Anatomy and Pathology of the Lateral and Posterior Skull Base, Dr. Suresh Mukherji (11-26-25)
HIDEInteractive Transcript
0:02
Hello and welcome to Noon Conference, hosted by Modality
0:05
Noon Conference connects the global radiology community
0:08
through free live educational webinars that are accessible
0:11
for all and is an opportunity
0:13
to learn alongside top radiologists from around the world.
0:16
Today we are honored to welcome Dr.
0:17
Siresh McCury for a lecture entitled Anatomy
0:20
and Pathology of the Lateral and Posterior Skull Base.
0:24
Dr. McCury received his undergraduate degree from Duke
0:27
University and his MD degree from Georgetown University.
0:31
He currently holds appointments at multiple academic
0:33
institutions and is a devoted educator
0:35
who has been an invited speaker on over 500 occasions
0:38
and written and edited 15 textbooks.
0:42
We are especially grateful for his supportive modality
0:44
and for serving as our head and neck neuroradiology advisor.
0:48
At the end of this lecture, please join him in a q
0:50
and a session where he will address questions you may
0:52
have on today's topic.
0:53
Please remember to use that q
0:55
and a feature to submit your questions so we can get to
0:57
as many as we can before our time is up.
1:00
With that, we're ready to begin today's lecture. Dr.
1:02
McCorey, please take it from here.
1:05
Okay, great. Again, thanks for having me.
1:07
It's a real pleasure to, to give this talk again
1:10
for modality on a brand new topic.
1:13
And, uh, thank all of you for joining.
1:15
Before I forget, uh, for those of us in the United States,
1:18
it is the United States Thanksgiving coming up tomorrow.
1:22
So for those of you in the US
1:23
and all around the world, I wanna wish
1:25
you a happy Thanksgiving.
1:27
Um, and also we started this a little bit earlier.
1:31
Uh, so I do have about, I left up to about 30 minutes
1:33
for questions at the end of it, it's really up to Ashley
1:37
and Ben how long they want to go.
1:39
But from my standpoint, I think part
1:41
of the really unique things about
1:43
having these webinars is kind of taking the time, uh, go
1:46
through something in detail
1:48
and then have the time to answer questions.
1:50
I, I know the, the meetings that I go to right now, so many
1:53
of the talks are almost down to 15 minutes
1:56
and sometimes you try to cover 30 minutes
1:58
of information in 15 minutes.
2:00
So I think this is one of the real, um,
2:02
unique things that we do.
2:04
So what I'm gonna do is the, the talk is gonna be anatomy
2:08
and pathology of the lateral, uh, um, posterior,
2:11
the lateral skull base.
2:12
And so the first thing that I want to discuss is exactly
2:16
what is the anatomy of the skull base.
2:19
Now I believe in prior talks we've given a talk on the
2:23
anterior skull base of Ashley would have to fact check me on
2:26
that, but we have a talk on the anterior skull base.
2:28
I know the last talk we gave a talk on the
2:30
central skull base.
2:32
So if you remember the central skull base,
2:34
we talked about the famous bird of the skull base.
2:37
And now what we're gonna do is
2:38
that we're now gonna move over
2:40
and we're gonna discuss the lateral skull base
2:42
and the posterior skull base.
2:44
Now based on the classification system
2:46
and kind of who you who you read,
2:49
there are different definitions of the lateral
2:52
and the posterior skull base.
2:53
So the, for the purposes of this talk,
2:56
I'm gonna predominantly talk about the temporal bone
2:59
and a little bit of the occipital bone
3:01
with the understanding that a lot of the pathology
3:04
that involves the posterior skull base
3:06
and the lateral skull base are very similar.
3:08
So we're predominantly gonna talk about this area right
3:11
here, which is the temporal bone.
3:14
And in particularly the majority of the pathology
3:18
that's gonna involve the temporal bone is gonna be in this
3:21
pyramid shaped structure.
3:22
So that's why I sort of have the great pyramids here.
3:25
So this is what we refer to as if you will the, the pyramid
3:29
of the petre portion of the temporal bone.
3:32
Now realize that there's a squamal portion,
3:34
there's a tepa segment.
3:36
There is, um, a uh, styloid process
3:39
that arises from the temporal bone.
3:41
We'll talk about that a little bit,
3:43
but predominantly this is where the action is going to be.
3:48
So the first pathology
3:49
that I'm gonna talk about is a little bit of a curve ball,
3:52
but I think you're gonna understand why I mentioned this.
3:55
Um, on the next couple of slides.
3:58
So this is a patient, excuse me, that has a mass right here
4:03
that's involving the central portion of the skull base.
4:06
Now this was a slide
4:08
that I showed I believe in the last lecture,
4:10
but it makes an I one important point, at least in my view.
4:14
And this is a mass that's invi in involving the central
4:17
portion of the skull base.
4:18
So if you look at the schematic illustration,
4:20
we can see the Petri bone right here.
4:22
This is where the petro clival fisher is gonna be.
4:25
And what we see here is an aggressive mass
4:27
that has increased T two signal and enhances with contrast.
4:32
So it almost has, if you will, a pseudo cystic appearance.
4:36
And when we look on the CT scan,
4:38
what we see here is this fragmentation of the bone.
4:41
So when we see something like this,
4:44
I think we can all make the diagnosis,
4:45
especially if you attended the my last talk of a chordoma.
4:50
Now remember a chordoma is what gives rise
4:53
to the central access of the spine
4:55
and the remnants of the chordoma end up forming the discs
5:00
between the different vertebral bodies.
5:01
So the bottom line is, is that these chords tend
5:04
to be midline and as you can see, it's high T two signal
5:08
and it enhances with contrast
5:10
and it can be associated with some bone erosion.
5:14
Now what I'm gonna do is I'm gonna show you this case.
5:17
So this is a case of on the T two weighted images we see
5:21
this aggressive mass that's not located centrally,
5:24
but it's located laterally.
5:27
And when we look at the non-contrast T one weighted images,
5:30
we can see it's involving a portion of the petre bone.
5:33
This is actually the hypoglossal canal.
5:35
So it's involving the hypoglossal canal
5:37
and it is involving the Clovis,
5:39
but it's only involving the lateral aspect of the Clovis.
5:42
So the bottom line is, is that this is a rising
5:45
and centered a pyramid midline in the region
5:49
of the petro Clival fisher or
5:51
otherwise known as the petro clival synchondrosis.
5:55
And this is the classical example of a chondro sarcoma.
5:58
So the chondro sarcoma is kind of the index tumor
6:02
that arises from the lateral skull base
6:05
and specifically at the level of the petroc clival fissure.
6:09
Now the classical example of a chondro sarcoma is going
6:14
to give you sort of this rings and circle appearance.
6:16
So if you see something like this,
6:18
especially in an older patient
6:20
and I unfortunately I have to include myself
6:22
as an older patient, we can see these rings and circles.
6:26
So when you see something like this,
6:27
I think chondra sarcoma is gonna be at the very, very top.
6:31
Now the reason I started off with the chordoma
6:35
and then I went to Chondro sarcoma is
6:37
that notice the signal pattern right here is high signal on
6:41
T two, low signal on T one and enhances with contrast.
6:46
So the bottom line is, is
6:47
that on Mr A Chondro sarcoma can have the exact same
6:52
signal characteristics as a chordoma.
6:55
So therefore if you're just looking at T one and T two
6:58
and enhancement, there's a lot of overlap.
7:01
A lot of that is due to the different histologic subtypes
7:05
of both chordoma and chondro sarcoma.
7:07
So what I've learned over time, there's an old saying
7:11
that says Good judgment comes from experience
7:13
and experience comes from bad judgment.
7:15
Unfortunately, I have a lot of experience.
7:18
What I've learned over time is that the,
7:21
because of the imaging overlap, what I look
7:25
for when I'm trying to make a diagnosis of these lesions,
7:28
whether it's midline or paraline, if I see something
7:31
that looks like this and it's paraline,
7:33
that's when I raise the possibility
7:35
of chondro sarcoma over a chordoma.
7:38
So the chondro sarcomas are paraline
7:40
and again, they're gonna be focused right here on the
7:43
petrich clival fissure.
7:46
Now this is a lesion that involves the Petra apex.
7:49
So if, now if you look at our Petra bone right here,
7:52
we're gonna get right at the top
7:54
of the Petrus pyramid, if you will.
7:57
So in this case, what we see here in a non-contrast T one
8:00
weighted image, we see this lesion that's high T one signal
8:03
involving the superior portion of the petre bone, right at
8:07
that petras apex.
8:09
And then when we do a CT scan,
8:10
what we see is an expanse lesion right at the petre apex.
8:15
Now this does not have the aggressive features
8:18
of a chondra sarcoma
8:19
and I think most of you will be able to make this diagnosis
8:24
because if you see something in the petris apex
8:27
and it's high T one signal, you can see that it does kind
8:31
of erode but also expands the bone.
8:33
Then we can make the diagnosis of this entity,
8:36
which is a cholesterol granuloma.
8:39
Now a cholesterol granuloma is not necessarily
8:42
a distinct entity.
8:44
A cholesterol granuloma really are byproducts in a way
8:49
of protein and blood that tends to degrade.
8:52
And as a result we can get this increased T one signal.
8:56
So cholesterol granulomas can, the entity
8:59
of cholesterol granulomas in this byproduct can really occur
9:03
anywhere where there's been prior hemorrhage.
9:06
So for 25 years I always thought
9:08
that cholesterol granulomas were sort of this unique entity
9:11
that arose in the petrich apex.
9:13
But literally I'm, I'm always learning.
9:15
The older I get actually the less I know.
9:17
So I always have to keep learning.
9:19
And then I noticed that um, my neurotology colleagues
9:23
that ended up doing mastoidectomy,
9:25
sometimes you would have an opacified mastoid bone
9:28
and they would go in and drain it
9:30
and it, they would say,
9:31
well there's a cholesterol granuloma there.
9:34
And I thought, well how can it be a cholesterol granuloma
9:36
because these things are supposed
9:37
to rise in the petris apex.
9:39
So the bottom line is,
9:40
is the cholesterol granulomas are a byproduct.
9:43
Now what actually causes a cholesterol granuloma
9:47
can be debatable.
9:49
Some people feel it's,
9:51
they occur in pneumatized petras bones in
9:55
where you have eustachian tube dysfunction
9:57
and you have chronic and recurrent hemorrhages.
10:00
And that's why it kind
10:02
of gives you this increased T one signal.
10:05
Now other people feel that there's some type of invasion
10:09
of the mucosa overlying the petri bone
10:12
and it kind of burrows itself into the petri bone
10:16
and eventually it results in blood products.
10:19
I think either one of those are possible.
10:22
I tend to favor the former rather than the latter.
10:26
Now just to emphasize that cholesterol granulomas are,
10:29
if you will, dynamic
10:30
for the longest time I thought they were static,
10:33
but this was an example of a patient
10:36
that initially had this CT scan
10:38
and uh, this MR scan on the non-contrast T one weighted
10:41
images, we can see a little bit of mucosal thickening.
10:44
That's T one shortening.
10:47
Now when you see something like this,
10:48
it really doesn't have the mass like effect
10:51
that you see in a cholesterol granuloma.
10:53
Rather it seems like it's conforming
10:56
to the expected morphology of the Petri bone.
11:00
But when it ended up happening about three years later is lo
11:03
and behold this same patient went on to develop this.
11:07
So this is why I tend to favor the theory
11:10
of multiple recurrent hemorrhages
11:12
because we can see now not only has the morphology
11:15
of the signal abnormality changed,
11:17
but it's also much brighter on the T one weighted sequences.
11:21
And this was another case I saw a few years ago.
11:25
This was the original study, excuse me.
11:27
We can see here on the CT scan this expansile oval lesion
11:32
involving the petre bone on the T two weighted images.
11:35
Here we can see it's high signal on T two,
11:39
but a few years later what ended up happening
11:42
and look at the same location
11:43
and notice where we are, we're anterior
11:45
to the internal auditory canal.
11:47
Lo and behold, all of that increased T two signal
11:51
actually turned into low signal.
11:53
So one thing that I've learned over time is
11:55
that cholesterol granulomas,
11:57
when we see them initially we think that they're static,
12:00
but they really are a dynamic process.
12:02
And I've seen several of these cholesterol granulomas over
12:06
uh, uh, appear and evolve over time.
12:09
And as illustrated in this case,
12:11
I've also seen the internal signal characteristics evolve
12:15
over time as well.
12:18
Now here's an example of another lesion
12:20
that's involving the petre apex.
12:22
So if you look at this,
12:23
it's on non-contrast T one weighted images, it's gray.
12:27
And then when we give contrast, we don't see a lot
12:30
of internal enhancement
12:31
but maybe a little peripheral enhancement.
12:34
So this by itself,
12:35
even though it's involving the petris apex, notice
12:38
how it doesn't have the characteristic increased T one
12:42
signal that we would like to see in cholesterol granuloma.
12:45
Now the interesting thing about this is
12:47
that when we do the T two weighted images,
12:50
it's high T two signal.
12:52
But when we look at the diffusion images, notice
12:56
how it's high signal on DWI.
12:58
And if I showed you the A DC map, it would be dark.
13:02
So when I see a lesion such as this
13:04
that's located in the petre apex, we can make the diagnosis
13:09
of a cholesteatoma slash epidermoid
13:12
involving the petre bone.
13:14
Now we're gonna be talking about epidermoids later in a
13:17
different location, but this is one of these rare cases
13:20
where there was actually an epidermoid involving
13:23
the petrus bone.
13:24
So when you first look at this, you say,
13:26
could it be cholesterol granuloma?
13:28
It's probably not 'cause it doesn't have the
13:30
increased T one signal.
13:32
And notice how this is bright on DWI signal
13:35
so we can make the diagnosis of
13:37
that coloma slash epidermoid involving
13:41
the petre pyramid.
13:45
Now what we're gonna do is we're gonna move a little bit
13:48
more posteriorly and we're gonna go to this area right here.
13:53
So what we've done so far is that we started with the
13:57
clovus, then we went to the petro clival fisher
14:00
and then we just talked about the petris apex.
14:03
Now what we're gonna do is we're gonna go a little bit more
14:06
posterior I medially
14:07
and we're gonna discuss this famous little angle right here,
14:10
which is called the cerebella pontine angle.
14:14
As we know the reason why it's called the cerebella pontine
14:17
angle, it's be because it's located at the junction
14:20
of the pons in the cerebellum.
14:23
And as we extend laterally from the pons in the cerebellum,
14:27
we see there are a variety of structures
14:29
that are located in the cerebellum pontine angle
14:33
that are going to give rise to the common pathology
14:37
that we will see in this location.
14:39
So when we're looking at this very nice coronal dissection,
14:43
first of all we'll look at the vessel.
14:45
So we see a vessel right here.
14:47
This is the anterior inferior cerebellar artery,
14:50
also known as iica.
14:52
When we look right above it,
14:53
we can see the various cranial nerves.
14:55
So this one is probably gonna be seven
14:58
'cause it's superiorly and this is the probably the eighth
15:01
nerve, either the superior or the inferior vestibular nerve.
15:04
We'll talk about this later.
15:05
But the bottom line is
15:06
that this is the seventh eighth nerve complex
15:09
extending into this opening right here,
15:12
which is the porous acoustics.
15:15
When we go down a little bit more inferiorly,
15:17
we can see three nerves right here, which are now combining
15:21
to extend through a foramen.
15:23
And that foramen is located down here.
15:25
This is gonna be the jugular foramen.
15:28
So this is cranial nerve nine, this is 10 and this is 11.
15:33
These extend to the jugular foramen
15:35
and this nerve that's coming more inferiorly is
15:38
gonna be the 12th nerve.
15:39
So we won't be talking about the 12th nerve today,
15:41
but we are gonna be talking about probably
15:43
that in a future lecture.
15:44
So these are the common pathology.
15:47
So again, I want you to remember artery, I want you
15:50
to remember vein and also these nerves.
15:52
Now what we've done in this case is
15:54
that we've did a beautiful dissection of these nerves, but
15:58
before you can see these nerves, you have to see
16:02
this glistening structure right here,
16:04
which lines the brain parenchyma and this is the meninges.
16:09
So the meninges covers all of the brain
16:11
and the meninges covers the cerebella pontine angle.
16:14
So when you're looking at cerebella pontine angle masses,
16:18
one of the common pathologies that you'll see arise here
16:21
is these type of masses.
16:23
So this is a large cerebella pontine angle mass.
16:26
We can see it's extra axial.
16:28
Now I do wanna point out the increased T two signal here.
16:31
This is involving the middle cerebellar peduncle.
16:34
This is not invasion,
16:36
but in this case just just happens to be edema that
16:39
resulted from this meningioma.
16:42
When we look at the non-contrast T one weighted images,
16:45
it's bland and once we give contrast we can see the
16:48
characteristic appearance of the meningioma.
16:51
So homogeneously enhancing,
16:53
we can see it has a broad base of attachment.
16:56
And oftentimes what these do is just sort
16:58
of cross over the porous acoustics.
17:00
When we talk about vestibular schwannomas,
17:02
which arise from the nerve,
17:04
we're gonna see a little bit more of a medial extension.
17:07
But because of that meninges kind of uh, completely uh, uh,
17:11
involves the surface of the brain.
17:13
That's why these meningiomas tend
17:15
to have a broad base of attachment.
17:18
Now what I showed was sort of the classical example
17:21
of a meningioma involving the cerebella pontine angle.
17:24
But what I wanna do is talk about the many faces
17:28
of the meningioma.
17:30
So this is an example of a meningioma.
17:33
So if you look real closely,
17:34
we can see this mass right here,
17:36
which is somewhat nonspecific.
17:38
But on the other hand what we see here is
17:40
diffuse dural enhancement.
17:42
Remember that slide I showed of the meninges
17:43
that completely covered the posterior fossa?
17:46
Well this is all this dural tail if you with
17:49
with the meningioma.
17:51
And if you have a really good eye, remember there's meninges
17:53
that extends into the internal auditory canal.
17:57
So this was actually spread of that meningioma
17:59
to involve the internal auditory canal.
18:03
Here's another example of a meningioma
18:05
and this case it's very, very dark
18:07
and in a couple of slides we'll show why it's dark.
18:10
The reason is, is
18:11
because these meningiomas can sometimes involve the bone.
18:16
Here's an example of a path proven meningioma.
18:18
When I saw this, I was thinking could this be a metastasis?
18:22
Could it be a condra sarcoma?
18:24
But on this CT scan we can see the relatively
18:26
homogeneous enhancement.
18:28
Now could I say that this was a meningioma for sure
18:31
because of this bone erosion?
18:33
Absolutely not. In fact, I wasn't sure what it was
18:35
until the biopsy came back,
18:37
but in this case it happened to be a meningioma.
18:41
This was another example of a meningioma.
18:43
This was extending into the jugular foramen.
18:46
Here we can see this uh, irregular calcifications.
18:49
Remember meningiomas can calcify internally.
18:53
This is an example of an intraosseous meningioma.
18:57
We can see it's completely expanding the bone.
18:59
Typically we see this type of experience, uh,
19:02
appearance in the talk that I gave previously.
19:05
Typically they arise from the sphenoid bone and
19:08
and the greater wing of the sphenoid sinus.
19:10
But here we can see intraosseous involvement.
19:13
And when they're completely ossified,
19:15
this gives you a complete signal loss.
19:18
So this was the case on actually a
19:20
contrast enhanced T one weighted image.
19:22
There was no enhancement whatsoever.
19:25
And when we look at the T two weighted images,
19:27
there was complete signal loss.
19:29
And the reason this was the case was
19:31
because this meningioma was completely calcified.
19:34
So in this case, there was no real enhancing component
19:38
that we could detect on our standard MR imaging.
19:43
Well here's another type of pathology
19:45
that can occur in the cerebella pontine angle.
19:48
So what we see here on a thin section T two weighted images,
19:52
we see the cystic mass right here
19:54
and notice the displacement
19:56
that it's having involving these nerves extending into the
20:00
cerebella pontine angle.
20:01
So this is the seventh to eighth nerve complex.
20:03
So this is what we're seeing anatomically normally.
20:07
And in this case we can see this mass anteriorly
20:09
displacing that complex.
20:12
This is that same lesion on the contrast
20:14
enhanced T one weighted images.
20:16
And in this case this was the DWI sequence.
20:20
So this was the diffusion sequences.
20:22
In this case, the diffusion sequence is not bright at all.
20:26
This lesion is low signal on DWI.
20:29
So if you see something that's purely cystic
20:31
and doesn't have any increased signal on diffusion weighted
20:34
images, well we can make the diagnosis of an arachnoid cyst.
20:39
So arachnoid cysts are relatively common in the
20:42
cerebellar pontine angle.
20:43
Typically I end up seeing in the floor the middle cranial
20:46
fossa or maybe along the convexity of the brain.
20:50
In theory it's felt to be due to splitting of the arachnoid.
20:54
As I mentioned before,
20:55
the most common area here is in the middle cranial fossa.
20:59
There a are typically fluid signal.
21:01
There's no enhancement
21:03
and there's no abnormal signal on DWI or flare.
21:06
So relatively classical appearance
21:09
of an arachnoid cyst involving the cerebella pontine angle.
21:14
Here's another example.
21:15
This is an example of a a lesion
21:18
that's involving the left cerebella pontine angle.
21:21
Again, it's high signal on T two weighted images.
21:25
When we look at the contrast enhanced T one weighted image,
21:28
look, there's no enhancement whatsoever.
21:31
But in this case what we have is a flare sequence.
21:35
So when we look at the flare sequence, notice
21:37
how there's increased signal within this lesion on
21:40
the flare sequence.
21:42
So this is a little bit unusual for this
21:45
to be a arachnoid cyst
21:47
because arachnoid cyst shouldn't have any signal within it
21:51
on the flare sequence.
21:52
And when we see something like this,
21:54
this in fact is characteristic for an epidermoid.
21:58
So an epidermoid or benign lesions are of derm origin
22:03
and they contain the keratin debris.
22:06
Now, previously I showed an epidermoid
22:08
that was located in the petris apex.
22:11
Now in my experience, these epidermoids
22:14
that extend all the way
22:15
to the petris apex are pretty unusual.
22:17
The only few times I've seen it have been huge middle ear
22:20
cholesteatomas that can grow into the petre bone.
22:24
More commonly I see these epidermoids located in the
22:27
cerebellar pontine angle.
22:29
It follows fluid signal on our standard sequences.
22:33
But the way that we can suggest the diagnosis is
22:36
that we look for the high DWI signal.
22:40
Here's another example of an epidermoid.
22:43
Again, if you just did standard brain imaging,
22:46
it's possible you could miss this.
22:48
Sometimes these patients may present
22:50
with dizziness high signal on T two when we give contrast,
22:53
there's no enhancement whatsoever.
22:56
But look at the a DC maps.
22:58
The A DC maps demonstrate this lesion to have low signal.
23:02
And then when we look at the heavily T two weighted images,
23:06
we can see this fron like
23:07
or papillary appearance, excuse me,
23:10
which corresponds pretty well to
23:12
what we see here on the schematic illustration.
23:15
So one of the things that kind of keeps me up at night is
23:18
that oftentimes we'll do standard brain MRIs in patients
23:22
that are dizzy and we won't do the he we won't do the
23:26
really thin IAC study.
23:28
So I always worry about missing epidermoids
23:31
because the standard brain MRI doesn't give you the thin
23:34
section heavily T two weighted images.
23:37
And sometimes you have to look really,
23:38
really closely in the cerebella pontine angle to see these.
23:42
So my sense is is that there are a lot
23:44
of epidermoids in patients with dizziness
23:47
that go undiagnosed.
23:49
So anytime myself
23:50
as a head neck radiologist makes the recommendation
23:53
what study to get in a patient with dizziness, I always like
23:56
to do an I-A-C-M-R-I as opposed to a just standard brain mr.
24:01
Now here's an example that sometimes we may not think about.
24:06
So when you look at the heavily T two weighted images,
24:09
draw a line down the middle,
24:10
compare the left side to the right side.
24:12
On the right side we can see the seventh
24:14
and eighth nerve complex, just like
24:16
what we do on this anatomic image.
24:18
But look at the left side.
24:20
This is sort of that fron like appearance
24:23
that we saw before, right?
24:25
So now you're thinking could it be an epidermoid?
24:28
But on the other hand, look at the DWI image,
24:30
there's no increased signal on the
24:33
diffusion weighted images.
24:34
So you're thinking, huh, that's
24:36
kind of an unusual appearance.
24:37
And then we give contrast and lo
24:39
and behold we have all of this enhancement.
24:43
Now epidermoids should not give you this
24:45
degree of enhancement.
24:47
So with standard neuroradiologist,
24:49
again we have our differential meningioma, we think
24:51
of arachnoid cyst, we think of epidermoids.
24:55
But in the back of your mind, remember the anatomy
24:59
of the cerebella pontine angle.
25:01
So we talked about the nerves, we talked about the meninges.
25:04
So if you see something like this
25:06
that has this dense enhancement
25:08
and it's also um, somewhat um, serpiginous, you have
25:12
to consider the possibility of a dural fistula.
25:15
So this was an example of a dural fistula
25:18
that was involved in the cerebella pontine angle.
25:21
Remember the difference between an A VM is what's felt
25:25
to be is that all the NIUs comes from the
25:27
intracranial vasculature.
25:29
Whereas the dural fistula, this sa,
25:31
you can still have a NIUs,
25:33
but that NIUs arises from the extracranial branches.
25:37
These patients oftentimes present with dizziness,
25:39
they can present with pulsatile tinnitus,
25:42
sometimes they can even present with hearing loss.
25:45
So this was another case of a patient
25:47
that had a dural fistula.
25:49
And here we can see this diffuse serpiginous enhancement
25:52
draining into the internal jugular vein.
25:55
Now these are somewhat rare,
25:57
but on the other hand, you know from myself, I used
26:00
to do neurointerventional about 20 years ago, I still go
26:03
to neurovascular conference.
26:05
So it's still not that uncommon to see this in pat,
26:08
especially in patients that are dizzy
26:09
and have pulsatile tinnitus.
26:11
And again, the only way we can make the diagnosis is
26:15
to think of the diagnosis.
26:16
So if you see something
26:17
that somewhat looks like an epidermoid
26:19
and you see this diffuse enhancement that's serpiginous
26:22
in the back of your mind, always consider the possibility
26:25
of a duro fistula.
26:28
So now what we're gonna do is that we talked about the
26:32
Clovis, we talked about the petris pyramid,
26:35
we talked about the cerebella pontine angle.
26:38
Now what we're gonna do is move our attention
26:40
to this little opening right here.
26:43
And this opening right here is the internal auditory canal.
26:48
Now again, sort of the way I look at these things, I sort
26:51
of have a somewhat strange way of looking at this is
26:53
that a lot of the structures
26:55
that we talked about were arising from the surface.
26:58
So we talked about the chondro sarcomas
27:00
and how they were pretty obvious.
27:02
You can see these looking down, we talked about some
27:05
of the dural fistulas and the meningiomas.
27:07
But when we really start
27:08
to talk about the internal auditory canal, to me it kind
27:12
of looks like a clamshell.
27:13
So the way I think about it is that a lot of the stuff
27:16
that we've talked about with sort of the shell itself,
27:19
but really in order
27:20
to look at these structures in the internal auditory canal,
27:24
we have to open the shell.
27:26
And all of a sudden we see this beautiful
27:28
pearl looking at us.
27:29
And when we see this pearl
27:31
and we remove the top of the Petra pyramid, all
27:34
of a sudden we start seeing this beautiful pathology
27:38
that's gonna be involving these wonderful structures
27:40
that run within the internal auditory canal.
27:44
And the first thing that we're gonna be talking about are
27:47
the vestibular schwannomas.
27:48
So this is the index case of these lesions
27:51
that involve the IAC.
27:54
So vestibular schwannomas have an incredible amount
27:58
of variability when it comes to their imaging findings.
28:02
When these vestibular schwannomas arise
28:05
and are located purely within the internal auditory canal,
28:08
this is what they look like.
28:09
They look like these oval shaped structures right here,
28:13
but sometimes based on where they arise from,
28:17
you can have vestibular schwannomas
28:18
that can arise right here at the porous ticus.
28:22
Now it's possible
28:23
that these vestibular schwannomas started here
28:26
and moved laterally.
28:27
On the other hand, when I was a resident it was felt
28:30
that vestibular schwans were felt
28:32
to arise from the porous ticus from
28:35
what we call the obermeyer Steiner line
28:37
because this is where the myelin changed.
28:39
I dunno if that was actually proven or not,
28:41
but that's how we learned it.
28:43
And this is an example of a patient
28:45
that had a very oblong vestibular schwannoma.
28:48
And again, notice a difference in morphology between one,
28:51
this one that looks more like a pebble versus this one
28:54
that looks like an ice cream cone.
28:56
And I have to say in the old days
28:59
before we had, when we started doing Mr, the way
29:01
that we would look for vestibular schwannomas was
29:04
to do a temporal bone ct.
29:06
And notice how when you have these vestibular schwannomas
29:09
that widened the pore acoustics,
29:11
that was the only way that we could tell that.
29:14
And if you were really suspicious, you had
29:16
to do a pneumoencephalogram to see whether
29:18
or not you could outline the vestibular schwannomas.
29:21
Certainly things have gotten much easier
29:23
and I can tell you I'm glad those days are over
29:26
because it wasn't fun for the radiologist
29:28
and it wasn't fun for the patient either.
29:32
So when we look at vestibular schwannomas,
29:35
please use the term vestibular schwannoma
29:38
because when I, when I was a fellow,
29:40
my attending Tony Mancuso would always really give us a hard
29:44
time if we use the term acoustic neuroma
29:47
because there's no real acoustic nerve.
29:50
And a neuroma is a post-traumatic uh, reaction
29:53
that happens in a nerve.
29:55
The proper terminology is vestibular schwannoma.
29:59
Now these schwannomas can arise from any
30:02
of the nerves involving the internal auditory canal.
30:06
So when we look at the four nerves involving the internal
30:09
auditory canal, we have this nerve right here,
30:11
which is the seventh nerve, we'll talk about this later.
30:14
These are the different segments, we'll come back to that.
30:17
Then we have this nerve that extends into the cochlear
30:21
through the cochlear canal.
30:22
This is the cochlear nerve.
30:24
And then we have two vestibular nerves,
30:26
one's the superior vestibular nerve
30:28
and one's the inferior vestibular nerve.
30:31
So if you're, do your imaging just right,
30:33
sometimes on these early schwannomas you can actually
30:37
identify the nerve from which they arise.
30:40
Notice this nerve,
30:41
this schwannoma right here is arising from the distal
30:45
aspect of this nerve.
30:46
Notice this nerve is extending into the cochlear canal.
30:49
So this is at the level of the cochlear nerve.
30:53
Remember seven up coke down,
30:55
coke down means the cochlear nerve is anterior and inferior
30:59
and posterior
31:00
and inferior to this is the inferior vestibular nerve.
31:03
How about this lesion right here?
31:05
Notice how this lesion right here is involving
31:09
the distal aspect of the internal auditory canal.
31:12
Notice how we're at the very, very top of the cochlea.
31:15
And this lesion right here is heading into the distal aspect
31:19
of the internal auditory canal through this little triangle,
31:23
this little apex right here, this triangle is the entrance
31:27
for the superior vestibular nerve.
31:28
So this was a vestibular schwannoma rising from the
31:31
superior vestibular nerve.
31:33
And in this case we can see there's a little lesion right
31:36
here that's involving the cochlear nerve.
31:40
So notice how this lesion was involving posteriorly,
31:43
this one's anteriorly.
31:45
And because we're at the level of the cochlear nerve,
31:47
we can see the inferior vestibular nerve.
31:49
So the bottom line is is
31:51
that these schwannomas can involve any of these three nerves
31:55
that are associated with hearing
31:57
and also balance which nerve it most commonly arises
32:02
from is debatable.
32:04
A few years ago I was told it was a superior vestibular
32:07
nerve, but more recently when I reviewed the literature some
32:10
felt it was the inferior vestibular nerve.
32:12
So the bottom line, it's just kind of hard to see.
32:16
Now here's the classical example of a vestibular schwannoma.
32:20
So we can see this sausage shape structure
32:22
that's involved in the internal auditory canal.
32:25
In situations like this, you don't know
32:27
what nerve it's arising from,
32:29
but I do wanna make sure
32:31
that you don't confuse the appearance
32:34
of a vestibular schwannoma with the meningioma.
32:38
So we talked about a a meningioma earlier notice in this
32:41
case this is involving the left cerebellar pontine angle.
32:44
Notice this vestibular schwannoma is involving the IAC,
32:48
but this meningioma, it's also involving the IAC.
32:51
But notice how this has this broad attachment
32:54
with this diffuse enhancement.
32:56
So this is that classic dural tail
32:58
that in this case is involving the posterior aspect
33:02
of the petre pyramid
33:04
but is also extending into the internal auditory canal.
33:07
So instead of this enhancement being centrally like we see
33:10
in the vestibular schwannoma, notice
33:12
how this enhancement is extending along the dura along the
33:16
posterior aspect of the IAC.
33:18
So that's one way
33:19
that we can separate this meningioma from a vestibular
33:22
schwannoma when they're kind of small
33:25
and located in the same area.
33:28
There are other pathologies
33:30
that involve cerebella pontin angle.
33:32
Some of these sometimes we just can't tell.
33:35
This was an example of lymphoma.
33:38
This was an example of metastases
33:40
and this was an example of sarcoidosis.
33:43
So in a case of lymphoma,
33:45
typically the patients are gonna have
33:47
some systemic disorder.
33:48
Rarely does lymphoma initially present as an IAC mass.
33:53
I have seen a few of these.
33:55
Uh, but in general it's pretty rare.
33:57
This was an example of metastases
33:59
and again, in general, patients have metastases
34:02
elsewhere in the body.
34:03
The most common metastases
34:05
that I've seen involving in the IAC have tended
34:08
to be breast breast cancer.
34:09
That's probably the most common that I've seen.
34:12
And this is an example of sarcoidosis.
34:14
So when we look at sarcoidosis,
34:16
we can see this plaque like enhancement.
34:18
If we saw this alone,
34:20
then maybe we could think of meningioma.
34:23
But if you look real closely,
34:24
we can also see this peel involvement
34:27
and also a little bit of wrinkle involvement as well too.
34:30
So if you said metastasis on these
34:33
or lymphoma completely fine,
34:35
but in this case this was just an usual case of sarcoidosis.
34:40
So now what we're gonna do is we're gonna now talk about
34:44
more other things that are involving a different nerve in
34:47
the internal auditory canal.
34:50
And this is the facial nerve.
34:52
So when we look at the facial nerve, patients that have
34:56
abnormal enhance from the facial nerve present
34:57
with an acute facial palsy
34:59
and then resolved between six weeks
35:02
and three months, then we have to consider Bell's palsy.
35:06
And this was identified and described by Sir Charles Bell.
35:10
Now Sir Charles Bell did not actually describe
35:14
what we now attribute to his name.
35:17
I read Sir Charles Bell's article.
35:19
You know I'm a very boring person.
35:20
I'd like to read articles that are 300 years old.
35:22
That's how I get my jollies if you will.
35:25
And this was actually the original diagram from his paper
35:29
about 250 years ago.
35:31
So because of this beautiful description
35:34
of the facial nerve, I think they paid homage
35:38
to Sir Charles Bell and they named this palsy after him.
35:42
So Bell's palsy, again, acute onset of facial nerve palsy
35:47
that resolves somewhere between six weeks and three months.
35:52
When you do your imaging just right,
35:55
you can actually see the different segments
35:57
of the facial nerve.
35:59
So we, before
36:00
what we did is we talked about the cochlear nerve
36:02
and the superior and the vestibular nerve.
36:04
Now we're gonna focus our attention on the facial nerve.
36:08
So this portion of the facial nerve right here is in the
36:11
internal auditory canal.
36:12
So we call that the canicular segment
36:15
and that's what we see here.
36:17
Then what happens, we have this segment right here which
36:20
runs through the bone
36:22
and this is referred to as the labyrinthine segment.
36:26
Then the facial nerve does a 180 degree turn.
36:29
And this area right here is called the anterior genu.
36:34
If you look real closely, there's a ganglion right here.
36:37
This ganglion right here is the GIC lid ganglion
36:40
and there's a nerve right here,
36:43
which is the greater superficial petroleum nerve.
36:45
So if you understand the anatomy,
36:47
you can see the jid ganglion here
36:50
and then we can see the greater superficial petrosal nerve.
36:54
Well what ends up happening is
36:55
that the facial nerve curves back on itself
36:58
and now it runs in the middle ear cavity.
37:01
So this is the anterior portion of that middle ear portion.
37:05
And here's that posterior portion.
37:06
And this is what we see on Mr.
37:08
Notice, this linear enhancement.
37:11
And this is the atic segment of the facial nerve.
37:14
Well what ends up happening in the facial nerve is
37:17
that eventually it has to exit the skull base
37:20
through the stylo mastoid foramen
37:22
and then eventually it goes in the parotid gland.
37:25
So this redirection of the facial nerve is
37:28
what we call the descending portion or the posterior genu.
37:32
So this is our posterior genu.
37:34
And now what this yellow arrow shows
37:37
is the descending portion of the facial nerve.
37:40
So this was an example of Bell's palsy
37:43
and I use it just
37:44
to nicely illustrate I believe the difference segments
37:47
of the facial nerve.
37:50
Now this is another case of a patient
37:53
that has abnormal enhancement of the facial nerve.
37:56
Now this patient also developed a seventh nerve palsy.
38:00
And when we look here on the contrast enhanced T one
38:03
weighted image, we can see abnormal
38:05
enhancement involving the fundus.
38:07
We can see abnormal enhancement involved in
38:09
the geniculate ganglion.
38:10
Here's abnormal enhancement involved
38:12
in the tympanic segment.
38:14
In these situations,
38:16
oftentimes the facial nerve doesn't come back spontaneously,
38:20
it needs a little help.
38:22
And if you've looked at the patient's ears
38:25
and you saw these vesicles,
38:27
then I think you can make the proper diagnosis
38:30
of Ramsey hunt syndrome.
38:32
So Ramsey hunt sun hunt syndrome
38:35
is actually the herpes varicella zoster.
38:38
The the bell's palsy was failed to be due to simplex.
38:42
Ramsay hunt is due to vari cellar zoster.
38:44
And it's the way that I sort of think about it,
38:47
it's chickenpox of the ear
38:49
where you have the varicella zoster kind
38:52
of take home here in the geniculate ganglion,
38:55
then it's reactivated
38:57
and that's why you end up getting these rashes
39:00
or these little papules in the paricular area
39:03
and then you end up losing your facial nerve function
39:06
because of this involvement of the facial nerve.
39:08
And I think those of you that like music if you will,
39:12
or in pop culture, I think everyone knows
39:14
that it's well documented.
39:15
Justin Bieber, bless his heart,
39:17
ended up having Ramsay hunt syndrome.
39:19
I saw a picture of him recently
39:20
so I think he's doing just fine right now.
39:22
But if you wanna remember Ramsay Hunt,
39:24
just think of Justin Bieber.
39:27
So the differential diagnosis
39:29
for lesions involving the facial nerve are gonna be
39:32
schwannomas that arise the GIC ganglion, this was an example
39:36
of a venous malformation.
39:38
We used to call 'em he angios.
39:40
Now they're venous malformations.
39:42
This was an example of a neurofibroma in a patient
39:44
with NF type two.
39:46
And one thing in the back of your mind,
39:48
if you have a facial nerve that goes out acutely
39:51
and never comes back.
39:53
So it's not Bell's palsy, you always have
39:56
to worry about retrograde perdu spread from a tumor
39:59
involving the parotid gland.
40:01
So this was a patient that quote unquote had Bell's palsy.
40:03
He was being treated for bell's palsy, but lo
40:06
and behold, no one remembered to look at the parotid gland.
40:10
And when you did that, we saw this aggressive tumor.
40:13
This was adenoid cystic carcinoma.
40:15
It could not be palpated 'cause it was too deep
40:17
and this grew all the way up along the facial nerve.
40:20
So in the back of your mind, you always have to remember
40:23
to look at the parotid gland.
40:26
Well now we're gonna move to the lateral portion
40:28
of the temporal bone.
40:30
The most common tumor to involve the lateral temporal bone,
40:33
at least in my practice, is squamous cell carcinoma.
40:36
So squamous cell carcinomas involving the external
40:39
laboratory canal are by far
40:41
and away the most common malignancy
40:43
that I see involving the temporal bone.
40:46
There are other tumors that have a propensity
40:49
to involve the lateral temporal bone.
40:51
Metastatic renal cell carcinoma
40:53
for some reason has a propensity
40:55
to involve the posterior skull base
40:57
on the lateral skull base.
40:59
This was an example of the diffuse enhancement
41:02
and if you look real closely, we can see the flow voids
41:05
because we know renal cell carcinomas are hypervascular.
41:09
So if I see something like this in the posterior foss,
41:11
I think of renal cell.
41:13
And in a child, if you see something like this
41:16
that's very aggressive involving the temporal bone,
41:18
obviously we have to think
41:20
of something like langer health cells histiocytosis.
41:25
So those are the most common tumors to involve the temporal,
41:29
the lateral temporal bone.
41:30
And the fact of the matter is, is these are pretty rare,
41:33
but really from a practical standpoint,
41:36
if you're reading out routine brain imaging or head
41:39
and neck imaging or anything,
41:41
the most common thing you'll end up seeing is opacification
41:45
of the mastoid aero cell.
41:46
So I do wanna comment real briefly to make sure
41:50
that we understand what this is
41:53
and what is the differential diagnosis.
41:57
So when we see something like this, this is not mastoiditis,
42:00
this is just opacification of the mastoid aerosol.
42:03
So please don't call it mastoiditis if you just happen
42:07
to see this incidentally.
42:09
And the patient has no symptoms
42:11
because mastoiditis is a clinical diagnosis.
42:14
If the patient did have a fever and the surgeon looked in
42:18
or the pediatrician looked in
42:20
and saw bulging membrane with fluid in the middle ear cavity
42:23
and the patient with symptoms and
42:25
and this patient had symptoms,
42:27
then this would be otitis media.
42:30
Sometimes what happens is
42:31
that when we look in the temporal bone,
42:33
we see diffuse opacification of the mastoid air cells.
42:37
And notice how this labyrinthine bone is very, very thick.
42:41
This indicates chronicity
42:43
and this is indicative of a longstanding disorder
42:46
of eustachian tube dysfunction.
42:49
Remember eustachian tube allows aeration
42:52
of the mastoid air cells
42:53
and if the eustachian tube is clogged
42:56
or it's not working right,
42:57
the mastoid air cell can never fully become pneumatized.
43:01
And as a result you end up having this opacity
43:04
and you end up having thickening of the labyrinthine bone.
43:08
Now on the other hand, if the patient is symptomatic,
43:12
they have pain over the mastoid air cells,
43:14
they have a low grade fever.
43:16
And now you look at the mastoid air cell,
43:18
draw a line down the middle,
43:20
compare the left side to the right side.
43:22
Notice the thin labyrinthine bone here.
43:24
Here it's completely opacified.
43:26
And again, if you have a good eye,
43:28
you can see the labyrinthine bone are eroded.
43:31
This is an example of coalescent mastoiditis.
43:35
Now what I say is that the findings would be consistent
43:38
with the clinical diagnosis of coalescent mastoiditis.
43:41
Again, remember this is still a clinical diagnosis,
43:45
but your radiological findings are supportive of that.
43:49
Always remember when you see unilateral mucosal thickening
43:53
involving the mastoid air cells.
43:55
Remember our friend the eustachian tube.
43:57
When we look at the normal surface anatomy, here's the tus
44:00
of tabius, this is our fossa Rosen Mueller.
44:03
And the opening of these station tube is here.
44:06
Remember the T tube runs from the nasal pharynx
44:09
through the skull base to the middle air cavity.
44:12
So when I see unilateral mucosal thickening,
44:15
especially in adult, I always have
44:17
to look at the nasal pharynx to make sure
44:19
that I don't have a nasopharyngeal carcinoma.
44:22
That's occluding the eustachian tube.
44:25
This is an example of a ification involving
44:28
the mastoid air cells.
44:29
You can see the mastoid air cells are not developed.
44:32
This tells me that there's some chronic eustachian
44:34
tube dysfunction.
44:36
And then when I look at the EpiPen, I just see the head
44:40
of the mals, no short process of the incus.
44:42
So when I see a soft tissue mass
44:44
and I see absence of an ossicle,
44:46
then I can make the diagnosis of cholesteatoma.
44:50
And this was an example of a ification
44:52
of the mastoid air cell.
44:54
This patient actually had trauma.
44:56
And now what we do when we look at our ice cream cone,
44:59
we can see the ice cream cone is abnormal
45:02
and there's actually dislocation
45:03
between the malus and the Inca.
45:06
So this is uh, inchi, malleolar disassociation,
45:10
and this was due to a temporal bone trauma.
45:12
So these are all different etiologies
45:16
that can give you the opacification
45:18
of the mastoid air cells.
45:19
And again, something that we commonly see
45:22
when we're looking at brain.
45:23
Mr. Now for the neuroradiologist in the audience,
45:27
I did specifically want to talk about this disease entity
45:30
because in my experience this is probably one
45:33
of those entities that is often overlooked.
45:36
Sometimes we end up having opacification
45:39
and we just mention it and we don't do anything else.
45:42
One of the things we always have to look for is whether
45:46
or not is it possible that this opacification is due
45:49
to a cephas seal?
45:51
So when you are looking for an opacified mastoid air cell,
45:55
please take a look at the teman
45:57
because sometimes what ends up happening,
45:59
we end up having these teman defects,
46:02
you end up having an encephalocele
46:05
and as a result this CSF is the cause of the opacification
46:09
of the mastoid air cells.
46:11
It is important to mention this
46:13
because this was a case that initially was unbeknownst
46:16
to have encephalocele.
46:17
Here we can see the mastoid opacification, it's chronic,
46:22
we see the dehiscence in the teman
46:24
and the beta two transferrin was positive.
46:28
As a result, this patient was then treated
46:30
and was went to the ser, went to the or
46:33
and they put bone cement in in order to fix
46:36
that teman defect.
46:37
And I've seen numerous patients this kind
46:40
of bubble along over time.
46:41
They call it opacification,
46:43
but no one ever looked at the teman.
46:46
So if you see something like this, look at the teman
46:49
and then if you do see this absence,
46:51
also raise the possibility of intercranial hypertension
46:55
because when you have intercranial hypertension,
46:57
this can also result in this defect of the teman.
47:02
Now here's an example of a case
47:04
that's involving now the posterior
47:06
portion of the temporal bone.
47:08
This is an ant mini.
47:09
What we see here is an expanse lesion involving the
47:12
posterior aspect of the temporal bone.
47:14
When we see something like this with this type of bone
47:17
and its high signal on T one,
47:20
this is the pathognomonic features.
47:22
So this is arising from the region of the endo lymphatic sac
47:26
and this is the characteristic periods
47:28
of an endo lymphatic sac tumor.
47:30
So how do we make the diagnosis where you sort of look
47:33
for this bubbly lesion right here involving the posterior
47:37
cortex of the petre bone.
47:39
And on non-contrast T one weighted images, it is one
47:42
of the very rare tumors to have high T one signal.
47:46
When you look at the T two weighted images, you can see
47:49
that there's a lot of peripheral signal loss.
47:51
This is susceptibility arising from these lesions.
47:54
These lesions are very hypervascular
47:57
and that's why you end up having a lot of blood products
48:00
and this is what results in the susceptibility.
48:04
Well the last couple things that we're gonna talk about
48:06
and you know I'm gonna talk about it.
48:08
So this is the time to uh, address this one,
48:11
these particular diseases.
48:13
And what we see here is a mass
48:15
that's involved in the jugular frame
48:17
and that's densely enhancing
48:19
and that has multiple flow voids.
48:21
And when we do the bright blood technique, we can see
48:24
that this lesion is very, very bright.
48:27
This lesion is located at the jugular foramen
48:31
and this is the classical appearance
48:32
of a paraganglioma jugular.
48:34
And when we do a conventional angiogram,
48:37
we can see the hypervascular mask corresponding
48:40
to this lesion here in the jugular foramen.
48:43
Now here's an example of a mass
48:45
that's located in the middle ear cavity.
48:48
It's at the level of the cochlear promontory.
48:51
And on this coronal image,
48:52
what we see here is dense enhancement of this mass.
48:56
So if we see something
48:58
that looks like this a very well-defined lesion
49:01
that's hypervascular, the surgeons can actually look in
49:04
and see it, they see a hypervascular mass.
49:07
This is what we see behind the tympanic membrane.
49:10
While they can make the diagnosis
49:12
of a paraganglioma tympanum.
49:14
So if they make a diagnosis of paraganglioma tympanum,
49:18
oftentimes they can just go through an end oral approach
49:21
and just pluck this thing out.
49:24
Where we really make a difference
49:26
is in situations like this, here's an aggressive lesion
49:30
that we can easily see at radiology,
49:32
we can see the diffuse enhancement,
49:34
we can see the flow voids,
49:35
but when the surgeon looks in, what they end up seeing
49:39
is this little mass right here.
49:41
So when they look in here, they're gonna see the mass
49:44
and they see aha, I can just pluck this out like I can here.
49:48
But in actuality,
49:49
what this lesion is right here is the classic tip
49:53
of the iceberg because this is a paraganglioma
49:56
jugular panicum.
49:57
If they try to pluck this thing
49:59
through an end oral approach, they're gonna have a holy mess
50:02
because this thing is gonna bleed like stink.
50:05
So from our standpoint, every time
50:07
that I see a paraganglioma
50:10
to panicum something in the middle ear, I specifically look
50:13
to see if it's eroding the skull base.
50:15
And if it is, then the surgeons are either gonna have
50:18
to do a formal skull base resection
50:21
or these patients may be treated with uh, radiation therapy.
50:27
So this was the example of the paraganglioma jugular.
50:30
Again, I want to emphasize the fact
50:32
that this is diffusely enhancing
50:34
and it has multiple flow voids.
50:37
Paragangliomas are not the only lesion
50:40
to arise from the jugular foramen.
50:43
Here's an example of a mass
50:45
that's involving the jugular foramen.
50:47
We can see it's densely enhancing,
50:49
but notice there are no flow voids.
50:52
So the other common lesions
50:54
to arise from the jugular foramen are jugular schwannomas.
50:58
So here's an example of a jugular schwan.
51:00
Typically these lesions arise from
51:04
the vagus nerve, the 10th nerve.
51:07
And unlike jugular paraganglioma jugulars which have this
51:11
aggressive erosion which involve the cortex,
51:14
the jugular schwannomas tend
51:16
to expand the jugular foramen without the permi of extension
51:21
that we see here in the paraganglioma Juul.
51:24
So there are different ways to separate these two.
51:28
One is to look for the presence or absence of flow voids.
51:32
One another way is to do the gradient echo sequences,
51:35
the bright blood technique.
51:36
You're not gonna see this enhancement in the schwannomas
51:39
and the other ways to do the CT scan,
51:42
the paraganglioma jugular and the jugular
51:45
and panicum are gonna erode that cortex,
51:47
whereas the jugular schwannomas are going to expand it.
51:52
And one of the things the Fullers
51:53
that we can get into is you see something like this.
51:56
Now I don't see this confused as much,
51:58
but this is just an example of just a normal jugular bulb.
52:03
So sometimes what ends up happening is
52:05
that when you're looking at the brain Mrs,
52:07
you can see the swirled appearance.
52:09
You're like, my gosh, is that a paraganglioma jugular?
52:12
But when you look at it, you can see it's kind
52:14
of a world appearance
52:16
and if you're not sure you can just do a CT venogram.
52:19
Here we see just an asymmetrically enlarged jugular bulb.
52:22
We can see nice diffuse uh,
52:25
enhancement within the jugular bulb
52:27
and the transverse sinus.
52:28
So this is just a normal appearance of a jugular bulb.
52:32
So again, try not to confuse this with some
52:35
of the more ominous differentials.
52:38
Well, I'm gonna end up with a few mimics.
52:41
So one thing that I've realized over time is
52:44
that when you are looking at lesions involving the
52:47
cerebellar pontine angle,
52:49
just realize other intracranial lesions
52:52
and brain tumors that can sometimes mimic some of the things
52:56
that we saw before.
52:57
This is an example of a choroid plexus papilloma.
53:00
Now when I looked at this, you can easily make the diagnosis
53:03
of meningioma, but notice there's not
53:06
a broad-based attachment.
53:08
And this lesion extends medially into frame and liska.
53:12
And so this arose from the normal choroid plexus
53:16
within foramen Luka.
53:18
This was an example of appendamoma.
53:20
Remember appendamoma can extend out through foramen Luka.
53:24
And this was an example of an atypical
53:27
roid tumor in a child.
53:29
So this looks a little bit more interal.
53:31
I don't think we'd confuse this
53:32
for cerebella pontine angle lesion,
53:34
but just realize they can extend to that location.
53:38
This was an example of pilocytic astrocytoma.
53:41
When you first look at this, you're like,
53:42
is that a schwannoma?
53:44
'cause we just spent 50 minutes discussing CP angles.
53:47
But notice this is arising from the middle
53:49
cerebellar P dunkle.
53:51
This was an example of a medulloblastoma.
53:53
Typically they are now dividing this in some
53:56
of the molecular mesoblast stomas have a propensity
53:59
to rise in the middle, cerebellar p dunkle
54:01
and the cerebellar hemisphere.
54:03
And this was an example of heman glioblastoma.
54:06
So just realize on rare occasions you can have primary brain
54:11
tumors mimic or extend into the cerebellar pontine angle.
54:15
So part of our job is to make sure
54:17
that we can triage these patients appropriately.
54:21
And the last case I'll show is this.
54:23
I started off our discussion with lesions
54:27
that were involving the clus and involving the petrus apex.
54:30
So here's a lesion right here
54:32
that's located in the proximity of the Petro Clival fissure.
54:36
When you look at this, we see this lesion is
54:39
calcified right here.
54:41
You can argue whether there's a rings in circles.
54:43
You know, I don't think I've truly
54:45
ever seen a ring or circle.
54:46
So when I see something like this,
54:48
I'm really kind of suspicious.
54:50
So notice where the location is, notice
54:52
where there's a little bit of bone erosion.
54:55
And when we look at the mr instead of a lesion,
54:58
what we see here is diffuse enlargement
55:02
of this flow void in the internal, in the cavernous sinus.
55:06
And notice how this is laterally directed.
55:09
When we give gadolinium, we can see a little bit
55:11
of peripheral enhancement.
55:13
So I think we can all make the diagnosis of an aneurysm.
55:17
So when you are looking at the skull base
55:19
and you are in the petro clival fissure, remember
55:23
occasionally you can have aneurysms arising from the
55:26
internal and carotid artery that can become calcified.
55:29
And you do certainly do not want to, um,
55:31
confuse an aneurysm involving the ICA
55:35
with a lateral skull base tumor.
55:39
So in summary, what we've done over the last 50 minutes
55:42
or so is that we talked about lesions involving the lateral
55:46
and posterior skull base.
55:47
So remember we talked about our petris pyramid.
55:50
We started centrally, went to the petrich clival fissure,
55:54
then we went to the Petras apex.
55:57
We worked our way down to the cerebella pontine angle.
56:00
Remember the IAC, we opened the clamshell
56:03
and we talked about the four nerves of the IAC.
56:06
The we then went laterally to,
56:08
I involve those lesions involving the lateral skull base.
56:12
We talked a little bit about lesions involving the posterior
56:15
portion of the petre bone.
56:16
Remember that that was the endo lymphatic sac tumor.
56:19
And then finally we ended up with a discussion, uh,
56:22
involving the uh, paraganglioma.
56:25
So thank you very much for your attention.
56:28
Um, again, most of my talks are, are on um, modality,
56:32
but we do have this YouTube channel if you wanna see some
56:35
more head and neck talks.
56:36
It's no charge to do it.
56:37
Um, you know, I'm not smart enough to create an iPhone.
56:40
Uh, so my small contribution to radiology is
56:44
through my educational platforms
56:45
and that just happens to be one of them.
56:47
So Ashley, thank you very much for your attention
56:50
and um, happy to answer any questions.
56:53
Thank you so much yet again for that awesome lecture.
56:57
We are going to open the floor for questions
57:00
and those are being put in the q and a box.
57:04
Dr. McCorey, if you can open
57:05
that up on your zoom screen right now,
57:07
it should be at the bottom and we got quite a few in there
57:10
already as I expected.
57:15
Let me know if you can't find it.
57:17
I got it, I got it. Awesome. The QA
57:19
One? Yeah, let's start there.
57:21
Wanna to start at the top?
57:22
Okay, so the first question, um,
57:26
is from an anonymous attendee
57:28
and they say, please explain how
57:29
to diagnose cholesterol granuloma
57:32
if it doesn't show increased T one hyperintensity.
57:35
So I think that's a really, really great question.
57:37
And so the way that I address that is the follows is that
57:42
for me there's a, what I've noticed is that there's a bit
57:45
of a spectrum to this.
57:46
So you can have a normally aerated petris apex, um,
57:51
and then you can develop the mucosal thickening.
57:55
And then if that aeration
57:59
or the drainage pathways of the petrus apex become occluded,
58:03
then you can actually potentially develop a mucosal.
58:06
Now whether or not mucus seals go on
58:08
to cholesterol granulomas, I think is debatable.
58:11
So from my standpoint, um,
58:14
if I see a lesion evolving the petre apex
58:16
and it's expanding the petre apex on MR.
58:20
And ct, even though it doesn't have increased T one
58:23
hyperintensity, it's the morphology
58:26
which makes it more oval.
58:28
And also the expansion of the bone.
58:30
And again, realize the signal intensities can be variable
58:35
based on the protein content.
58:36
So I do look at the bone morphology and the expansion
58:40
and give that, um, equal, uh, emphasis, um, as uh, uh,
58:45
uh, as much as the signal does.
58:49
Uh, do you want me to just go ahead,
58:50
Ashley and Just read 'em out. Yeah,
58:52
Go for it.
58:53
Okay. So the next question was from Bahir Al.
58:58
I, uh, if you get a chance, put where you're from.
59:01
It's always fun to see, um, where people are from.
59:04
So it's, uh, um, so his question is
59:07
how do you differentiate a cranial nerve seven neurofibroma
59:10
from a schwannoma?
59:11
Another great question,
59:13
and the answer is, um, we don't know.
59:15
Um, I think as, as everyone knows, if you have a single
59:19
lesion involving a nerve, um,
59:23
you don't know whether it's a schwannoma or a neurofibroma.
59:26
In that particular case that I showed,
59:28
this patient did have no neurofibromatosis type one,
59:32
he had neurofibromas elsewhere.
59:34
So therefore we can assume the diagnosis of a neurofibroma.
59:38
But if we just saw an isolated lesion, then it's really hard
59:42
for us to differentiate the two.
59:45
Um, the next one is from Dr. Osman Gabo. Amazing lecture.
59:49
Thank you, um, very much for the kind comments.
59:52
Um, can you comment on how to approach a brain MRI
59:57
or CT scan from where to where
60:00
and which sequences do I start first?
60:02
So, yeah, I can do that. I think from a, a brain mr.
60:05
In fact, I was just reading out with my resident yesterday.
60:08
When I'm looking at a brain, Mr.
60:09
The way that I look at it is the first sequence I look at
60:12
is a Sagal T one weighted image.
60:14
And if I look at the Sagal T one weighted image
60:18
and in my macro, I always look at the midline structure.
60:21
So I look at the corpus callosum,
60:24
I always look at the pituitary gland,
60:25
I look at the pineal gland and I look at the key
60:27
and I look at the posterior faucet
60:29
to see if there are low line tonsils.
60:32
Then I look at the diffusion,
60:34
then I look at the gradient echo,
60:37
and then I look at the flare in T two sequences and the pre
60:40
and post contrast T one sequences.
60:42
So that's my pattern,
60:45
but I always start off
60:46
with the sagittal T one weighted images.
60:50
Um, so a high writing jugular bulb.
60:53
How did diagnose on CT and MR and the clinical significance?
60:57
Yeah, that's a good question too.
60:59
'cause it's a little bit debatable from you are,
61:02
you're gonna hear different people give
61:04
different opinions on this.
61:07
I was always trained
61:08
and I still feel that a high writing jugular bulb should
61:11
extend to about the level of the cochlea.
61:14
I always use the basal turn of the cochlea.
61:17
Um, some people will say it's the internal auditory canal.
61:21
Uh, I think either one of those is fine.
61:24
The only thing I would say is that based on the angle on
61:28
how you acquired your images, uh, you,
61:32
it can be confusing.
61:34
So I think depending on the plane,
61:36
because the plane can make a big difference
61:37
regarding exactly what level you are.
61:40
So for me, I tend to use the basal turn,
61:42
the cochlea maybe extending to the middle turn,
61:44
but some people will say the, the internal auditory canal.
61:48
So it just depends on what you feel most comfortable with.
61:51
In general, it's not, um, in general, it's not, um, uh,
61:56
that significant unless the bone is descent
62:00
and the patient has puls tinnius
62:02
and maybe when the surgeons look in, they see a bluish mass
62:07
and they're worried about some other, um,
62:10
etiology resulting in that.
62:14
Okay. Um, great. So here we have someone from Zahir Ghana.
62:18
It's, uh, Zahir, uh, Zahir. Uh, thank you very much.
62:22
Um, so
62:23
how do we differentiate jugular dehiscence from
62:25
paraganglioma with confidence?
62:27
Um, again, it's sort of what I said
62:29
that the jugular bulb tends to smoothly expand, excuse me,
62:33
a high writing jugular bulb tends to smoothly expand
62:36
the jugular bulb,
62:37
whereas the paragangliomas are more permeable
62:41
and have more aggressive erosion of the cortex.
62:44
So that's how I can differentiate one's more
62:47
of a smooth expansion while the other one is more
62:49
of a perve expansion.
62:53
Um, let's see, let's see.
62:54
Should we always mention that the patient has an enlarged
62:57
or high writing jugular bulb
62:58
or only in patients with clinical symptoms?
63:01
And so this is from an anonymous attendee in Romania.
63:04
I've never been to Romania before.
63:06
I'd like to maybe make it there one day.
63:08
Um, so, uh, for me, uh, I think, uh,
63:14
I always try to remember it.
63:15
Um, I think it's one of these things that if I don't,
63:18
let's say the patient's being done
63:20
for conductive hearing loss
63:22
or sensor nearing hearing loss, uh,
63:24
and I don't mention it i's probably not significant,
63:28
but, um, I always do try to look for it.
63:30
I try to do mention it if I do happen to see it.
63:34
So, um, yeah, I, i I do try to mention it.
63:38
Um, so this is from Usman again,
63:41
my last question, Bell's palsy.
63:43
Is contrast mandatory? Yes, uh, I think it is mandatory.
63:47
I think, um, all of your IAC studies should be
63:49
done with contrast.
63:50
And if you see asymmetrical enhancement of the facial nerve,
63:55
especially on the side of the symptoms, then
63:59
that is confirmatory, that there is something wrong
64:02
with the facial nerve.
64:04
We, by ourselves can cannot make a diagnosis
64:08
of Bell's palsy.
64:09
What we can say is that the nerve is enhancing,
64:13
and that could be consistent
64:16
with the potential clinical course of Bell's Palsy,
64:20
realizing if the Bell's palsy does not go away, then we have
64:24
to think of more, uh, ominous causes of facial nerve palsy.
64:30
And these include things like herpes zoster
64:32
and it could be retrograde perineural spread of tumor.
64:36
So, um, yes, contrast is think is always necessary.
64:40
Um, okay.
64:43
On a similar note, we often see discrepancy in the jugular
64:46
bulb volume between the right and left sides.
64:49
Is this automatically high riding?
64:52
Uh, this is, uh, from my young, from Florida.
64:55
Um, hello from the us.
64:56
Um, for me, uh, no, they're completely different
65:00
because you can have different sizes of the jugular bulb,
65:03
but high riding jugular bulb means the
65:04
dome is a little bit higher.
65:06
So, uh, asymmetric enlargement of the jugular bulb
65:10
or asymmetry in size is pretty common.
65:14
Uh, so I tend not to mention that The only time
65:17
where I will mention that is that I work with some
65:23
neurotologists that tend to do resurfacing
65:26
of the temporal bone.
65:28
So if someone comes in with pulsatile tinnitus
65:32
and on the symptomatic side I see enlargement
65:36
of the jugular bulb
65:38
and there happens to be erosion of the
65:43
cortex of the sigmoid plate,
65:46
or if there actually is, uh,
65:49
dehiscence into the middle ear
65:51
cavity, then I will mention it.
65:53
So that is asymmetrical enlargement.
65:56
High writing jugular bulb just means the height of the bulb.
65:59
So you can still have jugular bulbs that are the same size,
66:03
but one's a little bit higher.
66:05
So I, it's a very good questions, uh, a little bit more
66:08
of a nuanced answer, but, uh, I hope I, uh, answer
66:11
that appropriately and didn't confuse you.
66:15
Um, the next question is from thank you very much,
66:20
fantastic lecture, uh, with the diagnosis
66:22
of Bells or Ramsey Hunt.
66:24
I always struggle with facial nerve
66:26
enhancement in various segments.
66:28
Can you briefly summarize which segment enhancement
66:31
is absolutely pathologic?
66:33
The literature conflicts, you're exactly right.
66:36
Also, how do you handle cases
66:38
where there is some perineural fat
66:40
along the course of the nerve?
66:41
Distinguishing this from enhancement?
66:44
So that is, uh, incredibly great question.
66:47
Um, and what I can do is, uh, you know, I'm old enough to
66:51
to understand that what I say is not dogma, rather it's, uh,
66:56
an opinion that's been accrued over about 35 years
67:00
and also keeping up with the literature.
67:01
So I agree with you, I have seen this evolve over 30 years,
67:06
so I can tell you, I can give you my experience
67:10
and then you can do with it what you wish.
67:13
So initially, when the papers
67:18
that came out on facial nerve enhancement were first
67:21
written, they were done with thick sections.
67:25
They were done with contrast agents
67:28
that were relatively low, T one relax activity,
67:33
and the original papers were tended
67:35
to be done on lower field magnets.
67:37
So maybe 0.5 1.0, or maybe 1.5.
67:42
And because the lack of resolution, the most
67:47
common areas where people had the most confidence
67:51
to discuss facial nerve enhancement tended to be
67:56
the area of the anterior genu and the posterior genu
68:00
and the icic ganglion.
68:02
'cause those were easiest to see.
68:04
They're also a little bit more prominent
68:07
vascular plexus there.
68:09
Now what I see is that over time,
68:11
and again, those papers were written in the late 1990s.
68:14
Now we're in 2025, almost 2026.
68:18
The way that we image the facial nerve
68:20
has dramatically changed.
68:22
The field strength has gotten lar um, stronger.
68:26
The slice thickness has gotten thinner,
68:29
and the contrast agents have better T one relax,
68:32
which means when we give contrast,
68:34
we can see things better enhance.
68:37
So when I do a sequence,
68:40
especially if I do a 3D GRE, uh, uh, uh, T one, um, uh,
68:45
t one sequence a 3D acquisition,
68:47
I see the whole facial nerve enhance.
68:49
So what I actually look
68:51
for is asymmetrical enhancement on the side of the symptoms.
68:55
So for instance, if I'm doing an IEC study
68:58
and I'm looking for sensory nerve hearing loss,
69:00
and the patient has no facial nerve dysfunction, you know,
69:04
I often times see both facial nerves hands
69:06
and I don't, I don't mention it.
69:08
But on the other hand, if the patient does have a facial
69:11
nerve palsy and on
69:13
that side there is a facial nerve
69:16
enhancement, then I will mention it.
69:18
So for me it's variable.
69:20
But if you do your imaging studies just right
69:23
with thin section imaging at higher field strengths
69:26
with a good, uh, contrast agent, for me,
69:29
I can see the whole facial nerve normally enhance.
69:34
Um, let's see.
69:36
Can you talk about neurovascular conflicts at the brainstem
69:39
and the posterior fossa?
69:41
Uh, sure. So, um, as I showed in that, uh, anatomic
69:46
slide in the cerebella pontine angle, there are lots
69:51
of vessels in the cerebella pontine angle.
69:53
There's typically aika, there are multiple veins.
69:57
Um, and so the rule of thumb that we
70:02
tend to, um, all agree on is that
70:06
we all see neurovascular
70:08
conflicts routinely on I-A-C-M-R-I scans.
70:12
We tend not to comment on those in those patients
70:15
that are asymptomatic.
70:17
And you may think that's cheating a little bit.
70:19
But the fact of the matter is, is that the people
70:21
that were referred these to us,
70:23
they really don't know wanna know about neurovascular
70:26
conflicts in patients that have a sensory or hearing loss.
70:29
They just don't care. But on the other hand,
70:31
if a patient does have glossopharyngeal neuralgia
70:36
or they have trigeminal neuralgia, then
70:39
specifically the surgeons are looking for a way to alleviate
70:43
the pain in those patients.
70:46
So in those particular cases, that's when we always look for
70:51
the neurovascular enhancement involving cranial nerve nine
70:55
or cranial nerve five.
70:57
Now, I'm sure someone is probably thinking about, well,
71:00
what about if the AI A
71:02
extends into the internal auditory canal?
71:05
If the AI C extends into the IAC in a patient
71:09
with pulsatile tin tinnitus
71:11
or hearing losses, that's significant.
71:13
And the answer is no.
71:15
I think there may have been one case
71:17
where I thought the a AI CICA was
71:20
actually causing pulse ATUs 'cause it was so big
71:23
and it was extending into the internal auditor canal.
71:26
I was actually lecturing at a skull base conference
71:28
and I showed my skull base surgeons this
71:30
and they said I wouldn't do anything about it
71:33
'cause I wouldn't even know how to get it out.
71:34
So that was the only time I'd actually seen it.
71:37
So the bottom line is, is that we don't really comment on it
71:41
unless the patient's symptomatic knowing full where Well,
71:44
that yeah, we see it fairly commonly.
71:48
Um, let's see. Thank you.
71:52
Um, I see these asymmetrical dimensions
71:56
and routine imaging without any history or context.
72:00
I'm an oral maxillofacial, uh, radiologist on cone beam ct.
72:04
Um, let's see, I'm not sure what you mean
72:06
by asymmetrical di dimensions.
72:08
I don't know if you mean by size
72:11
or, uh, so I don't know how to answer that question.
72:15
So I, I, I, I apologies, uh, apologies for that.
72:20
Um, let's see. Huh?
72:24
Can you explain crocodile tear syndrome? No, I don't.
72:27
I've never heard of that, but you know what,
72:28
that's why I like giving these talks
72:30
and these q and a sessions.
72:32
Um, so I'm gonna look up Crocodile Tears syndrome.
72:35
I know what Crocodile Tears are.
72:37
I don't, Ashley, do you know what crocodile tears are?
72:40
I don't know what Crocodile Tears syndrome is,
72:42
but, uh, I think, have you heard of Crocodile Tears,
72:44
Ashley? I've
72:45
Heard of Crocodile Tears, but not the syndrome.
72:50
All right. Um, the, uh, next one is how do, how does,
72:55
how do you approach the management of syn sneaky eye on Mr
72:59
after resolution of, of sagittal sinus thrombosis?
73:03
Um, I'm not sure what you mean by Signa.
73:06
I don't know if you mean fibrosis or not.
73:09
Um, to be honest with you, I don't know
73:11
how to answer that question.
73:13
I think if someone had superior sagittal sinus thrombosis
73:16
and you have a little bit leftover linear areas
73:19
and you still have flow in the sinus, um,
73:22
I don't think I would worry about that very much.
73:24
I would assume that the only way to resolve those is
73:27
through some type of endovascular procedure.
73:31
Uh, so I would have to defer that to the, uh, the, uh,
73:35
endovascular neuroradiologist.
73:38
Um, let's see. I mean, the jugular bulb,
73:40
asymmetrical volume.
73:42
Oh, um, yeah, if a patient's asymptomatic,
73:46
I probably, uh, I see what you're saying.
73:48
So you're doing a cone beam ct,
73:50
and then when you're doing a cone beam CT on the axial
73:53
images, sometime you'll see the jug or bulb.
73:56
So, um, my answer to you is, um, I have the privilege
74:01
of having a faculty appointment in the Texas a
74:05
and m Department of Oral Maxillofacial Radiology.
74:09
So, um, I do work very closely
74:11
with a incredibly talented group
74:13
of oral maxillofacial radiologists.
74:15
Um, so I am familiar with that.
74:18
The, uh, we just tend not to mention it,
74:20
if the patient's asymptomatic,
74:22
oftentimes these cone beam cts are being done
74:24
for completely unrelated etiologies.
74:27
I think the one thing where when I give them a curriculum
74:31
of lectures, uh, once a month, um, three
74:35
or four of those are on sinus imaging.
74:37
The one issue that does come up is
74:39
what if we see increased soft tissue involving the, uh,
74:42
nasal pharynx of the oral pharynx?
74:44
You know, that's something that I would mention
74:46
and that you should mention, especially if you see a lot
74:49
of soft tissue thickening in the
74:50
nasopharynx in a 60-year-old.
74:53
Um, and that I would mention,
74:54
but as far as, uh, looking
74:56
for asymmetry in the jugular bulbs
74:59
in which there's no bone erosion and
75:01
otherwise asymptomatic patient, um,
75:04
I don't think I would mention those is, uh, oh, here we go.
75:09
Crocodile tear syndrome
75:10
or gustatory ization is a rare disorder
75:12
where a person involuntary shed tears from one eye while
75:15
eating, chewing, or smelling food.
75:17
It's caused by misdirection
75:19
of regenerating facial nerve fibers, often
75:21
after an injury like Bell's Palsy, which causes these fibers
75:25
to stimulate the lacrimal gland instead
75:28
of the salivary gland.
75:29
Oh, that's terrific. So, yeah, thanks for doing that.
75:31
I haven't seen it. Um,
75:33
I don't know if we can really image it or not.
75:35
Um, but having said that, uh, every, um,
75:38
in about the reason I have
75:39
to leave at 1230 max is I'm gonna,
75:41
I usually see patients every Wednesday afternoon,
75:44
and today is my head and neck clinic day.
75:46
So I'm gonna ask our ENT surgeons
75:50
about crocodile tear syndrome
75:52
so I can get a better understanding.
75:53
So thanks for, uh, teaching me something new today.
75:56
I I appreciate that.
76:00
Um, let's see.
76:03
Thank you very much. Oh, go ahead, Ashley. Yeah,
76:05
There's a couple, if you scroll up on the q and a.
76:08
Yeah, there you go. You found it.
76:10
Uh, let's see, which one,
76:11
um, let's see.
76:17
Okay, did I find them there?
76:18
Um, neurovascular brain here.
76:23
Read me out a question. Can oh, can Omas coexist with other,
76:27
uh, so yeah, this is from Dan Philippe from the Philippines.
76:31
Um, yeah, that's another place I'd like to go.
76:33
I've never been in Manila, so
76:35
that would be kind of fun to go to.
76:36
Um, yes, a hundred percent koma can coexist
76:41
with granulation tissue.
76:43
Uh, and so really the only way to separate those two out,
76:47
uh, is probably with non EPI diffusion imaging
76:51
for me on CT scan.
76:53
If I see a focal mass with bone erosion, then I can say
76:58
that's likely due by cholesteatoma.
77:01
But yes, cholesteatoma
77:03
and granulation tissue can co insist.
77:06
It can be difficult to differentiate between the two.
77:10
But, uh, the only way that we can make the diagnosis
77:12
of OMA is look for, um, a erosion.
77:18
Um, yes.
77:20
Do you, do you do MR profusion routinely for
77:23
suspected intra AAL tumors extending into the skull base?
77:28
So not intra axial tumors.
77:31
We do use perfusion imaging,
77:33
but it's not the quantitative imaging
77:36
that you'll probably hear about when you go to meetings.
77:40
Um, years ago there was a paper written,
77:42
and I still quote it 'cause I thought it was a great paper.
77:45
Um, it was in the a g
77:47
and R, it was written by, um, uh, VJ Rao
77:50
and, um, oh, uh, uh, blanking on his name.
77:55
I'm having a senior moment.
77:56
But basically it was a qualitative imaging
77:59
where they did dynamic gradient echo sequences.
78:01
So it's not quantitative, but it's qualitative.
78:05
And I found that sequence to be terrific.
78:07
So I do do profusion, but it's qua, it's qualitative
78:12
and not the standard.
78:14
Um, um, profusion sequences that you,
78:17
that you oftentimes seen done, um, for, uh, brain imaging,
78:24
uh, let's see, from Indiana, oh, hey, Neil.
78:28
I know Neil. He was at our meeting a couple weeks ago.
78:30
Good to hear from you. Um, to be more general
78:34
with unilateral enhancement of both the seventh
78:36
and eighth nerves when the IAC without nodularity
78:39
be more secondary to infection or perineural spread?
78:42
That's a great question. I think, um, for,
78:45
for unilateral enhancement of the seventh
78:47
and eighth nerve in a patient
78:48
that's symptomatic without nodularity,
78:50
I think it's probably due to infection.
78:53
So typically we'll see this,
78:55
and in symptomatic patients, we just kind
78:57
of say it's probably due to some viral etiology.
78:59
Um, but on the other hand, if I showed those cases
79:02
that had more diffuse enhancement
79:04
and more nodularity, uh, then I would think of more
79:07
of a neoplastic process.
79:08
So I, I agree with you. Uh, thank you very much.
79:13
Um, thank you Ariana. I appreciate it.
79:19
Okay. Um, great. All right.
79:24
I don't see any more questions coming up on the q am I
79:26
missing 'em on the q on the q and a
79:28
or did we answer 'em all?
79:29
Ashley, I didn't look at the, I think we got
79:32
'em all. Yeah, there's a,
79:33
let me see if there's any in the
79:35
Chair. Oh, oh, here's
79:36
one. That's, what is the best modality
79:37
to diagnose Paraganglioma?
79:40
Um, of the middle ear? Of the middle ear.
79:42
So if we're looking at Paraganglioma temp panicum, um,
79:47
I think CT is usually fine.
79:49
Um, again, you can do mr,
79:52
and if you have a really good MR system
79:53
and you have a really good quality, um, study,
79:57
I think it's great.
79:59
But for, um, for middle ear paragangliomas,
80:03
specifically para gang, uh, Tim Panicum, that I think, um,
80:08
a ct, uh, non-con, non-contrast CT is fine.
80:13
Okay. Anything in the chat?
80:20
Okay. Um, um,
80:23
There's something here.
80:25
Um, uh, thank you Laslo. Great to see you. Uh, let's see.
80:30
Um, how would a meningioma with malignant trans, uh, yeah,
80:33
that's an interesting question.
80:35
Um, so this is from Wilham four E.
80:38
He asked how would a meningioma
80:39
with malignant transformation present?
80:42
Um, yeah. So basically when we talk about meningiomas,
80:46
I don't know if there's actual malignant transfer
80:48
transformation, but there are invasive meningiomas.
80:51
Um, they typically present with, um, you know,
80:55
more symptoms with more headaches.
80:57
And then when we look at the mr, uh,
80:59
oftentimes they have a lot of vasogenic edema.
81:02
Now, having said that, um,
81:05
if you have a meningioma in a younger patient,
81:08
that's pretty big, you can develop vasogenic edema
81:11
just from mass effect.
81:13
But if you have an older patient that have a meningioma
81:15
that has a lot of vasogenic edema, sometimes
81:18
that's due to peel invasion.
81:20
So the presence of edema from a meningioma in a younger
81:23
patient is not necessarily definitive for
81:27
an invasive meningioma.
81:29
But on the other hand, if it's an older patient
81:31
that I do see edema, uh, in irregular margins,
81:34
then I really do start worrying about, uh,
81:36
an invasive type of meningioma.
81:42
Oh, good. We have one of our, um,
81:44
maxillofacial resins here too.
81:46
Uh, let's see. Um,
81:52
I think the questions are getting thinner now.
81:55
Um, so are you following a AI models
81:58
for their effectiveness in this area?
82:01
Uh, not really.
82:03
You know, I think AI right now in the head
82:05
and neck is, um, still has a way to go.
82:08
It's, it's the old jokes, it's five years away,
82:10
it may always be five years away.
82:12
Uh, so I'm not really following much specifically
82:16
that are focused on head and neck.
82:17
What I do think is interesting is that,
82:19
and I've had some experience with this, when I do a neck ct,
82:22
um, neck CT sometimes catches part of the brain based on,
82:27
we have about 19 different AI algorithms that I use
82:30
between my two practices.
82:32
We are sending the head
82:33
and neck cts, um, to be screened with an AI algorithm
82:37
for brain aneurysms.
82:39
And I had a case of a, of a patient that had a, uh,
82:44
malignant parotid neoplasm that was resected.
82:47
And I did a great job describing the flap
82:51
and the surgical clips and the neck dissections.
82:54
And then lo and behold, about a week later I get this call
82:57
and saying, oh yeah, that one patient
82:59
where they just got the most inferior portion
83:01
of the brain had about a two millimeter, uh, aneurysm.
83:04
So I think, I think, um, there are benefits in head
83:08
and neck for, uh, for uh, ai.
83:12
Um, it may not be really focused on head and neck,
83:14
but I think certainly anything
83:16
that is gonna help me better screen for pulmonary nodules
83:19
or intracranial aneurysms in areas that are oftentimes, um,
83:25
blind spots because we're sort of focused on this area here,
83:29
I think it's really, really beneficial.
83:30
So that's where I see a lot of benefit when it comes to, um,
83:34
assistive slash pixel based m uh, ai.
83:38
Um, do you think three T
83:40
or 1.5 T is better for head and neck tumors?
83:43
Um, I think either is fine.
83:46
I think three T has more artifact.
83:48
Um, I think if you have a good coil you can use three T.
83:52
But you know, if, if I had a hundred different patients
83:55
that when three T or 1.5 T, my sense is, is that
83:59
overall the image quality is gonna be better at
84:02
1.5 T versus three T.
84:03
But again, it really depends on your, the texts, um,
84:07
the software, the coils, um, how comfortable you are
84:10
with your protocols.
84:12
To me, shorter protocols are better than longer protocols.
84:14
The longer my protocols are, the more patients move
84:17
and that degrades the image quality.
84:21
Um, hey Kermit, um, would routine, uh,
84:25
would routine head cts be sensitive to,
84:29
uh, teman defects?
84:30
And should we raise the suspicion where there's dehiscence?
84:33
That's a good question. So, no,
84:35
I don't think routine head cts are good enough
84:38
to look for dehiscence.
84:40
Um, I would say this is that if you do have a patient
84:42
that has unilateral opacification of the mastoid air cells
84:46
and they do talk about re um, then
84:50
in those patients I would, I always recommend testing
84:52
for beta two transfer
84:54
and then recommending a temporal bone ct, um, as indicated.
85:02
Um, yeah, so this one, the petris apex meningioma
85:05
with os osteo involvement looked like a
85:07
endo lymphatic sac tumor.
85:09
Actually, they're, they are different.
85:10
They're completely different.
85:11
So, um, I know we're running outta time right now.
85:14
What I would suggest, I'm gonna say this at the, at the risk
85:16
of being self-promotional,
85:18
we wrote the largest series on endo lymphatic sac tumors
85:21
about 20 years ago, 25 years ago.
85:24
So what I would suggest doing is, uh, uh, looking
85:28
for a paper that I wrote.
85:30
I hate to say that 'cause it's kind of, again, kind
85:32
of sounds goofy, but, um, we did have about th 25
85:36
to 30 cases of endo lymphatic sac tumor.
85:38
We showed the classical appearance
85:40
of endo lymphatic sac tumors.
85:42
So it's, you can, it's not digitized, you'd probably have
85:45
to, they, it is available on the internet.
85:47
It's a kind of a PDFed copy,
85:49
but that does show the appearance.
85:51
So the meningioma case I showed that was in the petris apex,
85:54
that was in the anterior petre apex.
85:57
The end lymphatic sac tumors were on the posterior
85:59
margin of the petre apex.
86:01
So they are um, different in appearance.
86:05
Um, so this is a good question.
86:09
Do you, if you find something suspicious for ecor doses,
86:13
saliro on cone beam ct,
86:15
what would be a good imaging identifier?
86:18
Um, so that's a really good case.
86:19
That's a great question
86:20
because there is a growing body suggesting
86:24
that histologically acidosis, saliro
86:29
is histologically the same as an early chordoma.
86:33
So actually they're the same.
86:35
And it's unclear whether
86:36
or not what we refer to as echo doses saliro,
86:39
which is actually not horal remnant will eventually go on
86:43
to progress to a chordoma.
86:46
So historically if you do pick up an uh,
86:50
ecor doses fiery, just kinda leave it.
86:53
But um, my own opinion is that given
86:55
that the histology is similar
86:57
and these paper just came out about three, four years ago,
87:00
um, I would recommend a follow up, uh, like every year just
87:04
to make sure it doesn't enlarge.
87:05
Because if it doesn't enlarge, um, then you could be dealing
87:09
with an early um, chord.
87:11
So for me, if you pick it up on a cone beam ct,
87:14
I'd probably recommend getting a follow up in about a year,
87:17
uh, just to make sure that it's stable.
87:23
I think you got through them all
87:24
and just in the nick of time.
87:27
Okay. Thank you so much for that lecture
87:30
and for hanging out for a little bit longer
87:32
to answer some questions.
87:35
No problem. I got a thanks for having me.
87:37
I'm glad got got, um, chance I got to use my new Zoom studio
87:42
with the new microphone and the lights.
87:43
So hopefully everyone heard me, Ashley,
87:45
and hopefully the lighting was good this time.
87:48
It was great. Everyone heard you loud and clear.
87:50
Thank you so much. Thanks for everyone else
87:53
for participating in our no conference reminder.
87:55
You'll get a link to this replay later today.
87:59
Be sure to join us next week on Thursday,
88:00
December 4th at 12:00 PM Eastern, where Dr.
88:04
Bernardo Tessa will deliver a lecture entitled Intercranial
88:08
Hemorrhage on CT and MRI.
88:10
You can register for that@modality.com
88:12
and follow us on social media for future noon conferences.
88:15
Thanks again and have a great day.
Suresh K Mukherji, MD, FACR, MBA
Clinical Professor, University of Illinois & Rutgers University. Faculty, Michigan State University. Director Head & Neck Radiology, ProScan Imaging
© 2026 Medality. All Rights Reserved.
