Interactive Transcript
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I'm Dr. Pomeranz
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here with neuroradiologist, Dr. Ben Lasar.
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And we are looking at a 77-year-old man
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with memory loss, cognitive decline,
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and also some mild motor dysfunction.
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The patient also had the history to rule out MS and
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rule out ALS or amyotrophic lateral sclerosis.
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On the left-hand side of the screen,
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we've got an axial conventional fast spin echo T2.
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There's extensive periventricular white matter hyperintensity.
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We also see innumerable hyperintense,
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little speckled foci in the inferior
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portion of the brain subfrontally,
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and in the basal ganglia, consistent with État criblé,
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which we'll explain.
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In the center,
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we've got a fluid-attenuated inversion
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recovery or a FLAIR,
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again demonstrating rather profound
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periventricular hyperintensity,
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but relative sparing of the temporal regions,
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especially the peritemporal white matter,
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which is important.
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And then on the far right,
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a susceptibility-weighted or blood-sensitive sequence,
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also known as SWI or Swan,
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which shows no evidence of siderotic change
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or hemorrhage.
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So, given the negative appearance of the susceptibility
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weighted sequence on the far right,
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what would be your differential diagnosis?
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Given the patient's history of memory symptoms,
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and cognitive impairment,
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my first differential consideration would include
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small vessel dementia,
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also known as Binswanger,
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also known as subcortical arteriosclerotic encephalopathy.
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And you know
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this is a condition which is an overlap condition
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related to underlying hypertension
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and underlying arteriosclerosis.
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And granted hypertensive patients
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do get little punctate hemorrhages
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in the perforating vessels, lenticulostriates,
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the thalamostriates,
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the perforators of the brain stem, et cetera.
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This patient doesn't have that,
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nor does the patient have evidence of
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lobar hemorrhages of varying ages,
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which you would see in amyloid,
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which might also be a consideration and is often
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commingled with other vascular disorders.
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Now, there's very extensive confluent white matter
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signal alteration, but on the axial T2,
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there are multiple speckly,
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or what I call twinkly little dots of hyperintensity.
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And you can see them in the subfrontal region.
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You can even see them a little bit in the brainstem,
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but mostly in the basal ganglia.
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And this is typical of the entity
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known as État criblé,
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where you have elevated blood pressure producing
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expansion of the perivascular spaces,
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a combination of underlying
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hypertension and arteriosclerosis,
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producing what we call the Binswanger's phenomenon.
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What's in the differential diagnosis here?
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Differential diagnosis for this type of appearance would
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also include MCI, Mild Cognitive Impairment Syndrome,
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or even early Alzheimer's.
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You could throw in the differential consideration.
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Sure.
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And I think you could consider that,
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and then I would probably throw it out.
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Now, 15% of all dementias are both vascular
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and neurodegenerative.
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But look how good the entorhinal cortex looks.
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It's not perfect, but it certainly
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not nearly as affected as the rest of the brain.
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So with this juicy entorhinal cortex
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and so much other disease elsewhere,
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that wouldn't be a strong choice of mine.
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Now, they asked us to rule out MS
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for I don't know what reason,
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but the fact that we've got sparing of the occipital
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region or less involvement of the occipital region,
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and the fact that we have very little to no
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periventricular white matter disease,
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and the fact the patient is a man,
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and he's in his 70s,
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that's probably a silly consideration.
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I think they were concerned about ALS because there is
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some change along the left corticospinal tract and
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that was not unreasonable from a clinical standpoint.
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But he's got severe gliosis in the brainstem pons.
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You kind of see it right,
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let's see if I can get to it.
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Right here.
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Maybe not severe,
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but definitely present, these areas of high signal.
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So, the combination of pontine disease and left
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corticospinal tract disease might have led them to
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that diagnosis.
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And you can get ALS at any age.
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It's usually bilateral. It isn't this lumpy,
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bumpy appearance,
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but rather one long strand-like area of hyperintensity.
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And he certainly doesn't have that.
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And you could use fiber tracking,
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which we do have to assess the status
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of the corticospinal tract.
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And we'll do that on the next vignette.
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So, this is subcortical arteriosclerotic encephalopathy
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or Binswanger syndrome.
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Incidentally noted,
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he's had both lenses replaced and there are a
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few other minor findings.
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Shall we move on?
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Let's.
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Let's. Pomeranz and Laser out.
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