP again because of
76:04
the perfusion abnormalities in the parietal lobes.
76:08
and the right occipital lobe
76:12
it did raise this suspicion for cerebral Venous Thrombosis, simply
76:15
because this territory is a little bit too big for posters
76:18
artery. It doesn't seem like a arterial territory seems
76:21
a little bit wider than that. And so we're gonna review
76:24
our CTA with an eye towards that and I know not all
76:27
the time on ctas. Do we have a good a Venus
76:31
evaluation, but in this
76:34
case we so happen to have a pretty good venous
76:37
evaluation. So
76:41
Yeah, but let it buffer
76:44
a little bit. So we see good contrast modification
76:47
in the straight sinus.
76:51
a pain of Galen kind of keeps herbal veins region, but
76:54
then nonopastication of the super sagittal scientists where we
76:57
saw that hyper density on CT and
77:03
It's taking a little bit for me
77:06
to load all these images and pull the thicker slice and
77:09
just to demonstrate that none of classification of the super sagittal
77:12
sinus transfer sinus.
77:14
right sigmoid sinus
77:16
extending into the internal jugular vein where we
77:19
see in the neck to expanded with clot.
77:24
All Upstream of this central venous catheter they have a chest port for
77:27
their rectal cancer chemo. And so
77:30
we have this thrombosis coming off
77:33
from the neck into the head along the
77:36
draw Venus sinuses. So that can confirms our
77:39
diagnosis of cerebral Venus barboses involving,
77:43
you know, drawing a sinuses and that explains
77:46
the prolongation of the time
77:49
to drain in the right posterior
77:52
cerebral hemisphere a little bit in the middle part
77:55
of the left cerebral hemisphere as well.
77:58
And this hyper perfusion area is chalked up
78:01
to be periodical hyper perfusion. Okay, so we have
78:04
in the periodic table period an elevation of
78:07
CBF and cbv in the
78:11
immediate kind of periodal and
78:14
postictal period and then it the cerebral blood
78:17
volume declines after that.
78:20
And so this is see here either as a
78:23
consequence of the several Venus
78:26
kind of thrombosis or it
78:29
can be due to irritation from that small amount of subarachnid hemorrhage
78:32
that we saw it's oligomy interrelated somehow the causation direction
78:35
of causation is not exactly clear
78:38
so
78:40
So once again just summarize in retrospect
78:43
we could see hybrid ends droving a sinuses
78:46
and non-con CT. We saw a little bit of hemorrhage. We see
78:49
some quarterly house calcifications that could
78:52
cause seizure. So we're on high alert for stroke mimics. In
78:55
this case. In this case. We saw hyper perfusion left parietal
78:58
lobe and this may be periyctal in nature. But
79:01
we also saw kind of bilateral abnormality
79:04
and delayed time to drain in the right occipital
79:07
and bilateral parietal lobes and and our
79:10
suspicion for Venous Thrombosis confirmed on
79:13
the CT angiography which which fortunately, you
79:16
know, kind of contaminated with a lot of venous phase but we
79:19
can make the diagnosis very confidently based
79:22
on the constellation of all these abnormalities this patient
79:25
did go on to get an MRI just to
79:28
confirm some of the
79:30
the vaster findings as well
79:33
as to better evaluate the brain parenchyma. So
79:36
here's our diffusion weighted image just
79:39
to see there are a few spots and
79:42
dots of dwr hyperintensity here. And there there's this cortical
79:45
area of slight DWI hyperintensity
79:48
in the left parietal region that corresponds to
79:51
some fire hyperintensity as
79:54
well. This is either post ictal swelling or
79:57
it could be a Venus in fart or result
80:00
of Venus congestion. And and
80:03
we did do a
80:07
Like I post contrast sequence to
80:11
win weighted gray and echo-based sequence that
80:14
re-identify is that feeling defect in the
80:17
superior sexual sinus extending all the way down into the right
80:20
transverse and sigmoid sinuses and down into
80:23
the neck as well confirming the diagnosis. So
80:26
so basically MRI redemstrating what
80:29
we could tell on close scrutiny of the
80:32
non-con CT the CTA and the CT perfusion.
80:36
This patient was managed with anti-seizure medications and
80:39
anticoagulation.
80:41
So in summary was this case about this is case of super
80:44
Venous Thrombosis and had related congestion
80:47
that we could see as elevated T Max
80:50
and time to train on our CT perfusion as well as superimposed
80:53
Perry ictal hyper perfusion that's elevated cbv
80:56
and CBF in that left Bridal region.
80:59
It was in a non-vascular non-arterial territory
81:02
and taking together with the clinical context of the
81:05
kind of transient symptoms was most
81:08
compatible with seizure recent
81:11
seizure following several Venus thrombosis. And
81:14
this is a stroke mimic. So here the take-home points
81:17
from the session on CT perfusion. Say number
81:20
one use non-con CT to
81:23
guide your interpretation of infarct core. The use
81:27
of CTP. CBF Maps is most helpful as
81:30
an adjunct for estimating the infrared core
81:33
in the late window of hyperacuse road.
81:36
It's like six to 24 hours outside this window.
81:39
It's a little bit less for Reliable in the early.
81:41
Will be aware of ghost infarct core
81:44
that is overestimation of what is actually
81:47
infarcted based on your CBF map that on follow-up
81:50
turnout not to be infarcted.
81:53
Beware of false negative situations that
81:56
can occur very late in acute stroke
81:59
into the Subacute window because that territory
82:02
has already reperfused. So you have normalization or
82:05
even high per perfusion on your
82:08
cvf and TMax Maps similarly
82:12
beware of bilateral perfusion
82:15
deficit which may mess up the computers analysis
82:18
of what is abnormally reduced relatives
82:21
removable blood volume. So you have to rely on
82:24
your quality of analysis. Okay. This territory is normal. This one
82:27
is abnormal on the ipsilateral side as well.
82:31
Beware of stroke mimics like seizure that
82:34
can be occurring in the case of press and several Venous
82:37
Thrombosis as we saw in our two cases
82:40
use CTP as a helpful guide to
82:43
augment your review of CT angiography, especially for
82:46
challenging areas, like medium vessel occlusions stenosis
82:49
or in our
82:52
last case Venus thrombosis, which can be easily missed
82:55
on a CT angiogram as well. There are
82:58
emerging uses for CTP for crowded stenosis, like
83:01
our case of near occlusion that we had as well as for
83:04
cerebral basis fathom after severeign hemorage about
83:07
caution you to interpret these not in the
83:10
same way that you interpret Lara's vessel occlusions Strokes, right the interpretation about
83:13
the threshold the CBF less than 30 team experience
83:16
doesn't really apply. It's not been validated in
83:19
these clinical contexts. So I would stick to remaining descriptive
83:22
about there are these areas of hypo perfusion
83:25
corresponding to the CT anger and your
83:28
graphic abnormalities and hopefully
83:31
That's in a helpful additional data point for the managing neurologists
83:34
neuro-interventional Specialists
83:37
to take to into
83:40
account when determining how to manage these very
83:43
complex patients. So with that having to
83:46
take any questions about the talking general or
83:49
this very last case.
83:52
Either a couple of questions if you're if you're game
83:55
for it.
83:57
TTP or TMax which is preferred. Is it
84:00
okay to evaluate only with TTP since some vendors don't
84:03
provide TMax and only give MTT and TTP. Yes, so
84:10
There's certainly disagreement in the literature about what is
84:13
the best parameter to use TTP and
84:16
TMax for relatively similar metrics and
84:19
just so happens that the dominant vendors
84:23
at least around my neck of the woods
84:26
use TMax primarily in determining what
84:29
is called the critical hyper
84:32
hypo perfusion Zone, but I
84:35
certainly understand that, you know, the the literature
84:38
is not 100% clear that team expert in
84:41
the six seconds is the best whatsoever in that some
84:44
vendors may choose to use TTP as well. But I
84:47
am agnostic about that. I think
84:50
there's there's
84:53
kind of a general
84:56
preference among these vendors to use team acts and
84:59
that's what I stick to and that's what I'm familiar with.
85:04
They should we always report the
85:07
hypodensity volume.
85:10
I think that's a stylistic thing. I like
85:13
to do that just because I like to communicate a
85:17
somehow the size
85:20
of infarx and that's
85:23
based on my experience of
85:26
seeing reports that say there's a MCA territory
85:29
infarc, but the infarct is actually like, you know, just the
85:32
basal ganglia plus the insula and just like, you know 10 milliliters
85:35
in Fargo. That's a very different story or the
85:38
patient compared to an MCA in Fargo. That's 200
85:41
milliliters. Right? And so just because
85:44
I like thinking quantitatively I try to estimate the
85:47
area of infarct some people like doing it kind of
85:50
semi quantity large medium small would have you but I
85:53
I if it's easy to
85:56
measure and just takes me a couple seconds once I'm fast
85:59
out with the measuring tools my packs I
86:02
Try to estimate the infarct volume.
86:06
Usually here because we get an MRI
86:09
and everybody I usually just provide it
86:12
for volume on the MRI. It's a better more reliable
86:17
way to measure it then trying to estimate it on the
86:20
first non-con has CT but in
86:23
general, you know, I think there is some relevance
86:27
providing a volume measurement at some
86:30
point because that is correlated with
86:33
their neurologic prognosis.
86:37
Or answering that one more question. This goes
86:40
all the way back to the first case. I didn't catch
86:43
it in time. Should we exclude a total region on
86:46
the aspect score even if a small part is involved?
86:52
Strictly speaking how the aspects score was
86:55
defined. Yes, if only
86:59
one part of say the
87:02
m6 section of the super
87:05
ganglionic, you know parietal cortex
87:08
was infarcted. Yes, he would say that
87:11
region is affected. It doesn't have to be the whole region is
87:14
affected.
87:15
Now I want to be clear that to count as affected
87:18
you have to have great white differentiation loss. It's not
87:21
enough to have cycle effacement. It's not
87:24
enough to have a white matter alone hypodensity. Even
87:27
if that's why matter if are you just don't know on non-conhead CT.
87:31
So you have to see great white differentiation laws somewhere
87:34
in that region to say
87:37
that it's affected. But yes any small
87:40
part of that region effective means that the region is affected. So
87:43
people have criticized to aspects score. It's not linearly scaled
87:48
to the infarctic volume, but this
87:51
is a relatively quick
87:54
and easy way to express
87:57
the extent of MCA territory
88:00
involved in Far That neurologists and
88:04
neuro interventionalists are familiar with
88:07
I think we'll end it there since we're overtime Dr. Dang.
88:10
Thank you so much for this incredible case review and everyone
88:13
out there for your questions. This was
88:16
really fantastic. Thank you so much. You can access the
88:19
recording of today's conference and all our previous new conferences
88:22
by creating a free MRI online account, and be
88:25
sure to join us next week on Thursday, April 20th at
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12 pm Eastern featuring Dr. Robin Roth for
88:31
a lecture on best of the breast cases. You can
88:34
register for this free lecture at MRI online.com and follow
88:37
us on social media for updates on future new conferences. Thanks
88:40
again, and have a great day.
Francis Deng, MD
Assistant Professor of Radiology and Radiological Science
Johns Hopkins University School of Medicine
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