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This is a 60-year-old gentleman with mental

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status changes and cognitive decline.

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We have the FLAIR scan,

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the T2-weighted scan, and the ADC map.

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As we scroll through this example,

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we note that the patient has relatively

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confluent white matter disease that is in the

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periventricular region,

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extending to the the external capsule

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and subinsular region.

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And it is relatively diffuse and

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bilateral and symmetrical,

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extending into the white matter of the corona

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radiata and the centrum semiovale,

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with some involvement to the deep white matter,

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possibly to the subcortical white matter

0:45

at the frontal lobe.

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So on the ADC map,

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we see that there are no areas of restricted

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diffusion on the ADC map.

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Just to confirm that,

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we pull up the diffusion weighted scan

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and we identify that there are no acute infarctions

1:04

amidst this diffuse white matter disease.

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On the susceptibility-weighted images,

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we don't see very much in the way of hemorrhage.

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There are a few subcortical areas

1:15

of hemosiderin deposition

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and on postgadolinium-enhanced scanning,

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no areas of enhancement.

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The key to this case is noticing

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the involvement of the

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anterior temporal lobes.

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So here on the FLAIR scan,

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I'll demonstrate this.

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You notice that there is prominent

1:44

high signal intensity,

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fairly selectively involving the subcortical

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white matter of the anterior temporal lobes

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on the FLAIR scans.

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And this is present as we scroll more superiorly

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out into the periphery of the

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anterior temporal lobe.

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This selective involvement of the anterior

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temporal lobes would be our best indicator that

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this patient has a diagnosis of CADASIL.

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And in fact,

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that was what was confirmed on the subsequent

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serology and genetic testing.

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So 60-year-old patient

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presenting with cognitive decline

2:25

with a diffuse white matter process that

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goes out pretty much to the subcortical

2:31

white matter of the frontal lobes,

2:33

but more importantly,

2:34

has a selective involvement of the anterior

2:36

temporal lobes,

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with some involvement also

2:39

of the external capsule,

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CADASIL disease.

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You note that the basal ganglia here are

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relatively spared of lacunar infarction,

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which is one of the distinguishing features

2:51

between CADASIL and Binswanger's

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or the subcortical arteriopathy with encephalopathy.