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Today we are honored to welcome Dr.

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Awesome Trry for a lecture entitled Pediatric Brain Tumors

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Latest Updates on the WHO classification revision.

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Dr. Trry is the chief

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of pediatric neuroradiology at Lab

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Bonner Children's Hospital.

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He's also a professor

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and associate chair of research Affairs in the Department

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of Radiology at the University

0:43

of Tennessee Health Science Center.

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At the end of the lecture, please join him in a q

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and a session where he will address questions you

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may 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.

1:00

Chaudry, please take it from here.

1:03

Thanks for joining.

1:09

So the goal today is to discuss an imaging approach

1:12

to pediatric brain tumors

1:16

and review updates to WHO classifications of CNS neoplasms,

1:21

focusing on clinical relevant changes

1:22

to pediatric brain tumor classification

1:26

and an emphasis on things relevant to the radiologist.

1:29

This is not a dedicated pathology lecture.

1:33

So pediatric brain tumors involve many entities, a lot,

1:37

a lot of which are not commonly seen in adults.

1:40

Tumor characterization has been historically classified

1:43

by histopathologic features.

1:46

In other words, looking under a microscope, molecular

1:50

and genetic characterization of tumors has augmented the,

1:54

um, tumor characterization methodology,

1:57

and in some places supersedes histologic characterization

2:01

in tumor diagnosis.

2:04

So why have classifications these classifications

2:08

if just for the sake of making a classification?

2:11

It just seems academic,

2:13

but classifications that allow optimized management is ideal

2:19

standardization of diagnostic criteria, AIDS

2:22

and clinical trials allowing similar entities to be grouped

2:27

and once similar tumors have been grouped

2:29

and used to assess treatments that can be used prospectively

2:33

to guide treatments in new patients.

2:36

And, uh, understanding the tumor types, um,

2:39

that we'll go over allows you to predict some patterns

2:42

of recurrence and metastasis,

2:44

which helps you guide initial imaging workup

2:47

and subsequent imaging surveillance.

2:50

The WHO or World Health Class Organization classification,

2:55

they began classifying central nervous system neoplasms in

2:58

1979, the fir, that's when the first edition

3:01

of their classification came out.

3:03

And 14 years later, they had a second edition,

3:08

a third edition, seven years later,

3:09

fourth edition, seven years later.

3:11

Now, there was a major update, um,

3:15

to the 2007 edition in 2016, which start,

3:20

they were waiting for the fifth,

3:22

but that's when some of this molecular data

3:25

that I'm talking about started to come in

3:27

and they felt they needed to give an update.

3:29

And the most recent version that we work

3:31

with is the fifth edition from 2021.

3:34

So it's five years old.

3:36

So again, while it was only five years old,

3:38

the next update is actually expected fairly, um,

3:42

soon in the next, uh, year or two

3:44

because of the rapid proliferation

3:47

of new information aiding in, uh, diagnosis.

3:51

So the, again, it is rapidly evolving

3:56

by shifting from just histopathologic basis

3:59

to molecular genetic basis.

4:03

Here's an article that summarizes

4:05

from a pathology in the oncologic perspective,

4:09

the 2021 classification of CNS tumors

4:13

if someone wants to learn more.

4:16

And then here's a two part series

4:20

of articles in the journal radiology

4:23

that go into more detail about the various entities in the

4:27

WHO, uh, 2021 criteria.

4:30

So these would be something for someone that wants

4:33

to delve a little bit deeper than

4:35

what we're going in this lecture,

4:37

that they find something interesting

4:38

and they wanna learn more about it.

4:40

Uh, these articles are very good places to start.

4:45

So why new classification systems?

4:47

So this is sort of one of the viewpoints that

4:51

you always wonder when the,

4:52

you hear updated classification systems and any standard

4:56

or classification system, you know, starts off,

4:59

there's multiple different ways of doing something

5:02

and people say, oh, we need a single unified way

5:06

that's better than all those other ones to, you know, adapt,

5:10

adopt new information, cover other use cases,

5:13

and that's great, but eventually it's just one more,

5:16

uh, classification system.

5:17

So there has to be a reason for this.

5:19

And as we'll see, the WHO has done this systematically,

5:24

uh, in a way that's actually helpful.

5:27

So what's the role of imaging?

5:29

We wanna spatially localize the tumor, see

5:31

where the boundaries are, the relationship

5:33

to the surrounding structures.

5:35

We wanna identify metastatic deposits.

5:37

Um, we wanna understand

5:40

what additional imaging might be needed.

5:42

So if you can predict the most likely entities,

5:45

it may help you determine

5:46

what additional imaging could be needed.

5:49

Uh, some brain tumors need spine imaging,

5:51

some need vascular imaging, some need a functional MRI

5:54

and some lesions may end up not being a tumor.

5:57

Once you characterize it.

5:59

You may think it is, but it may be something like tumor

6:01

effect, multiple sclerosis or something.

6:03

Uh, so, you know, understanding what these entities are

6:08

and how to appropriately characterize them on

6:11

imaging can be very helpful.

6:15

And one of the things that I do a lot

6:16

of is assisting in surgical planning.

6:19

So before we get to the specific entities, I want

6:22

to cover a topic that, um, I find very helpful.

6:26

It's estimating tumor cellularity with a DC maps,

6:30

because this becomes relevant in differentiating some

6:32

of the types of tumors that we're gonna be talking about.

6:36

So what's a cell? The cell has cytoplasm,

6:39

which is salt water with some

6:40

organelles floating around in it.

6:42

So it's mostly, um, equivalent of saline.

6:48

The nucleus is very densely packed with DNA

6:51

and regulatory proteins.

6:54

So in the grand scheme of things, water moves

6:57

around relatively freely in the cytoplasm

7:00

and water can't move as freely in the nucleus.

7:05

So my histology 1 0 1 CliffNotes version is for an h

7:09

and e stain cytoplasm is pink and the nucleus is purple.

7:13

So if we apply that to a pilocytic astrocytoma,

7:17

we see relatively speaking, a lot more pink

7:21

or cytoplasm than we do nucleus or purple.

7:25

There's a low nuclear to cytoplasmic ratio,

7:28

and this happens to be a WHO grade one tumor.

7:32

So it's a, a low grade tumor, very high amount of cytoplasm

7:38

in contrast, MedU Blas stoma we're seeing

7:42

largely we're just seeing nucleus.

7:45

Um, it's a very high nuclear to cytoplasmic ratio.

7:49

This is happens to be a Ws O Grade four tumor.

7:52

So remember as again, the hot,

7:55

the nucleus water doesn't move around

7:56

as freely the cytoplasm.

7:58

It does well. There was a great article by Dr.

8:02

Rumble and the, uh, Mauricio Castillo that

8:05

looked at pediatric posterior fossa brain tumors

8:08

and looked at the a DC values, the diffusivity

8:11

of a pilocytic astrocytoma,

8:14

which had the highest diffusivity.

8:16

Again, remember, it had the most amount

8:18

of cytoplasm relative to nucleus medulloblastomas,

8:23

where there was relatively reduced free movement of water

8:27

and appendamoma were in the middle.

8:30

This, this is one of my favorite papers, um,

8:33

that I've run across, because it's any paper that's

8:38

so simplistic that you can explain it in two

8:40

or three minutes and yet understand it

8:44

and apply it, is just very powerful.

8:48

So, as an example, here is a tumor in the fourth

8:51

ventricle, very large tumor.

8:53

You can see us causing obstructive hydrocephalus.

8:56

Here's another tumor. It's also in the fourth ventricle.

8:59

It's not as large. Um, so which is which, what,

9:04

what, what are these entities?

9:05

Well, if you look at the a DC map of this large tumor,

9:09

we're seeing relative facilitated diffusion,

9:12

even if we're not, even if we ignore the microcystic areas.

9:17

But this one, while it looks, you know, fairly bland on, um,

9:22

unassuming, it has relative reduced water diffusion,

9:26

low diffusivity, which would correlate

9:28

with a high nuclear de cytoplasmic ratio.

9:31

And this large one, despite it being large,

9:34

despite it causing hydrocephalus,

9:36

is the pilocytic astrocytoma of low grade tumor.

9:39

This is a blas stoma.

9:42

So this is an example of how some of these features can,

9:46

can work, um, to help characterize tumors.

9:49

So in my practice,

9:51

a DC maps are used in tumor characterization

9:53

and planning more,

9:55

much more often than perfusion

9:56

spectroscopy or other techniques.

9:58

And in some cases, it's actually even more important than

10:01

post contrast imaging.

10:02

I'm not saying we don't do some, some

10:04

of those other techniques, but I'm saying in terms

10:05

of making my final assessment,

10:08

the a DC maps are just highly important.

10:11

So I implore everyone make a habit of,

10:14

of reviewing the a DC maps on all brain tumors

10:17

and gain familiarity

10:18

with quantitative measures of diffusivity.

10:21

And approximately speaking, if you look at quantitative,

10:24

the cutoff separating a high grade in the low grade lesion

10:27

is often in the region of 1000.

10:29

Now, the units sometimes is measured as 10 to the minus six,

10:33

so it's a thousand, sometimes it's 10 to the minus three.

10:37

So it's one. Um,

10:41

this is a, um, a little primer on use of a DC

10:46

to estimate tumor cellularity.

10:48

So again, here's a patient with medulloblastoma.

10:51

It's the most common malignant, uh, brain tumor

10:53

of childhood, typically arises from the roof

10:55

of the fourth ventricle.

10:57

It's classified among oth other things

10:59

as a small rom blue cell tumor.

11:01

That's a way of saying high nuclear cytoplasmic ratio.

11:07

Now, this is sort of a classic appearance that, um,

11:12

in the histologic terminology, his histologically,

11:16

there was also a decimal plastic nodular subtype.

11:19

There was a medulloblastoma with extensive nodularity

11:22

and a large cell anaplastic.

11:24

So up until the two, 2016 WHO update,

11:28

these were the four categories of medulloblastoma,

11:33

and I'll say the desmoplastic nilar subtype.

11:36

Two interesting features about it.

11:38

One is often seen in the cerebellar hemisphere as opposed

11:41

to the fourth ventricle, and it can be seen in young adults.

11:44

So if you see, um,

11:46

a lesion in the cerebellar hemisphere in someone in their

11:50

twenties that restricts diffusion,

11:51

this is a very reasonable consideration.

11:55

Now, 2011, this article came out in Journal

11:58

of Clinical Oncology talking about

12:00

four distinct molecular variants of me neoblastoma

12:05

Two things to, no, this came out in 2011,

12:08

but as we know, there's been years of work

12:11

that went into this.

12:14

Um, but additionally, these molecular variants,

12:17

the grouping didn't have a one-to-one correlation

12:20

with the histologic grouping.

12:21

So there's sometimes two different tumors

12:24

with similar histology would be different molecular

12:26

subgroups, and that might actually account for some

12:30

of the difference in treatment outcomes and response.

12:35

So for the molecular subtypes, there's the WNT

12:39

or WINGLESS type activated.

12:42

There's the sonic hedgehog activated,

12:44

and there's two different variations of that,

12:46

whether it's a wild type or mutant of the TP 53 gene.

12:51

And then there's the nonw nons hedgehog, um, entities.

12:56

Now, those nonw nons hedgehog entities are further, um,

13:02

uh, categorized into group three and group four.

13:05

We, so this is a,

13:07

this is a very good article looking at Mr surrogates

13:11

of molecular subtypes, uh, of medulloblastoma.

13:16

And so the tumor location

13:18

and enhancement pattern were predictive

13:21

of the molecular subgroups of pediatric medulloblastoma.

13:25

Um, so that's in interesting

13:28

because you now are saying that MRI can actually

13:33

give you insight not just into histology,

13:36

but actually molecular the molecular basis of a tumor.

13:40

So it's not a one-to-one correlation,

13:42

but it, it is something to be aware of.

13:45

Now, in their paper, they looked at the went,

13:48

the Sonic Hedgehog, the group three, group four.

13:51

They subcategorized them by different age groups, um,

13:55

what the histology was.

13:57

And notice, um, for instance, group three,

14:01

they were the different classic and large ano plastic.

14:04

The sonic hedgehog could be classic nadu desal, plastic,

14:08

large cell anaplastic.

14:09

So there's not a one-to-one correlation

14:13

between the genetic subtype, molecular subtype,

14:16

and the histologic subtype.

14:18

Um, there are some findings that correspond

14:21

with the location, however, that start to come true,

14:24

like group three, group four were only seen in the fourth

14:28

ventricle on in their series.

14:31

Um, you know, the WINT one was, um,

14:35

sometimes seen in the CP angle,

14:37

and the cerebellar hemisphere was most commonly the

14:40

sonic hedgehog ones.

14:41

But the sonic hedgehog was not exclusively

14:43

in the cerebellar hemisphere.

14:46

So some of the molecular subtypes, the wind activated.

14:49

So we talked CP angle, foram of liska

14:53

sonic hedgehog activated often, but not always hemispheric.

14:57

Um, which, uh, the group three,

15:00

it was in the fourth ventricle and it tended to enhance.

15:04

And group four is in the fourth ventricle

15:06

and tends to not enhance.

15:08

So this right here already tells you

15:12

that the, where the mesoblast, um, might be

15:17

and how it corresponds to the molecular subtype.

15:21

This is a paper, um, uh, I have to call it. Uh, Dr.

15:25

Patai a wonderful person

15:26

who unfortunately we lost two years ago.

15:30

Um, the, the wint

15:34

or WINLESS subtype group specifically,

15:37

those are the ones in the CP angle, but the, the

15:41

or site of origin is along the framing of liska.

15:44

So it can go into the fourth ventricle, it can go up

15:46

to the CP angle so that the

15:52

molecular genetics

15:53

and the location of distribution of those genes

15:57

and the site of origin of the tumor all start to make sense.

16:01

So then it is not just random,

16:03

there's actually a basis for it.

16:04

And as we learn more, we'll, we will be able to hopefully,

16:08

um, get more information to help guide treatment.

16:13

So this is sort of a typical case

16:15

of MedU neuroblastomas in the fourth ventricle enhances.

16:20

Now there's some metastatic deposits we see here,

16:23

intracranial and metastatic deposit,

16:25

and a spinal metastatic deposit.

16:29

It fills the fourth ventricle,

16:31

and it notice it's relatively hyperintense on T two, um,

16:36

that we're, that's gonna be relevant.

16:39

It was also hyperdense on ct that's relevant

16:43

because if you think the,

16:45

these have a high nuclear cytoplasmic ratio,

16:48

so relatively low cytoplasm, cytoplasm is fluid,

16:51

which is bright on T two.

16:52

So less fluid, more cellular, darker on T two,

16:57

less fluid, more cellular, brighter on ct.

17:00

So this is now showing

17:03

that these MR imaging characteristics,

17:06

it's not just different images and something's bright, dark

17:10

or, you know, but they actually give you an insight into

17:14

the, um, the, you know, microcellular structure

17:19

of these, of these tumors.

17:21

And that can help guide us in figuring out what's going on.

17:25

There's low diffusivity, um, quantitative was six 50, um,

17:31

which is low.

17:32

If we look at re remember that chart from

17:34

before, only medulloblastomas were, um, were at

17:37

that level on that chart.

17:40

So low diffusivity implies a high nucleus cytoplasmic ratio,

17:43

and as I mentioned,

17:45

the high nuclear cytoplasmic ratio corresponds

17:47

to relative increased density on CT

17:50

and intermediate to hypo I intense appearance

17:51

on T two weight imaging.

17:53

So these are all different things that are related

17:56

and can be explained by the actual, um, uh,

18:00

histopathology of medulloblastoma.

18:04

And the imaging features

18:06

of this overall suggests group three.

18:07

It's a fourth ventricular tumor that's enhancing.

18:10

Um, I'll say this, uh, patient, um,

18:14

is from a wonderful family.

18:17

The family started at Go Lucy, go Foundation, uh,

18:20

which I'm lucky enough to, uh, have, uh, served on the board

18:24

for, and they do a lot of wonderful work

18:27

for pediatric brain tumors

18:28

and other pediatric neurologic disorders.

18:32

Here's a patient with a cerebral pontin angle lesion

18:36

extends laterally along the anterior margin

18:37

of the left cerebellar hemisphere has heterogeneous

18:41

intermediate, uh, appearance on T two.

18:45

Uh, the post contrast enhancement is also heterogeneous,

18:49

and there's heterogeneous areas of reduced diffusivity.

18:53

Now, there's some microcystic areas which are gonna have

18:55

facilitated diffusion,

18:57

but the solid portions definitely show reduced diffusivity.

19:02

And those solid portions also show relative increased

19:05

density on ct.

19:08

So this is a, a went activated medulloblastoma,

19:12

so it follows what we're, what we were seeing before.

19:17

Here's a patient with a mass in the periphery

19:19

of the left cerebellar hemisphere

19:22

with some internal microcystic areas.

19:25

There's a edema seen antra medially

19:27

to it in the left cerebellar hemisphere.

19:30

If you look on CT again, the, the mass,

19:35

the solid portions of the mass, uh,

19:38

have relative increased density on ct.

19:40

The microcystic areas are have, are hypot intense,

19:45

and the, there's also a hypo dense appearance

19:48

of the parenchyma that where there was, um, edema,

19:54

there's heterogeneous post contrast enhancement of this mass

19:59

and reduced diffusivity of the solid portions of the mass.

20:03

So the facilitated diffusion is seen in

20:08

the, um, cystic components as well

20:10

as in the cerebellar edema.

20:15

So overall, this is a sonic hedgehog activated

20:17

medulloblastoma, which in the hi, the, um,

20:22

histologic classification is typically going to be a, uh,

20:27

dem plastic nodular type.

20:32

Here's a patient with a fourth ventricular mass,

20:35

can actually see it's extending inferiorly through frame Mai

20:39

on this axial image.

20:40

It fills the fourth ventricle.

20:43

Has intermediate T two signal

20:44

characteristics, a little bit heterogeneous.

20:46

It's sort of bright here, here,

20:47

a little bit darker over here.

20:48

So there's some heterogeneity.

20:51

There's no significant post contrast enhancement.

20:57

There's intermediate diffusivity.

20:59

The quantitative was about 1150.

21:01

So that airs a little bit more on the

21:03

facilitated diffusion side.

21:05

Um, much higher than, uh, Dr.

21:08

Rumble's, uh, paper showed any of the me neuroblastomas.

21:13

The CT showed intermediate density of the solid portions.

21:16

We're not seeing the high density that we saw on those,

21:20

some of those other cases.

21:22

This patient also has obstructive hydrocephalus.

21:24

We can see on this image, on this, um,

21:30

balanced steady state free procession image.

21:31

We see extension through the bilateral foram of Monroe,

21:34

actually into the, um,

21:36

through the protruding into the porous acoustics towards the

21:40

internal auditor canals bilaterally.

21:42

And this is an appendamoma.

21:44

Um, so again, it's not as cellular, so it's not

21:48

as dark on T two, not as bright on ct, not as, um, high, um,

21:54

low diffusivity as a MedU bast stoma.

21:57

So those are, there's multiple differences.

21:59

So, um, now appendamoma is, in particular,

22:04

posterior foss pomas have been molecular subtype

22:09

into two main groupings.

22:11

There's type A PFA for posterior fossa.

22:14

A, they're often more asymmetric.

22:16

You know, a sometimes you can take asymmetric,

22:19

it may be unilateral cerebral pontin angle, for instance.

22:22

Uh, they more often have hydrocephalus

22:25

and they rarely enhance.

22:28

And this PFB poster, fossa, appendamoma type B,

22:31

they're central within the fourth ventricle,

22:33

often more spherically shaped.

22:35

Uh, a majority of them enhance.

22:38

They often have some cystic changes.

22:41

So here's a, another patient

22:44

with a left cerebral pontine angle mass.

22:48

In ENC case, there's, there's vascular

22:50

and cranial nerve encasement.

22:51

That's relevant because schwannomas, um,

22:55

and don't,

22:56

schwannomas don't typically encase vessels like this.

23:00

Meningiomas don't typically encase it like this.

23:03

They will displace them.

23:04

Again, there's always exceptions,

23:06

but typically speaking, you know, we're, we're thinking

23:09

of something that's encasing

23:11

and not just purely pushing on those neurovascular

23:15

structures has intermediate characteristics.

23:17

On T two 80 imaging. There's no significant enhancement

23:24

and there's intermediate to facilitated diffusivity.

23:27

The quantitative diffusion characteristics were 1225.

23:33

So this mass, this is an appendamoma,

23:36

and the imaging features are suggestive of, uh,

23:39

posterior fossa, appendamoma type B.

23:43

But, um, now just be aware

23:45

that non enhancing tumors will often have non enhancing

23:49

metastatic deposits.

23:50

They can be extremely challenging to identify.

23:53

So if you see that one, um, technique

23:58

to consider is post contrast flare imaging.

24:02

Now, the, um, diffusion can actually help

24:08

identify them sometimes, especially

24:09

for non enhancing me neuroblastoma, like the group four.

24:13

But for appendamoma, where the diffusion may not be

24:16

as clear cut in identifying the metastatic deposits,

24:19

post contrast flare imaging, T two flare imaging, uh,

24:23

can be helpful in finding leptin metastatic disease.

24:30

Here's an individual with a right cerebellar mass.

24:32

It's a mixed cell in the cystic lesion, in the medial aspect

24:35

of the right cerebellar hemisphere on flare,

24:40

there's, um, near complete suppression of fluid signal

24:44

with an cystic component.

24:45

Now notice this is the first time of use flare.

24:48

Um, flair is a great sequence.

24:50

We acquire it in all our studies,

24:52

but for a lot of brain tumors, I trust the T two

24:55

and the other sequences more lair is,

24:58

provides supplemental information here.

25:00

It tells, tells us about the fluid in here, that it's

25:05

probably proac fluid, but

25:06

otherwise, um, not overly complicated.

25:12

There's enhancement of this medial solid component

25:15

of this mass, but no enhancement of the cystic component.

25:19

No mural enhancement, no neural nodularity be, um,

25:23

along that periphery.

25:25

And there's facilitated diffusion in this solid component.

25:29

The diffusivity is 1850,

25:33

and it goes without saying this facilitated diffusion in

25:36

this fluid filled cystic component, uh, 27, 20, uh, 25.

25:41

So just very free movement of water.

25:43

So, um,

25:47

there's a hypodense appearance of the solid component on CT

25:52

and near CSF density of the cystic component, which goes

25:57

with, you know, what we're suspecting based on the flare,

26:00

probably some slightly proac fluid.

26:03

And this is a pilocytic astrocytoma.

26:09

Here's, here's a child with a, um,

26:13

they'll defined hypodensity in the

26:16

right cerebellar hemisphere.

26:19

See this on the coronal image looks fairly defined

26:23

when we get window it like this

26:25

and see it on this coronal, there's an ovoid circumscribed,

26:30

um, T two hyperintense lesion in the

26:33

right cerebellar hemisphere.

26:36

There's incomplete suppression of signal on flare imaging.

26:39

So this does not look like the

26:43

cystic component that we saw in that first case,

26:46

even though on T two it looks very

26:48

bright, almost like fluid.

26:50

But this is not a cystic component.

26:53

Um, this is solid just high water content.

26:57

This heterogeneous post contrast enhancement

27:03

and this facilitated diffusion,

27:05

the diffusivity is approximately 1650.

27:09

And this is a solid pilocytic astrocytoma

27:11

with no discernible cystic components.

27:14

So, um, textbooks

27:16

and some lectures often will suggest

27:17

that pilocytic astrocytoma will be cyst with a nodule,

27:21

but they very often can be solid.

27:24

Um, if they're solid, they look like this

27:28

very high water content, uh, facilitated diffusion,

27:32

some heterogeneous enhancement

27:33

that happens on delayed imaging.

27:36

Now, trying to link what we're seeing in imaging to, um,

27:42

clinical is, you know, the, it's starting to make sense

27:45

that we're getting an insight into these lesions.

27:49

So again,

27:51

this patient had a solid pilocytic astrocytoma,

27:55

intraoperative MRI demonstrate, uh,

27:59

achieved a gross total resection.

28:01

And at two year follow up, there's no signs of recurrence.

28:04

So this is essentially a, a cure.

28:07

So that's, um, a great, um, a great outcome.

28:11

Obviously they undergo surveillance for at least five years

28:14

and then maybe a more prolonged,

28:16

uh, surveillance after that.

28:19

But, um, this child's essentially cured.

28:24

Here's a patient

28:26

where the axial T two 80 image looks like a distended, but

28:30

otherwise unremarkable fourth ventricle.

28:32

That all, it just looks like

28:33

CSF although it looks a little bit large.

28:37

And, but if we look at this balanced,

28:40

steady state precession technique,

28:42

there's actually a solid lesion in there.

28:44

It just, that solid lesion just happened to be

28:47

very bright on T two weight imaging.

28:51

And on a DC maps, we see facilitated diffusion 1550,

28:56

uh, d uh, for the diffusivity, there's some mild areas

29:01

of post contrast enhancement along the periphery.

29:05

It's relatively hypo dense on ct.

29:08

And so, so far it's looking like a pilocytic astrocytoma,

29:12

but it looks like it's within the fourth ventricle, which is

29:15

not where we'd normally think of a biotic astrocytoma.

29:19

Well, if we go up a little bit higher,

29:21

there's either thickening and,

29:23

and involvement of the right superior cerebellar peduncle.

29:28

So it's, this is a possible site of origin of a lesion

29:31

that's exophytic into the fourth ventricle.

29:34

So intraoperative MR demonstrated gross total resection

29:37

of the fourth ventricular component of the lesion.

29:41

Um, and again, that high water content, um,

29:45

earlier I talked with me neoblastoma,

29:48

how the high gro cytoplasmic ratio corresponded

29:51

with the darker appearance on T two, which corresponded

29:54

with the brighter appearance on ct.

29:56

For this one, I will say the,

29:59

the hyperintense appearance on T two goes

30:02

with a high water content for this low grade tumor,

30:05

but that also for the surgeon implies it's very likely

30:09

that it's going to be very soft and suckable.

30:11

And it's, it was true that it, um, this was able to be,

30:16

um, that intraventricular portions of the tumor were able

30:20

to be sucked out, uh, with relative ease.

30:24

So again, it's corresponding the imaging to the histology

30:29

to what the, what information might help the surgeon.

30:34

Here's an entity,

30:35

A-D-I-P-G diffuse intrinsic pontine glioma.

30:38

These are not resectable, they're treated with radiation.

30:41

Um, they're not resectable 'cause they infiltrate.

30:45

Uh, we can actually see these striations,

30:47

these transversely oriented striations, which are, um,

30:56

uh, the transverse poncho cerebellar fibers.

30:59

We're actually also seeing here this,

31:02

these are the descending fibers

31:03

of the corticospinal tract here

31:05

and here confirmed on, uh,

31:07

directionally coated fractional antrop maps from DTI.

31:11

So you, this is not resectable,

31:12

so it's treated with radiation.

31:16

Historically atypical lesions were biopsied,

31:19

and these quote, typical lesions went straight

31:21

to radiation based upon just an imaging diagnosis.

31:27

Now for DIPG I'll mention, uh,

31:29

an organization called Mary's Magical Moment.

31:32

Um, they, among other things, uh, take children

31:36

with DIPG to Disney World.

31:38

And this is Mary.

31:39

This is, uh, IM image provided with permission.

31:42

Um, and this is Mary, uh, showing her strength.

31:47

Um, uh, Mary, uh, um,

31:52

courageously battled, uh, DIPG for 41 months, uh,

31:56

until March of 2024, unfortunately.

31:59

But, um, you know, Mary's magical moment, it is, um,

32:04

just something to be aware of

32:07

because it highlights the challenging outcomes

32:11

that these um, entities have.

32:14

Now, DIPG that w many of us have probably heard

32:17

of is currently classified under the heading

32:20

of diffuse midline glioma.

32:23

But there's still importance to understanding the imaging

32:26

of A-D-I-P-G growth pattern of a diffuse midline GLI glioma.

32:31

Um, and the abbreviation, DIPG is,

32:36

um, still commonly in use.

32:38

It will likely remain in use.

32:40

Um, so, you know, um, a purist may say, oh,

32:44

it's a diffuse midline glioma.

32:45

Well, histologically it is,

32:48

but that doesn't tell the full story.

32:50

For instance, if you just say someone has adenocarcinoma

32:53

from a biopsy, that doesn't give you adequate detail

32:56

for treatment planning, even if

32:58

that's a true pathologic diagnosis.

33:00

So just because this is a diffuse midline glioma,

33:03

in my mind, it, there's still relevance to understanding

33:08

that DIPG, um, pattern and presentation.

33:12

Now, the diffuse midline glioma, the reason I say

33:17

it's relevant to know the DIPG,

33:19

because this bi thalamic lesion

33:22

is also a diffuse mid L glioma,

33:25

and the,

33:30

these may be the same tumor on a molecular basis,

33:32

but the imaging and biopsy and radiation

33:35

and therapy considerations can be very different.

33:40

So this is the patient with an expansile brainstem mass

33:43

within the pons, it engulfs the basilar artery.

33:46

That is one of the things that was historically said

33:48

as very classic for A-D-I-P-G.

33:53

Um, now there's some smaller

33:55

internal T two hyperintense cystic appearing areas, um,

34:00

and there's some peripheral enhancement along those, um,

34:04

T two hyperintense areas

34:06

and even some subtle susceptibility hypo intensity,

34:09

which probably goes with microscopic blood products.

34:14

Now, there's a heterogeneous appearance on diffusivity

34:19

on, on a DC maps,

34:22

and there's facilitated diffusion in these sort

34:24

of cystic appearing areas, which are presumably necrosis,

34:27

but it's heterogeneous,

34:29

otherwise it's more hypo intense over here along the margin,

34:34

these margins of the, um,

34:37

these presumed necrosis, which would make sense.

34:40

So we use that to actually figure out a biopsy site.

34:43

Um, just to the left lateral aspect of these necrotic areas.

34:49

We didn't, the an areas anterior that are t

34:53

that are very a DC hypo intense would be a great target if

34:57

you want to just say, oh, I want

34:59

to get the most cellular part of the lesion.

35:02

But the problem is, is that that's also

35:04

where the corticospinal tract fibers are.

35:06

So the biopsy was made.

35:08

We, we selected a site, um, more posteriorly.

35:13

Um, this was a diffuse midland glioma, the DIPG pattern.

35:17

The area of necrosis

35:19

with the biopsy confirms A WHO grade four diffuse midline

35:24

glioma, the H three K 27 M mutant, uh, with necrosis

35:28

and microvascular proliferation.

35:30

Well, all that is stuff that needs

35:34

to be confirmed on hi on biopsy,

35:37

but all the imaging characteristics were

35:40

pointing in that direction.

35:42

Now, those molecular changes have made it where a lot

35:47

of patients with DIPG, even if it's imaging

35:51

features are classic, they will still proceed to a biopsy.

35:54

Now to get that molecular data,

35:56

which there may be targeted treatment, there may be,

35:59

you may find that it's actually a different entity

36:02

that responds differently.

36:05

Here's the patient with a brainstem expansile brainstem

36:07

mass, uh, striations corresponding to those, uh, pon

36:11

to cerebellar fibers that we talked about.

36:13

Um, the diffusion weighted image shows nothing specific

36:17

of interest, but there's a fo some focal areas

36:20

of hypo intense appearance on the a DC maps.

36:23

Now, some, uh, some, uh,

36:26

other advanced imaging was used multi vxl spectroscopy

36:29

and perfusion imaging.

36:31

Um, this multi vxl spectroscopy slightly higher level than

36:35

the, um, A DCI showed you, showed a hotspot area,

36:40

uh, in the, um, choline to NAA ratio right here.

36:44

The problem is that right here

36:47

and right here in those areas right next to it are

36:50

where the descending fibers of the cortex spinal

36:52

tract are so biopsying.

36:53

This hotspot area actually would, um,

36:58

not be very easy to do without risking, um,

37:02

uh, motor injury.

37:03

So the other area was, was targeted based on the a DC maps.

37:09

So this is a diffuse midline gliomas, A-D-I-P-G pattern.

37:13

Um, you know, those areas are suggestive of higher grade,

37:17

both on the spectroscopy

37:19

and the a DC maps and the needle biopsy.

37:22

Confirm the diagnosis.

37:24

Here's a patient with a brainstem lesion in the right

37:27

lateral aspect of the brainstem.

37:29

It's a very hyperintense on T two clear defined margin here.

37:35

Here's the appearance on T, one way of imaging.

37:37

And there's some heterogeneous central enhancement on, um,

37:41

post contrast T one, the fiesta imaging shows sort

37:45

of like an exophytic component,

37:46

so extending into the porous ticus.

37:50

Um, the direct encoded fractional antrop maps showed the

37:53

descending fibers of the corticospinal tract were actually

37:56

pushed over and not infiltrated.

38:00

So this patient underwent resection.

38:03

We did, did a subtotal resection.

38:05

Here's the intraoperative MRI, they went back and did more

38:08

and got a near total to gross total resection of the lesion.

38:13

So you can see the preoperative image,

38:14

the first intraoperative MRI, the second intraoperative,

38:17

MRI, they had a transient left-sided motor weakness,

38:20

but no permanent weakness and motor improved from baseline.

38:23

This was called the DIPG at other hospitals,

38:25

but the final diagnosis was a pilocytic astrocytoma.

38:28

So we felt comfortable based upon the other imaging features

38:32

that this was amenable to resection.

38:33

But this is another reason why, um, you know,

38:37

biopsying a lesion that may not be classic

38:40

or typical can really help guide you in the right direction.

38:44

Here's another patient with a discreet lesion in the

38:46

brainstem, it was called the DIPG, um,

38:49

but we felt it was discreet.

38:51

So, and not infiltrative.

38:53

We resected it by, um, here's the first intraop, MRI.

38:57

Here's the second intraoperative, MRI,

38:59

and this is a gross total resection.

39:01

These little bright areas here were actually present

39:04

on the pre contrast.

39:06

And this actually related to electrocautery use.

39:08

And this patient did not have A-D-I-P-G.

39:12

This was an embr tumor with multilayered rosettes.

39:15

Um, they got a gross total resection.

39:17

And, um, at four years, um, they had disease free, uh,

39:22

survival, which was the, in, in our series, the, um,

39:26

by far the longest, um, uh, survival

39:29

of any patient with this entity.

39:31

And that was guided by an understanding of the imaging

39:34

to help get, allow the surgeon to make the, those

39:38

that resection and then, which then allowed the oncologists

39:41

and, um, to have, you know, to not have to deal

39:45

with the whole tumor, but to only deal

39:46

with potential microscopic disease at the margins.

39:50

Here's an expanse cephalic lesion

39:54

involving both thalami left greater than right.

39:56

Um, it's one lesion.

39:58

They're connected through the mass intermedia can see it

40:01

spreads over to the medial aspect of the right thalamus

40:04

through the mass intermedia.

40:06

There's no appreciable post contrast enhancement.

40:09

There's heterogeneous, but mostly facilitated diffusion.

40:14

It's that this is a diffuse midline glioma,

40:16

but more of a hypothalamic pattern.

40:18

So again, that's why I think this is

40:22

just calling it a diffuse midline glioma.

40:25

This has almost nothing to do with that DIPG on a

40:29

gross macroscopic basis, just

40:32

because molecularly they're the same,

40:34

and that's very important.

40:35

But, so I would implore people to not just

40:40

ignore existing, um, descriptive, um,

40:45

terms like DIPG or bi thalamic glioma.

40:48

Um, but also not, don't be aware that there are, you know,

40:53

additional classifications that show the commonality

40:56

of those needle biopsy showed this as a low grade lesion.

41:01

Here's a patient with a, um, left al Pular tumor in the,

41:06

um, uh, left, uh, thalamus, uh, cerebral Pete uncle

41:11

and left aspect of the mesencephalon.

41:14

So it was a discreet lesion d um,

41:18

very different than the infiltrated emmic, um,

41:21

duse mid glioma that we saw, um, moment ago.

41:25

Some heterogeneous post contrast enhancement

41:28

facilitated diffusion and posteriorly.

41:31

We see it actually extends to the peel surface right there.

41:35

And we thought this is a possible opportunity of access.

41:39

Um, we, we looked at this interlateral margin, these,

41:43

the blue fibers here is the descending fibers

41:45

with the corticospinal tract,

41:47

and we're seeing, um, that there

41:52

comes down, comes down to the cerebral peduncle.

41:56

Now here it gets sort of this purplish or magenta.

41:59

And so, and then we see the fibers down here in

42:02

the pons below the lesion.

42:03

So, um, we proceeded to do a resection through that.

42:08

Um, vocally exophytic access point on,

42:13

on the right, uh, left, um, dorsal lateral aspect

42:16

of the mesencephalon.

42:19

And so a, a gross total resection was achieved.

42:22

Uh, the, the cortico spinal tract remained intact.

42:26

Um, so here's pre-op and post-op.

42:28

There some edema here that resolved on subsequent imaging.

42:33

So again, just

42:34

because you have a lesion in the g in the thalamus, it,

42:37

it doesn't mean that it's a diffuse midland glioma.

42:40

This was actually a pilocytic astrocytoma histologically.

42:45

Here's a patient with a right frontal abnormality.

42:47

It's hypo intense ill-defined.

42:51

Um, hyperintense signal on T two again goes with it.

42:55

I think water is bright on, uh, dark on, uh, CT

43:00

water is bright on T two.

43:01

So again, both those go with, uh, cellularity

43:05

or a tumor with cells that have a high, um,

43:09

amount of nu of, uh, cytoplasm relative to the nucleus,

43:14

which also goes with relative facilitated diffusion.

43:18

So this is a diffuse astrocytoma.

43:21

Diffuse astrocytoma is what the WHO criteria, um, refers

43:25

to that.

43:28

This one previously would've been called a fibrillary

43:30

astrocytoma, so it's,

43:33

but it's now called the diffuse astrocytoma.

43:36

Here's another patient with a left anterior insular lesion.

43:41

It's in the, um, an left anterior middle short insular gyri.

43:47

Um, can see here on this coronal image.

43:50

It, it's starting to skew around, um, the depth of

43:54

that sulcus right there

43:56

to the left inferior frontal, um, gyrus.

44:01

The functional MRI overlay here shows ex uh,

44:06

expressive language is immediately next to that little,

44:11

uh, corner right there.

44:12

So obviously this is very challenging

44:15

and this is the actual, like surgical planning.

44:19

Uh, you know, that was done instead

44:21

of blue going straight in.

44:23

The thought would be to go over and up.

44:26

So as opposed to going straight into this to go over

44:28

and up to spare some of the functional, um, uh,

44:32

characteristics of the overlying, um,

44:37

pars of peris of the left inferior frontal gyrus

44:40

where expressive language was, uh,

44:42

and a gross total resection was, was achieved.

44:46

Um, this was a diffuse astrocytoma, again,

44:50

previously referred to as a fibrillary

44:52

astrocytoma, a gross total resection.

44:54

There was no language deficit.

44:56

Now the reason I, I mentioned this in comparison

44:59

to the prior one is a diffuse

45:02

astrocytoma can actually appear to have discreet margins.

45:06

So that's one of the things that can be confusing.

45:09

So just because something has discre appears

45:12

to have discreet margins on imaging, um,

45:15

it still can be a diffuse astrocytoma.

45:20

Here's a patient with a expand extensive expansile,

45:25

T two hyperintense lesion involving the right temporal pole,

45:28

the right insula, um, the right inferior frontal gyrus,

45:32

the right inferior parietal lole.

45:35

And there's even extension across the body

45:38

of the corpus callosum to the left frontal lobe.

45:41

And there's facilitated diffusion within it.

45:44

There's no abnormal post contrast enhancement.

45:48

So this is a diffuse astrocytoma is confirmed,

45:53

but very different than those other two.

45:56

This is not discreetly marginated, this is not

46:00

discreetly resectable.

46:01

Um, again, previously referred to

46:03

as a fibrillary astrocytoma for this one also, um,

46:07

and this in my mind is more of a, a gliosis cerebri pattern

46:12

of spread of a diffuse astrocytoma.

46:15

The reason I say it like that is

46:16

because a biopsy would never sh show.

46:20

Oh, this is gliosis cerebri glioma, mitosis.

46:23

Cerebri is a pattern of involvement, um, that,

46:28

um, we now know can be achieved

46:31

by different histologic types of tumor.

46:34

Um, just like in pulmonary imaging,

46:37

I remember there's no biopsy that shows IPF, you get a UIP,

46:43

um, usual interstitial pneumonia biopsy result,

46:46

and then the macroscopic distribution would be,

46:50

can then be suggestive of an IPF diagnosis.

46:53

So similarly, there's a difference

46:56

between the histologic diagnosis in a given spot

46:59

and the pattern of spread for the disease process.

47:03

And I'm going, um, end on th this, uh, case.

47:08

This is about follow-up evaluation.

47:10

This pertains to all tumors, especially, you know,

47:13

some brain tumors, especially low grade tumors.

47:17

Here's a lesion, uh, it turns out to be a dnet

47:20

undergoes resection.

47:21

This is in 2003.

47:24

You get a follow up in 2004,

47:27

no change follow up in 2000 later 2004, no change.

47:30

2005, no change. 2006, no change. 2008, no change.

47:35

2011, no change. 2011, no change. 2013, no change.

47:39

2013, again, no change. 2013 later comes to our institution.

47:45

Fortunately, I didn't have any of the prior ones.

47:49

So I see this and I'm thinking, oh, I wanna see the priors

47:52

because this all here looks like local recurrence.

47:57

Well, here was the initial postoperative study,

47:59

here is the later postoperative study.

48:01

So for any tumor that you're looking at,

48:04

I personally think you should try

48:06

and see what the original tumor looked like, see

48:08

what the initial postoperative study looked like, see

48:11

what the resection cavity looked like.

48:12

And then now, now obviously if you can see along the way,

48:15

that's great because this patient had a, a lesion

48:17

that was growing by a millimeter or so every year.

48:20

And at no point would, did it register as being a change.

48:23

So this is just some, uh, you know, something

48:26

where just being attentive can really make a difference.

48:30

So select criteria to review MedU neuroblastoma,

48:34

removing on from just histo pathologic diagnosis.

48:36

The wind lesions are in the C can be in the CP angle,

48:39

the sonic hedgehog often in the hemisphere

48:41

hemispheric is group three.

48:43

They enhance in the fourth ventricle group four, they, uh,

48:46

less often enhance posterior foss pomas

48:49

type A in the CCP angle.

48:51

They less often enhance.

48:52

Type B is more spherically shaped in the fourth ventricle,

48:55

uh, diffuse midline glioma with this H three K 27 alteration

49:00

encompasses what was previously called DIPG

49:02

and hypothalamic gliomas diffuse astrocytoma,

49:06

which can spear appear discreet despite the diffuse name.

49:10

So overall, a systematic approach to imaging

49:13

of pediatric brain tumors can aid in structural

49:15

characterization and allow insight into

49:17

pathologic diagnosis.

49:19

A DC values are highly valuable

49:21

for detecting higher grade lesions

49:23

and can identify a high grade component

49:25

of a heterogeneous lesion possibly for biopsy planning.

49:28

And there are imaging characteristics that correspond

49:30

to some of the w updated WHO criteria

49:33

for classifying CNS neoplasms, in particular, subtypes

49:36

of medulloblastoma and appendamoma.

49:39

I wanna thank the neurosurgeons, neuro pathologists, MRI,

49:42

technologists, the radiologists.

49:44

Um, everyone that I work with,

49:46

uh, I'm lucky to work with them.

49:48

Um, and I wanna say thank you everyone.

49:52

Well, thank you so much Dr.

49:53

Charie for that awesome lecture.

49:55

We will now open the floor

49:57

for any questions from our audience.

49:59

You could submit those questions through that q

50:01

and A feature so we can try to get through as many as we can

50:04

before we need to close

50:09

and we'll wait a second, I don't see any in there right now.

50:20

I do see one in the chat.

50:21

Do you perform MRI on

50:24

a four week old baby with seizures?

50:28

If so, how do you perform that

50:31

and ensure safely the safety of the baby?

50:34

Great question. Uh, safety

50:36

of the baby is the number one thing.

50:38

If they're four week old, I'm assuming if they have seizure,

50:41

first of all, that they're getting a workup

50:42

for a perinatal infection.

50:44

So I wanna make sure that

50:44

they're safe from that perspective.

50:47

Four weeks old. Fortunately, um, many children are able

50:52

to, um, get a, uh, swaddle MRI after feeding.

50:56

Now that may make a difficulty of contrast,

50:58

but usually you can actually get initial basic information,

51:02

uh, without contrast.

51:04

Um, the DWI is extremely important in the, um, in

51:09

that age group

51:10

because, uh, in a neonate with seizure, uh,

51:15

um, the diffusion changes can actually be the, um,

51:19

the first presenting imaging finding of HSV encephalitis.

51:24

And note that HSV encephalitis in the newborn period is not

51:29

the medial temporal approach.

51:30

It is actually along the periphery of the hemisphere

51:32

because it's CSF and bloodborne

51:35

and not related to, um, oral facial HSV going back

51:39

to the gian ganglion, uh, in Meles Cave.

51:46

Okay, we've got a couple in that q

51:48

and a box, if you're able to pop that open.

51:51

I'm also happy to read it to you if you need that.

51:52

Okay. Can you have medulloblastoma

51:54

without restricted diffusion?

51:56

Um, the, the glib answer would be anything could happen,

52:00

but I'll say I haven't really seen it.

52:02

Um, though the exception being is if there's a lot of

52:07

microcystic changes, you will not be able to get an ROI

52:12

over an area that gets a, a low enough,

52:14

um, a DC value number.

52:16

So I personally, I think that men neoblastoma, just

52:20

by the nature of it, a solid representative portion is going

52:24

to restrict diffusion.

52:26

Um, but your ROI might not show it

52:29

because of inclusion of the cystic areas

52:31

where the fluid in there has facilitated diffusion.

52:36

Um, next, next question is, uh,

52:39

regarding what's the best sequence to give a diagnosis?

52:42

Reminding it says regarding brains.

52:45

Um, if it's, um, the question is

52:48

regarding brain stem lesions, um, you know,

52:51

axial T two I find to be very helpful.

52:53

And I think also, um, uh, in addition

52:58

to axial T two, um, uh, the diffusion,

53:03

um, and the for brainstem, DTI, if that's the question.

53:08

Uh, should children less than five

53:11

with ataxia have a CT before MRI?

53:14

Great question. Um, uh, one of the question, one

53:18

of the issues about that is going to be a balance

53:21

of radiation and sedation.

53:23

Um, we wanna minimize radiation.

53:26

We want to mini, um, which CT has,

53:30

but we also wanna minimize cost and sedation for MRI.

53:35

Uh, so I would actually say in a perfect world, uh,

53:38

those children would see with ataxia,

53:41

would see a child neurologist that can stratify the ataxia.

53:45

Uh, if you're talking about in the emergency department, um,

53:48

a CT is a very reasonable, practical thing

53:51

to do on a quick basis.

53:53

Um, how many days is recommended

53:55

to perform a postoperative control?

53:57

MRI? Does it depend upon the type of tumor in general?

54:00

Okay, that's a great question.

54:02

So historically it was said for your post-op evaluation

54:06

of residual tumor, try and do it within 36 to 48 hours

54:10

because otherwise you'll start to see granulation tissue,

54:12

which can enhance and, um, and can confound things.

54:17

We tend to do intraoperative MRI,

54:19

so we don't deal, deal with that.

54:21

If you want to get a good post-op baseline where some

54:25

of the post-op blood products are gone, some

54:27

of the pneumo ephalus is gone

54:28

or something, um, at least two weeks.

54:30

So we often will do it where, uh, right

54:33

before they potentially start radiotherapy.

54:35

Um, once they're healthy enough for that,

54:37

that will be a time to, to do it.

54:40

So there's other practical considerations like that.

54:43

Um, next,

54:44

how would one confidently differentiate hypoglycemia HYPO

54:48

glycemia from encephalitis and a neonate having seizures?

54:51

Wonderful question. Hi, neonatal hypoglycemia,

54:54

that's HYPO glycemia, uh,

54:56

very often has a bilateral occipital pattern.

54:59

Um, so, uh, the, um,

55:05

if so again, a, a blood glucose is going

55:10

to be the best, um, diagnosis.

55:12

So I'm assuming the question is saying if you have a child

55:14

that has hypoglycemia,

55:16

has diffusion abnormality in a seizure, um, you rever,

55:20

you know, you see about rev if it reverses when you

55:23

normalize the hypoglycemia.

55:25

Uh, so the clinical scenario is very

55:27

important for these cases.

55:29

You do not interpret in a vacuum at all, reach out to the,

55:33

uh, the referring clinician and um, stuff,

55:36

but the bilateral occipital pattern

55:38

of neonatal hypoglycemia is, um, is uh,

55:43

is somewhat characteristic.

55:45

Other patterns would be less pointing to hypoglycemia.

55:48

The other thing is, is that the severity

55:50

and duration of the hypoglycemia is going

55:53

to matter if the glucose goes down to 50 for an hour

55:57

and then is quickly corrected,

55:59

that's very different than it goes down to 30

56:01

and it's there for several hours.

56:02

So, uh, the clinical,

56:04

the clinical picture ends up being very important.

56:06

What do I think about spectroscopy?

56:07

Spectroscopy is a great study for, um,

56:11

ans for troubleshooting.

56:13

I don't use it for a routine basis.

56:16

Um, the, um, I don't like it

56:19

for high grade versus low grade glioma typically where I,

56:23

um, because there's a lot of other features

56:25

that we can usually get the information.

56:27

Um, where I find it heavy helpful the most is if you're wor

56:31

wondering about an inflammatory condition ver

56:34

that looks aggressive versus a high-grade glioma.

56:37

So if you have like a potential demyelinating lesion versus,

56:41

um, versus a high-grade glioma, that's

56:44

where spectroscopy can be somewhat helpful.

56:47

Next question, A wonderful question.

56:49

Are there differentiating features for MedU?

56:51

Neuroblastoma and A-T-R-T-A-T-R-T is atypical territory roid

56:54

tumor, A TRT diffusivity follows that of medulloblastoma

56:59

and it's actually potentially even, uh, more hypo intense.

57:03

Uh, I've been told that, uh, if you actually go

57:06

to the pathology lab for an A TRP patient,

57:08

if you look at the slide, you can visibly see

57:11

that it's just like dark purple.

57:13

Um, the A TRT can, it, it's something

57:18

at TRT is usually gonna be in the first year or two of life.

57:20

There's always exceptions to everything

57:22

and their blas stoma can occur at that young age.

57:25

So there are ca cases where it can overlap.

57:29

Um, but, uh, the younger age, um,

57:32

the slightly more atypical presentation like, uh,

57:36

and the extreme restricted diffusion, uh,

57:40

it can lead you towards an A TRT,

57:43

but it'd be, it'd be rare to have, um,

57:47

A TRT mentioned in a diagnosis without mentioning MedU

57:50

neoblastoma as a possibility.

57:52

Um, now oftentimes medulloblastoma if it,

57:56

especially if it fits one

57:57

of those characteristic appearances,

57:59

I won't necessarily mention A TRT as the possibility.

58:02

We always know anything's a possibility anytime,

58:04

but I try to balance, uh,

58:06

giving more comprehensive information

58:09

to giving focused information that can help them.

58:11

So if it looks very characteristic myoblast,

58:14

I will say imaging characteristics most consistent

58:16

with medial bost, and I don't give a

58:18

long differential after that.

58:20

Uh, if I, if I feel confident about that, um,

58:23

at TRT is the one where I would say if it pops up as that,

58:27

I'd say, okay, I, I could see

58:28

that it's just statistically it's not gonna happen as often.

58:31

Um, uh, at TRT um,

58:34

occurs has a much higher prevalence on multiple choice tests

58:38

than it does in real life.

58:39

Um, how can we differentiate imaging

58:43

between lesions extending to the fourth ventricle

58:45

and pure brainstem lesions on axial image?

58:48

That's a great question.

58:51

Um, you know, uh, lesions extending to the, um,

58:56

so I think there's not a single answer.

59:01

I tried to walk through a lot

59:03

of those cases showing you what I do.

59:05

I look at TT two, I look at the margins, I look at, um,

59:10

you know, uh, where it's going.

59:12

You can use a balanced, steady state free procession

59:15

technique like CIS or fiesta, uh, to actually

59:18

get higher resolution view of the brainstem surface,

59:21

what it's doing to cranial nerves.

59:23

Um, uh, there are times it can be it,

59:25

there are times it can be tricky.

59:27

Uh, that's, um, uh, it can be challenging,

59:31

but the cases I showed you here are representative

59:34

and usually you can sort of figure out one or the other.

59:36

But, um, uh, next question.

59:40

A TRT can have peripheral cysts describing the literature.

59:43

Great comment. I appreciate, uh, that comment.

59:46

Um, that can be a, uh, feature to use.

59:49

Um, as noted, uh, many MedU neuroblastomas can have,

59:54

uh, cystic changes, um, in,

59:58

in including the NI or desal plastic.

60:00

I should you an example of a wind, um,

60:03

one with cystic changes.

60:05

So those are possibilities.

60:06

Um, the one thing I didn't also mention

60:08

because it's not been as widely discussed in the literature,

60:11

is, um, that pattern with a low diffusivity

60:15

can be seen with anaplastic appendant as well, by the way.

60:22

Well, Dr. Charie, thank you so much for getting

60:23

through all those questions and for your lecture today.

60:26

Absolutely. Thank you everyone.

60:27

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60:29

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60:30

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60:32

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60:34

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60:36

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60:40

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60:45

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60:49

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60:52

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60:55

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60:57

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61:01

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