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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.