Interactive Transcript
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I wanted to show another example of
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neuromyelitis optica spectrum disorder.
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This case is particularly good because it identifies
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on the sagittal FLAIR scan,
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a nice demonstration of the area postrema.
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So on this sagittal FLAIR scan,
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one sees abnormally high signal intensity along
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the posterior aspect of the medulla
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below the fourth ventricle.
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This is seen right here in this bright signal
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intensity area, which is the area postrema,
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which is characteristic of brainstem or
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involvement with neuromyelitis optica.
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Now, the back of the medulla has an area
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where it kind of bulges outward at the junction
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with the cervical spine.
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And this area is called the clava,
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which is intimately associated
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with the area postrema.
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You notice that the patient also has a few
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additional lesions within the pons.
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On the axial scan,
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we see lesions within the midbrain
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as well as the pons,
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as well as the area postrema,
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more on the right side than the left side.
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And then we start to get into the cervical spine disease,
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which I'll describe momentarily.
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These lesions do not show contrast enhancement.
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The patient had incidental post-traumatic injury
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to the occipital lobe.
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That would probably
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also affect the patient's visual acuity,
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but was unrelated to the demyelinating disorder.
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Let's look at the orbits.
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We have T1-weighted,
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T2-weighted scan with fat suppression
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and post-gadolinium enhanced scan.
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In looking at the orbits,
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we should probably make sure
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that there's no mass first.
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So, this patient shows no masses in the orbits.
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Patient does show evidence
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of a previous lamina papyracea fracture
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with herniation of fat through there.
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On the T2-weighted scan,
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we see small optic nerves,
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which are bright in signal intensity centrally.
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And as we get to the optic canal, bilaterally,
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we see bright signal intensity,
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left greater than right,
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but bilaterally within the optic nerves.
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On post-gadolinium enhanced scan,
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as we get to the optic canals,
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we see both of the optic nerves showing contrast enhancement.
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Let me magnify once again.
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Here you see the anterior clinoid process.
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And medial to the anterior clinoid process,
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is where the optic nerves go through the optic canals.
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In this situation,
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what we have is bilateral optic nerve
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contrast enhancement with gadolinium.
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As I scroll through them,
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you'll probably see it a little bit better.
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Here is the optic nerve through the optic canal.
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Again, anterior clinoid process,
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and then coming to the optic chiasm.
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Both of these optic nerves are showing contrast
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enhancement at the optic canal,
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as well as on the T2-weighted scan,
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very bright signal intensity going
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through the optic canal.
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So we have white matter lesions in the brain,
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in the area postrema, as well as in the brain stem.
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We have small optic nerves,
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suggesting that this is a multiphasic
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process with optic atrophy,
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but active demyelination as evidenced
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by the contrast-enhancing optic nerves
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at the optic canal, bilaterally.
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The next thing to look at would be the spine.
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And here you can see that this patient has
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longitudinally extensive white matter lesions
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in the cervical spine,
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as well as the thoracic spine.
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When we look at the thoracic
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spine on this STIR image,
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we are struck also by the decrease in
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the caliber of the spinal cord.
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We usually say that the spinal cord should
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subsume around 50% or more
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of the total spinal canal AP diameter.
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This is less than that.
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So, this patient has cord atrophy from multiple
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episodes of transverse myelitis.
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You can see cord expansion further superior.
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We would not expect this portion
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to show contrast enhancement,
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but the more active demyelinating portion could
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potentially show gadolinium enhancement.
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Let's see how well I did.
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So, here on our post-gad T1-weighted scan,
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in point of fact,
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we see no contrast enhancement
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within the spinal cord,
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and we can confirm that,
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on our axial scans,
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that there is nothing showing contrast enhancement.
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So nonetheless,
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this is probably two different age disease,
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the one with the cord atrophy being more chronic
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than the one which is showing some cord
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expansion, yet without contrast enhancement.
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The combination of longitudinally extensive
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transverse myelitis, optic neuritis,
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as well as the imaging findings in the brain
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at the area of postrema,
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suggest a diagnosis of
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neuromyelitis optica spectrum disorder,
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and it would be confirmed with serology
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for the aquaporin-4 antibodies.
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