Interactive Transcript
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Well, this was a 21-year-old who had an acute
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neurologic episode and was presenting to
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the emergency room with new onset of
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tingling in the hands,
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as well as the legs.
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And on the scans that we're looking at,
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which are the axial FLAIR,
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the axial T2-weighted,
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and the axial ADC map.
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When we start to scroll,
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we initially look at the T2-weighted scans
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through the posterior fossa,
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and we see that there are areas of bright
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signal intensity along the periphery of the pons,
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as well as adjacent
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to the fourth ventricle.
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These types of peripheral
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brainstem lesions are
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not uncharacteristic of multiple sclerosis.
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So we don't just look in the
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central white matter,
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but we are looking at the periphery of the
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brainstem for demyelinating plaques.
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Here is a periventricular lesion,
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but periventricular around the fourth
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ventricle rather than our typical
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lateral ventricle,
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and very nicely seen on the T2-weighted scan
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and probably visible to most
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people on the FLAIR image,
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particularly if I put a lot
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of yellow lines around it.
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These lesions are not showing
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restricted diffusion.
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As we continue further superiorly,
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we see on the FLAIR scan of the
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supratentorial region,
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multiple demyelinating plaques,
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and they include those in
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the periventricular zone
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as well as ones that I would
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call juxtacortical.
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So, we have both periventricular
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and juxtacortical.
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Notice how well these are demonstrated
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on the FLAIR scans,
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whereas the T2-weighted scans,
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you would see them in retrospect,
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but certainly not as well demonstrated as
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having a pulse sequence that has dark
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signal intensity to the CSF.
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Let's continue to scroll further superiorly.
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Lots of demyelinating plaques.
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Again, ones that we would
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call periventricular,
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as well as one that's fairly deep and
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adjacent to the gray matter,
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and therefore fulfills juxtacortical.
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So we're already at the point where
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we have periventricular,
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we have juxtacortical,
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and we have infratentorial lesions without
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even looking at the spinal imaging.
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So, we have fulfilled the dissemination in
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space criteria as defined by
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the McDonald criteria.
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We are not seeing plaques that are dark in
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signal intensity or periphery
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on the ADC map.
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So right now, we have dissemination in
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space, but not dissemination in time.
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I want to pull down two
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more pulse sequences,
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and those are the postgadolinium-enhanced
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scans on your right and the susceptibility
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weighted scan in the center.
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Now, there is a differential diagnosis for
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multiple white matter lesions.
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This is a real good juxtacortical
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lesion here.
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So, there's a differential diagnosis that
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includes things such as collagen
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vascular disease,
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or vasculitis, or even migraines,
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or post-traumatic demyelination,
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which is in the differential diagnosis.
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However,
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if we look at the susceptibility
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weighted scan in the center,
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what we see on this particular
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slice is a very nice examination example
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of the perivenular nature of this
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patient's disease.
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So even here,
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at 1.5 or 3 Tesla scanning, we see the vein
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and we see the area of demyelination
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around the vein.
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Here we are seeing very nicely,
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the veins and the demyelination
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around the veins.
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So, this allows us to be even more specific
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within our differential diagnosis to
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suggest that this indeed represents
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multiple sclerosis.
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As we scroll through the scans,
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post-gadolinium,
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we do not see any enhancing plaques.
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Therefore,
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by McDonald criteria,
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the absence of seeing
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enhancing plaques or cytotoxic edema
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associated with demyelinating plaques,
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we have not fulfilled the criteria
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of dissemination in time.
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Now,
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the clinicians may have a patient who has
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multiple episodes of a neurologic deficit.
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In this case,
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it was in the emergency room
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with the first deficit.
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So this may not actually represent
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multiple sclerosis clinically,
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and we have not yet fulfilled those
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criteria by McDonald criteria
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for dissemination in time.
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So by virtue of the MR pattern,
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we would say that this is likely a
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demyelinating disorder with dissemination
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in space with multiple juxtacortical
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periventricular and infratentorial lesions
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without evidence of contrast enhancing
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plaques or cytotoxic edema to suggest
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dissemination in time.
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Clinical correlation for fulfillment of
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the McDonald criteria would be required
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in this particular individual.
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