Interactive Transcript
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Dr. Laser,
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we have a 73-year-old woman with severe memory disorder.
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She's got difficulty walking,
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slurred speech, and weakness for two months.
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She also has mixed hyperlipidemia and allegedly
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has a cerebral vascular accident.
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Let's scroll on the far left,
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we have an axial T1.
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In the middle, a T2, and on the far right, a FLAIR.
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So, some conventional sequences.
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Hard to pick out a macro infarction.
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And when we go up higher,
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and I know you pointed this out when
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we were scrolling the case earlier,
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a lot of cortical atrophy,
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and especially in the parietal area.
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Look at the interparietal sulcus,
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which goes into the postcentral sulcus.
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That's pretty profound atrophy affecting the
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parietal lobe,
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granted it's all involved.
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Then when we go down into the temporal region,
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the insula is dilated,
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so we've lost some temporal cortex.
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And then when we go to the temporal horns,
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they're not quite as dilated
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as I would have expected.
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It would have been nice to have a coronal
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to look at the entorhinal cortex,
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but we're certainly thinking about primary
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neurodegenerative diseases, Alzheimer's-like.
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Then we've also got white matter disease.
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And that white matter disease is really
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too much for a 70-year-old.
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We allow one area of gliosis per decade.
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Some of these are confluent.
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Maybe one goes off to the cortex,
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and there's certainly more than seven.
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They're more like 20 or 25,
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if you keep looking very carefully.
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So there is exaggerated gliosis.
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There is vasculopathic disease.
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15% of all cognitive declines are
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neurodegenerative and vascular.
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This is probably one.
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So let me ask you a question about catacil.
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This is a female, not a male.
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But what's a typical finding of catacil when
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you get down in the temporal region?
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So the most striking feature of catacil is there's
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a predominant white matter abnormality involving
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the anterior pole. Subcortical white matter.
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Yeah. So usually right about here, right,
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using my black pen to draw it.
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That's usually where I see it.
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And, of course, wrong gender.
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And there's often a genetic history.
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Not always,
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but if we consider just the phenomenon of
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dementia. When I look at a dementia case,
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I've got a laundry list of things
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that go through my head,
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especially if there is a vascular component,
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and that includes some very basic stuff.
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I want to know the triglyceride level,
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the cholesterol level.
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I want to know if the patient's a smoker,
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if they're diabetic, if they're on statins,
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renal disease, heart disease, liver disease.
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History of strokes? In this case, yes.
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Although we didn't find it bleeds,
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we'd pull up our susceptibility weighted image.
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Didn't see any. Didn't see any sclerosis.
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We'd pull up our diffusion weighted image
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to see if there had been an infarct.
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There hadn't.
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I want to know if the patient is hypertensive.
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I want to know the gender because of catacil and
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some other disorders like antiphospholipid
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antibody syndrome,
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which we see a little more frequently in women,
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maybe associated with SLE.
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Want to know if there's any history of
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coagulopathy, DVT. Are they homozygous for factor
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Five, lidn factor eight, antithrombin three.
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Do they have a known history of autoimmune
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disease? Do they have headaches?
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Do they have normal nutrition?
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Do they drink? If so, how much?
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These are all things that go into my thinking
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process, and I even drill down more granular.
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When I think about hypercoagulability,
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I have a list of about 20 things that
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goes through my head in a flash.
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Not just things like hypercholesterolemia.
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And I think about polycythemia and thrombocytosis
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and a number of other disorders that are
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on that list. So I'll stop right there.
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It's not just you look at it.
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You report the findings.
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You have to integrate everything that's going
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on with a patient. You got to drill very,
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very deeply,
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extract all you can from the information given.
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And when duty calls,
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you get on the phone and you talk to the clinician.
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Let's move on, shall we?
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Let's.
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Laser and P out.
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