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Case number eleven is a 62-year-old

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professional football player with symptoms

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of chronic traumatic encephalopathy.

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Now, CTE often presents with memory loss,

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which this patient had,

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mood changes, confusion and difficulty thinking,

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and this patient had all of those things,

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had obviously suffered multiple head hits over

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the years as a professional football player.

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They had an MRI of the brain in 2019.

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Here's the DWI.

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So, no evidence of acute infarcts.

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Here is the GRE sequence.

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There's no evidence of intracranial bleed.

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If you look at the FLAIR sequence here,

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I don't see any evidence of post-traumatic

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cortical encephalomalacia or gliosis.

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As the brain slides against the skull base,

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you typically have common characteristic areas

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where you can have post-traumatic

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cortical encephalomalacia.

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So, it's usually along the anterior,

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the inferior and lateral aspects

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of the temporal lobes,

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and then along the anterior aspect

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of the frontal lobes.

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And we don't see that in this case.

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However,

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I happen to notice that there are these foci of

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FLAIR hyperintensity scattered

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in the cerebral white matter.

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A few here along the colosal margins,

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and here's a few more here.

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Some of them are abutting the overlying cortex,

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like this focus here.

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So that is pretty characteristic in appearance

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for demyelinating disease.

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So this patient has multiple sclerosis,

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although they weren't aware of it,

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you know, until after I had interpreted this MRI.

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This is the T2-weighted sequence here,

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and we really don't see any atrophy

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at all in the temporal lobes.

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They just look completely normal.

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There are slight prominence of the

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sulci in the biparietal regions,

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but no temporal lobe atrophy, whatsoever.

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If we look here on the

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you know, sagittal sequence,

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you can see the patient does actually

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have a disc protrusion at C3-4,

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and it's probably causing some moderate canal

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stenosis at this level.

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Also, an incidental, partially empty sella here.

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So the patient then went on to have an FDG

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brain PET CT that same year in 2019.

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Here's the FDG brain PET CT,

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and this is completely normal.

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So you see here normal-looking metabolism

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throughout the brain.

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But the patient's memory loss was significant.

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So, they did come back also to have an amyloid

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PET in that same year in 2019.

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And to my surprise,

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the amyloid PET study was positive.

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So diffuse binding of that amyloid

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tracer throughout the cortex.

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So this is, again,

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a 62-year-old professional

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football player with CTE.

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This is the MRI brain study in 2019.

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Really pretty normal brain volume.

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You don't see any temporal lobe atrophy.

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But we did have findings of multiple sclerosis.

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The patient also had quantitative

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volumetric imaging in 2019.

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And these were really completely normal.

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Here's the icobrain, here's the Neuroquant,

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here's segmentation here.

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Normal hippocampal volumes,

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actually slightly above the

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mean for patient age.

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The HOC was normal and the ventricles were

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normal in size.

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Here's the FDG brain PET CT.

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And this was also completely normal.

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So, here's the PET CT image.

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And here is the FDG PET CT surface map.

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And is the PET MR fusion image.

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And again,

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normal metabolism in the temporal lobes.

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But here was the amyloid PET,

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which was diffusely positive.

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Here's the amyloid PET CT fusion.

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Here's the amyloid PET MR fusion,

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and diffuse binding of the tracer

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throughout the cortex. So,

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in the clinical setting of CTE,

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trauma has been suggested to demonstrate

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increased amyloid beta peptide levels,

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although the extent of amyloid deposition in CTE

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has really not been thoroughly characterized.

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But what we do know is there is amyloid deposition.

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Now, this is a different patient,

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but I just wanted to show you

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this so you could see.

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This happened to be an 18-year-old,

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unfortunate male who died 10 hours after a fall.

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And the autopsy revealed beta amyloid plaques,

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which we see right here,

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and amyloid precursor protein,

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which we see here and here.

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And those beta amyloid plaques were found within

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hours after the traumatic brain injury.

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So there is an epidemiological association between

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TBI and development of Alzheimer's disease,

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and that rapid beta amyloid plaque formation,

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we think,

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may result from the accumulation of this amyloid

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precursor protein in the damaged axons.

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You can see that APP tracking along the

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damaged axons here.

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And so, again,

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we had discussed previously about the disruption

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of the beta amyloid plaque genesis and

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catabolism following traumatic brain injury.

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And so, this is what can happen

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with traumatic brain injury.