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Alzheimer's Disease plus Cerebral Amyloid Angiopathy (CAA)

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Okay.

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So this first case is a 79-year-old

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with memory loss.

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We're looking here at an MRI of the brain in 2013.

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This is the DWI sequence, the GRE sequence,

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the T2 sequence, and the FLAIR sequence.

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Everyone has their own pattern

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in how they read studies.

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I tend to always look at the

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DWI and the GRE first,

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just because you don't want to use the DWI to

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detect acute strokes, and you don't want to miss

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that. In the GRE, we use to look for hemosiderin,

0:31

staining for blood products,

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and also you don't want to miss a bleed.

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So I tend to start with those.

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You see, the DWI here is negative.

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There's no evidence of acute infarct.

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The GRE actually, in the GRE.

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This is a subtle finding on this

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initial MRI from 2013,

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but there's a little focus of hemosiderin

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staining, old hemosiderin staining, by the way,

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on GRE susceptibility,

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weighted infarct can be hemosiderin

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staining or calcification,

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although hemosiderin staining is much more common

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scenario, unless you're in the basal ganglia.

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So there's a little punctate focus there.

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You see here along the lateral margin of the

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right pontomesencephalic junction,

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there's another punctate focus here.

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There's another little focus here in the region

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of the internal capsule on the right.

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If we look here at the FLAIR sequence,

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we see mild to moderate microvascular

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ischemic disease, little foci here,

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scattered throughout the cerebral white matter.

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Here's one in the right temporal subcortical white

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matter. And then if you look here at the T2,

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we see moderate cerebral atrophy with

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mesiotemporal and biparietal predilection.

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So you see here the temporal horns

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are kind of prominent,

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the psilsi are prominent in the temporal lobes.

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And again,

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SoCal prominence here in the bilateral parietal

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lobes. Now let's take a look at the MRI from 2016,

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and we will compare it to the MRI of 2013.

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This is the T2-weighted sequence from 2016.

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And you can see here this sort of significant

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progression in cerebral atrophy.

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We now have moderately severe cerebral atrophy

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in the bilateral temporal lobes.

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So there's a strong temporal predilection.

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Look at the size of the temporal horns

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here compared to the prior study.

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The parietal sulci are also larger in size.

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We'll compare here the FLAIR sequence.

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Here's the FLAIR sequence from 2016.

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And here is the FLAIR sequence from

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the earlier study in 2013.

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Microvascular ischemic disease has

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progressed since the prior study.

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Multiple new foci are now seen.

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So that has progressed.

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And now let's take a look at the GRE.

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On the left, I'm going to load the 2003 study,

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and then on the right-hand side,

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I will load the 2016.

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Study.

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Here we go.

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And now what you can see is there's multiple new

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foci of hemosiderin staining scattered

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throughout the brain.

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So here's one in the right temporal lobe.

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Here's another one in the left frontal lobe,

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at the gray-white junction.

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This wasn't present before, this was present,

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but is now more conspicuous.

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Here's a little punctate,

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one that wasn't present before,

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along the ependymal margin of the left lateral

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ventricle. Here's another one here.

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That's in the presential gyrus

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of the left frontal lobe.

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Here's another one here in the

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left superior frontal gyrus.

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These are often located at

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the gray-white junctions.

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And then you can see how much more conspicuous

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this one is here at the junction of the pons

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in the middle cerebral peduncles.

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Here's another one here in the high pons.

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We've got a couple here in the

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right cerebellar hemisphere.

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So this patient has cerebral amyloid angiopathy

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that has significantly progressed

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since the prior study.

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And this has all really happened over the past

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three years. Now, let's take a look.

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The patient then also had an amyloid PET in 2016.

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Here's the amyloid I'm going to invert,

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because this is how we view these.

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So this is the gray scale, and you see diffuse

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binding of that tracer throughout the cortex.

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This is a positive amyloid study,

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which indicates that this patient

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really has Alzheimer's disease.

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So this is again the 79-year-old with memory loss.

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We see here the MRI in 2013,

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where we had moderate cerebral atrophy

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with a right temporal predilection,

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and the patient had NeuroQuant at that time.

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And the NeuroQuant study did show

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some hippocampal volume loss.

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It also showed statistically significant

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enlargement of the inferior lateral ventricles.

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And then, in 2016, the patient came back.

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At this point,

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we have moderately severe bilateral temporal

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lobe volume loss, right, greater than left,

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and we see some rapid decline of the volumetric

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values off the normative curve.

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This is a heat map overlay here.

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This happens to be NeuroQuant.

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This is IcoBrain on the same patient.

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Here's a closer look at the NeuroQuant study.

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You can see the values of the hippocampus in 2013

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and how rapidly they've dropped off in 2016.

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So, as any person ages,

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they will get some hippocampal

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volume loss over time.

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But it tends to move very slowly when

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you see a rapid decline here,

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that's a big red flag for Alzheimer's disease

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or some other dementia syndrome.

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This is the hippocampal occupancy score.

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And this has dramatically decreased over time.

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And then here's the inferior lateral ventricles.

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You see where it went from 2013 to 2016.

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This is the IcoBrain report.

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In 2013,

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we had statistical significance less than one

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percentile on the normative

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percentile curve in 2013.

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And now the hippocampal volumes have dropped in

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And now we are getting statistical.

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Significance throughout the entire temporal

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cortex in the 2016 study.

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This is that Bullseye graph I mentioned

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for the IcoBrain report,

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where the points point towards areas of statistical

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significance. This blue zone, as you remember,

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is in the one percentile.

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Temporal cortex here is now statistically

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significant. The white dotted line, by the way,

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is the prior study, and the black

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is the current study.

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This is the segmentation where you see what the

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hippocampi looked like here in orange in 2013,

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and how they have become progressively atrophic

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by the 2016 study. This is a heat map overlay.

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NeuroQuant offers this.

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Anything that's red is increasing in size,

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so the ventricles and the psalci are increasing

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in size since the prior time point.

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This is an overlay of the current study with the

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prior, and the blue is anything that's decreasing.

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So you can see here that the cortex is decreasing

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in volume since the prior exam.

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Again, as a review from what we saw,

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this patient has cerebral amyloid angiopathy with

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multiple little foci of hemosiderin staining,

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which had significantly progressed

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over three years.

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And the patient had an amyloid PET CT study

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in 2016, which was diffusely positive.

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So this patient has both Alzheimer's disease

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and cerebral amyloid angiopathy.

Report

Faculty

Suzie Bash, MD

Medical Director of Neuroradiology

San Fernando Valley Interventional Radiology & Imaging (SFI), RadNet

Tags

PET

Non-infectious Inflammatory

Neuroradiology

Neuro

MRI

Idiopathic

Brain

Acquired/Developmental

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