Interactive Transcript
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We are proceeding with this patient who had a dense MCA
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sign on the non-contrast CT scan and then had a CTA.
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The CTA showed the occlusion of the M1 segment
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of the left middle cerebral artery, as well
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as a clot that was extending in the proximal
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A1 segment of the middle cerebral artery.
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Now, at that point, sometimes you will
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have a CT perfusion study to see whether
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the entire middle cerebral artery distribution is
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infarcted, or you may just have the CTA, and they're
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making a judgment about whether to proceed to
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thrombectomy based on the patient's symptomatology.
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In this case, the patient did not have a CT
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perfusion but did go on to thrombectomy.
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And that was considered successful.
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Two days later, the patient had this
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MRI scan that I'm about to show you.
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Now, if the thrombectomy was successful, we would hope
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that the speech areas would not have been infarcted,
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and we would hope that the vast majority of the motor
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cortex and the MCA distribution, again, would be spared.
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And we can also make that assessment
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based on the patient's symptomatology.
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If the aphasia went away after the thrombectomy,
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then there was good reperfusion. Nonetheless, in most
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cases—not in the emergency room potentially, but as
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an inpatient—the patient will have a follow-up MRI,
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because diffusion-weighted imaging still, to this day,
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is our gold standard for the imaging of a stroke.
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It's not the gold standard for determining
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whether the patient has neurologic deficits.
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That's the patient, and that's the clinical examination.
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However, for the imaging evaluation
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of the volume of infarcted tissue,
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it remains diffusion-weighted imaging.
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And that's what I would start in any
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case in which you are being asked about
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the BAT team—Brain Attack Team—or,
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uh, for an acute stroke. Go immediately
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to your diffusion-weighted imaging to
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see whether an acute stroke is there.
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So that way, you can make that call much earlier
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to the clinicians because time is brain, right?
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So, if they can save some brain, uh,
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then the patient has fewer neurologic
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deficits and a better long-term prognosis.
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So, here's an MRI scan when we scan the patient.
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Particularly in this setting, the very first clinical
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pulse sequence that we're going to do is going
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to be the diffusion-weighted scanning after a scout
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image to determine the location of those slices.
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So, for example, if I just show you this, this is
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the scout image—three images, basically—that take
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about, you know, 10 seconds, and then the next
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pulse sequence is going to be our diffusion-weighted
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imaging. For the diffusion-weighted imaging,
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remember that there is an initial B0 in which the
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diffusion gradients have not been applied, and then
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there is the B1000 in most clinical settings, where the
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diffusion gradients have been applied.
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And here we see the patient's diffusion-
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weighted scan on diffusion-weighted imaging.
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Imaging strokes are bright, so here
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we have the patient who had that.
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M1 segment occlusion and A1 segment thrombus.
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And what we see is a stroke, which is limited to
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the caudate nucleus and putamen on the left side.
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All of the remainder of the middle
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cerebral artery distribution on the left
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side was saved by that thrombectomy.
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So, there is an acute infarction here.
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It's affecting the basal ganglia, which
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likely will cause motor neurologic problems.
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But the speech centers of Broca's area and Wernicke's
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area have been spared, and therefore, one would suggest
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that this is a successful case in which, although
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a stroke was not avoided, the vast majority of the
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middle cerebral artery distribution has been saved.
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Now, after looking at this diffusion-weighted
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imaging, I'm on the phone with a clinician saying,
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"Hey, this patient has had an acute infarction.
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It's involving the caudate and the putamen, predominantly
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sparing the globus pallidus." So, you're on the phone
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early to give that information as soon as possible.
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The next thing they're going to ask you is,
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"Is there any hemorrhage?"
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So, the next pulse sequence that I would look at
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is going to be our susceptibility-weighted scan.
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The susceptibility-weighted scan is the scan
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that is most sensitive to the presence of
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hemorrhage. In this case, we see that
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the globus pallidus region has low signal
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intensity here, implying hemorrhagic products.
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However, this is likely hemosiderin because
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there's no edema surrounding it that I can see.
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So, remember that the patient had had a prior
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foraminal stroke, and this is probably hemorrhagic
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hemosiderin blood products rather than acute
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hemorrhage of deoxyhemoglobin.
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In any case, it's limited to the basal
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ganglia, not involving the distal middle
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cerebral artery distribution tissue.
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At that point, I would probably go to the FLAIR scans.
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The FLAIR scans are going to be our global
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view of what's going on in the brain.
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It identifies for us the old injury
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where there had been that craniotomy that
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we had seen on a non-contrast CT scan.
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So, this is gliosis.
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This is not an acute infarction.
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We know that because the DWI was negative.
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Here, we have loss of volume in the
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foraminal region from the prior stroke.
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Here, we have another area where
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there's cortical injury and scarring.
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But once again, this was negative on the DWI.
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So, let me just verify that for you
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by putting side by side the DWI.
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So, we're at the top of the ventricles here.
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This is this area here.
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However, this is likely hemosiderin because
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there's no edema surrounding it that I can see.
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So remember that the patient had had a prior
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foraminal stroke, and this is probably hemorrhagic
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hemosiderin blood products rather than acute
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hemorrhage of deoxyhemoglobin.
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In any case, it's limited to the basal
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ganglia, not involving the distal middle
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cerebral artery distribution tissue.
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At that point, I would probably go to the FLAIR scans.
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The FLAIR scans are going to be our global
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view of what's going on in the brain.
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It identifies for us the old injury
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where there had been that craniotomy that
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we had seen on a non-contrast CT scan.
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So this is gliosis.
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This is not an acute infarction.
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We know that because the DWI was negative.
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Here we have loss of volume in the
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foraminal region from the prior stroke.
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Here we have another area where
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there's cortical injury and scarring.
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But once again, this was negative on the DWI.
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So let me just verify that for you
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by putting side by side the DWI.
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So we're at the top of the ventricles here.
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This is this area here.
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No bright signal on the DWIs.
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This is an old injury.
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Similarly, this is an old injury on the FLAIR scans.
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The next thing I would look at is the T2-weighted scan.
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The T2-weighted scan is our better assessment
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of the posterior fossa structures.
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So I look at the brainstem, I look at
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the cerebellum, I look at the pons.
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Here, I look at the middle cerebellar peduncles.
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No injury in the posterior fossa on the T2-weighted scan.
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Again, we see
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the acute infarction as well as the old infarction.
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This is this area over here where
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there was a previous injury.
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There is a little bit of a small area
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going into the beam, but the vast majority
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of this shows evidence of chronicity.
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At this point, you may have an MRA.
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Most of the time, if you've had a CTA in
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advance of the MRA, there's really no need
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to duplicate the neurovascular imaging.
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You go with the CTA.
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So in summary, for this case, the correct diagnosis is a
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left middle cerebral artery M1 segment occlusion with a
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proximal left A1 segment small area of clot as well,
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associated with a basal ganglionic
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infarct and older injuries to the brain
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in the left frontal lobe and left putamen.
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The thrombectomy avoided involvement of a large
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portion of the middle cerebral artery with
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preservation of Broca's motor speech area,
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as well as Wernicke's receptive speech area
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on the diffusion-weighted MRI scan.
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So congratulations if you got all
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that on your analysis of this case.
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