Interactive Transcript
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This was an elderly gentleman who had bilateral visual loss.
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Let's start with looking at the magnified
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views of the optic nerves.
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These are fat-suppressed T2-weighted imaging, and we
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see very nicely the optic nerve sheath
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and the optic nerve intraorbitally.
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Here we are seeing the globes,
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and now we come to the optic nerves.
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And at first blush,
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the optic nerves and the optic nerve sheath look good,
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demonstrating the dark signal intensity of the optic nerve
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contrasted by the bright signal intensity
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of the CSF within the optic nerve sheath.
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Remember, as I said previously, the optic nerve,
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because it is a portion of the white matter of the brain
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should have similar signal intensity to the white matter
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elsewhere in the brain. And these look normal initially.
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However, as we scroll more posteriorly,
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we're going to find some abnormality.
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We are at the level of the optic canal.
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How do we know we're at the level of the optic canal?
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Once again,
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we identify the dark signal intensity of the anterior
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clinoid process, and we note that the optic canal is going
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to be medial to the anterior clinoid process.
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Here we see the optic nerve,
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and we note that the signal intensity has changed.
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It is no longer the same as the white matter of the brain.
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It is brighter than the white matter and seems as if it's bilateral.
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So we would consider, once again,
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could this patient have neuromyelitis,
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optica or another cause of bilateral optic neuritis?
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We're going to continue to scroll a little bit more
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posteriorly, and we continue to see the bright signal
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intensity of both optic nerves
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as they come intracranially.
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And now, we're within the brain substance and in the
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subarachnoid space, and we're coming to the optic chiasm,
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which has normal signal intensity.
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The next thing to do is to look at the
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postgadolinium-enhanced images.
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These are magnified views of the postgadolinium fat
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suppressed images of the optic nerves and the orbits.
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And what one sees is somewhat fluffier enhancement
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around the optic nerve sheath, potentially better seen
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on the left side than the right side on this image.
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So, what I'm describing is the abnormal contrast
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enhancement that seems to be beyond the normal thin
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enhancement of the optic nerve sheath, on the left side,
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and it looks as if it's going into the intraorbital fat.
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Let's see if that persists as we scroll more posteriorly.
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On this image as well,
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we see that the enhancement of the optic nerve sheath
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seems somewhat ragged in appearance and is a little
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more prominent than what I've demonstrated in the
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normal optic nerve sheath previously,
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but it's not as thick as one would expect
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for an optic nerve sheath meningioma.
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So right now, we have abnormal signal in the optic nerves,
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as well as fluffy enhancement around the optic nerve sheath.
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On this image, we are at the level of the optic canal.
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How do we know we're in the optic canal?
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We identify the anterior clinoid process.
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So, the anterior clinoid process has
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its bone marrow signal and cortical signal,
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seen as the dark and bright signal intensity here.
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And we are identifying the optic nerve as showing
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contrast enhancement bilaterally.
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In this case,
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we also start to see some abnormalities associated
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with the intracranial compartment.
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For example,
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we note that there does appear to be some enhancement
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along the frontal horns of the lateral ventricles.
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So, let's shift at this point to the contrast
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enhanced images of the brain.
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This is a standard post-gadolinium non-fat
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suppressed image of the brain.
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So you note that the orbital fat remains bright.
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And as we scroll through the brain,
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we come to the more superior aspect of the brain,
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and we note abnormal enhancement in the
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subarachnoid space of the brain.
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This is a bilateral process
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with abnormal enhancement in the subarachnoid space,
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looking as linear areas deep to the sulci of the brain.
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And this goes to the superior aspect of the brain, as well.
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So, how do we wrap this all together?
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So, this is an instance where we might suggest that
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there is a process of the subarachnoid space,
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either infectious inflammatory or neoplastic,
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that could be affecting the optic nerve sheath
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complex and affecting the optic nerve, secondarily.
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In my report on this case,
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I recommended evaluation of the cerebrospinal
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fluid by lumbar puncture.
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This patient ended up with a final diagnosis of leukemia
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with subarachnoid space involvement of the leukemia,
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as well as the optic nerve sheath complex,
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leading to bilateral optic neuritis.
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