Interactive Transcript
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The MRI protocol for evaluation of the
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patient for head trauma should include T2
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weighted FLAIR imaging, diffusion-weighted
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imaging, and susceptibility-weighted imaging.
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This is a study that there's very little
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role for post-contrast imaging.
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And this was a great example of
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the benefit of MRI for diffuse axonal injury,
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a rotational acceleration-deceleration injury.
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In this case, what we see is a hematoma over
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the right parietal-occipital region, and this is
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likely where there was the original contact injury,
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the so-called coup injury on this FLAIR scan.
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However, we notice that the suppression
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of the cerebrospinal fluid to make
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the CSF dark on FLAIR is not present.
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It's bright CSF.
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That means there's abnormality in
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the CSF and in the trauma setting.
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This is going to be subarachnoid hemorrhage.
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So the patient has bilateral subarachnoid
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hemorrhage over the upper convexity.
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Not only that, but we see that there is abnormal
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signal intensity in the splenium of the corpus
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callosum, manifested as this bright signal intensity.
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It's not only affecting the splenium, it's going
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anteriorly to affect actually the septum pellucidum.
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And here we are at the top of the corpus callosum as
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well, where we see the bright signal intensity.
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So this in and of itself would suggest that
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This is a pretty gross traumatic injury.
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You notice also that the patient has
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high signal intensity in the occipital
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horns of the lateral ventricles.
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The normal frontal horns have dark signal intensity.
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Why is this bright in the occipital horns?
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This is blood layering in the occipital horns of the
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lateral ventricles.
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As you go further inferiorly, you notice
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that the posterior aspect of the midbrain
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shows high signal intensity, maybe worse
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on the left side than the right side.
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And there is spillover into the cerebellar folia,
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where there is bright signal intensity in the
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subarachnoid space of the upper vermian structure.
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So there's hemorrhage also in the posterior fossa,
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as well as injury to the midbrain and pons junction.
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Now let's look at the patient's gradient
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echo scan for hemorrhagic products.
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So normally, we would recommend going
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with susceptibility-weighted imaging.
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If your MRI scanner does not have SWI pulse sequences,
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the next best thing is to go with a low flip angle
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gradient echo scan. Here on this gradient echo scan,
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what we see is an area of dark signal intensity
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crossing into the left side of the midbrain,
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identifying hemorrhagic products in the
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midbrain, associated with that amount of edema.
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As we go further inferiorly, we see blood products,
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also the dark signal intensity in the subarachnoid
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space of the vermis, and then going further.
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Superiorly, blood products layering in the
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occipital horns of the lateral ventricles.
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And then here we have this very black area, this
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dark area in the corpus callosum, the junction
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between the splenium and the septum pellucidum, which is seen
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here, the posterior septum pellucidum, and corresponding
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just to the right of midline, more hemorrhagic
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products in the top of the corpus callosum.
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And...
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Farther superiorly, at the gray-
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white junction, on this gradient echo
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scan, more areas of hemorrhage.
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So this is grade three diffuse axonal injury.
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Why grade three?
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Grade one—
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we have the foci at the gray-white junction
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for shearing injuries at the fixation point
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of the gray matter to the white matter.
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We have the involvement of the corpus callosum,
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identifying it as grade two hemorrhage and injury, and
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the presence of brainstem edema and hemorrhage is the
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criterion for grade three diffuse axonal injury—
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the worst grade.
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So this patient has a very poor prognosis.
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When you just look at the brain, it doesn't
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look... you know, there's no midline shift.
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The ventricles look pretty good.
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The parenchyma doesn't look all
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that horrible on the FLAIR scan.
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But when you combine that with the gradient
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echo scan for blood products, you see that the
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patient actually has a fairly severe diffuse
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axonal injury, grade three, and therefore
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a very poor prognosis.
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This patient has additional pulse sequences.
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The diffusion-weighted scan, as I mentioned previously,
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is useful for the identification of whether or
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not the patient has cytotoxic edema secondary
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to glutamatergic outpouring of neurotransmitters
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that can lead to a diffuse cerebral edema pattern.
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In this case, all we're seeing is the cytotoxic
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edema associated with the shearing injuries,
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rather than the diffuse involvement
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of the brain. The patient had an MRA.
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The MRA is not useful.
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It's not part of our traditional trauma
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protocol. I think it was done because they were
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unsure whether the patient's hemorrhage in the brain
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was secondary to a vascular etiology versus trauma.
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Uh, you might think, "Oh, how
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that... that's pretty obvious."
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But unfortunately, a lot of times what happens is
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that the patient gets in a motor vehicle accident
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and is unconscious, and the clinicians will say,
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"Well, did the patient have an aneurysm that bled,
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which led to loss of control of the motor—"
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"—the car, which led to a motor vehicle collision,
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as opposed to just a motor vehicle collision?"
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And that sequence is, uh, sometimes
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obscured when the patient is unconscious
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and can't give you a clinical history.
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So when they see subarachnoid hemorrhage,
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we would say as radiologists, "Well, it's
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most likely secondary to the trauma."
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But they sometimes ask the question, "Well, could the
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patient have had an aneurysm that bled, which led
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to them being unconscious and crashing their car?"
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So that's why sometimes you will see an MRA
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or a CTA, uh, performed even in the setting of
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trauma. In this case, that, uh, MRA was normal.
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