0:02

Hello, and welcome to Case Crunch Rapid Case

0:04

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

0:11

best choice via the live polling feature.

0:14

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

0:20

of today's case review and previous

0:22

case reviews by creating a free account.

0:24

Questions will be covered at the end if time allows.

0:27

Please remember to use the Q&A feature

0:29

to submit your questions so we can get

0:31

to as many as we can before time is up.

0:33

Without further ado, please enjoy this case review.

0:36

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

0:59

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.