Interactive Transcript
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Hello, and welcome to Case Crunch Rapid Case
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Review for the Core Exam, hosted by Medality.
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In this rapid-fire format, faculty will
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show key images, and you'll respond with your
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best choice via the live polling feature.
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After a quick answer explanation,
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it's on to the next case.
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You'll be able to access the recording
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of today's case review and previous
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case reviews by creating a free account.
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Questions will be covered at the end if time allows.
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Please remember to use the Q&A feature
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to submit your questions so we can get
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to as many as we can before time is up.
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Without further ado, please enjoy this case review.
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Thank you very much.
0:37
Well, my goal today is to get through a lot of cases,
0:41
as many cases as possible, and poll the audience for
0:45
their answers and make it interactive and fun if we can.
0:49
So, we're going to take off here with spine case review.
0:52
These are all new cases that I just loaded up
0:55
recently, and they are in addition to the 100 spine
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case review cases that will be available for board
1:02
review. So, let's dive right in and see what we've got.
1:06
All right, here is case number 101.
1:07
Again, the first 100 are
1:09
going to be offered through MRI Online.
1:11
Um, I'm letting you see a T2-weighted image,
1:15
a post-gadolinium-enhanced axial scan,
1:19
and then a sagittal T2 STIR image—Case 101.
1:26
And, uh, I'm going to start the polling.
1:30
So what do you think is the
1:31
best diagnosis for this case?
1:33
Is this a Pancoast tumor, a neurofibroma,
1:38
a schwannoma, a lymph node, or a synovial cell sarcoma?
1:43
So those are your choices, one through five.
1:46
Number one, Pancoast tumor.
1:47
Number two, neurofibroma.
1:49
Number three, schwannoma.
1:51
Number four, lymph node,
1:54
and number five, synovial cell sarcoma.
1:58
So we've, uh—once I hit a hundred,
2:00
uh, answers, I'll, uh, stop the polling
2:03
so you can see what people have said.
2:05
So you gotta be fast
2:08
in your answering.
2:09
Uh, the majority of people put in choice
2:12
number three, but the correct answer
2:15
was—by 39 people—answer number two.
2:19
So this is an example of a patient who had a
2:23
neurofibroma, and you should know that this is a
2:26
lesion that is associated with the brachial plexus.
2:28
This is the anterior scalene muscle,
2:31
anterior to the lesion, posterior
2:33
middle scalene muscle behind it.
2:35
And within brachial plexus lesions,
2:38
neurofibromas outnumber schwannomas.
2:41
Most of the time, schwannomas are
2:43
much more common than neurofibromas.
2:45
And this does have what we call the
2:48
target sign—lower signal intensity
2:50
centrally, with a periphery that is brighter.
4:11
get ready to relaunch my poll.
4:14
So here we have a T1-weighted, T2-weighted,
4:17
post-gadolinium-enhanced T1-weighted, and
4:20
axial. This is actually a T2-weighted
4:22
image looking at the lesion at L4-5.
4:26
So, case 102, what do you think this is going to be?
4:29
What's the best diagnosis here?
4:31
Is this a protrusion, an extrusion, a sequestrated disk,
4:37
an epidural hematoma, or does this represent lymphoma?
4:42
So go ahead and start answering the questions.
4:44
Would you say that this is most likely a
4:46
protrusion, extrusion, sequestration, sequestrated
4:50
disk, epidural hematoma, or number five, lymphoma?
4:55
So we're polling for those
4:58
options behind the L5 vertebra.
5:02
So, we've got our 100 answers, and the
5:04
most common answer is sequestrated disk.
5:08
And that is indeed the correct answer. By
5:12
virtue of this lesion—this piece of disk no
5:17
longer communicating with the parent disk.
5:19
And that's probably most obvious on the post-GAD scan.
5:23
Sequestrated disks—these disk fragments often
5:25
have a little bit of a peripheral enhancement.
5:28
And you can see that that peripheral
5:29
enhancement separates it from the parent
5:31
disk, identifying this as a sequestration.
5:35
So, in the North American Spine Society, American
5:38
Society of Neuroradiology, and American Society of
5:40
Spine Radiology, we have agreed to the nomenclature
5:43
of protrusion for that lesion that has a wider
5:46
base than its peripheral portion, the extrusion,
5:49
which kind of looks like the mushroom cloud with a
5:52
narrow base and a more wide peripheral portion,
5:56
and then a specific type of extrusion where the disk
5:59
is no longer communicating with the parent disk.
6:02
And that is the sequestration or sequestrated disk.
6:05
The importance of this is that if you were to
6:07
consider chemonucleolysis to dissolve the
6:11
disk, that would not work with a sequestrated
6:14
disk because it no longer communicates with
6:16
the disk at the, in this case, the L4-5 level.
6:20
So the correct answer here: sequestrated disk.
6:23
Let's move on to case 103.
6:25
Oh, I forgot to share the results.
6:27
Um, stop sharing.
6:29
Let's relaunch.
6:31
Okay.
6:32
Case 103.
6:34
We have the CT scan and the MR scan.
6:36
This is a STIR image, and this is a
6:38
post-gadolinium T1-weighted image.
6:41
Case 103.
6:44
The question here is: the patient has prostate cancer.
6:47
What's the most likely diagnosis of this lesion?
6:51
Is it myeloma?
6:53
Is it a metastasis from a second primary?
6:58
Is it more likely to be a chordoma?
7:01
A giant cell tumor? Or is this a prostate metastasis?
7:05
Again, our choices in a patient who has prostate
7:07
cancer: is this going to be more likely myeloma,
7:11
a second primary (not prostate metastasis),
7:15
chordoma, giant cell tumor, or prostate metastasis?
7:21
So the audience is feverishly putting in answers.
7:25
We'll end the poll, and this time
7:27
I actually will share the results with you.
7:28
It's kind of split here, and appropriately so,
7:32
but the most frequent answer was choice number
7:35
five, which is actually the correct answer.
7:38
And this was biopsy-proven prostate cancer.
7:42
Why is this a difficult case?
9:20
So, axial, sagittal, and the coronal reconstruction.
9:28
So, what is the best diagnosis for this lesion?
9:30
Would you call this a hemangioma?
9:33
A giant cell tumor?
9:35
A chondroid neoplasm?
9:38
Is this just DJD, degenerative disease-related
9:44
to the ligamentum flavum, or none of the above?
9:50
So, our choices here are: number one, hemangioma,
9:54
two, giant cell tumor, three, chondroid
9:57
neoplasm, four, DJD, or none of the above.
10:03
So, our, um, poll is, we hit our hundred
10:08
people.
10:09
And, um, number three, which is chondroid
10:14
neoplasm, was the most common, uh, answer.
10:19
Uh, this turned out to be biopsy-proven hemangioma.
10:22
So, uh, only 16% of you got that one right.
10:26
But why is it a hemangioma?
10:28
This, this bubbly bone lesion could
10:31
be from, uh, a number of these
10:33
options.
10:34
The hemangioma—it's much more well-defined and benign.
10:39
If we had done a T1-weighted scan, I think we would
10:42
have settled this as bright on a T1-weighted image.
10:47
So, the correct answer here was indeed a
10:49
hemangioma, a very common spinal lesion.
10:54
But let me ask the follow-up question.
10:56
So, I'm going to stop sharing.
11:00
Okay.
11:03
So, at the boards, the majority of the cases will
11:07
just be cases on imaging and then diagnosis.
11:08
There are follow-up questions
11:10
on a minority of the cases.
11:12
So, with regard to the term hemangioma,
11:15
is that the right term for this
11:18
lesion?
11:19
Yes, it's a spinal hemangioma.
11:21
No, we should be using the term cavernous malformation.
11:24
No, we should be using the term
11:25
venous vascular malformation.
11:27
No, we should be using the term
11:29
venolymphatic malformation, or no,
11:31
we should be using the term varix.
11:33
Is hemangioma the correct term
11:37
for this lesion?
11:39
This is the terminology of the case.
11:43
So, um, we've hit our hundred. Let's share results.
11:46
So, choice number three—it's actually true.
11:49
You know, we all use the term hemangioma of
11:53
the spine, but we should know that this is
11:56
not in our, you know, uh, classification.
12:00
It is not a neoplasm.
12:02
And, you know, the hemangiomas
12:06
with the Mulliken classification
12:08
are supposed to be GLUT-1 positive.
12:11
These lesions are not GLUT-1 positive, and they're
12:13
not related to infantile hemangiomas, for example.
12:17
These are capillary or venous vascular malformations, they're not
12:24
truly neoplasms, despite the fact that they're usually
12:27
classified as such, and we use the term hemangioma.
12:31
So there has been a movement to change our
12:34
terminology on these lesions, but the common
12:37
vernacular is just to call them hemangiomas.
12:39
And as you probably know, one of the
12:41
differential diagnoses often is, um, just fatty
12:46
infiltration of the vertebral body.
12:49
And, you know, when you see enhancement on a post-GAD
12:54
FatSat scan, it kind of cinches the diagnosis of a
12:58
venous vascular malformation, a.k.a. hemangioma of bone.
13:05
All right.
13:06
Did I share?
13:07
Okay.
13:07
Stop sharing.
13:10
All right, we're moving on to Case 105.
13:12
Let me relaunch the poll.
13:15
Okay, Case 105.
13:16
So, we're looking in the cervical spine.
13:18
I've got a T1 post-GAD.
13:20
This is the same as the T1 post-GAD.
13:22
I just magnified it for you.
13:26
And let's see what the question is.
13:29
All right.
13:29
This patient has prostate cancer.
13:32
What's the best diagnosis in this
13:34
patient with prostate cancer?
13:35
Is this a prostate metastasis?
13:37
Is this a hemangioblastoma?
13:39
Is it an ependymoma?
13:40
Is it an astrocytoma?
13:42
Or most likely a multiple sclerosis plaque?
13:45
So, which do you think is, um, in this patient who has
13:48
prostate cancer, what's the most likely diagnosis?
13:52
Prostate metastasis, hemangioblastoma,
13:55
ependymoma, astrocytoma, or an MS plaque.
14:02
All right.
14:02
We've got 333 participants, and we're
14:07
doing pretty well with getting over
14:09
a hundred, uh, results and choice
14:12
mumber three was ependymoma,
14:14
and that is
14:15
reasonable, but incorrect.
14:19
So, this is, in fact, a hemangioblastoma.
14:23
And why is it a hemangioblastoma
14:26
rather than an ependymoma?
14:28
I have to say that it certainly looks
14:30
like it's a cyst with a nodule here.
14:32
If we go back to the previous
14:34
and look at the magnified view here,
14:36
you have the cystic portion as
14:38
well as the nodular portion.
14:40
When it's this small—cyst and nodule—I'm
14:43
much more likely to call this a hemangioblastoma.
14:47
When it's a larger lesion, more extensive,
14:50
with a larger area of enhancement, then I would
14:54
be more likely to call it an ependymoma.
14:56
So, if it's under one vertebral body segment,
14:59
I think you should really go with hemangioblastoma,
15:02
even though it is true that hemangioblastomas
15:05
are less common lesions than ependymomas.
15:09
Um, and astrocytomas also can have solid enhancement.
15:13
We just don't look for it to be quite as small and
15:15
quite as well-defined as with hemangioblastoma and,
15:20
uh, the occasional ependymoma.
15:22
So, which of these five items—
15:27
well, let me stop sharing here.
15:32
Which of these five items does
15:36
not fit with the other ones?
15:38
Okay.
15:38
One of these doesn't fit with the others.
15:42
Is that hemangioblastoma,
15:45
renal cell carcinoma, pancreatic cysts,
15:49
endolymphatic sac tumors, or adenoma sebaceum?
15:54
Which one of these doesn't fit with the other
16:00
um, items?
16:02
So, um, hemangioblastoma, renal cell
16:05
carcinoma, pancreatic cysts, endolymphatic
16:07
sac tumors, or adenoma sebaceum.
16:10
Okay, so this one, uh, y'all did pretty well with.
16:14
It is indeed choice number five.
16:16
The numbers one, two, three, and four are all
16:22
associated with von Hippel-Lindau disease, right?
16:26
So, you remember that von Hippel-Lindau disease
16:28
is an autosomal dominant disorder with the
16:32
VHL gene, which is on chromosome 3.
16:42
You may have hemangioblastomas
16:44
or angiomatous lesions as well.
16:47
They may cause retinal detachment,
16:49
for example. In the abdomen, I don't usually
16:53
talk about, but you may have your pancreatic
16:56
cysts or tumors. Clearly, you have
17:00
renal cell carcinomas and your kidney
17:03
cysts associated with von Hippel-Lindau disease.
17:06
Um, endolymphatic sac tumors.
17:08
So, endolymphatic sac tumors, about 10 to 15
17:10
percent of patients with Von Hippel-Lindau
17:13
disease will have an endolymphatic sac tumor.
17:16
For those of you who are unfamiliar with this,
17:17
these are tumors in the
17:20
temporal bone, usually along the plane
17:23
of the petrous portion of the bone, even though
17:25
it's, um, more in the mastoid portion. And they are
17:29
unique in that on pre-contrast T1-weighted images,
17:34
they are bright on the pre-contrast T1-weighted
17:36
scan, a very, uh, fluffy lytic lesion.
17:39
They do enhance, um, and they, in fact, obviously
17:43
the vestibular aqueduct or endolymphatic sac.
17:47
Um, you should also remember that Von Hippel-
17:50
Lindau disease is also associated with
17:52
pheochromocytomas and other cystadenomas.
17:57
Um, the criteria for making the diagnosis is:
18:00
If you have a family history of
18:02
Von Hippel-Lindau and one of these tumors
18:07
that I've mentioned, that's sufficient.
18:10
But if you don't have the family history, but you have
18:13
two or more of these types of lesions, then, um, you
18:17
can make the diagnosis of Von Hippel-Lindau disease.
18:20
So, I have another question
18:21
about Von Hippel-Lindau disease.
18:22
Let me stop sharing.
18:25
Again, a follow-up question, which, um, probably
18:29
about 20 percent of the cases on the boards will
18:32
have follow-up questions to just the diagnosis.
18:35
So, which is not true?
18:36
Patients with Von Hippel-Lindau have a 25 to 35
18:39
percent chance of having a spinal hemangioblastoma.
18:42
Patients with a spinal hemangioblastoma have a 25
18:45
to 35 percent chance of having Von Hippel-Lindau.
18:48
Number three, 25 to 35 percent of cases
18:50
of Von Hippel-Lindau occur sporadically.
18:53
Number four, all of the above are not true.
18:56
Or five, none of the above, which
18:59
means that all of them are true.
19:02
Okay.
19:02
So, tricky wording, be careful.
19:05
Um, I'll let you think about
19:08
that, but which is not true?
19:11
Patients with Von Hippel-Lindau have a 25 to
19:12
35 percent chance of a spinal hemangioblastoma.
19:16
If you have a spinal hemangioblastoma, you have a
19:18
25 to 35 percent chance of having Von Hippel-Lindau.
19:21
25 to 35 percent of cases of Von Hippel-
19:24
Lindau occur sporadically as opposed to
19:27
through the genetic autosomal dominant route.
19:31
All of those are wrong for number four,
19:34
or one, two, and three are all correct.
19:36
And therefore, the correct answer is none of the above.
19:40
All right.
19:40
Oh, I see whether I completely confused everybody.
19:44
I did indeed.
19:45
So, uh, answer number one is correct.
19:49
We usually say the one-third rule of Von Hippel-
19:52
Lindau and spinal hemangioblastoma. That is,
19:55
one-third of VHL patients have a spinal
19:58
hemangioblastoma, and one-third of patients who
20:01
present with a spinal hemangioblastoma end up
20:04
having the diagnosis of Von Hippel-Lindau disease.
20:08
Answer number three is actually incorrect.
20:11
Only 20 percent of cases of
20:14
Von Hippel-Lindau occur sporadically.
20:16
Most of these are genetic—80 percent occur
20:19
through that VHL chromosome 3 gene.
20:22
So, the correct answer to something
20:25
that's not true is number three.
20:27
Only 20 percent of cases of
20:30
Von Hippel-Lindau occur sporadically.
20:33
All right.
20:38
Case number 106.
20:40
So, every once in a while, they'll put in a case
20:42
that's not perfectly obvious visually and try to
20:42
423 00:20:42,115 --> 00:20:46,500
20:46
see whether you can make the diagnosis.
20:49
This is what we call an eye case.
20:52
What is the mechanism of injury for this lesion,
20:54
and we're not identifying the lesion yet.
20:57
Is it an acceleration-deceleration injury?
20:59
Is it a high-energy rotation injury?
21:02
Oh my gosh.
21:04
Re-poll.
21:06
Okay, what is the mechanism
21:07
of the injury for this lesion?
21:08
Is it an acceleration-deceleration injury?
21:10
Is it high-energy rotation?
21:12
Is it high-energy axial compression?
21:14
Is it hanging, or is it an assault?
21:17
So, for this lesion that is depicted, and
21:19
I'm not pointing it out for you, what is the
21:23
mechanism of the injury for the lesion?
21:26
So, this is not a diagnosis question.
21:29
It's a mechanism question.
21:31
Is it an acceleration-deceleration injury?
21:32
Is it a high-energy rotation injury?
21:35
Is it high-energy axial compression?
21:37
Is it a hanging injury, or is it status post-assault?
21:43
So, lots of people are putting in their answers
21:46
as if they know something is correct.
21:48
And, um, the correct answer here is number
21:51
three—high-energy axial compression.
21:55
This is an occipital condyle
21:59
avulsion injury.
22:01
Let me see what I had previously.
22:03
Oh, I only had one image.
22:05
So, this is the lesion here from the occipital condyle.
22:08
I have to admit that, um, in the 25 years of doing
22:12
neuroradiology, uh, twice, the resident on call
22:17
picked up the occipital condyle injury on the
22:19
spinal CT, and I was like, "Oh, man, I missed it."
22:23
So, good for the residents for looking at this.
22:25
And this is something that you will see with
22:27
motor vehicle collisions as well as falls.
22:30
And it is considered a high-
22:32
energy axial compression injury.
22:34
It's not rotation.
22:36
And it's not a back-and-forth injury, and it
22:39
doesn't occur with hanging or assault.
22:42
There is a classification.
22:44
And I think that asking a question
22:47
about the type of occipital condyle
22:50
lesion might be something that could be asked
22:53
in the neuroradiology subspecialty certification
22:56
test, but it would be, I think, punitive for the
23:00
residents, um, taking the diagnostic radiology boards.
23:03
But nonetheless, here are the different types
23:06
by the Anderson-Montesano classification.
23:10
Type 1 is a comminuted impaction fracture,
23:12
which you see the comminution here.
23:15
Type 2 is associated with other skull base fractures,
23:19
and/or a linear fracture.
23:21
And then what we saw was Type 3.
23:24
Here, it's avulsed off of the, um, off of the occipital
23:31
condyle, and it may or may not be, uh, displaced.
23:34
So, an avulsion fracture with tension from the
23:37
alar ligament is one of the mechanisms here.
23:42
Okay, we're moving ahead.
23:46
Case number 107, right on target
23:50
here with where I want to be.
23:52
Okay, so you're seeing a post-myelogram CT scan.
23:57
This is with a kind of a bone window.
24:00
The medial, the middle image
24:03
is more of a soft tissue window.
24:06
And this is a coronal reconstruction
24:09
through the thecal sac, Case 107.
24:15
You can see the patient's already been
24:16
operated on, but that's irrelevant to the case.
24:23
And poll.
24:27
Okay.
24:28
Um, these images demonstrate what? A pseudo-
24:32
meningocele, arachnoiditis, scoliosis,
24:40
root avulsion, or cord atrophy?
24:44
What are you seeing on these three images?
24:47
A pseudomeningocele, arachnoiditis,
24:53
scoliosis, root avulsion, or cord atrophy?
25:00
What is being demonstrated here?
25:05
So, we've hit our magic number.
25:08
Uh, indeed, the correct answer is root avulsion.
25:11
What you see are the normal nerve roots
25:14
here and here, but if you notice, on the
25:17
right side, we don't have any nerve roots.
25:20
We've got the anterior and the posterior rootlet here.
25:24
Nothing on the contralateral side,
25:26
and the cord looks a little funny here.
25:28
This is not such a great coronal reconstruction,
25:31
but here we have a nerve root, and here we have a nerve
25:33
root, and here we have a nerve root. On the other side,
25:36
it's not just that we're not in plane—
25:38
those nerve roots have been avulsed.
25:41
So, the correct answer is number four, root avulsion,
25:45
with absence of seeing the nerve roots on
25:48
the right side, which is the pathologic side.
25:56
So, here's the follow-up question
25:58
for root avulsion injuries:
26:04
Klumpke—associated with C8-T1, which is correct?
26:07
Klumpke—associated with C8-T1.
26:09
Klumpke—absent biceps reflex.
26:13
Erb palsy and triceps reflex.
26:16
Erb palsy and C6-C7 injury.
26:19
Or Dubersy paralysis and C5-C6 injury.
26:24
Which of these is correct?
26:26
Klumpke associated with C8-T1 injury, Klumpke
26:29
absent biceps, Erb's, absent triceps reflex,
26:35
Erb's, C6-C7, and Dubersy paralysis, and C5-C6.
26:40
Which is the correct?
26:42
Um, so, a little bit slower on answering this one
26:47
as everyone's checking the internet and doing the
26:50
Google search for what, what is a Klumpke paralysis?
26:56
All right.
26:56
Well, it looks like it's a little bit
26:57
slowed down, so I'll share the results.
27:00
Uh, the most common answer is indeed
27:03
number one, and it is the correct answer.
27:06
So, Klumpke's paralysis is a root
27:09
avulsion of C8 and T1 nerve roots.
27:13
It's an injury of those nerve
27:15
roots at C7-T1 and T1-T2.
27:18
And as such, it is most commonly associated
27:23
with intrinsic muscles of the hand weakness.
27:26
So, they talk about the claw hand of Klumpke paralysis.
27:31
This most commonly occurs.
27:34
We see it with shoulder dystocia
27:37
around, um, birthing process.
27:41
However, in young adults, we see it most
27:44
commonly in motorcycle injuries, where the
27:47
motorcyclist goes flying over the handles
27:49
and reaches out the arms as they land.
27:53
And that kind of yanks the shoulder
27:56
back, and you get root avulsions.
27:59
So, there's two different types.
28:00
There's the Klumpke, um, which is that
28:03
C8-T1, and then you have, and that, that
28:08
may also be associated with Horner's syndrome.
28:10
So, the, the avulsion that's associated with
28:13
Horner's syndrome is Klumpke paralysis.
28:15
The Erb—whoops.
28:16
The Erb-Duchenne, um,
28:17
568 00:28:18,887 --> 00:28:22,754 palsy is a C5-C6 palsy,
28:23
where you lose the biceps reflex,
28:25
and you havve this, sort of, waving hand, um,
28:27
characteristic.
28:29
So, it's, it's not the intrinsic muscles of the
28:32
hand, but it's—I'm sorry—it's more the, um, um,
28:39
more the, um, the limp arm rather than the hand.
28:45
So, the biceps reflex is lost with the Erb palsy.
28:51
Okay.
28:52
Dubersy paralysis—
28:54
I made this up.
28:55
Uh, thank you to the five
28:56
people who went with that one.
28:58
I just made up some term.
29:01
Okay.
29:03
Let's move on.
29:03
So, this is case 108.
29:05
Um.
29:12
This was a patient who had
29:14
abrupt onset of quadriparesis.
29:26
Let me relaunch the poll here.
29:27
Sorry about that.
29:28
So, what is the best diagnosis?
29:31
Is this most likely to be multiple sclerosis,
29:35
neuromyelitis optica spectrum disorder,
29:39
myelin oligodendrocyte glycoprotein disorder (MOG), um, spinal cord
29:45
stroke, or acute disseminated encephalomyelitis?
29:48
Abrupt onset of quadriparesis in the patient.
29:53
Best diagnosis: multiple sclerosis,
29:56
NMO, neuromyelitis optica.
29:58
Used to be called Devic's syndrome, um, MOG
30:02
disorder against the oligodendrocyte protein,
30:06
stroke, or acute disseminated encephalomyelitis.
30:16
All right.
30:16
So, let's see, share the results here.
30:19
So, the most common answer is stroke.
30:23
You should recognize that this
30:24
is diffusion-weighted imaging.
30:26
How do we know this is diffusion-
30:27
weighted imaging? Really bad.
30:29
Look at the spine.
30:30
It's not—you know, the vertebral bodies here don't
30:33
look anything like a T1, or a T2, or a STIR image.
30:38
What you're seeing is a sagittal DWI/DTI
30:42
sequence.
30:43
And you've got these bright
30:45
areas within the spinal cord.
30:47
So, this is a spinal cord stroke, and the history
30:49
of abrupt onset should have led you to that.
30:53
Most of the other things—multiple sclerosis and
30:56
all the other demyelinating disorders—are not
30:58
presenting like that. Um, ADEM is the
31:03
post-viral or post-vaccination autoimmune
31:07
demyelinating disorder that can occur in the spine.
31:11
Those are long-segment diseases.
31:13
Remember that we talk about long-segment
31:15
disease when we're talking about NMO.
31:18
These are little—you know, dots here,
31:21
which would not go for multiple vertebral
31:24
body segments of either NMOSD or MOG.
31:28
It could be MS, um, but this is a DWI
31:32
suggesting that this is ischemic injury.
31:37
Which is the—let me stop sharing here.
31:43
Which of these is the least
31:45
likely etiology of a cord stroke?
31:49
I'm not necessarily saying the one that I showed
31:51
you, but of all cord strokes, what's the least
31:55
likely etiology? Aortic surgery, aortic
31:58
dissection, genetic causes, vasculitis, or trauma?
32:03
Which of the five of these is the least
32:06
likely source of a cord stroke?
32:08
Is it aortic surgery?
32:10
Is it aortic dissection?
32:12
Is it genetic causes?
32:14
Is it vasculitis?
32:16
Or would it be trauma?
32:17
So, what?
32:21
Okay.
32:21
So, a vast majority of you got the
32:23
correct answer of genetic causes.
32:25
Aortic surgery, unfortunately, is the most common
32:28
of the iatrogenic etiologies for cord stroke.
32:32
It doesn't happen very often, thank goodness.
32:34
But remember that we do have that supply
32:37
of the Artery of Adamkiewicz, which is
32:41
the most common source of the stroke.
32:45
This one up top in the cervical spine is very uncommon.
32:48
You can see that with vertebral artery
32:50
dissections occasionally, um, and sometimes
32:53
surgery, but the vast majority of these
32:56
are really in the thoracolumbar junction.
32:59
And they're secondary to either aortic surgery,
33:01
or aortic dissection, or aortic coarctation, or aortic
33:05
aneurysms that they're operating on.
33:08
And unfortunately, they pick off one of the
33:10
supplies of the, um, Artery of Adamkiewicz,
33:15
through the intercostal arteries, for example.
33:19
Genetic causes.
33:20
I'm not really sure where I came up with that.
33:22
Um, you know, theoretically, Marfan
33:25
syndrome, I guess, but that's the least
33:27
common. Vasculitis is a common cause.
33:29
And in fact, this patient that had that
33:31
cervical spine stroke actually had lupus and a mixed
33:36
connective tissue disorder and had lupus,
33:39
um, antibody—the lupus anticoagulant
33:42
factors—and that was presumed to be the
33:45
source of the patient's cervical spine stroke.
33:47
And as you would imagine, it's very devastating.
33:50
This was a 26-year-old, I believe.
33:52
Trauma occasionally will occur if you
33:55
have aortic, um, transection, for example.
33:59
But genetic causes was the correct answer.
34:01
Let's move on to case 109. Let me stop sharing here.
34:07
Stop sharing.
34:08
Okay.
34:10
Okay.
34:11
Okay.
34:11
So we are on case 109.
34:13
This patient had left-sided back pain.
34:16
You're seeing a coronal
34:17
reconstruction of the axial scan.
34:19
Here's one of the axial scans. You're seeing
34:22
a sagittal reconstruction through the sacrum.
34:25
And this is an axial scan with a soft tissue
34:28
window, as opposed to the bone window, case 109.
34:34
Best diagnosis for this lesion.
34:35
Is it spondylolysis?
34:38
Is it spondylolisthesis?
34:41
Is it Baastrup's disease?
34:43
Is it Bertolotti syndrome or none of the above?
34:49
Best diagnosis here.
34:51
Spondylolysis, spondylolisthesis, Baastrup's
34:55
disease, Bertolotti syndrome, or none of the above.
35:04
Alright, you guys are hitting home runs these days.
35:07
Okay.
35:08
So the correct answer was indeed
35:10
number four, Bertolotti syndrome.
35:12
Bertolotti syndrome is a syndrome in which
35:16
one or both of the transverse processes
35:19
of L5 articulate with the sacrum.
35:25
And via this unusual articulation, you have
35:30
abnormal spinal mobility, and that can lead
35:32
to either unilateral, bilateral, or midline
35:36
low back pain.
35:37
And, um, this, uh, believe it or not, there is a
35:42
gene that predisposes you to Bertolotti's syndrome.
35:46
It's called the HOX10 gene.
35:50
Strange thing, but, um, we, we walked
35:54
by this quite a few—quite a bit.
35:56
And, you know, this is the best diagnosis in an outpatient
36:00
setting. For a patient who has low back pain, you
36:01
get a CT scan or MRI of the lumbar spine.
36:05
First off, on the MRI, it's gonna
36:06
be very hard to pick this up.
36:09
Um, on the CT, this is what you're
36:11
looking at—this communication between the
36:15
transverse process of L5 with the sacrum.
36:19
And, you know, I suspect that we walked by this
36:22
quite a bit in our practice.
36:26
Um, in the emergency room, for those
36:29
residents taking ER call, you want to
36:31
make sure you don't call this a fracture.
36:34
You can see that the edges are actually quite bright.
36:38
And this is a congenital deformity
36:40
rather than an acute traumatic deformity.
36:46
Okay.
36:47
We're moving on to case 110. Stop.
36:49
737 00:36:53,310 --> 00:36:53,430
36:53
Alright. Case 110.
36:54
We have a sagittal T2-weighted image.
36:56
Doesn't look like it's STIR
36:58
because the fat is still preserved.
37:00
Here's an axial T2-weighted scan.
37:09
Which does not fit with this case.
37:13
B12, copper, folate,
37:19
nitrous oxide, or none of the
37:22
above? They all fit. Which does not?
37:26
Let me go back just to show
37:28
the axial scan one more time.
37:30
So here's case 110, sagittal and
37:33
axial. Which of these does not fit?
37:38
Is it B12?
37:39
Is it copper?
37:41
Is it folate?
37:42
Is it nitrous oxide, or none of the above?
37:46
The preceding four options all fit together.
37:53
So, all right.
37:56
Almost evenly split.
37:58
I stumped quite a few of you on this one.
38:02
So this is, um, let's just go
38:05
back to the previous image.
38:06
This is pretty classic for subacute combined
38:09
degeneration, in which you have the high signal
38:12
intensity in the posterior aspect of the spinal cord.
38:15
And you notice the two posterior columns here.
38:18
And there's often a little spared portion right in the
38:21
midline of the raphe there, but these are indeed in
38:24
the posterior columns bilaterally of the spinal cord.
38:29
So we—the diagnosis is subacute combined degeneration.
38:33
Now we have to ask, what are the various
38:35
causes of subacute combined degeneration?
38:40
And the answer is that B12 deficiency, copper
38:44
deficiency, and folate deficiency all can cause subacute
38:50
combined degeneration in a pattern just like that.
38:53
Often, the folate is in conjunction with the
38:55
B12, but before this morning, I checked and
38:59
said, can folate in and of itself, without
39:02
B12, cause subacute combined degeneration?
39:05
I looked online and said, yes,
39:07
that is, um, that does occur.
39:10
The other thing that can lead to the pattern of subacute
39:14
combined degeneration is nitrous oxide overdose.
39:19
This is, um, laughing gas.
39:21
And when, when, when I was young,
39:24
many years ago.
39:26
Uh, we used to have these things called little
39:28
whippets, and it was like a little canister-
39:30
sized laughing gas that you could get, you know,
39:33
illicitly and, uh, have a good time at the party.
39:37
So, um, nitrous oxide overdose or use, uh, whippets,
39:42
as we called them—these are the things that
39:44
can cause subacute combined degeneration.
39:46
This pattern of posterior involvement of
39:49
the spinal cord, uh, can also be seen in
39:53
demyelinating disorders, such as your NMOSD.
39:56
It's a little bit too long for us to be
39:59
thinking in terms of multiple sclerosis,
40:01
because of this, um, you know, longitudinally
40:04
extensive transverse myelitis appearance.
40:06
The other thing is vacuolar myelopathy,
40:10
which has, in recent years, has been most
40:13
commonly associated with HIV infection.
40:16
Um, so there is a differential diagnosis,
40:19
but when you see this, you know, two little bright
40:22
stuff right in the posterior columns of the
40:24
spinal cord, that's, you know, we're going to
40:27
certainly raise these issues in the report.
40:31
So that way the clinicians check,
40:33
check those values and supplement.
40:35
Um, this is, um, in particular, um, because the
40:39
number of vegetarian and vegan Americans has been
40:43
rising—not rapidly enough, according to my wife,
40:46
who's a strict vegan, but it has been rising.
40:49
And therefore, B12 deficiency is something that can be a,
40:52
um, a complicated—or not a complication, but something
40:55
that vegans and vegetarians have to be careful about.
40:59
Okay, stop sharing this.
41:04
This is case 111.
41:05
Um, you're looking at a sagittal T2,
41:11
CISS image, high-resolution CISS image.
41:19
Which does the patient have?
41:23
Chiari I, syringohydromyelia, achondroplasia,
41:30
hydrocephalus, or all of the above?
41:33
Which does the patient have?
41:36
Chiari I.
41:37
Syringohydromyelia, achondroplasia, hydrocephalus,
41:45
or all of the, uh, all of the above?
41:49
Okay, so, I mean, most of you would recognize the,
41:54
the syrinx here, the, uh, the syringohydromyelia.
41:58
We use the term syringohydromyelia because
42:01
purists will say that hydromyelia is just
42:03
central canal dilatation, whereas the syrinx is
42:06
not in the central canal but peripheral to it.
42:09
A lot of times, we can't tell the difference.
42:11
You might also look at the ballooning out
42:13
of the third ventricle, and we've lost our
42:18
infundibular recesses of the third ventricle.
42:22
We've got a big lateral ventricle.
42:24
So we have hydrocephalus, and we have syringohydromyelia.
42:27
So you got to go with all of the above.
42:29
If we look at the size of the
42:31
foramen magnum here, it is small.
42:34
And so that will go along with achondroplasia.
42:37
If I had shown the head size,
42:39
you might have figured that out as well.
42:41
And, um, eh, on the, um, on the Chiari I.
42:48
Uh, it's a little soft, so I might
42:49
want to change this question.
42:51
Uh, this patient actually had,
42:53
in addition, aqueductal stenosis.
42:57
So, the correct answer here—and I'll share the result—
43:00
was indeed choice number five, all of the
43:03
above. Although soft on the Chiari I, we want
43:07
to, you know, when we draw that line from the
43:10
opisthion to the basion, we want to see
43:15
tonsillar herniation more than five millimeters.
43:17
I'm not sure what would have gotten there.
43:19
Let's move on to case 112.
43:26
Okay.
43:27
Case 112 is a trauma case.
43:31
And it's a craniocervical junction trauma case.
43:40
Which ligament—
43:44
you already got answers coming out of me.
43:46
Let me re-re-poll because I
43:48
didn't even show the question yet.
43:50
Okay, which, uh, ligament
43:53
is injured in this patient who had
43:56
cranio-cervical junction trauma?
43:58
Is it the tectorial ligament?
43:59
Is it the anterior longitudinal ligament?
44:02
Is it the posterior longitudinal ligament?
44:06
Is it the atlanto-occipital ligament or membrane?
44:09
Or is it the apical ligament?
44:11
This is a T2-weighted scan in a patient
44:14
with cranio-cervical junction trauma.
44:16
Which ligament is demonstrated to be injured?
44:19
Is that the tectorial
44:21
membrane or ligament?
44:22
Is it the anterior longitudinal ligament?
44:25
Is it the posterior longitudinal ligament?
44:27
Is it the atlanto-occipital ligament or membrane?
44:30
Or is it the apical ligament?
44:34
All right.
44:35
So people are having a little
44:36
bit of difficulty on this one.
44:39
All right.
44:39
Well, um, I would recommend that for those of you
44:43
who are about to take call, uh, in the emergency room,
44:47
that you might want to relook over the anatomy here.
44:50
So the most common answer was choice number
44:53
four, which is the correct answer, but we
44:55
only got a 29% correct response rate.
44:59
Um, the atlanto-occipital membrane or ligament is that
45:03
extension of the anterior longitudinal ligament,
45:06
where it comes to the skull base and the C1-C2 level.
45:11
So that's the area where we have our injury.
45:15
I put up a diagram here.
45:17
So remember that the tectorial membrane is
45:20
this guy right here, and that's the extension
45:22
of the posterior longitudinal ligament.
45:25
Um, but up here, this bright area here—
45:29
represents the anterior atlanto-occipital membrane.
45:33
And that is, again, the extension of the
45:36
anterior longitudinal ligament, which we usually
45:38
say ends at the C1-C2 kind of junction there.
45:42
You have the transverse ligament behind the
45:45
C1-C2, so back here would be our transverse ligament.
45:51
So, what is the—uh, let me stop sharing
45:56
and then ask the next question.
45:58
Name the extension of the posterior
46:00
longitudinal ligament to the clivus.
46:02
Is that the tegmental ligament?
46:03
Is that the tectorial membrane?
46:04
Is that the apical ligament?
46:06
Is that the cruciate ligament? Or is that
46:08
the posterior longitudinal membrane?
46:10
What is the term for the extension of the posterior
46:12
longitudinal ligament as it connects to the clivus?
46:15
Is that the tegmental ligament, tectorial membrane,
46:19
the apical ligament, or the cruciate ligament?
46:21
Or the posterior longitudinal membrane?
46:24
So this is what I call, for the residents,
46:26
your five-minute recall question,
46:31
since I just mentioned that to y'all.
46:34
Okay.
46:34
So...
46:35
Here, again, the tectorial membrane—this arrow should
46:39
be right here—this tectorial membrane is the extension
46:43
of the posterior longitudinal ligament, and then this is
46:48
the tectorial membrane going to the—this is our clivus.
46:51
We're a little bit flipped in our usual orientation.
46:55
The apical ligament is this guy right
46:57
here, which goes from the top, or the apex,
47:00
of the odontoid process to the clivus.
47:04
That's the apical ligament.
47:05
And then remember that the anterior atlanto-occipital
47:08
membrane is the extension of the anterior
47:10
longitudinal ligament up to the clivus.
47:14
So, case 117, we're going to stick with
47:17
this theme just to push you on it.
47:21
We launched a poll here.
47:22
So, here's another trauma case, another injury case.
47:27
Craniocervical injury.
47:29
Which is the non-injured ligament?
47:32
Is it the tectorial membrane?
47:34
Is it the anterior longitudinal ligament?
47:38
Is it the apical ligament?
47:39
Is it the atlanto-occipital membrane?
47:41
Or none of the above—all of them injured?
47:45
So, which of these is not
47:47
injured?
47:47
Would that be the tectorial membrane?
47:50
Would it be the anterior longitudinal ligament?
47:52
Would it be the apical ligament?
47:55
The atlanto-occipital membrane?
47:56
Or none of the above?
47:58
They're all injured.
48:02
All right.
48:02
So, if you look here, there's this displacement,
48:07
and the ligament that should be going from the
48:09
top of the odontoid process to the clivus, which
48:12
is the apical ligament, is involved, right?
48:15
The anterior longitudinal ligament is all
48:17
this stuff here with the bright stuff.
48:19
And then...
48:20
This—There should be a ligament connecting
48:24
from here to here at the C1-C2 junction.
48:27
This is all bright.
48:29
So, this atlanto-occipital membrane, and I
48:31
would argue that this goes down further.
48:34
You can see this darker signal here of the
48:36
anterior longitudinal ligament where it was intact.
48:39
So, this is involved. This is involved, and this is above.
48:41
The next question is, is the
48:43
tectorial membrane involved?
48:44
So, here's the tectorial membrane going,
48:48
as I said, the extension of the posterior longitudinal
48:51
ligament to the clivus, and I would say this is intact.
48:55
So, the correct answer should be number one.
48:58
We'd want to see it on multiple views.
49:01
You know, some people might say,
49:04
"Well, what about right at the attachment of the clivus?"
49:07
Questionable, but usually, if it's going
49:10
to tear, it's like on this portion,
49:12
not at its junction with the clivus.
49:14
So, the correct answer was tectorial membrane.
49:18
All right, case 114.
49:20
We're still rocking and rolling here.
49:22
Oh, I forgot to show these ones.
49:24
Um, let me relaunch.
49:28
Okay, so we have case 114.
49:33
And, um, this is a gradient
49:38
echo scan and a T2-weighted scan.
49:43
T1, not much seen there.
49:45
T2, the lesion is here on the sagittal.
49:54
Given everything—one, two, three—
49:59
and this, what's the best diagnosis?
50:03
Would this be an ependymoma, multiple sclerosis,
50:08
post-traumatic myelomalacia, a cavernoma?
50:12
Or none of the above?
50:15
Given everything, what do you
50:16
think this most likely represents?
50:17
Is this going to be an ependymoma,
50:19
an MS plaque, post-traumatic myelomalacia,
50:22
a cavernoma, or none of the above?
50:23
Woo-hoo!
50:27
Woo!
50:27
Knocked it out of the park.
50:29
Good job.
50:30
So, this little dot of darkness here
50:34
in the spinal cord is indeed a little
50:36
focus of hemosiderin in the spinal cord.
50:39
You notice that the cord is not expanded,
50:41
so there's not going to be an ependymoma.
50:43
It's negative on T1.
50:46
Here, it actually has a rim of dark signal around it
50:50
on the T2-weighted sagittal scan, which is
50:54
typical of a cavernoma, with the bright signal
50:58
intensity—the dark signal intensity
51:00
of the hemosiderin around the periphery of it.
51:03
So, this is not an acute injury.
51:04
You don't see any edema in this spinal cord.
51:06
This is an old injury with
51:07
hemosiderin deposition in a cavernoma.
51:14
Okay.
51:17
All right.
51:17
Next case, case 115. T2, T1, post-GAD.
51:17
1028 00:51:27,375 --> 00:51:32,225 T1, or the sagittal plane, case 115.
51:33
Best category of disease?
51:34
This is most likely neoplastic,
51:37
degenerative, metabolic, infectious, or iatrogenic—
51:41
something that we did as physicians.
51:45
What is the best category of disease?
51:46
Do you think this is neoplastic, degenerative, metabolic,
51:49
infectious, or something one of the doctors did?
51:57
All right.
51:57
So, um, choice number four—overwhelmingly,
52:01
this is indeed diskitis and osteomyelitis.
52:05
And you also see this extradural enhancing tissue.
52:11
Um, you know, I wouldn't necessarily
52:15
call this an epidural abscess.
52:16
I still like to see some central
52:18
necrosis to call something an abscess.
52:20
I'm more likely to use the term phlegmon for this
52:24
enhancing tissue that is associated with the infection.
52:27
So, you've got enhancement in the disk,
52:29
you've got abnormal signal in the disk.
52:31
The endplates are all eroded, T1
52:33
darkened signal intensity.
52:35
So—infectious diskitis-osteomyelitis complex.
52:39
So it is, uh, 12:55
52:42
with me, so I'm going to stop the share.
52:47
And start, um—there's some chat questions.
52:52
I'll try to get to the chat
52:53
questions, and I'll go to Q&A.
52:55
So, uh, would the size of the sequestration
52:57
point to an acute or chronic process?
52:59
I don't think the size helps at all with making that
53:03
differentiation. For a sequestration, they can
53:06
be small, they can be large, but what you do see
53:08
is a—tend to be for a peripheral rim of enhancement.
53:12
Chat. Can you mention injuries
53:14
expected with other mechanisms, please?
53:17
I think this is—what we were, uh, when we were talking
53:20
about the occipital condyle fracture.
53:24
So, the rotational injuries—
53:26
you can have rotatory subluxation at the C1-C2
53:29
junction, and specifically talking about that.
53:32
Obviously, we know the mechanism for the
53:34
Hangman's fracture, with the pedicle fracture
53:37
of C2, and you have the Jefferson fracture
53:40
of C1, where it's kind of a burst fracture.
53:43
So there are different mechanisms,
53:44
specifically for what we usually talk about—
53:46
cranio-cervical junction injuries.
53:50
Can degenerative changes mimic a type 1 occipital
53:54
fracture?
53:56
Um, type 1 is comminuted.
54:00
I don't—I don't think—that's not
54:03
where you usually have degenerative change
54:05
that you would have little ossicles, for example.
54:08
Question 106—not sure what that's about.
54:10
Hyperacute MS plaques can show restricted diffusion.
54:15
Um, I would agree in the brain. Um, we don't
54:21
have, I think, enough experience in the spinal
54:24
cord to be able to say that they're restricted.
54:27
They're usually so small, and DWI is
54:30
so, um, is— is so low resolution that I
54:35
don't— I haven't seen literature about
54:39
spinal MS plaques showing restricted diffusion.
54:41
I would still be very worried about a cord infarct.
54:43
5, 1, 2, 5, 4. Thank you for that.
54:46
I don't know what that means.
54:47
Thank you for attending.
54:48
Very good.
54:48
Thank you for your time.
54:49
Okay.
54:50
Looks like that's, um, again, uh, let me go to the Q&A.
54:53
Can you address ectopic gas in the spinal canal?
54:59
So ectopic gas in spinal canal usually
55:01
means, obviously, vacuum phenomenon.
55:03
It can occur
55:04
in the intervertebral disk, but it
55:06
can also occur in the facet joints.
55:09
And therefore, you might see it laterally.
55:11
You may see it, um, centrally. Um, it is an
55:17
indicator of, uh, degenerative change.
55:21
Not only that, but there's a statement that
55:24
people make, and that is— you should not see vacuum
55:26
cleft phenomenon in fused spines because it
55:31
shouldn't be moving in it and trapping nitrogen.
55:34
So, if you see ectopic gas in a spinal fusion
55:39
case, it usually means that the spinal fusion
55:41
has not taken, and it's not truly fused.
55:44
Can you please tell me in detail
55:45
about gradient coils used in an MRI scan?
55:47
That's a little bit removed from what, um,
55:53
from what, um, I wanted to talk about, but you
55:57
know, there are a lot of— we, we tend to
55:59
use small coils in tandem in order to maximize
56:04
signal-to-noise and yet have enough coverage to
56:07
be able to cover the cervical-thoracic region.
56:10
For example, in an MS case, usually we're doing it
56:13
with, like, 30 centimeters— 24 to 30 centimeters— field
56:17
of view, and you have to have a lot of parallel coils
56:20
used for the spine. It fits right
56:23
in with us, and Maria, thank you very much.
56:25
I hope so.
56:25
How— how— how might you make a difference
56:28
between an apical ligament injury and an atlanto-
56:30
occipital one, one behind the other?
56:33
So, the atlanto-occipital membrane is anterior
56:36
to the apical ligament. The apical ligament, you would
56:39
see at the top of the odontoid process, going to the
56:43
clivus, as you saw in the diagram. The atlanto-occipital
56:47
one follows the anterior longitudinal ligament.
56:51
It's anterior to the apical ligament.
56:53
Thanks so much.
56:53
Great.
56:54
Do you put that in your report
56:56
the potential for spontaneous
56:57
regression of the disk extrusion.
57:00
So, um, with respect to the sequestrated disk,
57:04
over the course of time, they do, um, uh, resolve.
57:10
And in fact, the presence of that enhancement
57:13
around that sequestrated fragment is a
57:15
good sign because it means granulation
57:17
tissue is growing in, and it can resolve.
57:19
Basically, it doesn't matter what
57:20
we're showing on the imaging.
57:22
What's the patient’s symptoms?
57:23
Is it referable to that, uh, disk herniation?
57:26
I've seen horrible disk herniations in patients who are
57:28
symptomatic at a different level and a different side.
57:31
Can you get degenerative gas in a vertebral body?
57:33
When you get degenerative gas in the
57:34
vertebral body, you worry about Cosmos
57:36
syndrome, which is potentially from
57:41
avascular necrosis of the vertebral body.
57:43
However, the most common source of gas in
57:46
a vertebral body is from the disk going up.
57:48
But if you don't have degenerative change and you
57:50
have the disk—the gas in the center of the vertebral
57:53
body, consider caisson disease, sickle cell
57:56
disease, or avascular necrosis of the vertebral body.
57:59
What do you think about resorption of a herniated disk?
58:01
What is the criteria for full resorption?
58:04
I'll pass on that one.
58:05
I don't know what you mean by full
58:07
resorption, but obviously, if you don't
58:09
see it, um, I guess that means resorption.
58:12
Uh, can you explain in the last
58:14
case why it is not a metastasis?
58:16
So, the last case is centered on the disk.
58:19
It has high signal intensity in the disk.
58:21
It has enhancement in the disk.
58:23
That's not a site where we usually see
58:25
metastases, and it had the epidural phlegmon,
58:28
which is unlikely to be with a metastasis.
58:33
Most metastases are to the bones.
58:36
They're not to the spinal cord,
58:38
and they're not to the epidural space.
58:40
All right.
58:41
I think, well, I did pretty well
58:43
with answering all those questions.
58:44
Let me see.
58:44
Can you please describe the traumatic injuries and
58:46
rheumatoid arthritis regarding craniocervical junction?
58:48
So, um, not so much the trauma, but clearly
58:51
the transverse ligament, um, becomes lax.
58:53
You have that possibility of a atlanto—uh,
58:56
atlantoaxial subluxation greater than three
58:58
to five millimeters at the C1-C2 junction.
59:01
And, um, it's more of an inflammatory
59:04
process rather than a traumatic injury.
59:06
Does it predispose you to having some laxity at C1-C2?
59:10
It does, um, but that combination
59:13
of trauma and RA is not
59:14
as much.
59:16
Thank you.
59:16
What is the incidence of solitary spinal
59:18
hemangioblastoma in VHL without intracranial lesions?
59:21
So, it wouldn't be VHL if it's only a solitary
59:24
spinal hemangioblastoma without a family member.
59:27
So, that's what makes it VHL is—the family
59:30
history with a single hemangioblastoma.
59:33
As it were, I would say it's probably less than 5%
59:37
will present as just spinal hemangioblastoma
59:41
and family member with von Hippel-Lindau.
59:43
That's pretty uncommon.
59:47
All right, I think that's all the questions.
59:50
I, I commend you.
59:52
Uh, 15 cases, 15 questions.
59:54
That was—that was fantastic.
59:56
Thank you so much for this case review
59:57
and for everyone in the audience for participating.
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