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Hello and welcome to Noon Conference, hosted by Modality

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Noon Conference connects the global radiology community

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through free live educational webinars that are accessible

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for all and is an opportunity

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to learn alongside top radiologists from around the world.

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You can access the recording

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of today's conference in previous noon conferences

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by creating a free account.

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Today we are honored to welcome Dr.

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Sally Aisa for a lecture entitled Introduction

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to Pet Imaging of the Brain.

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Dr. Aisa is a radiologist nuclear medicine specialist

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and academic based in Sydney, Australia.

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She serves as a specialty lead

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for medical imaging at the University of Sydney

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and has special interests in oncology imaging

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and thoracic radiology.

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At the end of the lecture, please join Dr.

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AA in a q and a session

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where she will address questions you may

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have on today's topic.

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Please remember to use the q

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and a feature to submit your questions so we can get to

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as many as we can before our time is up.

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With that, we are ready to begin today's lecture. Dr.

1:01

Asa, please take it from here.

1:04

Good morning everybody, and I'll just, um, unmute my mic

1:08

and start my video.

1:10

And thank you so much to modality for having me along today.

1:14

It's a real pleasure. And this is the first time I've had

1:16

the privilege of presenting at noon conference.

1:18

Um, it is 9:00 AM in Australia's,

1:20

and so I apologize for the interesting time

1:23

that you're all joining us with today.

1:25

Um, but thank you for coming

1:26

along at the end of your workday.

1:27

I really appreciate you being online.

1:29

Um, so, um, as the introduction mentioned,

1:32

I'm a nuclear medicine and, um, nuclear medicine specialist

1:35

and radiologist from Sydney, Australia.

1:37

And, um, today we're gonna be talking about a bit

1:39

of an introduction to PET imaging of the brain.

1:42

And, um, I report a lot of pet, um, I really enjoy it,

1:45

so hopefully you enjoy this introductory talk.

1:48

Um, so I do have a couple of disclosures, um,

1:50

mostly just from teaching, um, at different outlets, um,

1:53

including Siemens Radio Pedia and Modality.

1:56

So as we jump in, I'm very conscious that a lot

1:59

of you will be joining from different places

2:00

around the world, including North America,

2:02

where modality is based, but also all around the globe.

2:05

So just a little bit about where I'm joining you from today.

2:07

Um, I'm from Sydney, which is on the east

2:09

coast of Australia.

2:11

And here is our map of Sydney.

2:13

And if you've heard of the Sydney Opera House

2:14

that is about here.

2:16

And I work up here at Royal North Shore Hospital

2:19

and down here at the University of Sydney,

2:21

and then living out in a place called the Hills District in

2:24

Northwestern Sydney, which is a really

2:25

beautiful part of the world.

2:27

Um, this is near where I live.

2:28

Um, these are Sydney Blue Gums,

2:30

so it's a big theme here today.

2:32

Um, they're a bit, they're actually a threatened species

2:34

because they grow so tall

2:35

and straight people using them for telegraph poles.

2:38

Um, but this is a really beautiful part of the world.

2:40

Um, and here's the, one of the most, um,

2:43

historic buildings at the University of Sydney.

2:44

This is our quad, um, with the Grand Hall.

2:46

Unfortunately, I don't have an office in this beautiful part

2:48

of the university, but it is the most iconic shot.

2:51

And here is the original Royal North Shore Hospital,

2:54

which no longer looks like that, it looks like.

2:56

Well, although that building does still stand.

2:58

I only took that photo about three weeks ago.

3:00

But here is where I work.

3:02

I work in the yellow part of this building,

3:04

not quite in the basement on level two

3:05

above radiation oncology at the back

3:07

of Royal North Shore Hospital in Sydney's North.

3:10

Um, I'm very lucky, I'm part

3:12

of the Australian National Total Body PET Facility.

3:14

So we have a fantastic camera, um, which allows us

3:16

to do really high-end, um, um, pet imaging,

3:20

and we do that in com, um, in conjunction

3:21

with the National Imaging Facility in the University

3:23

of Sydney with Sydney Local Health.

3:26

So that's a little bit about me.

3:28

Um, and today we're going to be talking about, um,

3:30

different ways that we can image the brain using PET scans.

3:34

So starting with some neurodegenerative conditions.

3:36

And traditionally this has kind of been where a lot of the,

3:40

um, I guess where the meat of what we do is come from,

3:43

but also brain tumors, which is going to be our second part.

3:46

And initially when I wrote this lecture, um,

3:48

and thank you very much to Medical College Wisconsin,

3:50

who I helped me develop, which I developed this lecture

3:52

initially from, and then we've revamped it and re um,

3:56

and reworked it for our noon case conference today.

3:59

They were, um, really interested in, you know,

4:01

how we can use different traces to image the brain.

4:04

And you may be familiar with F 18 FDG

4:07

or our Glucose pet, which is what we use

4:08

for all of our oncology.

4:09

Well, not all of our, sorry for a gra large proportion

4:13

of our oncology imaging.

4:15

Um, and so that's been the workhorse,

4:16

but we are so blessed to be living in a time at the moment

4:19

where we have so many different traces to be able

4:22

to demonstrate different pathological

4:23

and physiological processes through the brain.

4:27

And just because we are kind of head

4:29

and epigenesis, we're going to finish off with, um, F 18

4:33

choline with and looking at parathyroid adenomas,

4:35

which can be a diagnostic challenge in the head and neck.

4:38

Not quite brain, but something really interesting

4:39

and I had to throw it in there at the end.

4:42

So for those of you who may be unfamiliar with PET

4:44

or just learning, um, PET is positron

4:46

and mission tomography.

4:48

So, and I'll just restart that animation actually.

4:51

So we, if we restart it, so we have our radio nuclei,

4:55

and as the positron emitted decay, it throws out a positron,

4:58

which is an antimatter particle.

5:00

It's an anti electron when antimatter meets

5:03

matter it each other.

5:05

So when a positron meets an electron,

5:06

it annihilates each other

5:07

and then throws off two gamma photons at 120 80 degrees

5:12

or 180 degrees to each other called coincidence photons.

5:15

They always have 511 KV energy.

5:18

And then when we put this tracer into the patient,

5:21

so the radiopharmaceutical being F 18 or flu eight 18

5:24

or gallium 68 into a patient, it, it's a poron.

5:29

And then when that annihilation reaction happens

5:31

and those photons are sent out at 180 degrees to each other,

5:34

the camera detects both of those

5:35

and they know that that reaction

5:37

happens somewhere along that line.

5:38

When this happens millions and millions of times,

5:40

and we get millions and millions of

5:41

what we call coincidence photons, we're able

5:43

to build up a three dimensional image,

5:45

which gives us the distribution

5:47

of the radiotracer within the patient.

5:49

Now, I've thrown out a few different words,

5:51

and for some of you need a pet might be a little bit

5:53

confused with all the terminology

5:54

I know I was when I started.

5:56

So we have a radioisotope, which is decaying

5:59

to throw out a particle or a gamma away gamma

6:01

or a gamma ray, and then it's tagged onto a pharmaceutical

6:04

and together that's called the radiopharmaceutical.

6:06

Your pharmaceutical might be FDG or Fluor DEOXY Glucose

6:09

or dotatate or PSMA for prostate cancer.

6:13

So they're some ones you might come across.

6:15

So it's something that can interact with the body,

6:17

like a drug with a tag, radioactive tag on it.

6:19

And that is our radiopharmaceutical

6:21

and that is the, the basis

6:23

of nuclear medicine and PET imaging.

6:25

So let's move on.

6:28

So we're going to be starting with dementia imaging

6:30

and the largest proportion of cases

6:32

for today are going to come into this section.

6:34

And because dementia imaging of the brain with, um,

6:36

PET is just such a big part of what we do

6:38

and where we can help is PET scans for the brains.

6:41

Are we usually a first line investigation? Not really.

6:45

Um, you know, it, we can't compete with something like,

6:47

you know, CT brains or MRI for certain pathologies,

6:50

but PET is an excellent problem solver, particularly

6:52

for difficult cases and also

6:54

for neurodegenerative conditions where you need some, the,

6:57

the best diagnostic certainty we can get.

6:59

Looking at the patterns of uptake can be really useful.

7:03

So when we assess dementia on F 18 FDG, we're ma trying

7:07

to map glucose uptake in the brain.

7:09

So the brain itself takes up a lot

7:11

of sugar on a, on a regular PET scan.

7:13

Even if you do it for lung cancer,

7:15

the brain is always going to be hot.

7:17

So you are going to be looking

7:18

to see if the brain is taking up the glucose

7:20

and using the sugar normally or abnormally.

7:24

So basically, and the principle of this is

7:26

that glucose uptake reflects neuronal and synaptic function.

7:31

So then if there's hypometabolism,

7:32

and when I say hypometabolism,

7:34

it means there's less metabolism

7:35

and less sugar being taken up than we expect.

7:38

That can be a sign of neurodegeneration

7:40

and certain types of dementias will demonstrate

7:43

characteristic patterns of reduced uptake of the tracer.

7:47

But why does it matter? And it matters

7:49

because the treat, the way that we treat, um,

7:51

neurodegenerative conditions,

7:52

including Alzheimer's, is changing.

7:54

We now have medication options

7:56

and if we can detect neurodegeneration

7:58

and Alzheimer's disease early, potentially

8:00

by administering these medications, we would be able to, um,

8:04

modify the disease course.

8:06

And then also if somebody may have Alzheimer's

8:09

or may not, you also have to be mindful

8:11

that we wanna be certain that they do have Alzheimer's.

8:13

Because if you start 'em on a medication which potentially

8:15

may have side effects and they don't actually have the

8:17

condition you're trying to treat, there's

8:19

that risk benefit in there

8:20

as well that we need to think about.

8:25

So just a, as we go in, um,

8:27

just a note about total body pet, um,

8:29

and the challenge that we have with brain imaging is that

8:32

with total Body pet, you're imaging the whole body at once

8:35

when traditional PET scanners

8:37

and digital PET scanners have a scanning bed,

8:39

which is about 30 centimeters, which is perfect, top

8:41

of the head down to, you know, the neck, great,

8:42

you're only imaging the brain.

8:44

But we've ended up with a bit of a challenge

8:46

that we are capturing the whole person,

8:48

and this is the head holder up here,

8:50

but we can't, if we image this

8:51

whole body, then what do we do?

8:52

What is the ethics of having to interpret that whole body

8:55

the pictures of that person's entire body?

8:57

So we've ended up sliding our patients down a little bit.

9:00

We're still getting part of thorax though,

9:02

and we can end up with conditions like this.

9:05

So with, as a patient who has had a dementia brain study,

9:08

but now we've got a lung nodule and what do we do?

9:10

This person could be 90, 95, a hundred years old.

9:13

And so what's the ethics of finding things

9:15

that we might not be exposed to that we may not have found

9:17

otherwise if we were only doing dedicated brain imaging?

9:20

So I'll just leave that one with you, just there. Okay.

9:25

So as we jump in, I'm gonna show you a do two,

9:27

two main different ways of how we, um,

9:29

display the images when we are looking at dementia brains.

9:32

So the first thing is our 3D reconstruction

9:35

and PET data is, um, reconstructed exactly like MRI

9:38

and CT as a scroll level stack.

9:40

You can adjust the levels and we,

9:42

but we do a lot more with fusion.

9:44

So PET CT is always acquired with a pet,

9:46

which is our functional data

9:47

and a ct, which is our anatomical data.

9:50

And the CT is useful not only for anatomical correlation,

9:53

but also attenuation correction,

9:55

which means getting the levels of the tracer correct, um,

9:58

and reducing artifacts.

10:00

So this is how what we do and the,

10:03

but we can see that the brain is very, very hot.

10:05

So I'm constantly adjusting these levels to see more detail.

10:08

So you can see that I've just, um, moved that up and down

10:11

and now we can see more detail in the brain

10:13

and I can see that there are some red

10:14

areas and some are less areas.

10:16

Um, so there are less red.

10:18

So, but what does that color scale really mean?

10:21

So we are going through, and I'm adjusting it down

10:24

and similar to when you're looking at lung windows,

10:25

you're constantly adjusting your windows, you're trying

10:28

to look in vessels, exactly the same with pet,

10:30

but what does the color scale mean?

10:33

So on this particular, um, on, in this particular image,

10:36

the red is where there is most

10:38

uptake or greatest metabolism.

10:39

And I can adjust it to make it look like anything.

10:41

But the red means that there is the greatest metabolism,

10:44

which is often in, this is gonna be normal into mentor

10:47

imaging, um, if it's blue.

10:49

So it kind of, it goes down in a rainbow scale, red, orange,

10:53

yellow, green, blue.

10:54

So once we're blue, that's least uptake.

10:57

So what I'm looking at in these regions is areas

10:59

of reduction, like here, where it should be red,

11:01

but instead we're getting down towards yellow, green, blue.

11:04

So reduced uptake.

11:07

And just keep in mind that this is different to another type

11:09

of way that we display the images in pet dementia,

11:12

brain dementia brains, which is like this.

11:14

And this is a brain mapping

11:15

or a statistical analysis

11:16

where we push the data against a normal population.

11:20

So we are looking for is there reduction in the uptake

11:23

or the metabolism in certain areas of the brain compared to

11:25

what we would expect for a normal person in this,

11:28

the color scale is flipped, red is bad,

11:32

blue is blue, is blue to green is mild reduction, yellow,

11:37

um, and orange is moderate reduction

11:38

and red is severe reduction.

11:40

So it's flipped compared to those, um,

11:43

the gray scale is essentially just normal.

11:44

You can see here that the cerebellum is normal,

11:46

but through here all these red areas,

11:48

they're the most abnormal.

11:50

So just keep that difference in mind as we go

11:52

through and look at the cases.

11:55

And we're gonna start with Alzheimer's,

11:57

which is got a very characteristic pattern.

12:00

But that said, it's very, very common.

12:02

And we all know in radiology

12:03

that not every single patient is going to read the textbook.

12:06

Um, so not every Alzheimer's patient is going

12:08

to look like this, but this is a nice textbook example

12:10

of the characteristic findings

12:12

that we are looking for with Alzheimer's.

12:14

We're looking for reduced uptake in the precuneus,

12:16

the imperial parietal lole, middle temporal gyrus

12:18

and posterior cingulate cortex.

12:21

But I'm not gonna throw it at that.

12:22

I think that would just be mean. Let's go back

12:24

and review the anatomy

12:25

because I've found that this,

12:26

that reading dementia brains has really forced me

12:29

to improve my anatomy

12:31

to understand these different areas of the brain.

12:34

So firstly, looking at the medial cortex, we'll look

12:37

for the um, the cingulate gyrus

12:39

and then the posterior cingulate gyrus is the back here.

12:42

And this is a really important structure in Alzheimer's

12:44

'cause the, um, the posterior cingulate gyrus should be the

12:47

hottest or um, most red part of the brain on those, um,

12:52

on those standard reconstruction images,

12:54

it should be chewing up the most glucose.

12:56

So if the posterior cingulate gyrus is not the hottest part

12:59

of the brain, then we need to be start thinking

13:00

about Alzheimer's disease.

13:03

And then we also want to think about the precuneus as well,

13:07

which is here marked in blue.

13:09

And when we put it overlaid onto our um, statistical map,

13:14

you can see that there is yellow, red, um, and blue

13:17

and green through the posterior cingulate gyrus

13:20

and the pecs, which corresponds to those anatomical areas.

13:23

I will just jump back quickly to um,

13:26

the posterior cingulate gyrus as well

13:28

because when we are diagnosing Alzheimer's,

13:30

you really just don't wanna see just decrease in the

13:32

posterior cingulate gyrus.

13:33

Um, because you, this can indicate an,

13:36

an alternative diagnosis

13:37

or amnesic, mild cortical, um,

13:39

my cognitive rather impairment, um,

13:41

which is a separate diagnosis.

13:43

But one quarter of these patients will go

13:45

on to Alzheimer's disease.

13:46

So it may very well be a precursor situation,

13:49

but if you're starting to see precuneus like we see here

13:52

and these other regions seen at the lateral cortex,

13:54

then you can be more confident in your

13:56

diagnosis of Alzheimer's.

13:58

So here, inferior parietal lole here marked in yellow,

14:01

and then the middle temporal gyrus marked in purple

14:03

that when we look at the map with reduction in these areas,

14:06

it almost gives you this kind of draping look, this kind

14:09

of draped pattern down the lateral aspect of the brain.

14:15

So how do I go about reading these?

14:16

Um, so here's a little video that I captured

14:18

of me making my adjustments.

14:20

So we always get kind of gray scale to start with

14:22

and then you can apply your color maps.

14:23

I love to look at the gray scale first

14:25

because I think it's more sensitive in the brain when,

14:27

or sensitive for looking at pet scans.

14:30

But keeping in mind with the brain,

14:31

the color scale is really useful

14:33

'cause you're looking for degradations of reduction.

14:35

I like to use pet rainbow.

14:37

My colleagues like to use this one.

14:38

And so I'm very strange in my department

14:40

'cause I like to use rainbow, whereas warm, um,

14:42

warm metal is favored by my colleagues.

14:44

They love the purple, um, the purple orange white one

14:48

and white is the area of greatest metabolism

14:51

or most normal where things start to go pinky purple, that's

14:54

where you're worried that there's a reduction.

14:56

So coming through here, if we look in the region

14:58

of the posterior cingulate gyrus, when we go back to my

15:01

favorite color scale here, which is pet rainbow, you can see

15:04

that it's should, it's not red.

15:06

And I'm going to go through, there we go,

15:08

we're making my adjustments and we're constantly adjusting.

15:11

So right where the arrow is here now these are the, um,

15:14

the lateral parietal lobes and the,

15:16

and we'll see precuneus in a moment,

15:18

but really that posterior cingulate gyrus, which is just

15:22

through here, um, it's not, it's got a little bit of uptake,

15:25

but here it's not the hottest part of the brain.

15:28

And so that's where coming back

15:30

and looking at my statistical map as well was really useful

15:32

because what I was seeing visually,

15:34

I could confirm it on the statistical map almost like

15:36

having a second reader.

15:40

So here again, this is, um, the full vision of this case.

15:43

And then, so this was considered, um, consistent

15:46

with Alzheimer's disease.

15:47

And then here's a comparison case as well,

15:49

which demonstrates all those findings that we saw before.

15:52

Actually more marked reduction in precuneus

15:54

and posterior cingulate, again, with that draping pattern

15:57

through the lateral parietal lobe through

16:00

to the middle temporal gyrus coming

16:01

through here, that draping look.

16:03

But you can notice it's asymmetrical and it can be,

16:06

but there's also, if you'll notice there's

16:08

other areas of reduction.

16:09

So frontal lobes as well, you know, different parts

16:11

of the temporal lobe can have reduction too

16:13

in severe Alzheimer's.

16:15

So that won't dissuade me from the diagnosis

16:17

because we've got those quite typical features.

16:22

So I've just got a question in the chat

16:23

and I'll try my best to keep up with them as we go.

16:25

Any suggestions to distinguish volume loss

16:27

versus true reduction?

16:29

Sometimes it's hard to know which came first.

16:30

Reduced metabolism or loss of volume leading to this.

16:32

That's a really tough one.

16:33

And I think kind of that's more coming

16:35

down to the pathology.

16:36

So when I'm looking at PET scans, I don't really look,

16:39

not the anatomical imaging isn't

16:41

at the forefront of my mind.

16:42

I'm really looking at the, um,

16:45

I'm really looking at the functional data.

16:47

Um, so I'm sorry I don't have the answer to that.

16:49

Um, but I, I dare say that they probably go hand in hand.

16:52

The reduced metabolism is reflective of

16:54

that neurodegeneration.

16:56

Um, and therefore the cortical loss is

16:58

mimicking that pathology.

16:59

But I do will tell you

17:00

that sometimes we do see metabolism loss in, you know,

17:04

fairly normal looking brains.

17:06

Um, so I, if I were to hazard a guess

17:08

and please don't quote me on it, maybe we are seeing

17:10

that reduction earlier

17:12

and when we go, um, so Natasha, when we go actually go

17:14

to look at amyloid, um, pet in a few um, slides time,

17:18

you'll get kind of get a sense of well

17:19

that we're also seeing more precursors as well.

17:21

Sometimes the brains when we're looking at amyloid pets.

17:24

So looking for amyloid plaque deposition,

17:26

you have, um, preserved volume.

17:28

Um, okay, so Alex has asked, are there confounds for PET

17:32

with CSF pulsation variations?

17:34

Would motion artifacts reduce apparent

17:35

uptake adjacent ventricles?

17:37

That's a great question.

17:38

Um, I don't, I had, hasn't something I come across, I think

17:42

with pulsation as well, you know, the movement is kind

17:45

of going to be quite small and

17:47

because with MRI, yes, you know, they,

17:49

they it's much more sensitive and the boxer size is smaller,

17:51

but pet is pet and nuclear medicine inherently has a

17:54

lower spatial resolution.

17:55

Um, what we do see sometimes with our, um,

17:58

with this statistical map

17:59

that we have up on the screen at the moment

18:01

is some misregistration.

18:03

So, um, so you can,

18:05

if if it the brain's very atrophic you have might,

18:08

it might fall off it a little bit.

18:09

And I kind of noticed through here,

18:10

sometimes you've gotta stripe even though the

18:12

cingulate gyrus is normal.

18:13

And that's just from the atrophy, just pulling it off a bit.

18:15

So every time I'm reading these

18:17

and co probably says a little bit more advanced is I'm

18:19

always looking at the three dimensional data first I'll make

18:22

a decision and then I'll go and check myself on the neuros

18:24

stat and that helps me to determine artifacts

18:26

and also, um, you know, quality assure my work.

18:30

Um, so yeah, hopefully that helps. Okay, great.

18:33

Just double checking. Um, we can see my mouse as well.

18:36

Hopefully I've, I'm sharing the right screen.

18:38

I always just dive in and hope, hope for the best,

18:40

but that should all be fine.

18:43

Um, okay, great. Let's keep going.

18:48

Okay, so we're gonna move on to frontotemporal dementia.

18:50

We'll go through these next ones a little bit quickly

18:52

so we can get to the back of the, um,

18:54

the presentation with some new traces.

18:56

Um, frontotemporal dementia is massive.

18:58

There's so many different patterns of how it can present

19:02

and the different differences in metabolism.

19:04

Um, and it, that's just

19:05

because it's multiple neurological syndromes which overlap.

19:08

There's multiple sub classification, um,

19:10

and in over 50% it's associated

19:12

with abnormal tau deposition as the protein.

19:15

Um, so here is kind of what we would typically kind

19:18

of think, you know, frontotemporal this patient,

19:21

this on our statistical map, noting

19:23

that the red areas are the most severely affected.

19:26

We can see that in this, um, temporal lobe here.

19:28

Um, there is reduction, um, there's,

19:31

but it's also present on the contralateral side as well.

19:36

Um, sorry, particularly, yeah, so right and left.

19:39

Um, and then also reduction medially within the

19:42

frontal lobes as well.

19:44

We're seeing preservation

19:45

of uptake in the posterior singular gyrus.

19:47

And precuneus looks pretty okay as well.

19:49

A little bit of this kind of blue and

19:51

and green kind of dotted through

19:52

that's gonna be mostly statistical noise.

19:54

Um, so, but that just comes with a lot of reading these

19:57

and I, and I wish that I could say

19:58

that every single time I open a case

19:59

and go, yep, that's frontal demand,

20:01

that's frontotemporal, that's Alzheimer's.

20:03

Realistically, I have to look really carefully

20:05

and I've picked you great cases today,

20:07

but it's not uncommon for me to go

20:08

and get a second opinion as well if these do

20:10

look a little bit confusing.

20:11

Um, because that's how we roll in our department.

20:13

We're quite collaborative. But I have picked a couple

20:16

of variants which have really nice imaging findings.

20:19

So primary progressive aphasia has three subtypes

20:22

and we're going to have a quick look at semantic dementia

20:25

and lope progressive aphasia.

20:27

'cause I found two really nice cases in our collection.

20:30

So semantic dementia, it's a type

20:32

of frontotemporal dementia, which is characterized

20:34

by marked unilateral anterior lobe atrophy.

20:37

Um, and it's typically affecting the left side of the brain.

20:40

So these patients will present with, um, fluent,

20:42

they'll have, um, fluent speech,

20:44

but they'll have ev loss of word and object knowledge.

20:47

Um, and they might have anomia or surface dyslexia and word

20:51

and object associated agnosia.

20:52

Lots of big words there, lots of, um, tongue twisters there.

20:55

Um, but they do have preserved episodic memory.

20:58

Um, and this is a really classic case here.

21:00

So we've got the intermedial temporal lobes, um,

21:03

and more pronounced on the left as we can see here.

21:06

And here's our three DI collected as a couple

21:08

of slides, um, slices.

21:10

You can really see that

21:11

that temporal lobe has asymmetric reduction in uptake.

21:14

We are seeing these red areas through here

21:17

and it's much more gray style

21:18

and more yellow coming through.

21:19

And you can really see that visually, um, reflecting

21:23

that dementia even here.

21:24

Not quite normal lope progressive aphasia, um,

21:30

or is similar but not quite the same left, um,

21:32

lateral temporal parietal region.

21:34

And this is really striking the semantic.

21:37

Yes, it was kind of a bit patchy and it was reduced,

21:38

but here it's really striking that this part

21:41

of the brain is most affected.

21:42

It really kind of jumps out and hits you.

21:45

And then when we look at our, um,

21:47

at our three dimensional fused imaging as well, we can see

21:50

that there's also further reduction

21:51

through the parietal lobe through here.

21:53

It's not as red as we would like it to be.

21:55

And significant market reduction in the anterior temporal in

21:58

the temporal lobe there I thrown

22:03

in some cases of dementia with Lewy bodies

22:05

because I think the patterns of this are really interesting.

22:08

Um, so Lewy body dementia is secondary to accumulation

22:10

of Lewy bodies in the brain with intracellular inclusions

22:13

and aggregates of misfolded a, um, solan.

22:17

And this is that frontal dementia that give, um,

22:19

there's little in the way of memory deficits, um, which, um,

22:22

early in the disease, but you can get these kind

22:24

of fluctuating cognitive impairments

22:26

and visual hallucinations.

22:28

Um, I remembered it from medical school as kind of,

22:30

it was called the pixies at the bottom of the garden.

22:32

So people would see kind of pixies and hallucinate visually.

22:35

Um, and it can have a lot of overlap with dementia,

22:39

um, with Alzheimer's disease.

22:40

And that's probably the most common indication I see.

22:43

Um, on, on my request forms is query Alzheimer's,

22:46

query Lewy body dementia.

22:48

So if we can distinguish between those

22:50

or even say that there isn't a clear pattern to in,

22:52

to determine either way, that can be really useful

22:55

for our referrers.

22:57

So with dementia, with Lewy bodies,

22:59

you get reduced uptake in the occipital lobes and frontal

23:01

and temporal lobes as we're seeing here.

23:03

Lots of kind of stipulated, um, blue green and yellow

23:07

and a little bit of red coming through those regions.

23:09

And it does have a mimic of Alzheimer's dementia.

23:11

But the big difference is the preservation

23:14

of the posterior singular gyrus, which gives rise

23:17

to the most characteristic.

23:19

Um, and eponymous imaging feature

23:20

of dementia with Lewy bodies.

23:23

So just coming through here, looking at our statistical map,

23:25

you can see here at the back, um, it's pro,

23:27

it's certainly got a predilection

23:29

for the occipital lobes here.

23:31

See the, it's the greatest reduction,

23:33

but the posterior cingulate gyrus in here is preserved, um,

23:36

which was confirmed on visual inspection

23:38

as we'll see on the next slide.

23:40

Um, and this is what it looks like in the fusion.

23:42

Um, and you can see that there's the postero,

23:44

cingulate gyrus is the hottest part of the brain

23:46

as we see here, but there's relative reduction

23:49

in the occipital lobes.

23:50

Did I put those in? I did not.

23:52

Um, so the occipital lobes just through there.

23:57

Um, but the cingulate island sign wasn't nicely

23:59

as nice as I would've liked on that one.

24:01

So I've got you the best case I could find

24:02

of the cingulate island sign, which is the most common kind

24:07

of textbook appearance of dementia with Lewy bodies.

24:10

So here a island of preserved uptake corresponding

24:14

to the posterior cingulate gyrus

24:16

with corresponding reduction in uptake in the occipital

24:18

CORs, which is driving that presentation

24:20

with those visual hallucinations

24:22

and cognitive cognitive disruption

24:27

finishing up with, um, a relatively new entity, um, and late

24:31

or limbic predominant age related

24:33

TDP 43 encephalopathy or late.

24:36

It's been a bit of a new kid on

24:37

the block in terms of dementia.

24:38

It's really come into more diagnostic, um,

24:40

might more diagnostic practice within the last five years.

24:43

Um, and it is often seen in the, um,

24:47

in the population of patients who are presenting

24:50

for Alzheimer's related, um,

24:53

or Alzheimer's related, um, present, um, presentations

24:56

with memory impairments.

24:58

But often patients who are found to have late are older.

25:01

Um, the presentation is memory predominant

25:03

and there's a slower rate of decline, um,

25:05

with Alzheimer's it can be steeper,

25:07

so late is more prolonged.

25:09

Um, so, and they've also got lower a OE four as well.

25:14

And um, also some genetic changes in comparison.

25:17

So what does late look like

25:18

and why is it not Alzheimer's

25:20

so late has reduced uptake in the medial temporal

25:22

lobe and hippocampus.

25:24

And I think this one's a video. That's right.

25:25

So we're looking at the posterior cingulate gyrus

25:27

that looks okay, nice

25:28

and hot, really red, hottest part of the brain.

25:31

But as we start to look down, um,

25:33

at the medial temporal lobes here, um,

25:36

and I'll just move on to the next slide.

25:37

You can see that they are green. Here's the side by side.

25:40

So I'll annotate the right

25:42

and you can see that that medial aspect

25:43

of the temporal lobe is very green.

25:45

There's a sign, there's reduction medially compared

25:48

to even laterally and certainly

25:49

compared to other parts of the brain.

25:51

Like look how nicely these, um, occipital cortices, um, are,

25:54

um, have preserved metabolism.

25:57

And this exactly matches on what we see with the um,

26:00

Arab bios statistical analysis,

26:02

particularly on the left hand side here,

26:04

you can see significant reduction with that red area, um,

26:06

and mild reduction there on the right.

26:14

Okay. Um, so this is just a nice bit of a summary paper.

26:17

I wish I could go through and spend hours teaching your old

26:20

dementia today, but it's just, um, not enough time.

26:22

Um, but we will pop in the, um, the chat,

26:25

um, a link to this paper.

26:26

Um, there's a QR code coming up,

26:28

but we'll be able to um, give you the PDF.

26:30

This is a really nice one from the Journal

26:32

of Nuclear Medicine that just gives the different patterns

26:34

of uptake associated with the different dementias.

26:38

Um, and so just we'll pause there

26:40

and I'll just have a quick look at the questions.

26:44

What software do we use for the 3D maps? We use MIM neuro.

26:47

Um, so we use a package called MIM seven.

26:50

Um, and that has um, a nearest neuro analysis.

26:53

We've formally used Neuros stat, um,

26:55

but at the moment we're using MIM neuro.

26:57

Um, and what is the role of PET CT in diagnosing ms?

27:01

Great question. We don't have a role.

27:03

Um, so we, MS is really kind of the realm

27:07

of MRI PET CT doesn't really,

27:10

we don't kind of factor in there.

27:12

Occasionally we'll do some brain tumor imaging

27:13

and I know sometimes tumor factor MS is in then the

27:16

differential, but because there's inflammation as well,

27:19

we, we don't really help.

27:20

So m MRI is certainly the gold standard.

27:22

Great question though.

27:27

Okay, so moving on to um, other regions

27:31

of neurodegenerative imaging including amyloid pet.

27:34

Um, and thank you to a, um,

27:36

associate professor Jeff Shery and Dr.

27:38

Ash Raghavan, who's my resident, um, for helping with um,

27:40

some of the information and cases on these slides.

27:44

So Amyloid pet, really exciting.

27:46

I like, they're really pretty

27:47

studies as you'll see in a moment.

27:48

Um, and there are several different agents including F 18

27:51

Flo Bein floe and Flut edol.

27:54

Um, we use Flo Bein at Royal North Shore in Sydney.

27:56

Um, and what we're looking for is imaging

27:58

of amyloid plaque deposition, which is that that's

28:01

that hallmark of Alzheimer's disease.

28:02

We're looking for abnormal amyloid plaque deposition within

28:05

the cerebral cortices.

28:06

And if that's there at a certain degree,

28:08

then we can diagnose Alzheimer's disease.

28:10

Essentially a normal amyloid pet is going

28:13

to exclude Alzheimer's, which can be so useful in some

28:16

of these patients who are presenting with cognitive issues

28:17

and memory impairment.

28:20

So this is, um, a normal study.

28:22

I like to start normal 'cause then I can show

28:24

you what we should be looking for.

28:26

And what you can see, it's really almost like a beautiful

28:27

outline of the white matter

28:29

and you can see the ventricles in the middle ventricles.

28:32

And what we are looking for is a few hallmarks.

28:34

So here we're looking for an arboreal pattern.

28:37

So if I draw the outline, it should be really spiky looking,

28:40

um, because we shouldn't see anything in the cortex.

28:42

If we see cortex, then the brain's gonna look more

28:44

cloud-like lobulated, but we should be seeing this nice

28:47

and um, spiky.

28:48

And this is called an arboreal

28:49

pattern or like a tree pattern.

28:51

So here's another animation to kind of help you remember.

28:55

The other thing we wanna see is cortical separation.

28:57

We wanna see a line between the cortices,

29:00

particularly at the top of the brain

29:01

because there should be gray matter in there.

29:03

So the white matter should be separated.

29:05

So we wanna see cortical separation.

29:08

And the other um, thing we use,

29:10

and this is also using MIM Niro, um, is a package

29:12

for aloid analysis.

29:14

Um, and a aloid is, um, we'll come up to the next slide,

29:18

is a standardized scale looking for the degree of amyloid,

29:21

um, plaque deposition

29:22

or tracer uptake in certain areas of the brain.

29:26

Zero is suspect, what we would expect in normal

29:28

young, healthy patients.

29:29

And then a hundred or above, we getting up to a hundred

29:31

and above is where we are confident that we are looking at,

29:34

um, a typical case of Alzheimer's.

29:37

Um, so we essentially the package will do this analysis.

29:41

You can see these areas where it's looking at certain areas

29:43

in the brain, including the posterior cingulate

29:45

gyrus and the pros.

29:46

Those areas where we would expect abnormality in Alzheimer's

29:50

as we know from our anatomy

29:51

that we saw in the previous section.

29:53

Um, and it can be useful in, in helping aiding

29:55

with our diagnostic certainty really useful.

29:58

Um, and also tracking amyloid plaque progression.

30:00

And sometimes you'll have equivocal cases, you know,

30:02

they might be borderline, we're not quite sure

30:04

and you'll re-scan 'em in five years and that will increase.

30:07

So that progression is really useful.

30:09

We tend to use thresholds of significance of 10 to 20.

30:12

Um, so if you're getting above 10 to 20,

30:14

but even those cases as well, you know, a good proportion

30:16

of those, um, it may be very well precursor

30:19

and they may increase over time.

30:20

So we may be seeing like a pre-Alzheimer's.

30:22

Um, but often I, the, in my experience,

30:25

the vast majority are going

30:26

to be pretty clear cut one way or the other.

30:29

So 50, as I said, sorry, 50 is our cutoff for diet, um,

30:32

being consistent with Alzheimer's disease as we describe it.

30:36

Um, and then the computer spits out this table

30:38

and we look at this cental load value

30:40

here and it's almost zero.

30:41

So this is negative, um, a negative study.

30:45

So that's a negative study and this is a positive study

30:49

and hopefully you can kind of see that we've lost

30:51

that arboreal pattern.

30:52

It does not look spiky.

30:54

So I'll pop in that it's hard for to

30:55

to know first off the bat.

30:56

So I'll pop the normal next to it.

30:58

So here is our normal comparison

31:01

and you can see that we've lost that spikiness

31:03

and instead we've got a smooth cortex.

31:05

So smoothing

31:06

because there's abnormal tracer uptake in the gray matter.

31:11

And also we've lost that normal cortical separation.

31:14

So here's our normal comparison

31:16

and here the cortis are almost touching.

31:18

So that is again an abnormal study.

31:22

So what does the aloid look like in this patient? Different.

31:27

So here our centel value is over a hundred,

31:30

134.79, which is consistent

31:35

with Alzheimer's disease

31:37

and really useful for patient like this.

31:39

And we had that question earlier about, um, about kind of,

31:43

you know, diagnostic certainty and, and things like that.

31:45

And you know, some, I, it's not uncommon

31:47

to see any mild cerebral atrophy

31:48

and not typical CT structural features

31:50

of Alzheimer's in these patients

31:51

or even significant neurodegeneration or atrophy.

31:55

Um, so our amyloids can be really useful evening younger

31:58

patients for that diagnostic certainty.

32:02

Great. Okay. Feel free

32:04

to keep asking questions in the chat, um, as well.

32:06

But we'll move on to Parkinson's disease

32:08

and nuclear medicine has been doing

32:10

DAT scans for a long time.

32:11

You know, we've had agents in general nuclear medicine, um,

32:14

but I always found that was so hard to, to read.

32:16

The spatial resolution wasn't great.

32:18

The signal to noise wasn't great.

32:19

But now we have a PET tracer, which is FPC,

32:22

another flu 18 base tracer.

32:24

Um, and it's great because it binds

32:26

with really good affinity to the dopamine transporter

32:28

and we enable in in vivo assessment of the Niagara

32:31

salal pathway, which is so important in um, Alzheimer, in,

32:35

I'm sorry, in Parkinson's disease.

32:37

And we are looking for that structural target.

32:39

Sorry, one moment,

32:53

sorry, apologies for the sneezes there.

32:55

Um, so we're looking at a structural

33:04

apologies one more time.

33:05

Um, so we're looking at a structural target

33:07

and interestingly FPC is an analog of cocaine, so we need

33:10

to be quite, um, in other stimulant medications.

33:13

So we need to be quite careful about

33:15

what patients are on when they come in for this scan.

33:17

So there'll be a medication checklist.

33:19

The advantages of this particular tracer does is

33:21

that it has fast kinetics

33:22

and we get this great high, um, signal to noise ratio,

33:25

which gives us really nice clear images.

33:28

And you'll see what I mean in a moment.

33:30

But let's start with the anatomy.

33:32

We are really looking at, um, the,

33:34

we are really looking at this part of the brain,

33:36

so the putamen, um, and then the coordinate coming around

33:39

and keep note of the Amy, um, amygdala body as well.

33:43

'cause you can sometimes just see that on the studies.

33:45

But the putamen and the preservation of the an

33:48

of the ventral end dorsal putamen is important,

33:50

important area for us to assess.

33:53

So I'll just play this little video of

33:56

how I use, how I set this up.

33:59

And this isn't mim, um, I couldn't take a screen cap.

34:01

This is just using a, um, another viewer called Radiant,

34:04

but we can still work with it.

34:05

Um, just mimicking what I do. So I adjust my levels.

34:08

You can really see that we wanna kind of play up

34:10

and down until we can see the internal detail

34:14

of the chordate amputate.

34:16

Great. And then I'll line it up along it.

34:19

And I like to use MIPS as well.

34:21

I find MIPS are super useful,

34:22

particularly if you line them up along the body

34:24

of the putamen and you get a real sense of

34:27

what we look like.

34:28

So there we are. So I'm lining it up along like that.

34:31

And then I'm gonna put on the MI tool

34:34

and then kind of scroll in in a moment.

34:36

But already I'm scrolling back

34:37

and forward looking at the chordate, comparing side to side,

34:41

considering that asymmetry

34:43

and then well you'll see on the mit,

34:46

but just how nicely we can capture.

34:49

I'm gonna turn it around that morphology.

34:54

And so what you can see there quite beautifully

34:59

is this nip here and you can always see the amyloid

35:01

body, which I just think is so gorgeous.

35:02

So putamen coordinate wrapping around,

35:04

coming down all the way here.

35:06

Um, and that is a normal study.

35:07

That is what you expect to see.

35:09

Um, and I like to think it looks like a bunny.

35:11

Um, but we've gotta give bunny much longer ears,

35:14

um, to account for that.

35:18

And there we go. There's our anatomy again.

35:20

And just to overlay it, that's

35:21

what we're looking at in comparison.

35:26

This is an abnormal study

35:27

and you can see that the, um, the back of the bunny of the,

35:30

or the um, or the dorsal aspect

35:32

of theam payment has essentially reduced uptake.

35:35

Um, and here if I draw it out for you.

35:38

So this is a nice normal study, whereas here

35:41

you can also see reduction in the, um,

35:43

the tail of the chordate as well.

35:45

And I'll be looking at these side by side,

35:47

um, particularly on a rainbow.

35:48

I use rainbow. My, my colleagues will use more metal,

35:50

that purple scale that we saw before.

35:52

And we're looking for symmetry.

35:55

So in a normal study, we're looking for that symmetry.

35:57

So cord eight head is just up here.

35:59

This is the cord eight head and this is the putamen.

36:01

Um, but here you'll notice the tails

36:03

of those putamana are decreased

36:05

and it can be asy asymmetric.

36:07

And we can also see reduction in the chordate

36:08

as well in the ventral part of the putamen.

36:10

But we are looking side to side looking, um,

36:12

for loss of that normal pattern.

36:14

And this is consistent with Parkinson's disease.

36:17

Um, there's a few different ways to remember this as well.

36:20

I would think about them as commas and full stops.

36:23

Um, comma, you know,

36:24

we're seeing the tail, um, and full stops.

36:26

We not seeing the tail on the commas,

36:28

so commas and full stops.

36:29

Um, but when I was over at um, MCW, um,

36:31

I had a new one which was, um, shrimp and scallops.

36:36

So if you have the tail of the shrimp, um,

36:38

all the scallops being round us.

36:39

So however you you read it locally, um,

36:42

whether it's tech commas, um, or bunny rabbits

36:44

and full stops or shrimps

36:46

and scallops, whatever helps you to remember the morphology.

36:50

Um, and just to throw in another case here as well,

36:52

so normal and Parkinson's disease, that case that we saw

36:55

before, and this one is an atypical Parkinson's disease,

36:58

we're not only seeing that, you know,

37:00

we're losing kinda the more ventral aspect of theam,

37:02

but the cord eight is down to, there's a bit

37:04

of preserved uptake here, but we've really

37:05

lost that beautiful signal.

37:07

And even that signal to noise ratio is less

37:09

because the tracer isn't being taken up where it should be.

37:12

Um, so this is an abnormal study

37:14

and not all

37:15

that we see on these fp sit stands is necessarily going

37:18

to be Parkinson's disease.

37:19

Um, it can help us with the assessment of a range

37:22

of neurodegenerative conditions and including MSA, both P

37:25

and c, progressive supra nuclear palsy,

37:28

even diffuse Lewy body dementia, um,

37:30

or um, corticobasal degeneration.

37:33

But um, essentially we,

37:34

we use these in conjunction with other modalities.

37:36

Um, is EFPC gonna be the first

37:38

line for a lot of these cases?

37:40

Probably not. Like they'll have, they'll often come to us

37:41

with MRIs and cts

37:43

and we are certainly a problem solving, um, investigation

37:46

and often for patients who have had they then maybe

37:48

presenting younger or with atypical symptoms

37:51

or refractory to treatment.

37:57

Okay, so we're going to move on to some brain tumor imaging

38:00

and we're going to no questions.

38:01

Great. Feel free to keep putting the chat,

38:03

the questions in the chat box as well.

38:05

So let's move on to brain tumors

38:07

and we're gonna briefly stop at FDG.

38:09

FDG has been used in the brain,

38:11

it was actually brain imaging with FDG PET was

38:13

what probably one of the earlier applications

38:15

of PET program railroaded by oncology and body imaging.

38:18

Um, so brain tumor imaging for with this has been, you know,

38:21

a store walk for such a long time.

38:23

Um, but that's had assessment can be difficult

38:25

because we know that the brain takes up so much sugar so

38:28

that signal to noise ratio can be reduced.

38:30

Um, so we need to be very careful with our scale adjustments

38:33

and also correlating it with the diagnostic imaging, whether

38:36

that be MRI ideally

38:37

or a CT note as well,

38:40

that certain different brain tumors

38:42

can have variable metabolism.

38:43

Often high grade disease will have, um,

38:46

higher uptake glioblastomas grade three,

38:48

um, who grade three lesions.

38:49

Um, even some metastases will be hotter,

38:52

but small lesions are difficult to detect.

38:54

We don't have that spatial resolution, we don't have

38:56

that signal to noise ratio.

38:57

We don't have the contrast resolution that MRI does.

39:00

And so in no case I, in no way am I'm advocating

39:02

that we should be taking over for those modalities.

39:05

Um, but we are useful in problem solving.

39:07

Um, but so if you see a lesion we can kind of help with the

39:12

decision making and leading down one path or another.

39:15

Um, so, and then also keep in mind

39:17

that some benign neoplasms and inflammation

39:19

and infection will also be FDG AVID as well.

39:23

So encephalitis we don't help a lot.

39:25

Encephalitis first tumor, both can be hot.

39:27

So that's a bit of a tricky one.

39:29

Um, so here again,

39:30

this is actually the, the kind of the norm.

39:32

The case that we were looking at earlier.

39:33

This patient came in with, um, for dementia assessment.

39:36

And I just like it because it shows

39:38

how when we turn down the brain we really need to look

39:40

through because you need to be looking

39:43

through the background metabolism for um,

39:48

for increased, um, for increased uptake.

39:51

And if you look down towards the base

39:53

of the brain here in the

39:55

pituitary fossa, we'll come back up again.

39:57

You'll notice that there is something popping up right there

40:00

in the middle that is bright red above background.

40:02

And this was a case of a

40:04

incidentally detected pituitary

40:06

macroadenoma in this patient.

40:07

So they can also be really hot occasionally you'll also see

40:10

them on body imaging too,

40:11

which is why you've always gotta look through the brain.

40:15

Um, this is a nice case I took from radio pedia, um,

40:18

which is a good example of

40:20

where FDG can be used for problem solving.

40:22

Um, this was a patient with an optic HIAs and glioblastoma

40:25

and then if you look through here,

40:26

there's corresponding abnormal uptake through that.

40:29

So that was useful in,

40:30

in problem solving a difficult region.

40:32

Um, and you could see that that could be used for surgical

40:35

or um, radiotherapy planning

40:36

depending on what was happening.

40:38

And another useful case.

40:40

And this leads right onto our next part,

40:41

our next section on FET.

40:43

Um, and this was an, um, a grade three oligo dendro glioma,

40:47

which didn't have a lot of enhancement at the beginning.

40:49

And so a debulking surgery was performed.

40:52

You can see it there with flare hyperintensity,

40:54

cortical expansion, not a lot of enhancement, but

40:57

after the patient underwent their debulking surgery,

41:00

they wanted their progress MRIs

41:01

demonstrated in enhancing nodule.

41:02

Unfortunately I don't have that image,

41:04

but this is what on the MRI.

41:06

But let's have a quick look at what the pet showed.

41:09

So just scrolling through, you can see that as we go up

41:12

and we're gonna ignore the bright spot for a moment.

41:14

I'm just gonna show you the surgical cavity

41:16

as this relative area of low, um, low signal.

41:20

Um, and that's, and then low tracer uptake.

41:22

So this is just all what we expect

41:24

to see post-surgically and normal brain.

41:26

But here above normal background is this right spot.

41:30

Um, so this was concerning for tumor recurrence.

41:33

The patient had not had radiotherapy,

41:34

which is an important diagnostic

41:36

consideration as we'll see in a moment.

41:37

Um, and unfortunately this patient did progress, um,

41:41

and they recurred the higher grade component

41:43

of the lesion was seen as the FDG avid, um, a abnormality.

41:48

Okay, just looking at our questions,

41:50

a great one from mattes.

41:52

Um, it's not one that I don't think I can answer well now,

41:56

um, and it's a little bit kind of outline of outside

41:59

of the the scope,

42:00

but I'm gonna take it down, um, if you'd like to.

42:03

So for the question about amlo, her BAPL scores, um,

42:06

and also FPC in terms of PD

42:08

or PD plus syndromes, um, if you'd like

42:11

to shoot me an email, um, I'll put my email at the end

42:13

as well and I'll um, I'll, I'll be able to answer

42:16

that one offline for you

42:17

with a little bit more nuance I think.

42:19

So thank you. That's a really great question.

42:23

Okay, so, ah, excellent.

42:26

So Katie has has anticipated the next part of my my talk.

42:30

So is there a differentiation between radiation necrosis

42:32

and tumor necrosis using FDG

42:34

or other alternative radiant traces?

42:36

That is a great question.

42:38

Um, and one of the hardest things

42:39

that we can do is determine, is trying

42:41

to determine whether it's radiation necrosis

42:43

or true progression.

42:45

Really tough. Yes,

42:46

no, no, I got what you were talking about.

42:47

Um, perfect, thank you Katie.

42:48

Um, yes, so is it recurrence or is it radiation necrosis?

42:52

Um, because both can be hot.

42:53

FDG, it's a very sensitive but not a very specific tracer.

42:56

So inflammation can certainly be hot on pet of the brain

42:59

as it can elsewhere in the body.

43:01

Um, and so what do we do?

43:02

Um, because on MRI, radiation necrosis

43:05

and progression can look the same.

43:07

So we've been, one of the things tools

43:09

that we have in our arsenal at Royal North Shore is FET.

43:13

Um, and that's another agent, um,

43:14

called um, floral ethyl tyrosine.

43:16

It's an amino acid pet and it is taken up by glial tumors

43:20

and we'll often use it in conjunction with FDG as well.

43:22

And also some, um, time activity curves to see, to try

43:27

and distinguish between, um,

43:28

radiation necrosis and recurrence.

43:30

Are we perfect? No,

43:32

but no imaging modality is

43:34

so often our radiation oncologists, um,

43:36

and our medical oncologists

43:37

and our neurosurgeons will sit down with us

43:38

and we'll try to, you know, work it

43:40

and almost like, you know,

43:41

problem solve based on which one is more likely as well.

43:45

Um, so that's a fantastic question

43:46

because that's one of the,

43:47

the challenges that we're working on.

43:49

Um, so FET, um, it's a molecular we,

43:53

it's a molecular imaging agent.

43:54

Um, and it's a supplement to MRI, it does not replace MRI.

43:57

Um, so we use it altogether.

43:59

Um, and the few reasons that we use this is for monitoring,

44:02

um, um, patients clinical features, um, imaging

44:06

features will all come into it.

44:07

Um, and FET and um, FDG PET are often an adjunct.

44:13

So here's a nice example of just a, a straightforward one.

44:16

Um, so this is a patient who had multifocal

44:18

glioblastoma on both sides of the brain.

44:20

So a left temporal lesion, um,

44:22

and a right paral region lesion here, here and here.

44:26

So these enhancing lesions.

44:27

And then they had a pre-treatment FAT scan, um,

44:31

just for delineation.

44:32

And you'll notice that when I play the video it's coming up,

44:37

we'll have that spot here just in, did I indicated it, yes,

44:40

there in the parietal region corresponding to

44:42

that ribbon enhancing lesion

44:44

and then intense FET uptake medially within

44:47

that temporal lobe

44:47

corresponding to the more dominant lesion.

44:50

So we already know that we've got multifocal disease

44:52

and this patient went on to have therapy radiation

44:54

to both of those regions.

44:57

Um, and unfortunately recurred.

44:59

Um, so in the parietal region, which was different distant,

45:02

um, with these mass like areas of enhancement,

45:05

there was a question, could this be radiation?

45:07

Um, but this was very, um, FET avid, um,

45:12

and with the distribution, um,

45:13

and the correlation with the radiotherapy fields being

45:16

outside of it, um, the areas of boosting

45:18

that this was thought to be recurrence and yes it was.

45:21

Um, so here's actually, this is the baseline, uh,

45:24

a diagnosis and here's the recurrence as well showing

45:26

that the FET distribution help them to map the disease

45:30

and come down with more diagnostic certainty.

45:34

And moving on to dynamic imaging,

45:36

which is one thing that we really do.

45:37

If the clinical question is, um,

45:39

recurrence versus pseudoprogression or radiation necrosis

45:43

and we are looking at something called a time activity curve

45:46

where the, um, the tracer

45:48

washes in and washes out over time.

45:49

So we're looking at blood flow similar to what we do

45:51

for dynamic imaging in breast cancers, you know,

45:54

even in arterial enhancement and hepatocellular carcinomas.

45:57

So that malignant kind of pattern of washing wash out, um,

46:01

as opposed to inflammation which should theoretically just

46:03

accumulate tracer over time.

46:06

And so we use this information,

46:07

we take measurements over 40 minutes of continuous imaging

46:10

and then create a time activity curve which can have

46:13

three different morphologies.

46:17

Um, yes Avastin, if it does decrease the blood supply,

46:21

yes it will in impact things we haven't, we don't tend

46:23

to image patients on Avastin, um, prednisone index,

46:27

I'm not too sure, but most patients will come to us

46:29

with prednisone index, so I don't think so,

46:31

but fact check me on that one.

46:32

Thanks again Katie for a great question.

46:34

Um, so let's look at those three, um, time activity curves.

46:38

Um, so here is a type one increasing curve

46:42

and this is typically our inflammation curve.

46:44

So it's continuously outgoing like this

46:48

and then a plateau curve which is going up

46:50

and then it's staying flat.

46:51

And now we're starting to get worried.

46:52

Plateau curves can be seen in high grade glial tumors.

46:55

Um, so this is coming to get concerning

46:58

and then a type three

46:59

or decrease in curve, which is very

47:00

concerning for high grade tumor.

47:02

So over time we're getting a peak

47:04

and then starting to decrease off.

47:06

And so this is the pattern

47:07

that the textbook says is most consistent

47:09

with tumor recurrence, whereas the type one curve,

47:12

which is this one, is more consistent

47:13

with radiation necrosis on FAT.

47:16

There is some overlap

47:17

'cause FAT can be taken up in areas of inflammation.

47:20

Um, but it's just a, as we said, it's just another tool

47:23

that we have in our problem solving

47:24

arsenal, which can help us here.

47:26

And a bit of a demonstration case.

47:28

Here's a patient with a tumor cavity.

47:30

They've already had it resected,

47:31

they've had local radiotherapy,

47:32

they've had this patchy enhancement posteriorly to this.

47:35

The question was whether this is tumor recurrence

47:37

or is this um, radiation necrosis or pseudo-progression?

47:42

And yes, it was FAT avid

47:43

but we could we call it based on this FAT alone.

47:45

'cause both can demonstrate uptake. No, we can't.

47:48

So let's have a look at our curves

47:50

and the curve demonstrates that morphology that up going up

47:54

and then down curve

47:56

or like I I, I know with an eye faith looks a bit plateau

47:59

but I think there was an up and we considered

48:00

that was going down with our peak kind of around the 15

48:03

to 20 minute mark and then slowly decreasing.

48:06

So this study was reported as concerning

48:08

for high grade malignancy with

48:09

and that diagnosis was confirmed on progress imaging.

48:14

Okay. Um, so stopping briefly at gallium 68 dotatate,

48:17

which a lot of you might kind of come across as um,

48:19

a neuroendocrine tumor marker.

48:21

So this is a patient with metastatic small bowel

48:22

neuroendocrine tumor with a dotatate scan.

48:25

This spot in the brain is the pituitary.

48:26

So we just need to keep that in

48:27

mind looking at brain imaging.

48:29

Um, and also this was a nice example I had of a, um,

48:32

pancreatic insulinoma look at that.

48:34

Just gorgeous. Um, but we can use dotatate in the brain

48:37

because meningiomas have somatostatin receptor expression,

48:40

um, which means that they are avid on dotatate scans

48:44

and sometimes we detect these incidentally,

48:47

but where does pet, if we, someone does have an meningioma,

48:49

where does PET dotatate add value?

48:51

Where does gallium 68 dotatate add value?

48:54

Um, 'cause we know meningiomas are well characterized on CT

48:57

and MRI MRI especially.

48:59

So you don't wanna be doing a dotatate scan for everyone

49:01

with a meningioma, but if you are looking to treat

49:04

or you're looking to characterize atypical lesions like on

49:07

plaque meningiomas or where there's bone involvement

49:09

or osseous meningiomas, that pituitary is normal.

49:12

But this is all on plaque

49:13

and into osseous meningioma through the sphenoid.

49:16

Um, or this really nice case here of this, um,

49:20

of this one at the orbital apex

49:22

where there was this thickening and then there was

49:23

focal do uptakes.

49:24

This was a little tiny ingio at the, um,

49:27

at the optic canal or the optic nerve.

49:30

There we go. Nice.

49:32

Um, and so we can use it in some patients,

49:35

some select patients for predictions of growth

49:36

and outcome for therapy, planning for radiotherapy

49:38

or surgical resection and also for theranostics.

49:42

We'll come back to Theranostics in a moment,

49:44

but I will just show you some nice radiation contours

49:46

that the dotatate have used just from

49:48

a nice article I found.

49:49

So contouring the lesion based on the dotatate uptake

49:52

and then being able to deliver more targeted radiotherapy

49:55

to these atypical meningiomas.

49:58

And just a little quick couple

50:00

of animations about lutetium therapy,

50:03

which you would've seen with prostate cancer,

50:05

neuroendocrine tumor elsewhere.

50:06

But there is an application in meningiomas.

50:09

So with diagnostic imaging,

50:11

gallium 68 is our positron emitter with dotatate,

50:13

which is our pharmaceutical, but you can swap it out

50:16

for Lutetium 1 77, which is a beta emitter.

50:19

So particle radiation can be used for targeted radiotherapy.

50:23

And how does it work?

50:24

We've got our receptors on these cells.

50:26

In this case it's gonna be gonna be a somatostatin receptor.

50:28

Um, and then we send in our somatostatin receptor, um,

50:32

agonist, sorry, my bad.

50:34

I just press play. There we go.

50:37

Um, so then the radiopharmaceutical will come in

50:41

and for diagnosis it will come in

50:43

and then it will send off our gamma photons

50:46

for us to be able to image it.

50:47

But in treatment it will be taken into the cells as well.

50:50

So this is our diagnostic,

50:51

but if we've got a particle radiation

50:54

and it's in there, then it's gonna be throwing

50:55

out these electrons.

50:57

What type of damage is that going to do to the cells?

51:00

Well, if we get it in the cell, then it can hit the DNA.

51:03

And so the electron, it's a big particle, it causes damage.

51:06

Um, and then it can cause double stranded breaks within the

51:10

DNA and this can be fatal to the cell

51:14

and then cause apoptosis.

51:16

So same therapy of radiotherapy elsewhere.

51:18

So apoptosis, getting the

51:20

beta emitter into the cells exactly where it needs

51:22

to be and causing cell death.

51:25

And here's a nice case. So on the top is the dotatate.

51:28

This is a patient with multifocal meningioma who'd had

51:30

multiple craniotomies but just kept coming back.

51:33

This was an atypical histopathology.

51:35

And then on the bottom is lutetium dotatate therapy.

51:37

So really good targeted therapy

51:41

just running through to the end.

51:43

A brief stop on FMI OI don't have any um, diagnostic cases,

51:46

but just to know that this is in the research realm.

51:48

It's an imaging of, um, hypoxia.

51:51

So we're looking for, um, you know,

51:53

changes in oxidation pathways and cell hypoxia.

51:55

So this is firmly in research.

51:56

Um, but detection of hypoxic tumor cells can help

51:59

with our detection of necrosis and upstaging and comp

52:01

and, um, considering about re um, the patients

52:05

and how they will interact to therapy and respond.

52:08

Um, and this was complimentary to MR as well

52:11

and that's just a nice example of an F miso scan.

52:17

So in the last three minutes, just a bit of a show

52:19

and tell about F choline just

52:21

'cause I've got some such beautiful cases of, um, of pittu,

52:25

of parathyroid adenomas, um, which, so choline,

52:29

transporters, um, it's operated upregulated in pituitary

52:32

adenomas and it's incorporated into the cell membranes.

52:35

And so it gives us a really nice signal to noise

52:36

and really clear imaging.

52:38

Traditionally we've used aceta, me and other gen

52:41

and um, four DCT

52:42

and ultrasound for assessment of para of um,

52:44

parathyroid adenomas.

52:46

Um, but sometimes because parathyroid adenomas can be

52:49

multiple, they can recur, they can be in strange places

52:51

because of variant anatomy.

52:53

Um, we are looking for better agents all the time.

52:55

And this is one of the CHO studies.

52:58

And you can see this patient actually had multiple surgeries

53:01

already, um,

53:02

and they were still having refractory hypercalcemia.

53:05

Um, so if I spin the patient,

53:06

you'll notice in the chest there are three dots

53:08

and they should not be there.

53:10

The muscle uptake, the glib bowel, that's all fine.

53:12

Slide glands, that's fine,

53:14

but those dots should not be there.

53:16

And so here superiorly, we've got one kind

53:19

of typically located parathyroid adenoma in the

53:21

tracheal esophageal groove.

53:23

Another spot posterior to a surgical clip

53:25

after one had already been resected.

53:27

And then moving a little bit further down, inferior,

53:30

the aortic arch is alar, very large parathyroid adenoma

53:33

with intense tracer accumulation, which may not have,

53:36

which definitely would've been caught off al on ultrasound.

53:39

And you'll say, well Sally, you know,

53:41

surely this would've been caught on esta maybe scan.

53:43

Well actually no it wasn't.

53:45

Um, so here's the sesam maybe on, um, screen on,

53:48

on screen left and the choline on screen, right?

53:51

And there's, oh my gosh, you can just see maybe a bit

53:53

of uptake through there on the MIBI study,

53:56

but so much better on choline.

53:59

Um, and just so you believe me

54:01

that there's a few other examples

54:02

and I just haven't given you one.

54:04

Here's one more. There's one coming through here

54:08

and another one just in the neck in the

54:10

tracheal esophageal groove here.

54:14

And the last one, more anteriorly,

54:16

we can see the variable uptake based on the scanning times

54:18

that really nice, um, study.

54:21

And it is in a lot of the,

54:23

is showing really good positive predictive value

54:25

and also, um, good sensitivity above 90%, um, compared

54:29

to four DCT and system may be used in isolation.

54:32

So watch this space and some nice some cases to finish up.

54:35

Great. So it's 9 54. Well, where I am, it's 9 54.

54:39

Thank you for everyone else you are joining

54:41

a few references and a few thanks.

54:43

Um, I'd like to thank the team at Modality

54:44

who have invited me along today.

54:46

It's been a real pleasure, um, to, um,

54:48

associate professor Jess s Shery, Dr.

54:50

Sophie too, and Dr. Ash Raghavan who have, um, helped me

54:52

with some of the content in the cases, um, my workplace,

54:55

university of Sydney, Royal North Shore Hospital,

54:57

and the Australian Total Body Fit for PET Facility on behalf

55:00

of the National Imaging Facility

55:02

and also Medical College, Wisconsin and Dr.

55:04

Mohit Agarwal, um, for the inspiration, um,

55:07

and some great feedback on curating these cases.

55:10

So I'd like to open the floor.

55:11

Is there any questions or anything?

55:13

Um, I can comment and I know that there was that question,

55:16

um, about, um, the PD plus.

55:19

Um, I'd love to be able to chat more about that,

55:21

so please email me, um, who wants it.

55:25

So, um, Natasha, I, if you'd like to send me an email,

55:28

that would be fantastic and I'll also bring in my, um,

55:30

the local experts as well who'll be able

55:32

to give you a really great, um, a really great explanation.

55:35

Um, but are there any other questions, comments, feedback,

55:38

um, that I can help with this, um,

55:41

today at the end of the talk?

55:44

Yeah. Thank you so much Dr.

55:46

AA for sharing your lecture with us today.

55:48

And yeah, it looks like, oh,

55:49

we just had one question pop into the q and a.

55:52

Oh, excellent talk says, thank you.

55:54

Very nice talk. Thank you very

55:55

Much. Um,

55:56

we can wait a few more seconds

55:58

to see if any questions pop in,

56:00

but you were answering so many during your lecture,

56:03

it was great and it was extremely helpful to the learners.

56:06

Um, wonderful. I hope that you all found it useful.

56:09

Um, as I said, there's my emails

56:11

and my content, so if you've got any questions, comments,

56:14

feedback, things I could do better, um,

56:16

please don't hesitate.

56:17

Um, and I'm looking forward to kind of, you know,

56:20

meeting a few of you in the real world. So thank you.

56:22

Awesome. Thank you so much again, Dr. Aa.

56:25

And thank you to everyone

56:26

for participating in our noon conference today

56:29

and asking such great questions.

56:31

You can access the recording of today's conference

56:34

and all our previous noon conferences

56:35

by creating a free account.

56:37

We'll also be emailing out the link

56:39

to the replay later today.

56:42

Be sure to join us next week on Wednesday,

56:45

December 18th at 12:00 PM Eastern, where Dr.

56:48

Asim Chowdry will deliver a lecture entitled Pediatric Brain

56:52

Tumors Latest Updates on The WHO Classification Revision.

56:56

You can register for it@mmrionline.com

56:58

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57:00

for updates on future noon conferences.

57:02

Thanks again and have a great day.