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Anatomy and Pathology of the Central Skull Base, Dr. Suresh Mukherji (9-25-25)

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0:02

Hello and welcome to Noon Conference, hosted by Modality

0:05

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 a recording of today's conference

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and previous noon conferences by creating a free account,

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and today we are honored to welcome Dr.

0:24

Esh McCury for a lecture entitled Anatomy

0:26

and Pathology of the Central Skull Base.

0:29

Dr. McGurty received his undergraduate degree from Duke

0:32

University and an MD degree from Georgetown University.

0:35

He currently holds academic appointments at multiple

0:38

institutions and is a devoted educator who's been an invited

0:42

speaker on over 500 occasions and written

0:44

and edited 15 textbooks.

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We're especially grateful for his supportive modality

0:49

and for serving as our head and neck neuroradiology advisor.

0:52

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

0:54

and a session where he will address questions you may have

0:57

on today's topic.

0:59

Remember to use that q and a feature

1:00

to submit your questions so we can get to as many as we can

1:02

before our time is up.

1:04

But that we're ready to begin today's lecture. Dr.

1:07

McCury, please take it from here.

1:09

Great. Okay. Alright, well,

1:10

thanks again for having me here.

1:12

It's, it's great to have so many people attend.

1:14

Uh, I know, I think we had over 1500 registrants if

1:16

that's, I have that right.

1:18

So it's fantastic to have, uh, that degree of interest.

1:21

Um, I usually, I, uh, I will be taking q and a afterwards.

1:25

I do have to leave for the airport

1:27

after this so I can take maybe about

1:29

15 minutes of questions.

1:30

I'm actually heading to the, um, American Society of Head

1:32

and Neck Radiology meetings.

1:33

So if, uh, guys wanna do something this

1:36

weekend, it's gonna be in Las Vegas.

1:37

It's, it's gonna be a terrific meeting.

1:39

I was passed, I was president, that organization in 2012,

1:43

so, uh, I can, uh, attest to how great it is.

1:46

Thank you. Excuse me.

1:48

So over the next, um, 15 minutes

1:49

or so, we're gonna talk about anatomy

1:51

and pathology of the Central skull base.

1:55

And the outline

1:56

of this talk is we're first gonna start

1:58

talk about the anatomy.

2:00

So we'll spend a fair amount

2:01

of time talking about the anatomy,

2:03

then we'll talk about different neoplasms.

2:06

We'll talk a little bit about dysplasias

2:08

and then maybe a little bit for congenital.

2:11

Quite frankly, each one of this is sort

2:12

of a topic on its own,

2:14

but I think for this audience, we're going to try

2:16

to cover a little bit in each one

2:18

and spend the for more majority

2:20

of our time talking about anatomy and neoplasms.

2:23

So when we talk about the central skull base,

2:26

there are different aspects of the skull base.

2:28

I think we've given a talk on the

2:29

anterior skull base in the past.

2:31

Today we're gonna focus on the central skull base,

2:34

and I think we have a session set up in November

2:37

where we're gonna discuss the lateral

2:39

and the posterior skull base.

2:40

So in today's talk,

2:41

we're predominantly gonna talk about the central skull base.

2:46

Now the central skull base is formed, predominantly formed

2:49

by this bone, and this bone is the sphenoid bone.

2:53

And I gotta tell you, this bone has been perplexing me

2:56

for years and years and years.

2:58

I've, I've, you know, I've seen it.

3:00

Um, when I looked at it, especially on the axial images,

3:04

people would talk about a lesser wing and a greater wing,

3:08

and they would talk about the OID plates

3:10

and they would talk about the body.

3:12

And for me it was incredibly confusing.

3:16

Um, but one day, probably about 10 years ago,

3:19

maybe even less than that, I had my epiphany.

3:22

And my epiphany was is

3:23

that when they actually looked at the central skull base,

3:28

we have to remember that there was life before CT and MR.

3:31

So when the anatomists backed in the beginning of the, like,

3:35

I don't know, 10th century

3:37

or something like that, when they first started describing

3:40

the bones of the skull

3:41

and the calvarium,

3:43

they actually looked at the individual bones

3:45

themselves on phos.

3:47

So they didn't really look at,

3:48

obviously they don't look at cts and Mrs

3:50

but they looked at the bone such as this,

3:53

and this is the sphenoid bone.

3:56

And if you look at the sphenoid bone on Foss,

3:59

and then you kind of ask yourself, you know,

4:01

are there lesser wings and greater wings?

4:04

And so on and so forth.

4:06

I realized that the sphenoid

4:08

bone actually looks like a bird.

4:10

And once I had this bird concept, all

4:13

of a sudden the sphenoid bone kind of jumped out at me.

4:15

So for instance, if you look at the bird,

4:17

and now you look at the sphenoid bone, all

4:19

of a sudden you can see this structure right here

4:21

that literally looks like a wing.

4:23

This is the greater wing of the sphenoid.

4:25

And with the leap of faith, you can see the feathers here.

4:28

Now this little wing right here is gonna be the

4:31

lesser wing of the sphenoid.

4:32

So when we look at this anatomic image,

4:34

here's the greater wing, and this is the lesser wing

4:37

and the lesser wing conforms,

4:39

this little anterior glenoid process.

4:41

And if you look anteriorly,

4:43

there's a little framing right here,

4:44

and that's the optic framing.

4:46

Then we have the body of the sphenoid bone,

4:49

which is located here.

4:51

You need to have a head.

4:53

And this head right here is where the pituitary gland lives.

4:56

We'll talk about that later.

4:58

And then if you have a bird, it has to be able to land.

5:01

And the way it lands, it lands on its feet.

5:04

And when it lands on its feet, these are what we refer to

5:07

as the tevo plate.

5:09

So unlike regular birds that have two legs,

5:12

the sphenoid bone is pretty special

5:14

and has four legs, so two paired legs.

5:16

So this is the medial OID plate,

5:19

and this is the lateral OID plate.

5:21

And right between the medial

5:23

and the lateral ter plates is what we refer to

5:26

as the oid fossa.

5:28

So if you can kind of remember the bird analogy.

5:31

Now when you go back and look at this axial image right

5:33

here, we can see the greater wing,

5:35

we could see the lesser wing.

5:37

Here's the anterior C glenoid process,

5:39

here's the optic canal,

5:41

and here's the body of the sphenoid bone.

5:43

So we're gonna talk a lot about this anatomy in

5:46

the upcoming slides.

5:49

Now here's a, I have a riddle for you.

5:51

Now, you're not live right now, but, but,

5:53

but here's a riddle.

5:54

So, so the riddle is, um, um, how many,

6:00

uh, why is the sphenoid bone the most

6:02

religious bone in the body?

6:04

Now, I I, no one can really answer that.

6:06

I don't know, Ashley, I, you can't jump on right now.

6:08

But if I ask you why is the sphenoid bone the most

6:11

religious bone in the body?

6:13

The answer is because it's so holy.

6:17

You get it Holy. Because when we look at the swen,

6:20

isn't that a great joke, Ashley?

6:22

I'm sure you're laughing. But if, if you look at this bone,

6:25

if you look at the bone right here,

6:27

there are lots of foramen.

6:28

Now these freemen were actually described in the importance

6:32

of these freemen were described about 200 years ago,

6:35

believe it or not, by Leonardo da Vinci.

6:37

And da Vinci was one of the first ones

6:39

that described the cranial nerves

6:41

and the communications of the cranial nerves as they pass

6:44

through the skull base.

6:46

And the way these nerves, many of these nerves pass

6:48

through the skull base is through the sphenoid bone.

6:52

So if we look at this area right here, we talked about this

6:56

before, this foramen is the optic canal

6:58

and this extends anteriorly

7:00

to innervate the components of the orbit.

7:03

This foramen right here is going

7:05

to go from anterior to posterior.

7:08

And when we look at the sagal images,

7:10

this is foramen rotunda, our famous round for round foramen.

7:14

And you can see V two extending through the round foramen.

7:18

And then it's gonna extend into this area,

7:20

which we'll talk about later.

7:22

So don't worry about the anatomy,

7:23

we're gonna go over this in great detail.

7:25

We have another foramen right here,

7:27

which looks like an oval foramen.

7:29

We even see it better on the opposite side.

7:32

We call it frame in oval.

7:34

And this is where V three runs through.

7:36

And then we have another round frame right here,

7:39

which is frame and spinosum.

7:41

So you've probably seen all of these various freeman

7:45

before, you just may not have concentrated on it.

7:48

So this is an example of a coronal image through the sinus.

7:51

So I know I've given a talk on sinuses before.

7:54

So when you're looking at the sinuses, most

7:57

of the times you concentrate on the sphenoid

7:59

sinus and the aeration.

8:01

But when you look at the sinus, all

8:03

of a sudden you start seeing these processes right here.

8:05

So this is the anterior crinoid process

8:09

as we see on the top left.

8:11

This area lateral to is is gonna be in the region

8:14

of the the para juxta cell or paracellular region.

8:18

And this little framing right here,

8:19

which we're now looking at in the coronal image, corresponds

8:23

to this frame and right here and this frame and right here,

8:26

and this is foramen rotunda just here.

8:29

And then medial and inferior to it is gonna be this frame.

8:33

And this forin corresponds to this nerve.

8:36

And this is the nerve of the vian canal.

8:39

So when you're doing a normal sinus ct,

8:41

if you look real cl carefully, you can always see foramen,

8:45

rotund and inferior medial to that is gonna be the nerve

8:48

of the videon canal.

8:50

Now remember when we talked about the bird,

8:52

the bird has to land, right?

8:53

And now when we look at the base of the sphenoid sinus,

8:57

now we can see the medial and the lateral oid plate.

9:01

So these are the feet of the bird as you, if you will.

9:05

So this is the normal appearance of these frame.

9:07

And here again, V two frame and rotunda excuse, excuse me.

9:11

Uh, yes, frame and rotunda.

9:12

And here's the nerve of the vian canal.

9:15

Now if you look at the right side, this was a patient

9:17

that has neurofibromatosis.

9:19

So if you draw a line down the middle,

9:21

compare the left side to the right side.

9:23

Here is the normal appearance of foramen rotunda.

9:26

Here's the nerve of the vian canal.

9:28

Now look at the right side.

9:29

Here we see diffuse enlargement and expansion of V two.

9:34

So this is frame rotunda and inferior

9:37

and medial to this is gonna be the

9:39

nerve of the videoing canal.

9:40

So this neurofibroma, this is an example

9:42

of neurofibromatosis,

9:44

and these likely represent plexiform neurofibromas, which

9:48

as we know is affiliated with NF two.

9:52

So when we are looking at lesions involving the central

9:56

skull base, based on what we said

9:58

and the orientation of these various nerves, we can come up

10:03

with specific diagnosis based on

10:06

where the tumors are located and the orientation.

10:10

So here's a T two weighted image demonstrating a mass right

10:13

here that's involved in the superior aspect

10:16

of the cerebella pontine angle.

10:18

But notice how this is coursing anteriorly.

10:21

And when we look anteriorly,

10:22

we can see the carotid artery here.

10:24

This is extending through the region of mecca's cave.

10:28

And because of this orientation,

10:29

it corresponds very nicely with V two.

10:33

So here's the main course of the fifth nerve,

10:35

here's the trigeminal ganglion, there's V two.

10:37

So when we see this orientation, we can come up

10:40

with the diagnosis of a fifth nerve schwannoma.

10:44

Here's another example.

10:45

Now in this case we have a oblong sausage shape enhancing

10:50

mass, which is involving the masticator space,

10:53

but notice how it's extending

10:55

superiorly through the skull base.

10:57

So on the left hand side, here's the floor

10:59

of the middle cranial fossa.

11:01

Remember the floor of the middle cranial fossa is formed

11:03

by the greater wing, the sphenoid.

11:06

This structure right here, which is frame oval,

11:09

allows the third division of the fifth cranial nerve

11:11

to extend through frame oval

11:13

and extend into the masticator space.

11:16

So when I see something like this

11:18

that's involved in the masticator space

11:19

and it's growing soup purely through the central skull base

11:23

and extending intracranial, then I start thinking

11:26

of lesions involving V three.

11:28

And then when I see the sausage shaped lesion like this,

11:32

this is pretty typical

11:33

for a schwannoma involving the third division

11:36

of the fifth cranial nerve.

11:38

So if you remember what I said, the religiousness

11:40

of the central skull base

11:41

and the sphenoid bone, you'll always be able

11:44

to at least consider the possibility is, is the pathology

11:48

that you're seeing possibly of, of neural origin,

11:52

of which the, the main two things are gonna be schwannoma

11:54

and neurofibroma, um, when you can see some

11:57

of these lesions involved in the central skull base.

12:01

So to continue this theme,

12:03

when we look at the central skull base,

12:06

and we're looking at this phen bone again,

12:08

we spent a fair amount

12:09

of time talking about the normal anatomy.

12:12

So when we look into the orbit here,

12:15

we see the superior orbital fissure

12:18

and the inferior orbital fissure.

12:20

Now this anatomic relationship here is caused by the anatomy

12:25

of the sphenoid bone.

12:26

So this is the greater wing and this is the lesser wing.

12:29

And between these two is the fissure.

12:32

Now, one thing that we can see, again in patients

12:35

with more advanced forms of neurofibromatosis,

12:38

and in this case NF one is

12:40

that these patients typically have a dysplasia involving

12:44

the sphenoid wings.

12:45

Now I have to tell you, when I trained in neuroradiology

12:49

back in the last century, the way

12:50

that we would make this diagnosis is

12:53

that we would actually look at a plain film.

12:55

And one of the things that we were always warned about when

12:57

we were taking our oral boards is

12:59

that if they showed you a plain film, a frontal plane film

13:02

of the orbit, we were always taught

13:05

to look within the orbits themselves

13:08

and look at what we refer to as the MT orbit sign.

13:12

So the normal orbit is the greater wing or the lesser wing

13:15

and superior and inferior orbital fissure.

13:17

And notice we don't have the normal anatomic uh components

13:22

and the landmarks in the right orbit compared to the left.

13:25

And this is the empty orbit sign. Now what causes this?

13:29

Well, the reason it's caused is

13:31

that we have an abnormality here involving the greater

13:34

wing of the sphenoid.

13:35

Notice a normal anatomy on the left compared to the right.

13:38

And what we see here is a diffuse plexiform neurofibroma

13:42

that's involving the right orbital apex.

13:46

Now, whether or not this mesodermal dysplasia is inherent

13:50

to neurofibromatosis type one

13:52

or whether it's due

13:53

to regressive remodeling from all these plexiform

13:56

neurofibromas, I'm not sure if it's been completely figured

14:00

out yet, but just realize these are the

14:02

characteristic findings.

14:04

So this is what we see on ct and this is what we see on mr.

14:07

So here's an axial T two weighted image

14:10

and wanna call your attention the normal appearance

14:13

of the sphenoid bone here on the left hand side.

14:15

See it looks like a triangle here.

14:17

And look at the nice separation

14:19

between the bone and the orbit.

14:21

Now look at the patient's right side.

14:23

There is no triangular bone right here.

14:26

It's completely gone.

14:27

And what we see here is that the anterior portion

14:31

of the right temporal lobe

14:32

and the CSF is extending into the

14:34

posterior portion of the orbit.

14:36

In all of these areas

14:37

of increased C two signal are the plexiform neurofibromas.

14:41

So this is just an example of the congenital lesion

14:44

that can involve the sphenoid bone, phen wing dysplasia.

14:48

And historically these patients typically present

14:51

with pulsatile opals.

14:54

Why do they have opals?

14:55

Because the neurofibromas are extending behind the orbit

14:59

and it's anteriorly displacing the globe.

15:02

And the reason it's pulsatile is that the bone acts

15:05

as a natural barrier

15:06

between the CSF pulsations in the back of the orbit.

15:10

If there's absence of this bone, there's no separation.

15:14

And these CSF pulsations are now transmitted directly

15:17

behind the orbit.

15:19

And that's why these patients have this pulsatile ex talus

15:22

as an initial presentation.

15:25

So we spent a fair amount of time on the sphenoid bone,

15:30

but now we're gonna take it to that next level.

15:32

So we already talked earlier about the greater wing,

15:35

the lesser wing, the superior orbital fissure,

15:38

the inferior orbital fissure.

15:39

We talked about the body.

15:41

And now what I wanna do is talk about the feet

15:43

of the sphenoid bone.

15:45

So when we talk about the feet

15:47

or the legs of the sphenoid bone, these are

15:50

what are referred to as the OID plates.

15:52

So we have a medial and a lateral OID plates.

15:56

So on the sagittal image,

15:57

the OID plates right here are defined

16:00

by this green right here.

16:01

And notice the greenness right here,

16:03

they're vertically oriented.

16:04

And those are the OID plates that are contiguous

16:08

with the sphenoid bone.

16:10

Now one of the bones that we oftentimes

16:13

forget about is this little blue bone right here.

16:15

And this blue bone right here forms the posterior

16:19

aspect of the palette.

16:21

So you can see the palette right here.

16:23

The anterior portion of the palate is actually formed

16:25

by the maxilla and the posterior portion is formed

16:28

by the palatine bone.

16:30

So we have this palatine bone here,

16:32

which has a horizontal component

16:34

and then it has a vertical component.

16:37

So this is the foot of the palatine bone

16:39

and there's the vertical component.

16:42

So we have the palatine bone anteriorly,

16:44

we have the OID plates posteriorly.

16:47

So then what do we call the space between the OID plates

16:52

and the palatine bone?

16:54

Well, this is our famous tego palatine fossa.

16:57

So when we look at the normal anatomy of this area,

17:01

we have the sphenoid bone

17:02

and our palatine bone is located here.

17:05

As we extend laterally, we get to the OID process

17:09

of the sphenoid bone.

17:11

And because this is the OID process,

17:13

and this is the palatine bone,

17:15

this is the ter palatine fossa.

17:17

And as we extend laterally the fissure

17:20

between the tego process

17:22

and this maxillary sinus is referred to

17:25

as the tego maxillary fissure.

17:27

So within this tego palatine fossa, the roof

17:30

of this is formed by V two.

17:32

So this is V two forcing anteriorly through foramen rotund,

17:37

and it runs in the roof of the tego palatine fossa.

17:40

This fossa contains lots of little nerves right here.

17:44

And the ganglion here is a s phenyl palatine ganglion.

17:48

Now when you look at the tego palatine fossa,

17:51

remember you have a s pheno, palatine foramen,

17:54

tego palatine fossa and tego maxillary fisher.

17:57

And if you like to play soccer

17:59

as we call it in the United States

18:00

or fall, this is the Voo Zela.

18:03

So if you've ever been to the World Cup,

18:04

I know the World Cup is coming to the United States.

18:07

Next year, you're gonna hear this annoying

18:09

sound in the background.

18:10

That's the voo ala.

18:12

And I always remembered that the mouth

18:13

of the V voo zela is this pheno Palatine Freeman.

18:16

The shaft is the tego palatine fossa.

18:19

And the flame right here,

18:20

this phalanges right here is the tego maxillary fissure.

18:24

So that's our tego Palatine foso.

18:27

So why do I spend so much time on this?

18:29

It's to give you a better understanding of one

18:32

of the most common pathologies

18:34

that you'll see involving in this area.

18:37

So here we have a adolescent male that presents

18:40

with nasal stuffiness and also epistaxis.

18:44

So what we have here is a mass right here involving the

18:47

nasal cavity extending laterally to involve the posteriorly

18:51

to involve the central skull base

18:53

and laterally through the senal palatine foramen.

18:56

Notice the posterior wall

18:57

of the maxillary sinus is not really eroded,

19:00

but it's regressively remodeled and placed anteriorly.

19:04

This is a different patient,

19:05

but when we do an MR on this, we can see diffuse enhancement

19:09

and we can see multiple flow hos.

19:12

So I'm sure all of you on the the call right now and

19:15

and this program understand

19:17

that this is the classical appearance

19:19

of a juvenile angio fibroma.

19:22

So here's our juvenile angio fibroma.

19:25

They arise from the tego palatine fossa

19:28

and the artery

19:29

that extends into the tego palatine fossa is a branch

19:33

of the external carotid artery.

19:35

And this is the internal maxillary artery.

19:38

So here's an example of a conventional angiogram.

19:41

Here's the internal maxillary artery here,

19:44

it supplies this juvenile angio fibroma,

19:46

and we can see this hypervascular lesion.

19:49

So I spent a little time on this

19:51

because I want you to understand the classical appearance

19:54

of the juvenile angio fibroma, both on CT and mr.

19:59

So the classical appearance is gonna be

20:01

that centering in this pheno palatine foren,

20:04

there's relative preservation of the bone.

20:06

And on mr, we can see the diffuse enhancement

20:09

and the multiple flow void.

20:11

So why do I spend so much time on this?

20:13

Because juvenile angio fis typically present

20:17

with epistaxis and they present with nasal stuffiness.

20:22

Now this is another pathology

20:24

that can involve the same age group.

20:27

So these patients can also present with epistaxis

20:31

and nasal stuffiness.

20:33

If you tell the pa, the doctor, the referring physician

20:36

that this patient has a juvenile angio fibroma,

20:39

well they're gonna get some type of vascular study.

20:41

And now obviously in 2025 they're gonna do a CT angiogram

20:45

or an MR angiogram.

20:47

But on the other hand, if you tell them

20:49

that this is a solid tumor

20:50

and in this case this is a rhabdomyosarcoma,

20:54

then they're going to biopsy it.

20:56

So notice a difference here.

20:57

It's an aggressive mass, very aggressive bone destruction

21:01

distinct from juvenile angio fibroma.

21:03

Here's the rhabdomyosarcoma here.

21:06

Again, this has a similar location,

21:08

but notice how there are no flow voids in

21:10

the rhabdomyosarcoma.

21:12

So if you tell them that you think

21:13

that this is a rhabdomyosarcoma, they're gonna biopsy this.

21:17

So what you don't wanna do is mix up juvenile angioma versus

21:21

rhabdomyosarcoma because if you call this a rhabdo sarcoma,

21:26

they're gonna biopsy this

21:27

and the patient's gonna have a substantial amount

21:29

of bleeding, which is not good.

21:31

And oftentimes that's done in the office.

21:33

So the bottom line is, is that I want you

21:36

to understand the anatomy of this area right here.

21:39

I want you to understand the appearance of the normal

21:42

juvenile angio fibromas.

21:44

And then I also want you to be able to distinguish the CT

21:47

and the MR appearance

21:49

because it makes a big difference on

21:51

how these patients are worked up,

21:53

whether they should be biopsied

21:54

or whether they should be sent for an angiogram.

21:59

So the next area that we're gonna talk about

22:02

is the nook cord.

22:03

Now, like I said

22:04

before, I'm not the sharpest tool in the shed.

22:07

I kind of get it eventually.

22:08

And when I thought about the nook cord, you know,

22:11

because this has cord in it,

22:14

although it's not spelled CORD,

22:15

it's spelled C-H-O-R-D-I was under the impression

22:18

that the Noor formed the spinal cord, which is not correct.

22:22

The no cord actually a uh, it affects

22:26

and initiates the ululation of the, of the spinal cord

22:30

and the adjacent structures.

22:32

But eventually the remnants

22:33

of the no cord end up forming the spine

22:35

and specifically the nucleus pulposus.

22:38

So the Noor is not the cord itself,

22:41

but in it's involved in creating the spinal column

22:44

and eventually regresses into the nucleus pulis.

22:48

Now this Noor has specific remnants

22:51

that we will occasionally encounter when we're looking at

22:56

various imaging of the brain and the spine.

22:59

And in this case, we oftentimes see this when

23:01

we're evaluating the neck.

23:03

So this is an example of a mass right here

23:05

that's located in the nasopharynx

23:08

and it's high signal on a T one weighted image.

23:12

This is located between the uh, uh,

23:15

longest coline muscles

23:18

and this is the classical appearance of a torn wall cyst.

23:21

The reason why this is important to understand is

23:24

that these patients sometimes present with halat ptosis,

23:27

sometimes they'll present with nasal stuffiness.

23:30

When the surgeon looks in with a nasal pharyngeal scope,

23:33

what they can see is a submucosal lesion right here.

23:37

So they're not sure whether

23:38

or not that there's a tumor underline

23:40

this or it's something else.

23:42

So if you see something like this on a,

23:44

it's high signal on T one, you can make the diagnosis

23:47

of a torn wall cyst.

23:48

In fact, today is Wednesday.

23:50

I just saw an incidental case

23:52

of a torn wall cyst just two days ago on Monday.

23:55

So this is something that I'm sure

23:56

that you'll run into your practice.

23:59

So this is a a not cordial remnant, a benign remnant

24:03

that we call a twin wall cyst.

24:05

Now this is a lesion that we sometimes encounter

24:09

that's located along the dorsal aspect of the clus.

24:13

So what we see here is when you're looking at the studies,

24:15

what we see is a scalloped lesion

24:18

that's involved in the dorsal aspect of the clus.

24:20

And notice it's not a foramen,

24:22

but it's actually something

24:24

that is giving some erosion here involved in the posterior

24:27

aspect of that colvis.

24:28

When we look at the MR study, what we see here is an area

24:32

of increased T two signal.

24:34

And on the sagittal images we can see

24:36

that this is not a cystic lesion,

24:37

but it's actually a solid lesion.

24:40

Now the sometimes this lesion may have a stalk

24:43

and it, if it has a stalk, that's great, I'm not,

24:46

sometimes it happens and sometimes it doesn't.

24:49

But when you see this type

24:51

of lesion involving the dorsal aspect of the clus,

24:53

it's high signal on T two but is not cystic,

24:56

but it's actually solid.

24:58

This is the entity that we refer to as OSIS Saliro.

25:03

And what this is again, it is a no cordal remnant

25:07

and the reason why it's called saliro is

25:10

that histologically, this contains saliro cells

25:13

and we'll talk about that a little bit more

25:15

on the next slide.

25:17

But the bottom line is, is that

25:19

historically this has been felt to be a benign etiology.

25:24

But the challenge that you run into is that when I talk

25:28

to the pathologist,

25:29

they have a hard time distinguishing a true echo doses

25:33

saliro from an early other tumor that can arise here,

25:38

which is a classic chordoma.

25:40

So as of the few years ago, there has been some suggestion

25:44

that we shouldn't necessarily call this osis saliro

25:49

and completely say it's benign.

25:51

But now what has the term

25:53

that has been suggested over the last couple years is

25:56

to call this a benign horal cell tumor.

26:00

Now again, it's a bit of a waffle in the sense

26:02

that it's in the middle, but the challenge

26:04

that you run into is that if you see something like this

26:07

and the pathologist doesn't know whether it's actually a

26:10

benign or a malignant lesion

26:12

and they can't separate it from a chordoma,

26:15

then I think we're gonna have

26:17

to change our approach to this.

26:18

Typically we would just kind

26:19

of dismiss it and say forget it.

26:21

But if we see something like this, I think in the back

26:24

of our minds we have to say, Hey,

26:26

could this actually be the early stages of a chordoma?

26:29

So we are now we're some people are now advocating

26:32

to use the term benign OC cordal cell tumor.

26:37

Now this is one of the classic lesions

26:39

that you'll end up seeing.

26:40

So here's a lesion right here

26:42

that involves the central skull base.

26:45

You can see it's located in this at the area

26:48

of the cranial vertebral junction.

26:50

You can also see this etiology all the way back

26:53

into the sacrum.

26:55

And this is just a schematic illustration

26:57

demonstrating these lesions.

26:58

I wanna highlight that this lesion typically arises at the

27:02

lar ends of the spine, the top or the bottom,

27:05

and it's usually midline.

27:07

So if we see something like this,

27:09

and especially if patients presents with a six nerve

27:12

or possibly a Guelph nerve palsy,

27:14

and this is the classic example of your chord.

27:18

So I alluded to this a little bit earlier.

27:20

This is a malignant tumor that arises from our friend,

27:24

the nodal cordal remnants.

27:26

They either arise from either end of the nodal cord

27:28

and I mentioned before they tend to involve the six nerve.

27:31

So you have a six nerve palsy.

27:33

And the reason they involve the six nerve is

27:36

because the six nerve extends from the brainstem

27:41

into the cavernous sinus through this little fissure,

27:44

which is the petro clival fissure.

27:46

Because these chordomas are midline, they have a propensity

27:51

to extend anteriorly.

27:52

And when they extend anteriorly,

27:54

they can knock off the six nerve.

27:57

If it involves a sacral area, it can present

27:59

with weakness in bowel function.

28:01

Typically they arise in between 50

28:03

and 60 years old,

28:05

a little bit more common in men than in female.

28:08

And the treatment tends to be surgery with

28:10

or without proton beam therapy.

28:13

So this is the classic CT appearance

28:15

and here's the MR appearance.

28:17

Now these chordomas present

28:20

or are comprised of what we refer to as the fifer cells.

28:24

The reason why that is important to at least understand is

28:29

that these fists lior cells contain mucins and are VAs.

28:33

So as a result, they tend to be high signal on T two.

28:37

So it's possible if you looked at the sagittal T two

28:41

weighted image and you see this mass, you could say, wow,

28:43

was that a cephas seal that's extending anteriorly

28:47

through the skull base to involve the nasal Ferris?

28:49

And even when you look at the axial T two

28:52

weighted image is bright.

28:54

But when we look at the contrast enhanced T one weighted

28:56

images, we can see that this is a solid mass

28:59

that's enhancing with contrast.

29:01

So it almost has this pseudo cystic appearance to it.

29:05

So if you see this mass right here, don't be confused

29:08

by the T two weighted sequences.

29:10

Always look at the T one weighted sequences with contrast

29:14

and this distinction

29:16

or this discrepancy between

29:18

what you think is possibly fluid versus a solid mass.

29:21

This is the characteristic of this fists cells.

29:25

So the bottom line is the chordomas tend

29:27

to be midline structures.

29:30

Now here's another type of tumor

29:32

that can involve the central skull base.

29:34

So in this case we see a mass right here that's not midline,

29:38

but it's paraline.

29:39

And when we look at the axial images right here

29:43

on the bone algorithms, we can see something

29:45

that looks like rings in circle or some type of matrix.

29:49

And this is the typical example of a chondro sarcoma.

29:53

So chondro sarcomas again are malignant lesions typically

29:57

between 40 and 50 years old.

30:00

And these are felt to arise in the synchondrosis

30:04

between the petre bone and the clovus.

30:06

So in the petro clival fissure.

30:09

So here's this uh, normal anatomy here,

30:11

here's our petro clival fissure here,

30:14

and here's a schematic illustration of

30:16

where these chondro sarcomas arise from.

30:19

So in these case, they can sometimes be difficult

30:23

to differentiate from a chordoma,

30:26

but the characteristic findings that I look

30:28

for is whether it's off midline.

30:31

So here's an example of a chondro sarcoma here.

30:33

This is the normal clus here,

30:35

here's the petro clival fisher.

30:37

And notice on the T two weighted images,

30:40

it's actually high signal.

30:41

And in fact when we look at the T one pre

30:44

and post, both of these enhance with contrast.

30:48

So on something like this you can say, is it a chordoma

30:51

or is it a chondro sarcoma?

30:53

And in this case, because it's off midline,

30:56

I would put chord a chondro sarcoma number one

30:59

followed by chordoma.

31:00

And I just saw a case about three months ago, had a very,

31:03

very similar appearance.

31:04

It was high signal on T two, it was just off midline.

31:08

And the issue was, is it chordoma or chondro sarcoma?

31:11

And that particular case, I leaned on chondro sarcoma

31:15

and the path came back.

31:16

So for me, when I look at something like this,

31:19

I really put a lot of attention on whether

31:22

or not it's paraline.

31:24

If I see it overlying the synchondrosis,

31:27

then I favor the chondro sarcoma.

31:30

So here's another tumor

31:32

that can involve the central skull base.

31:34

So here we have a lesion that is not midline,

31:37

but it's paraline.

31:39

And when we look at this, we can see it's involving the

31:42

region of the petro clival fissure.

31:44

But notice how it's extending posteriorly

31:46

and has a plaque like configuration

31:49

and has a linear area of enhancement,

31:51

almost looks like if you will, a tail.

31:55

And then we can see the tumor is extending anteriorly

31:59

to involve the area of mecca's cave

32:01

and also involve the cavernous sinus.

32:04

So here we have a lesion, petroc clival fissure extends

32:08

to involve the dura with almost looks like a tail

32:11

and then involves the cavernous sinus

32:13

and encase the internal carotid artery.

32:16

So when you put all of that together, then we can come up

32:19

with the diagnosis of meningioma.

32:22

So the reason why I show this anatomic image is remember

32:24

there are meninges all the way surrounding the brain

32:28

and there's clearly meninges overline,

32:30

the central skull base and also lining the capita sinus.

32:34

So when you see something like this, the iso intends

32:38

to T one densely enhances the dural tail in the man case.

32:41

The carotid artery always remember

32:43

to consider meningioma in the diagnosis.

32:47

Now what I showed before was a more classic

32:49

case of meningioma.

32:51

When we are dealing with the central skull base,

32:54

you can actually have intraosseous meningiomas.

32:58

So this is an example of a patient that presents

33:01

with unilateral proptosis, in this case the left globe.

33:05

And then when we look at the greater wing of the sphenoid,

33:07

we can see this expansile intraosseous mass

33:11

that almost looks like it has from

33:13

spicules extending from it.

33:15

And on the choroidal images there's that diffuse thickening.

33:18

When we perform an mr, we can see the high T two signal

33:22

with expansion of the greater wing of the sphenoid

33:25

and posterior wall of the orbit.

33:26

And there's the diffuse enhancement with the dural tail.

33:30

So in situations like this,

33:32

this was an interosseous meningioma.

33:35

Now there are other things that can mimic this.

33:38

If I know that the patient has a history of breast cancer,

33:41

this could be metastatic breast cancer,

33:43

it could also be potentially metastatic prostate

33:46

carcinoma as well too.

33:48

In a child, if I see something like this

33:50

and I start thinking about metastatic neuroblastoma,

33:54

I also think about Ewing sarcoma

33:56

and possibly uh, leukemia as well too,

34:00

or some type of lymphoproliferative disorder.

34:02

So it's not 100% specific at all.

34:05

But on the other hand, if I do have an adult

34:08

that has no prior history of a malignancy

34:11

and I see something that has this typical CT

34:13

and MR appearance,

34:15

then I will strongly favor a sphenoid wing meningioma.

34:20

Now here's an example of a patient

34:23

that has a mass right here involving the nasal pharynx.

34:26

We can see that extending posteriorly

34:29

to involve the petro clival fissure

34:31

and the lateral aspect of the central skull base.

34:34

In a different case, we have a mass right here

34:37

that's involving this, uh, the sphenoid bone

34:41

and we can see it's high signal and DWI signal.

34:44

So it has high DWI signal, which means it's going

34:46

to have low a D, C.

34:48

So when I see something like this,

34:50

it's essentially nonspecific

34:52

because a lot of tumors can have this appearance.

34:56

The main thing, the question that you have

34:57

to ask when you see this is the age of the patient

35:01

and if I told you that this was a child,

35:03

then the most likely diagnosis is gonna be rhabdomyosarcoma.

35:07

So when something like this, this could be a wide variety

35:11

of things, but the way that we can come

35:12

and make the diagnosis of

35:14

rhabdomyosarcoma is based on the age of the patient.

35:18

So these are another example

35:20

of a rhabdomyosarcoma in a child,

35:22

we know it's the most common soft tissue sarcoma

35:26

and most common tumor in the head and neck area.

35:30

There are various histologic types, there's embryonal,

35:33

body roid, pleomorphic and alveolar.

35:36

And there are various genetic associations.

35:38

Yes, in general I find it very difficult

35:42

to predict the actual pathology If I,

35:45

this occurs in an a little bit of an older patient

35:49

and possibly it could be alveolar,

35:51

but you know, quite frankly the pathologist every year

35:55

or every five years in the WHO criteria,

35:58

they always change the goalpost, new terminology comes out

36:02

and now everything has some type of tic basis to it.

36:06

So for me, I try to give the diagnosis of rhabdomyosarcoma.

36:10

Sometimes I try to guess the histology,

36:13

but quite frankly right now

36:15

because of all the moleculars, I kind

36:17

of let the pathologist determine exactly

36:20

what the specific subtype is.

36:23

So so far what we've talked about is

36:25

that we talked about the greater wing of the sphenoid,

36:29

we talked about lesions, intraosseous meningiomas,

36:32

we talked about the body of the sphenoid

36:35

and we talked about uh uh, chordomas

36:38

and also paraline structures like chondro sarcomas.

36:41

And we talked about the feet of the sphenoid bone,

36:44

which are gonna be things such as where uh,

36:47

juvenile angio fibromas arise from.

36:51

Now what we're gonna do is that we're gonna look at the top

36:54

of the sphenoid bone, which is where we now refer

36:57

to the head of the sphenoid bone,

36:59

or I should say the head that lives in the cell.

37:02

And that's the pituitary gland.

37:05

So I think all of us can make this diagnosis.

37:07

This is the classic example of a pituitary adenoma.

37:11

We know that it's living in the cell

37:13

and right below this is gonna be the sphenoid sinus.

37:18

Now interesting things about pituitary adenoma is

37:21

that they can have different variations

37:23

that can occasionally be quite aggressive.

37:26

So here's an example of a pituitary adenoma

37:30

that extends superiorly.

37:31

This is the classic pituitary macro adenoma.

37:35

It has a little waste right here

37:36

because the reason of the waste is formed by the cell

37:39

and the diaphragm marcela,

37:41

which gives us this natural waste.

37:43

So it sort of has this dumbbell appearance

37:45

or figure eight appearance.

37:47

And if it gets big enough,

37:48

it can abut the optic chiasm as we see here.

37:53

So this is the classic pituitary macroadenoma

37:56

and I'm sure you're familiar with that.

37:58

But there are some interesting variations

38:00

that can involve the central skull base.

38:03

So this was an aggressive mass right here

38:05

that involved the lateral aspect of the cell

38:10

extended into the cavernous sinus.

38:12

You can see it's encased in the carotid artery extending

38:15

into the floor, the left middle cranial fossa

38:18

and it's actually extending inferiorly

38:20

through foraminal valley.

38:21

Here's normal F valley on the right here, it is on the left

38:24

and it's involving the masticator space.

38:27

And this was pathologically proven

38:30

to be pituitary macroadenoma.

38:32

So this is a large pituitary macroadenoma

38:36

that actually can extend extra intracranial.

38:39

And then in this case it extended inferiorly

38:42

through the masticator space.

38:43

So I've seen a few of these are kind of rare,

38:46

but occasionally we'll run into something like this.

38:49

And this is an entity

38:50

that's a little bit more common than you think.

38:53

So this is an example of a pituitary adenoma

38:56

that involved the Clovis.

38:58

So in pituitary gland normally extends superiorly from the

39:02

oral Imodium and that can extend into the Clovis.

39:05

Now the way you can suggest this diagnosis

39:08

that if you see a mass like this that's expanding the Clovis

39:11

but you don't see a pituitary gland,

39:13

if you see no pituitary gland with expansion of the Clovis,

39:17

then you have to consider the possibility

39:20

of a pituitary adenoma.

39:21

And some people would call this an invasive

39:24

pituitary adenoma.

39:25

So always keep that in the back

39:27

of your mind when you see something like this

39:29

and your eye should see whether

39:30

or not there's a normal pituitary gland.

39:33

And if it's not there, consider the possibility

39:35

of pituitary adenoma.

39:38

Well, when we look at pituitary macro adenomas,

39:41

there is a classification

39:43

to determine the lateral involvement

39:45

of the claf claf cavernous sinus.

39:47

This is what's referred to as AOPs criteria.

39:50

You draw a line here along on the medial aspect

39:52

of the internal carotid artery.

39:54

If it's medial to this, it's a zero.

39:56

You draw a line in the midline.

39:58

If it's within the medial wall

40:00

and the midline, it's a one then laterally it's a two.

40:03

And then if it extends all the way to the lateral wall

40:06

of the cavernous sinus, it's a fork.

40:09

So for me, this is really a surrogate to determine whether

40:12

or not the cranial nerves are involved.

40:14

And I would argue that I think I do use this criteria

40:18

occasionally some of our surgeons ask for it.

40:20

But if you really understand your anatomy,

40:22

you can say specifically which nerves are involved.

40:25

So here's a large macroadenoma, there's the third nerve,

40:28

there's a sixth nerve.

40:30

So in this case we can see this lesion is involving the

40:33

third nerve and the sixth nerve.

40:35

Similarly, the third nerve is located here in the

40:38

upper outer quadrant.

40:39

There's a sixth nerve. And we can specifically say

40:42

that this tumor extends all the way to the lateral wall.

40:45

You can see it's encased in the carotid artery.

40:48

So I think the knobs criteria is a good criteria,

40:51

but if you understand your anatomy,

40:52

you could actually be a little bit more specific when you

40:56

look for this lateral extension.

40:59

So here's an example of a child that presents

41:01

with the super cell mass.

41:02

You can see it's high T one signal

41:05

and normal uh, pituitary gland here.

41:08

And this is the classical example of a cranio phn.

41:11

So cranio PHNs are neoplasms.

41:15

They are derived from what we refer to as rathke pouch,

41:18

which again is a remnant of the oral odium.

41:22

They have a bimodal age group between five and 15 years old

41:26

and 50 to 60 years old.

41:29

The classical appearance

41:30

of a cranial PHN is a super cell mass

41:33

that on CT can contain cyst and calcification.

41:37

So this is the classic appearance of a cranio on CT

41:41

and on mr, what we expect to look for is fat.

41:46

Sometimes we can see the fat right here,

41:48

sometimes they can be cystic

41:50

and they can also have this high T one signal, which is felt

41:54

to be proteinaceous material.

41:56

And when I was growing up as a resident, the term

41:58

that I was always taught was crank case oil.

42:01

Now back now with Teslas

42:03

and all the electric cars, we don't have a lot

42:05

of crank cases anymore,

42:06

but in general it was that sort

42:08

of pro nastious gooey material in cranial PHNs

42:12

that would give us that T one shortening.

42:15

So cranial PHNs are divided into two types.

42:19

In general, if they recur in younger patients

42:21

that have the classic cyst and calcification

42:24

and possibly the fat, this is the adenomas type

42:28

and that they occur in adults, these tend

42:30

to be a little bit more solid.

42:32

This is the papillary type.

42:34

So there is a subdivision histologically for cranial PHNs.

42:39

Now here's the case that I just completely missed.

42:42

I looked at this case, I guarantee I always remember this in

42:45

my differential diagnosis.

42:47

So what we have is an expansile lesion involving the dorsal

42:52

aspect of the clus and the body

42:54

and the posterior aspect of the sphenoid bone.

42:56

So I went through a differential diagnosis,

42:59

I thought it could be metastasis,

43:00

I thought it could be lymphoma, so on and so forth.

43:03

But the key thing here is that it's expansile,

43:07

it's involving the Clovis and it's low signal on T one.

43:10

So if I see something like this, I now think

43:13

of plasma cytoma.

43:15

So I completely missed this. This was a plasma cytoma.

43:19

So I always now remember this in the diagnosis

43:21

and if I see something that is low signal on T two,

43:25

then I shark to favor plasma cytoma.

43:28

And notice how we can see the pituitary gland.

43:31

So plasma cytomas are tumors of the plasma cells.

43:34

They are malignant, they have an identical pathology

43:38

to multiple myeloma, but in general they

43:41

form a discreet mass.

43:42

So the way that I think about it is almost like a

43:45

unifocal multiple myeloma.

43:47

Instead of being diffused, it forms a discreet mass.

43:51

And the typical treatment for this is radiation therapy.

43:54

So when you see these lesions, think plasma cytoma,

43:58

here's another lesion involved.

43:59

The central skull base on T one, it's low signal.

44:03

When we give contrast, there's no enhancement.

44:06

When we look at the T two weighted images, it looks cystic

44:09

and you're thinking, hmm, is it possible this could be an

44:12

arachnoid cyst?

44:14

But when we look at the DWI, it's high signal on DWI

44:18

and notice on flare on flare, if it was fluid,

44:21

it should be dark, but it's not.

44:23

So when you look at this combination of

44:24

what you think is probably cyst,

44:27

but then it high has high signal on the DWI signal,

44:31

then we can make the diagnosis of an epidermoid.

44:34

So epidermoid as we know are benign lesions, they're

44:37

of epidermal origin, they tend to be soft and pliable

44:41

and they can occasionally extend into the region

44:43

of the lateral and the central skull base

44:46

and we can make a specific diagnosis.

44:48

Again, I'm trying to focus on

44:50

how we can make specific diagnoses.

44:52

If you see the cystic area with the increased DWI signal,

44:56

then we can make the diagnosis of that epidermoid.

45:01

Now here's a case I saw years ago in the middle

45:03

of the night, it was like three in the morning

45:06

and I was reading this out.

45:07

I came in to do an angiogram when I was doing interventional

45:09

neuro and I saw this patient

45:11

that had a mass right here involving the sphenoid bone.

45:15

Now when I looked at this I'm like, huh, that's interesting.

45:18

It looks kind of aggressive.

45:20

But what kind of was interesting

45:22

to me is notice in this older patient,

45:24

the patient was about 50 years old,

45:26

there was no high signal involving the Clovis

45:30

and when we gave contrast there was diffuse enhancement.

45:33

So the bottom line is, is that if I see a mass right here

45:36

that's involving the central skull base

45:39

and I see replacement of the Clovis, then one

45:42

of the things I have to think about are various lesions

45:45

of hematopoietic uh uh, disorders or lymphoproliferative.

45:50

In this case I thought it was gonna be lymphoma

45:53

and this was one of the few times I was right.

45:56

So how can we suggest this diagnosis If we see a solid mass,

45:59

then we look at the bone marrow

46:01

and there's replacement of the bone marrow, then we have

46:04

to think of some type of infiltrative process

46:07

and we can make the diagnosis of lymphoma.

46:11

So when we are looking at lymphoma

46:13

and we start to see different aspects of marrow replacement,

46:17

we also have to think about this entity.

46:20

And this is one of these entities.

46:21

There's an old saying, you only see what you look for

46:24

and you only diagnose what you know.

46:27

So this is a patient that presents with the six nerve palsy.

46:31

Remember the six nerve exits at the

46:33

ponto medullary junction.

46:34

It extends anteriorly through Dores canal

46:37

and extends at adjacent to the colvis.

46:40

So here we have this lesion right here

46:43

that's involved in the Clovis

46:44

and with the leap of faith we can see the sixth nerve

46:47

extending right into that mass.

46:49

Here's another patient. This patient presented

46:52

with a 12th nerve palsy.

46:53

I know I almost missed this

46:54

because I was about to dictate it out as normal.

46:57

I think it was actually a brain Mr.

47:00

But then when I went back in there I

47:01

said, now hold on for a second.

47:03

This patient was an older patient,

47:04

they should have high signal here involving the clus.

47:08

And then lo and behold, when we look at the tongue,

47:10

if you draw a line down the middle,

47:12

compare the right side to the left side.

47:14

Notice my normal vis tiger stripes.

47:17

If you've heard me talk before,

47:18

you know I love my tiger stripes.

47:20

So there's white, there's black,

47:22

there's white and there's black.

47:23

Here's the geno gloss muscle.

47:26

Notice on the right side we don't have this muscle

47:29

and this is due to denervation atrophy of those muscles.

47:32

So if you see someone that presents with a 12th nerve palsy,

47:36

here's the classic what we would see in the tongue.

47:38

Make sure you look at the region of the skull base

47:42

because the 12th nerve exits the brainstem

47:45

and it extends through the hypoglossal foramen,

47:48

which is right at the bais sphenoid.

47:50

So the bottom line is in the sixth nerve and the 12th nerve.

47:54

When you're looking at the central skull base, please,

47:56

please, please take a close look at the marrow

47:59

because these are both example of metastases.

48:02

And again, sometimes the only time you'll see this is on

48:05

brain MRIs.

48:06

You know, you're quickly looking for intra AAL lesions.

48:10

But again, anytime

48:11

that you have those lesions involving the cranial nerves,

48:14

I guarantee you you're gonna be start seeing these

48:17

metastases involving in these areas.

48:20

So here's an example of a case.

48:22

I think we can all make the diagnosis here.

48:24

Here we have this expanse lesion involving,

48:28

in this case the lateral skull base.

48:30

Here we have a lesion involving the sphenoid bone.

48:33

Here's our lesser wing, here's our greater wing,

48:36

and we can all make the diagnosis here of fibrous dysplasia.

48:39

So I think this is a fairly classical appearance

48:43

of fibro dysplasia with the expansile lesion.

48:46

Um, and also this woven bone, uh, if you will.

48:49

So fairly classical appearance of fibrous dysplasia.

48:53

But the point that I wanna make,

48:54

sometimes it can be really confusing.

48:58

So here's a mass here

48:59

that's on the axial T two weighted images.

49:01

It looks kind of bad on the

49:03

non-contrast T one weighted image.

49:05

It looks like the skull base is completely replaced,

49:08

but when we give contrast, there's diffuse enhancement.

49:12

Now we're thinking about a really,

49:13

really aggressive skull base tumor, right?

49:15

Are we thinking about a chondro, sarcoma,

49:17

metastasis, so on and so forth.

49:20

But the point of this case is I always want to emphasize

49:23

that CT and MR are complimentary

49:26

and in this case just just happened to turn out

49:28

to be an extensive fibro osseous lesion.

49:31

And I believe this was pathologically proven

49:34

to be fibrous dysplasia.

49:36

So if you ever are confused when you're looking at MR

49:39

and you see something that just doesn't make sense

49:41

or maybe you see an abnormality that doesn't correspond

49:45

with the patient's clinical symptoms, remember

49:48

that CT can be incredibly helpful.

49:51

And these two entities,

49:53

these two modalities are very complimentary

49:55

for the skull base.

49:58

Now these are a couple of things

50:00

that are a little bit of a fooler.

50:01

Here's a lesion right here that's involved in the Clovis

50:05

and I see this pretty frequently.

50:07

So we see this abnormality here involving the Clovis

50:10

and we talked about lesions that can sort of give you,

50:13

and I don't wanna use the term lytic appearance,

50:16

but an irregular bony appearance involved in the colvis.

50:20

And if you look closely here, notice

50:21

how the bone is actually intact.

50:23

So this is predominantly involved in the interior

50:26

portion of the clus.

50:28

Now in something like this, I just show, oops,

50:30

I I showed earlier that

50:34

CT can help you figure out weird MR lesions as we saw here,

50:38

this is an example where the MR can help.

50:41

So in this case we see this abnormality here

50:43

and you're trying to think to yourself,

50:45

is it possible this could be a chordoma?

50:47

Is it possible it could be a metastases?

50:50

When we do a non-contrast T one, what we see here is a lot

50:54

of increased T one signal and increased T two signal.

50:58

And this actually is fat.

51:00

So this is an example of incomplete pneumatization

51:04

and sometimes it's called arrested pneumatization.

51:07

It's been called uh, intraosseous sphenoid lipomas lesions.

51:11

There's about six names to this.

51:13

I just call it incomplete pneumatization.

51:16

So in this particular case,

51:17

if you see something like this on uh, CT

51:20

and you see this preserved fat right here, then you can say

51:24

with a pretty high degree of confidence

51:26

that this is incomplete.

51:27

Pneumatization another example here,

51:30

when you look at the sagal images,

51:32

you see the scallop lesion right here involving the anterior

51:35

portion of the sphenoid bone.

51:37

Here it is on the coronal. Here it is on the axial.

51:40

Again, notice how the cortex is pretty well intact

51:44

in the same place we perform an MR here we have

51:47

that transition right here we can see

51:49

increased T one signal.

51:51

This is the fact this tells me

51:53

that this lesion was a sphenoid bone

51:56

or sphenoid sinus that was supposed to pneumatized

51:59

but it never did.

52:00

So again, I'll call this arrested pneumatization

52:04

or incomplete pneumatization.

52:06

Now look, if you're uncomfortable with this,

52:09

it's totally appropriate to get a follow-up CT

52:12

to confirm that, that's fine.

52:14

But if you do have this combination of CT

52:16

and mr, then I think you can be pretty confident

52:20

that this is the disease entity that you're looking at.

52:23

And finally, I'm gonna leave you with this case.

52:25

So this is something you should always

52:28

remember in the back of your mind.

52:29

So what we have here is a P paracellular lesion right here

52:32

that's located a pyramid midline, right?

52:35

It's located the petro clival fissure.

52:38

And when we look at this, we can see some

52:39

increased attenuation.

52:42

So now we're thinking to ourselves, hey,

52:44

is that a new matrix?

52:45

Is it potentially conroy or bony or so on and so forth.

52:49

But always remember anytime that you have a jux or cellar

52:52

or a PARACELLULAR lesion, the first thing that you have

52:56

to exclude is this specific disease entity

53:00

and that's an aneurysm.

53:01

So when we look at the MR right here,

53:04

here we see focal dilatation of the distal aspect

53:07

of the internal auditory canal.

53:09

And when we give contrast,

53:11

we can see a little bit of enhancement.

53:13

And on the conventional angiogram we can see

53:16

that this is a laterally directed aneurysm.

53:18

So remember aneurysms, especially when they're giant

53:21

that they can calcify.

53:23

And in the back of your mind, anytime

53:25

that you see a lesion here, the first thing that you have

53:28

to exclude and you can do it pretty quickly is

53:31

that you always have to exclude the possibility

53:33

of an aneurysm.

53:35

So with the last 55 minutes, what we've done is

53:38

that we talked about the central skull base,

53:40

we talked about the anatomy, we talked about the neoplasms,

53:44

we talked about dysplasia and congenital lesions.

53:47

And remember when you're looking at that central skull base,

53:50

always remember to look at my friend the sphenoid bone.

53:55

And if you remember that the bird,

53:56

the sphenoid bone looks like the bird

53:58

and you remember the, the wings, the greater wing,

54:01

lesser wing body and the plates right here.

54:05

I think it's actually gonna make skull base a lot of fun.

54:08

So thank you very much for your attention

54:10

and uh, happy to answer any questions.

54:12

Well thank you so much for this great

54:14

lecture yet again, Dr.

54:15

McCury. We will open the floor for some questions.

54:19

So go ahead and place your questions in that q

54:22

and A feature so we can get to as many as we can.

54:27

Yeah, so I can go and take these questions.

54:29

So like I said, I got about 15 minutes

54:30

and then I gotta run to the airport.

54:32

So, um, so the first question that we have is, uh,

54:35

if you see something like EID doses on ct,

54:38

do you always recommend an MR?

54:41

And how often do you follow it? So that's a great question.

54:45

I think if I see something that looks like acidosis on ct,

54:48

I think I would just get a follow-up ct.

54:51

Now, if there was extension into the sphenoid sinus,

54:55

then I think, I think getting an MR is probably fine.

54:59

Um, now I have to say too, because we're in the US and

55:04

because of my background as a a consultant in public policy

55:08

and healthcare, I tend to think about

55:11

how patients sometimes pay for these.

55:13

So for instance, if you were in area like in Europe where

55:17

you know a lot of everything your healthcare is paid for,

55:20

then yeah, I don't think there's any harm in getting an mr.

55:22

But I, in, in general, I always think about, okay,

55:26

if we're gonna get the MR who's going to pay for it,

55:29

is it really gonna add a lot of value?

55:31

So in general, if I seen something

55:33

that looks like acidosis on ct, um, based on

55:38

what I've talked to the pathologists are is

55:40

that you can't separate the benign acidosis, if you will,

55:43

from an early chordoma.

55:45

I think I would follow up, I'll probably just follow it up

55:47

with the ct, but if you wanna get an

55:49

mr, that's completely fine.

55:51

Um, someone said aneurysm question mark,

55:54

so I'm not sure what that was.

55:56

I think maybe you were just

55:57

answering the question that I had.

55:58

So, um, you were right. That was a, that was an aneurysm.

56:03

Um, so here's an uh, question.

56:05

Why does the incomplete ization have fluid?

56:08

So, uh, you know, I don't

56:11

a hundred percent know the answer that all I can tell you is

56:15

what I think is the answer.

56:17

And that is normally when the bone starts to pneumatized,

56:23

my sense is that the matrix within that bone that's about

56:28

to be pneumatized is if you will, within a normal range.

56:33

And my sense is, is

56:34

that sometimes there's an abnormality in the creation of

56:37

that bony matrix that eventually gets pneumatized.

56:41

And if indeed there's fluid there

56:44

or something that's, that is unable to be pneumatized,

56:48

then I think that's why it has fluid.

56:50

So the bottom line is it's like the chicken

56:52

or the egg, is it does the fluid form

56:55

because of the abnormal pneumatization

56:57

or does the pneumatization not occur

57:01

because that bone

57:02

that should be resorb is actually abnormal.

57:05

And I have to admit that I think it's probably the latter,

57:08

at least in my opinion as opposed to the former.

57:11

So that's the best I can give you on that uh, someone asked,

57:15

is chondro sarcomas always T two Brighten?

57:17

The absu is absolutely not chondro sarcomas, uh,

57:21

typically have, um, a heterogeneous T two signal.

57:25

So it can be low signal, it can be high signal,

57:28

it can be heterogeneous.

57:30

The reason I specifically show the lesions

57:33

that were T two Bright is

57:35

because in the real world you're gonna be trying

57:38

to figure out the difference between a chordoma

57:41

and a chondra sarcoma.

57:43

If that lesion that I showed you was low signal on T two

57:47

and it was off the midline in the synosis,

57:50

then chondra sarcomas would be the number one.

57:53

But oftentimes both chondra sarcomas,

57:56

which may have a con a a um, more of a fluid

58:01

or a mucinous component to a can mimic a chordoma.

58:04

But a hundred percent are chondro Sarcomas are not always T

58:08

two bright, and typically they can be low signal on T two

58:12

because of the matrix, or they can be heterogeneous.

58:17

Um, how do we deal

58:18

with the incidental echo acidosis, faus regions?

58:21

I think I just answered that one so, um,

58:24

I'll go on to the next one.

58:26

Um, would features

58:27

of chondro sarcoma you described here be seen in chondro

58:30

sarcoma in jaw lesions?

58:32

Um, and the answer is yes.

58:35

So, uh, one of the privileges I have is that, uh,

58:40

I, I do have a joint appointment in oral

58:42

maxillofacial radiology.

58:43

So we do see chondra sarcomas in that area.

58:46

And then also I, I read out with my colleagues from Tanzania

58:49

and they have these really very, very large

58:53

chondra sarcomas of the jaw.

58:55

So they're gonna have a similar appearance to it.

58:57

They're gonna have the conroy matrix to it

59:00

with potentially rings and circles.

59:03

The challenge that I run into when I don't know the answer

59:07

is that when these lesions get really big in the jaw,

59:12

sometimes for me it's hard to differentiate

59:15

the conroy matrix from the osteoid matrix.

59:19

So from, I sort of include both

59:22

of those in the differential diagnosis.

59:24

Um, if I see something

59:25

that's a classic conroy matrix, then I'll favor that.

59:29

If I see something that's more

59:31

of the classic sunburst appearance,

59:33

then I'll favor an osteosarcoma.

59:35

But oftentimes you can't tell the difference.

59:39

I sort of include 'em both.

59:41

Now I will say that if I have a lesion

59:43

that's involving the jaw in a younger patient,

59:46

let's say a female who's 25 or 26

59:49

and it's paray fial,

59:51

then I will consider a NAIC osteosarcoma

59:54

'cause they do have a, a propensity

59:56

to involve the jaw in that area.

59:59

Um, how long do I follow up arrested Pneumatization?

60:03

So if I do a CT

60:04

and mr it has a classical appearance, um,

60:07

I don't follow it up at all.

60:09

If you are doing a CT scan

60:11

and you wanna follow up arrested pneumatization,

60:14

then I would say maybe, uh, maybe uh, one

60:18

to two years just doing a CT scan, non-contrast CT

60:21

and you should be done with it.

60:22

So I would say maximum two years I think.

60:25

And if it's stable and it has a typical appearance

60:28

to it, I think you're done with that.

60:31

Um, any particular protocol that we would do

60:33

for the central skull base?

60:35

Yeah, um, I think what I like to do, uh, is first

60:39

of all, in order to look at the central skull base,

60:41

you really have to do thin section images.

60:44

And one of the biggest challenges that I see, um,

60:48

in the real world and not in a tertiary RY care

60:52

academic center, but is that people are trying

60:55

to evaluate the central skull base

60:58

and the skull base based on brain mrs.

61:01

And it's just not gonna work that way.

61:03

So in general, uh, I like

61:05

to do maximum three millimeter thick section.

61:08

So I like to do axial T ones pre and post contrast,

61:11

and then I like to do a post contrast fat suppression.

61:15

Then I do an axial T two, then I do a, um,

61:20

some type of heavily T two weighted thin section imaging

61:23

like a KISS or a fiesta or whatever.

61:27

And then I'll do a coronal T one post contrast.

61:32

Personally, I like to keep my

61:35

se my MR sequences short to try to have a shorter study

61:40

because what ends up happening is

61:42

that the longer longer the patient is on the magnet,

61:44

the more likelihood they are to move.

61:47

So for me, I personally would like

61:49

to keep the patient on the magnet less,

61:52

do the highest quality study that I could do

61:54

and that's gonna provide me the most information.

61:58

Um, I also will occasionally do, if it's a tumor,

62:01

I think you can do some type of profusion imaging,

62:04

whether you like to do a qualitative gradient echo T one

62:08

profusion or whether you wanna do more

62:10

of a quantitative technique.

62:11

It's really up to you.

62:13

But I don't think that should be the primary driver.

62:16

And by the way, I always do diffusion imaging as well too.

62:19

So I did want to make sure I mentioned that.

62:22

Um, hemangioma versus mening, I'm not sure

62:26

what you're asking, uh, there.

62:29

Um, maybe you're asking about intraosseous, he angios, um,

62:35

in, I think that's a, if you're asking about some

62:37

of the bony changes in a,

62:39

in an intraosseous heman in general,

62:42

I don't think the intraosseous he angios versus intraosseous

62:46

meningiomas, I don't believe the he angios have that um,

62:50

hair on end appearance or that expansile abnormality.

62:54

And also if it's arising from the greater wing

62:57

of the sphenoid, at least in my experience, they tend not

63:00

to have the classic dural tail, um,

63:03

that we see in meningioma.

63:05

So that, uh, helps me,

63:07

I believe separate the meningiomas from Heman Omas.

63:11

Uh, would you consider lymphoma

63:13

and plasma cytoma in your differentials?

63:16

Uh, when do I consider? So the answer is yes.

63:19

Anytime that, as I mentioned in the talk, anytime that I see

63:23

a pathology that's involving the central skull base

63:27

and there's a substantial amount of marrow replacement

63:32

than I consider lymphoma.

63:33

So lymphoma to me is more of a, if you will,

63:37

marrow replacement process without the bone expansion.

63:41

So if I see marrow replacement, then I start thinking

63:44

of lymphoma and metastases.

63:46

If I something, see something

63:48

that's predominantly intramedullary

63:50

and then there's expansion of the bone like I showed

63:53

before, then I think of plasma cytoma.

63:57

So again, as you allude to lymphoma

63:59

and plasma cytoma are actually both

64:03

hematopoietic slash lympho proliferative processes,

64:07

but the fact that one is more expanding the bone makes me

64:10

think that it's more plasmacytoma.

64:14

Um, what are the most common lesions

64:15

that arise in the sphenoid bone

64:17

and how do we typically present?

64:19

I think we sort of covered that, um, in the last talk.

64:22

So I'm sure you can go back to modality and,

64:24

and kind of see that, uh, um, on the,

64:27

on the lectures and take your notes.

64:29

Um, the follow-up, uh, interval for EID dose is saliro.

64:34

I probably would say I would probably do the three months,

64:38

six month, one year, then two years.

64:41

So if, if you go from one month, uh, three months

64:45

and it's stable, then six months,

64:47

that's the doubling time that we see.

64:49

That's probably sufficient.

64:52

But as I mentioned before, they can be very variable.

64:55

But I think if you go to a two year period

64:57

and it's stable, then I think you can feel pretty

65:00

comfortable that you're not dealing with a very,

65:04

very aggressive, uh, highly aggressive, um, chord.

65:11

Um, oh my pleasure.

65:13

Kai Kim, how much weight for DWI

65:15

for diagnosing chondro sarcoma versus chordoma?

65:20

Uh, that's a good question.

65:21

I don't think, I don't put

65:25

that much weight on it for a couple reasons.

65:29

Um, I think DWI is good. I mean I use it all the time.

65:33

I use it as a problem solving technique.

65:35

Like for instance with the epidermoid, the challenge

65:38

with DWI is that

65:41

when you are looking at the skull base, um,

65:44

and you are looking at the interfaces

65:47

and especially with chondro sarcomas

65:49

'cause it can contain uh, a conroy matrix.

65:53

Um, you can the DWI can be fraught with a lot

65:57

of artifact from the bone

66:00

and also from the adjacent structure.

66:03

So for me, the DWI doesn't really help me out trying

66:07

to differentiate a chordoma from chondro sarcoma.

66:11

Now you may see instances where it does,

66:13

but again, that's why wanted to emphasize

66:16

for me it really is the location, the location location, um,

66:21

really makes a difference.

66:23

And then also, um, the signal characteristics,

66:26

so was talked about before if you have something

66:27

that's paraline

66:29

and it's low signal on T two, um, again

66:32

that favors chondro Sarco as well too.

66:36

Um, and we large, so I'm an oral maxillofacial radiologist

66:40

and we largely read cone bean cts.

66:42

I was comfortable in calling fiber dysplasia the greater

66:46

weighing, but compared that case

66:47

that you showed at the iNOS meningioma,

66:50

is there a specific feature that I should be careful about?

66:53

That's a great question. Yeah.

66:55

So, you know, I think in the cone beam cts,

66:58

I don't know if you're, I don't know if you're one

66:59

of my residents at Texas a and m or not,

67:01

but I do have a joint appointment in oral maxillofacial

67:04

radiology at Texas a and m.

67:06

Um, if you see the typical features of fibrous dysplasia

67:11

with the woven bone, then I think you're fine.

67:14

But on the other hand, if it becomes densely sclerotic

67:18

or if you look at the cortex of the bone

67:21

and that cortex of the sphenoid bone is irregular

67:24

or we start seeing a spiculated appearance, then you have

67:29

to think of something more ominous arising from the bone.

67:32

So if it's just the classic intraosseous

67:36

or intramedullary expansion, I think you're fine.

67:39

But if you see that cortical irregularity, then you have

67:43

to worry that you're dealing with something else.

67:44

So that's a great question.

67:48

Um, is it possible that trigeminal neuralgia can be related

67:52

to enlarged meles cave or meningocele?

67:55

Uh, so I, it's a great question.

67:58

Um, I don't think it's necessarily due

68:02

to an enlarged meles cave or meningocele rather.

68:07

I've seen the opposite.

68:09

So I've, I remember I had a case years ago

68:12

back in the 1990s.

68:13

It was the first time I saw it.

68:15

And then since then I've seen numerous reports of this.

68:18

And that is if you have an atrophic

68:21

or an absent meles cave, I have seen patients that present

68:25

with trigeminal neuralgia if they have a

68:28

hypoplastic meles cave.

68:30

Why? That's the reason, I don't know.

68:32

Um, and I think it's somewhat debatable,

68:35

but I can tell you the case that I had, you know,

68:37

30 years ago, um, clearly had trigeminal neuralgia.

68:42

And again, I've seen I think three

68:44

or four cases since then, not only in my own practice

68:47

but at meetings where they have associated hypoplasia

68:51

of meles cave with trigeminal neuralgia.

68:55

Uh, can nasopharyngeal carcinoma invade the Clovis

68:59

and do they figure in the differential diagnosis

69:01

of a chordoma?

69:02

And the answer is yes.

69:04

And so I don't know, let me pull that up

69:07

because I think I, just to be honest with you,

69:09

I think I just ran out of time.

69:12

But uh, just gimme a second

69:13

and then I can pull, I'll show you that example

69:16

'cause it's uh, it's a great point.

69:18

I just gave, um, this talk, uh,

69:22

recently is a brand new talk I put together.

69:25

Um, this is more of a global thing on skull base.

69:27

It's not as drilled down as we're getting now,

69:30

but uh, let me show you this case.

69:34

Yeah, so this is more of a, a more of a more, uh,

69:37

a high level view.

69:38

But yes, here's an example of nasopharyngeal carcinoma

69:42

that's extending into the sphenoid bone.

69:44

So this is, yes, so you can have really,

69:47

really aggressive nasopharyngeal carcinomas

69:50

and they can have this spread pattern which extends

69:53

posteriorly to involve the colvis.

69:55

So this is just a sagittal,

69:57

a reformatted CT demonstrating this big nasopharyngeal

70:01

carcinoma that's involved in the colvis.

70:03

So the answer to your question is yes. Um, absolutely.

70:10

Um, let's see.

70:11

So the next one question that I have is canals, uh, canals,

70:16

bais medias related to Noor two.

70:20

So it is, uh, these foramina involving the skull base.

70:25

So I did not get into normal variants just based on time.

70:28

So there are various types of framing

70:30

that involve the sphenoid bone.

70:32

They can either be on the dorsal or the ventral surface.

70:35

To be honest with you, I always have to to read up on 'em.

70:38

Um, you know, I'm editor of neuroimaging clinics, uh,

70:42

and uh, I think about three years ago,

70:44

gold muni wrote a really nice

70:45

article on the different framing.

70:47

So the canal is bais is not related

70:51

to an abnormality involving the Noor.

70:54

Now it is a developmental malformation.

70:57

So in theory, because the

71:01

Noor potentially could give rise to some

71:03

of these mesodermal elements, it's possible,

71:07

but it's not, um, due to the horal remnants

71:12

that we talked about, specifically the torn wall cyst

71:16

or the, um, OSIS saliro.

71:19

So it's not related to that.

71:22

You got 'em all and with time to spare.

71:25

Okay, great.

71:27

Well thank you so much and um, we will plan to have your

71:31

part two, the anatomy and pathology of the lateral

71:34

and posterior skull base talk on November 26th.

71:38

So everyone please look out for that invite. Dr.

71:42

McCury, thank you so much for being here

71:44

and thank you so much for everyone else

71:45

for participating in today's NOOM conference.

71:48

As a reminder, you can access the recording

71:49

of today's conference

71:51

and all our previous ones by creating a free account.

71:54

And we'll also email out a link to the replay later today.

71:57

Be sure to join us next week on Wednesday,

71:58

October 1st at 12:00 PM Eastern, where Dr.

72:01

Lacey Macintosh will deliver a lecture entitled Resist 1.1

72:05

Principles, pearls and Pitfalls.

72:07

You can register that for that@modality.com

72:10

and follow us on social media

72:11

for updates on future NOOM conferences.

72:13

Thanks again and have a great day.

Report

Faculty

Suresh K Mukherji, MD, FACR, MBA

Clinical Professor, University of Illinois & Rutgers University. Faculty, Michigan State University. Director Head & Neck Radiology, ProScan Imaging

Tags

Neuroradiology