0:00

This next patient had some memory loss, and what we see here is

0:05

multiple foci of old hemosiderin staining on the GRE sequence. So This looks

0:11

like a cerebral amyloid angiopathy case. But on the T2 weighted image here,

0:15

we see extensive T2 hyperintensity surrounding these zones of GRE susceptibility

0:20

artifact. So this is actually cerebral amyloid angiopathy with inflammation.

0:26

On the FDG PET here, we had some cortical hypometabolism in the bilateral

0:32

parietal lobes, which you see more profoundly here on the right hand side.

0:36

And as we mentioned before, APOE4 is a significant risk factor for cerebral

0:41

amyloid angiopathy. One interesting fact is cerebral amyloid angiopathy

0:46

is found in 5% of the general population, but in 80%

0:51

of patients with Alzheimer's disease. So that's a really big number.

0:54

Again, I believe it comes down to the pathway of a beta amyloid

0:59

deposition from the APOE40 and the APOE42 with disruption of that pathway

1:06

in terms of either production or degradation of those products and then

1:11

accumulation along the vessel walls in the cortex.

1:16

This is another case here of cerebral amyloid angiopathy with inflammation.

1:21

Here's the initial presentation where we have this big bleed in the right

1:24

temporal lobe. We also have multiple other little foci of old hemosiderin

1:28

staining. And then on the FLAIR sequence, we see surrounding FLAIR hyperintensity.

1:33

So this was a CAA with inflammation. One week following steroid therapy,

1:39

the blood products are still there, but that surrounding inflammation has

1:42

gone down. So steroids are very helpful when you have inflammation with

1:47

CAA. This patient happened to be a 71 year old woman with headache

1:51

and cognitive change. Now, this type of appearance is very similar to an

1:55

ARIA appearance. ARIA stands for amyloid related imaging abnormalities,

1:59

which we're going to talk about very shortly.