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ADC Negative Multiple Sclerosis

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This is another examination of a patient

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who had known multiple sclerosis

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and was being evaluated for the effectiveness

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of therapy.

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As I stated earlier,

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I'd like to have up initially the axial

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FLAIR, the axial T2-weighted scan,

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and the diffusion-weighted scan.

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In this case, on the right hand side,

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you're seeing the ADC map that allows us

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to look for areas of cytotoxic edema without

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having the issue of T2 shine through.

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So we can see right from the bat

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that this patient has a large

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volume of demyelination.

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As we scroll through the posterior fossa,

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initially, we're going to let our eyes stray

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to the T2-weighted scan

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as the most accurate for identifying

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demyelinating plaque.

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As I said, though,

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demyelinating plaques are better

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seen on the T2-weighted scan.

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And it's also because of the prevalence of

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CSF ghosting artifact that

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you see on FLAIR imaging.

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FLAIR is particularly susceptible to CSF

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pulsation artifact, and therefore,

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what we're seeing going through the brain

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stem on the left hand side

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is actually CSF ghosting artifact

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rather than demyelination.

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It's not seen on the T2-weighted scan.

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Yet another argument for using the

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T2-weighted scan in the posterior fossa.

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Now, if we look at the T2-weighted scan

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at this juncture,

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we are identifying a central area within

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the pons of demyelination,

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which is quite hard to see here

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on the FLAIR imaging.

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Let's continue to scroll further superiorly.

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Again, we're seeing some areas in the central

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pons on the T2-weighted scan

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that I would call areas of demyelination

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in this patient,

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but not really reliably seen on the FLAIR imaging.

1:52

I think I've made my point.

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As we scroll further superiorly,

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we come to the supratentorial region.

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Now, we're going to focus a little bit more

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on the FLAIR imaging going back and forth,

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and we see that there is a large volume of

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demyelination in the periventricular regions,

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as well as in subcortical regions.

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I generally am not that critical with

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regard to whether something is subcortical

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or juxtacortical or deep in the white matter.

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So, for example,

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here on the FLAIR scan, we have the pia,

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the sulcus,

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and in this example,

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I would call this a juxtacortical

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demyelinating plaque.

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I would call that one as well juxtacortical.

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I would call this one juxtacortical.

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Some people,

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when they're looking at the centrum semiovale

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in lesions that are not

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adjacent to the gray matter,

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will use the term deep white matter lesions

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rather than using it juxtacortical.

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Why is this...

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Why do I bring this up?

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Why is this important?

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Well, the McDonald criteria specify that the

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four locations are juxtacortical

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or subcortical,

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periventricular,

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infratentorial and spinal cord lesions.

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So, if you just had lesions like this

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that are in the deep white matter

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without being close to the gray matter,

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would you include them and say that it

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does indeed fulfill the criteria

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of two or more locations,

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i.e., juxtaportical and periventricular or not?

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So, depending upon what a stickler

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you are for the nomenclature,

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you may count these as juxtacortical or not.

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Again, as we look at these lesions,

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we're going to be looking both at the ADC map

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to see whether there is any area

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of cytotoxic edema,

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as well as the post-gadolinium-enhanced scans.

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Now, just looking at these white matter lesions,

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can I predict which ones are going to

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show contrast enhancement or not?

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That's not something that is easily

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done on T2 or FLAIR scans.

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Sometimes, you think,

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"Ah. This one seems a little different

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than the other one,"

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so it might show contrast enhancement and

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and be an active plaque.

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That is very hard to predict.

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And hence, we have to do the

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post gadolinium enhanced scans,

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certainly for the initial evaluation of the patient.

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However,

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the fulfillment of the criteria

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of being spaced out in time,

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that is a polyphasic disorder,

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a disorder in which there are different aged lesions.

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One can fulfill that criteria by having a

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prior study and showing new lesions on

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FLAIR scan that were not present

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on the prior study.

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So the two ways we say that the patient

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has demyelinating plaques of different ages

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is by showing whether the plaques are

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enhancing or not,

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and whether or not

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they preexisted on a prior study.

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So, let's eliminate the drama

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and let's see what looks...

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how the patient looks on the

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postgadolinium enhanced scan.

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Well, I'll scroll them together

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and we'll try to fix that in a moment.

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So here, we have a patient who has

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multiple enhancing plaques,

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some of which are showing more

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of an open arc appearance,

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some of which are showing a complete

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rim of enhancement,

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some of which are showing

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solid enhancement,

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and I would even say some of which show

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more of a linear pattern of enhancement.

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At this juncture,

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we can see that there are some plaques

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that are enhancing.

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And let's just stop here.

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These are fairly analogous sections.

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Here we have

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the hand knob area,

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and what we're seeing is a plaque here

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that does not enhance versus

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multiple other enhancing plaques.

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So once again,

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here we have a non-enhancing plaque.

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Here we have a non-enhancing plaque,

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here we have non-enhancing plaques.

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So these, we would say,

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no active blood-brain barrier breakdown.

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And therefore, we would assume that these

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are more chronic,

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as opposed to those that

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are showing contrast enhancement,

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which are demonstrated also

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on the FLAIR scan.

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So, spaced out in both location

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as well as in age,

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defining it as multiple sclerosis

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by McDonald criteria.

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I'd like to pull down the coronal scan

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just to remind you of the value of

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scrolling through the orbits to ensure

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whether or not the patient has

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active optic neuritis.

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This is an example of a patient whose

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optic nerves do not show contrast enhancement.

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So, please utilize all the pulse sequences

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because to demonstrate the optic nerve

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demyelination on the axial FLAIR or

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T2-weighted scan is quite hard.

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I'm pulling down the sagittal.

7:39

Again,

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the sagittal FLAIR scan, very useful.

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It shows us that the patient has

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atrophy of the corpus callosum.

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And this is a little bit more ragged

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in the colossal septal interface.

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So, let me demonstrate that.

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As opposed to the previous case where I

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showed a fine linear area of bright signal

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intensity at the colossal septal interface,

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this has a more ragged area,

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identifying the demyelination

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at the colossal septal interface.

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And that, again,

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is characteristic of multiple sclerosis as

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opposed to other demyelinating disorders.

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And you also get a better sense of just

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how dramatic the demyelination

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is on the sagittal

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FLAIR scans.

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If one were to make a coronal

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reconstruction from the sagittal scan,

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you may be able to identify demyelination

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in the optic nerves.

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That would be another option.

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So, yet another example of a patient who has

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pretty robust active multiple sclerosis

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with both enhancing and non-enhancing plaques,

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in this case,

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none of which showed cytotoxic edema on

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the diffusion-weighted scan,

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but multiple ones showing contrast

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enhancement in the brain.

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On the sagittal FLAIR scan,

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you might also get a chance to look at the

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cervical spine, if that has not been

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separately scanned.

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In this case,

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there's nothing dramatic seen in the

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cervical spine in this patient.

Report

Description

Faculty

David M Yousem, MD, MBA

Professor of Radiology, Vice Chairman and Associate Dean

Johns Hopkins University

Tags

Neuroradiology

Metabolic

MRI

Brain

Acquired/Developmental

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