0:02

All right, it is now 12:00,

0:04

and we are going to get started.

0:05

So, I just wanted to say hello and welcome to the 7th of

0:09

many live stream noon conferences hosted by MRI Online.

0:12

In response to the changes happening around the world

0:14

right now and the shutting down of in-person events,

0:16

we have decided to provide free daily noon conferences

0:19

to all radiologists worldwide.

0:20

Today we are joined by Dr. Stephen J. Pomeranz.

0:24

He is the founder of MRI Online,

0:26

CEO and medical director of ProScan Imaging.

0:28

He has authored numerous medical textbooks in MRI,

0:32

authored numerous MRI texts,

0:33

including the MRI Total Body Atlas.

0:35

He is an avid conference lecturer,

0:37

chairs fellowship training programs

0:39

in MR and advanced imaging.

0:41

A reminder that there will be time at the

0:42

end of this hour for a Q&A session.

0:44

Please use the Q&A feature to ask these questions and

0:47

we'll get to as many as we can before our time is up.

0:50

That being said, thank you so much for joining us today.

0:53

Dr. P, I will let you take it from here.

0:55

Dr. Pomeranz: Welcome to everybody around the world.

0:57

Hope you're all doing well.

0:59

Today, we're going to talk about

1:00

critical concepts in spine imaging.

1:03

And I'm going to predominantly stay away from disc disease,

1:07

which is a commonly understood subject and

1:10

one that we will cover at a later date.

1:13

Although there will be some description and discussion

1:16

of this matter as it relates to contact or collision events.

1:21

These are my faculty disclosures.

1:23

I have nothing else to declare.

1:26

And I'd like to begin with my first case,

1:30

which is a

1:33

middle-aged individual with back pain.

1:37

And I'm going to scroll on the left,

1:40

a T1 spin echo image.

1:42

In the center, a T2 spin echo image.

1:46

And on the far right,

1:48

I've got a fat suppression proton density image.

1:52

And these three images demonstrate a cardinal MR finding

1:56

in an entity that you should all recognize,

1:59

and that is discovertebral osteomyelitis.

2:04

Now, there are several highlighted abnormalities that make

2:08

this diagnosis and is pathognomonic

2:11

and diagnostic on MRI alone.

2:15

First, on the T1-weighted image,

2:17

we have completely lost the normal endplate.

2:21

I'm going to draw the normal endplate for you,

2:24

or I'm going to highlight it for you

2:25

with a few little tick marks here.

2:29

And the endplate is this very subtle...

2:34

Actually, I'm going to draw it with my little arrow here,

2:37

this very subtle area of low signal intensity right

2:40

there, between the vertebral body and the disc.

2:43

Now, this line is composed of both the cortex and the

2:48

osteochondral endplate. So it's a summation of both.

2:51

And look at how it is completely destroyed on the

2:55

T2 weighted image and completely destroyed

2:57

on the proton density fat suppression image.

3:00

In its wake is an area of diffuse inflammation,

3:04

increased signal in the disc space,

3:07

and an area of prespinous soft tissue inflammation.

3:12

This pattern of endplate destruction.

3:15

And I'm going to scroll a little bit so you get a better feel for it.

3:18

It's typical and diagnostic of discovertebral osteomyelitis

3:23

and allows it to be differentiated from

3:26

microinstability, sterile spondylitis.

3:30

Now, let's go back to our PowerPoint and talk about Discitis.

3:37

I want to focus on three key issues.

3:40

One, understanding the pattern of endplate effacement.

3:46

Regardless of whether the patient

3:47

has had an operation or not,

3:49

this effacement of the endplate is still diagnostic of

3:55

an infectious Discitis and is best appreciated on

3:59

the T1 and the fat-suppressed proton density image.

4:04

Issue number two.

4:07

Discitis is an MRI neuroclinician, neuroimaging diagnosis.

4:12

It is not a diagnosis that you should necessarily

4:15

be making by aspirating the disc space,

4:18

by relying on the sedimentation rate,

4:20

or by relying on the white count. In other words,

4:25

this is an imaging diagnosis.

4:27

And finally,

4:28

what are the constellation of signs for Discitis

4:32

and how to slam the door open,

4:35

making the diagnosis,

4:37

or closed,

4:38

shutting down the diagnosis

4:40

in a patient who has endplate swelling,

4:43

but one of those two diagnoses.

4:47

Now, there are three key findings that allow you to

4:51

differentiate inflammation at the disc endplate complex

4:56

that is infectious versus mechanical or noninfectious.

5:00

The first,

5:01

increased signal in the disc space

5:04

without a vacuum phenomenon favors infectious Discitis.

5:11

Vacuum phenomenon, on the other hand,

5:14

favors sterile spondylotic mechanical disease.

5:18

Number two.

5:19

As already shown,

5:21

endplate destruction or erasure of the end plate

5:25

is typical of discitis versus swelling or edema,

5:29

but still, sharply defined low-endplate signal that is

5:33

marginated by reactive fat in the vertebral body.

5:38

Reactive fat is an excellent sign around the disc endplate

5:42

complex that you are not dealing with an infection.

5:46

Number three.

5:48

Disproportionately long elongated and high signal intensity

5:53

on water-weighted imaging,

5:55

pre and paraspinous masses that does not represent a SPIR

6:00

or fibrous tissue, or a ligament.

6:03

This is another supportive sign of infectious discitis.

6:07

And I'll add one more to that.

6:09

The amount of edema in the vertebral body.

6:12

More than 50% of the vertebral body edematous or even

6:17

holo vertebral edema is typical of infection,

6:20

whereas laminar or linear small volume edema is typical of

6:27

noninfectious mechanical spondylitis.

6:30

Clinically, any patient with inordinate pain that is so severe that

6:36

even bumping the patient or the patient coughing,

6:40

so-called 'Tuss of back pain'

6:42

is typical of infectious discitis.

6:48

Aspiration.

6:50

Sometimes performed in situations

6:52

where you have a walled-off abscess

6:56

is positive only 15% of the time.

6:59

So culture positivity is not going to

7:03

be found in 85% of aspirations.

7:06

So we empirically treat with antibiotics

7:08

based on the MR findings.

7:10

Only occasionally will you feel the need

7:14

to drain a walled-off abscess

7:16

in patients who are immunosuppressed,

7:18

such as diabetics and patients with renal insufficiency.

7:22

Check for air or gas.

7:25

Gas in the soft tissues, bad infection.

7:30

Air in the disc space or air in the facet,

7:34

good, so-called vacuum phenomenon.

7:37

So where the air or gas is located really matters.

7:41

Fourth point.

7:43

MR has a very poor correlation temporarily with

7:46

the clinical improvement of the patient.

7:49

In fact, the patient may get better,

7:52

but the MR may not show improvement

7:54

for six to nine months or more.

7:57

So MR is not necessarily used to ascertain

8:02

the efficacy of antibiotic treatment.

8:05

Perhaps most challenging for the more advanced

8:08

practitioners of you out there

8:10

is the postoperative spine.

8:13

You would think that when someone has a cage placement

8:16

and a fusion that you would get inordinate amounts of

8:20

edema at the disc endplate complex, but in fact,

8:24

you don't.

8:24

And any endplate and what I call non-marginated

8:28

vertebral edema, which I'm going to show you,

8:31

should be viewed with suspicion, even around cages.

8:35

Let's take this case.

8:37

Sagittal T1-weighted image on the left.

8:41

Sagittal T2-weighted image on the right.

8:45

The cages are obvious as oblong areas of low signal intensity.

8:52

But look at the vertebral signal.

8:55

Look at a normal vertebra, the T2-weighted image,

8:58

not as valuable

9:00

for T2 imaging is not that water-sensitive.

9:03

But compare L3 with the subtle loss of vertebral signal,

9:09

the entire vertebra, holo vertebral edema

9:11

should absolutely not be present, even with this cage.

9:15

And look at the loss of the endplate

9:18

low signal intensity stripe,

9:20

and it's even more severe and worse at L5.

9:24

Yes, the simple T1-weighted image,

9:27

any scanner can do it,

9:30

tells the story of non-marginated edema with loss of

9:34

the disc endplate complex or linear low signal stripe,

9:39

both at L4-5 and L3-4

9:44

in a patient who has sustained

9:47

a postoperative infection.

9:50

Contrast-enhanced MRI has limited value in this setting.

9:54

In expert hands,

9:56

one should be able to make and differentiate

9:58

the diagnosis of sterile reactive edema

10:01

and sterile reactive endplate change

10:04

from infectious destructive aggressive

10:08

discovertebral osteomyelitis.

10:11

So it's not that often that we feel the need to deliver

10:14

contrast, and you can see that it doesn't add a lot.

10:17

It does show enhancement of this prespinous mass,

10:20

which was present on the non-contrast portion of the study.

10:24

It shows enhancement of the disc,

10:26

it shows enhancement of the vertebral bodies,

10:28

but so what? It adds nothing to the diagnosis.

10:34

Let's take a look at

10:37

noninfectious discospondylitis.

10:41

The first thing you should note

10:43

is the listhesis present at L4 on L5,

10:48

on the Sagittal T1 and proton density

10:51

fat suppression image.

10:52

The very presence of listhesis should make you

10:55

suspicious that these changes are mechanical.

10:59

Now, at first glance,

11:00

you might assume that the disc endplate

11:04

complex is effaced or erased.

11:06

But when you look at the water-weighted image,

11:09

you actually can still see it on the right.

11:13

And above it is a linear area of edema.

11:16

The rest of the vertebral body is relatively low in signal.

11:20

And even around that low signal intensity area,

11:23

is a high signal-intensity area of fat.

11:28

Fat marginating this area of low signal on T1

11:33

is a very strong sign as opposed to a fadeaway.

11:37

In musculoskeletal MRI,

11:39

we call this a narrow zone of transition abnormality,

11:43

whereas in our postoperative patient,

11:45

you saw a wide zone of transition edema.

11:49

This is a critical differentiator of infection

11:54

from mechanical inflammation.

11:57

And in this case,

11:58

we do have mechanical inflammation.

12:00

So we do have a high signal intensity disc.

12:04

So the disc signal, in this case,

12:06

doesn't necessarily help us, but everything else does.

12:10

And at the bottom,

12:11

you have a summation of all of the findings that support

12:15

the diagnosis, not of infectious discitis,

12:18

but of sterile mechanical discospondylitis.

12:23

Sometimes in patients like that, we'll actually do

12:27

standing lateral flexion and extension views, to see just

12:30

how unstable they are.

12:32

Here's the T2 weighted image.

12:34

You saw the T1 and the proton density fat suppression.

12:37

Look how bland appearing the T2 weighted image is.

12:41

On the T2 weighted image,

12:42

the disc is not so bright anymore, is it?

12:46

There's no disc abscess.

12:47

There's no real disc swelling on the T2.

12:51

We do see the low signal intensity of the endplate.

12:55

And the vertebral edema that we saw an infectious discitis

12:59

is not visible on the T2 weighted image.

13:03

Although, T2 signal intensity of the vertebral bodies

13:07

is a very variable finding,

13:10

it's less reliable than the pattern of edema on

13:13

the proton density, fat suppression, SPIR, STIR,

13:18

SPAIR or special images, which are required

13:21

in the assessment of the spine,

13:24

especially when you're looking for discovertebral osteomyelitis.

13:28

So T2 alone with T1 is not sufficient.

13:32

Here's a dramatic example.

13:35

At the L3-L4 level,

13:38

we have completely lost the disc endplate complex.

13:42

We have holo vertebral edema at L3 and L4.

13:47

We have soft tissue masses anteriorly and posteriorly.

13:52

We see the normal disc endplate complexes

13:56

at more proximal levels,

13:58

low signal intensity as a stripe all

14:00

the way from anterior to posterior,

14:03

even at this level where a small node exists.

14:07

Now, let's go to the T2 weighted image.

14:10

We already said that the pattern of vertebral edema

14:13

on the T2 weighted image is not reliable in discriminating

14:18

whether you have infectious or non-infectious inflammation.

14:22

But the pattern of disc anatomy,

14:26

endplate anatomy and disc signal is,

14:29

you saw a T2 weighted image in a

14:32

mechanical spondylitic case that

14:34

was low in the disc space.

14:37

But now you see this puffy area of signal alteration

14:41

that has completely destroyed and effaced the center of

14:45

the disc endplate complex with the vertebral bodies

14:48

low above and below,

14:51

and some inflammation that is extending anteriorly.

14:56

This is the typical pattern that one sees in chronic

14:59

discovertebral osteomyelitis on the T2 spin echo image,

15:04

even though fat suppression is on board.

15:07

Now, let's turn to the all-important proton density

15:12

fat suppression, SPIR, SPAIR, or Special image.

15:16

It's an edema party. It's an edema explosion.

15:20

Look at the center of that disc space.

15:24

This is all inflammatory material.

15:26

And sometimes you can even have an abscess or pus

15:30

that may require aspiration,

15:31

but that's the minority of cases.

15:33

The disc is completely destroyed.

15:35

You're not seeing an endplate here.

15:37

You're seeing what's left of the cortex-to-cortex.

15:41

The disc and endplate are now completely gone.

15:45

And anteriorly,

15:46

there's a tremendous amount of swelling that is

15:49

not fibrous tissue. It's not just a SPIR.

15:52

It's not just a ligament. It's inflammatory material.

15:56

So the end is up on this diagnosis, namely,

15:59

discovertebral osteomyelitis.

16:03

We've given you some cardinal signs to differentiate it

16:06

from sterile mechanical spondylitis.

16:09

Let's move on, shall we?

16:14

I'd like to turn our attention to example number two.

16:23

So now I have three sagittal images.

16:27

A sagittal T1,

16:29

a sagittal T2,

16:31

and a sagittal proton density fat suppression image

16:35

in a 14-year-old who is complaining of chronic back pain.

16:41

He plays American football,

16:43

not European football or soccer.

16:45

And he also wrestles,

16:48

both sports that involve hyperextension activities.

16:52

What's another sport that involves hyperextension activities?

16:56

Gymnastics.

16:57

I'm sure you've all seen women on the beam.

17:02

These are individuals who are very prone

17:04

to this diagnosis. So, let's scroll.

17:08

Let me see if I can get my pointer working.

17:10

But while we're scrolling,

17:11

I'm going to ask you to look at every single laminal

17:15

pedicle complex. On the left is a T1.

17:18

In the middle is a T2.

17:20

On the right is the PD SPIR

17:22

Keep looking.

17:22

I'm going to scroll from right to left,

17:25

and you should see a change in the signal intensity at one level.

17:30

And that is L4 right there.

17:34

Now, let's see if I can get my pen working here.

17:38

Take a run at it.

17:44

I'm going to draw it for you.

17:50

And here we go. Right there.

17:53

Nice high signal intensity

17:55

throughout the pedicle laminal complex.

17:58

Let's take that even one step further.

18:00

Right there, where my pointer is,

18:02

does everyone see the crack?

18:04

I'll bet you do.

18:06

Not so easy to see on the T2-weighted image.

18:10

Not as easy to see on the T1-weighted image,

18:16

but present.

18:18

Excuse me.

18:19

Present involving the upper cortical surface

18:23

of the L4 lamina pedicle complex.

18:27

What are the two most common causes of back pain

18:29

in a 14-year-old who's involved in sports?

18:32

They are facet arthropathy or facet inflammation,

18:37

capsulitis, and spondylolysis syndrome.

18:41

This is Spondylolysis Syndrome.

18:45

Now let's see if I can tactfully get out of my drawing tool

18:53

and do some clearing here.

18:57

And now let's bring down a couple of other images.

19:01

Let's bring down our axial. Let's scroll the axial.

19:05

And I'm going to focus on the T1 axial.

19:09

I want you to keep looking because a very confusing

19:13

thing for many young radiologists and

19:15

non-neuroradiologists, is differentiating

19:18

a swollen facet from true spondylolysis.

19:22

Now, this arc shape with intermediate signal intensity

19:26

is the cartilaginous unit of the right facet.

19:30

There's the slightly irregular cartilaginous

19:32

unit of the left facet.

19:35

And then as we scroll up, right there is a crack.

19:40

Right there is sclerosis with your crack.

19:42

I'm going to blow it up for you.

19:44

Everybody see the crack right there?

19:46

There it is.

19:47

It's horizontal.

19:50

Now let's go back to our facet. The facet is arc-shaped.

19:55

Facet.

19:57

Crack.

19:59

Horizontal crack with sclerosis,

20:02

facet arcuate shaped with cartilage intervening.

20:07

Now, let's return to our PowerPoint.

20:12

Let's talk about spondylolysis.

20:16

I'm trying to feed you information that you can't

20:19

necessarily get out of the book.

20:21

Yes, you can study spondylolysis in a book,

20:25

but what you don't hear about is the overuse and abuse

20:30

of CT lumbosacral spine with obliques and nuclear

20:35

bone scintigraphy to make this diagnosis.

20:39

Would you want three millisieverts or one year's worth

20:42

of background radiation with the target organ being the

20:46

testes and the ovaries delivered to your child?

20:49

To your teenage child?

20:51

Of course not.

20:53

And these patients,

20:54

not only do they get an X-ray or a CT or a nuclear study,

20:58

they get them again and again and again to see if it's healed.

21:03

A big mistake.

21:05

Let's stop radiating our children for this diagnosis.

21:08

I'm going to talk about the four stages of spondylolysis

21:13

that occur in bone as point number two.

21:16

And as point number three,

21:19

I want to emphasize, in every child,

21:22

in every adolescent,

21:23

in every individual where you suspect this diagnosis,

21:27

the T2-weighted image, even with fat suppression,

21:30

doesn't cut the mustard. It is not sufficient.

21:34

You must have proton density, STIR, SPIR, SPAIR, Special,

21:39

or an equivalent with the fat very black to

21:43

pick up some of the most subtle cases.

21:46

And here I put a nice white arrow to highlight a step off

21:51

of the lamina pedicle complex of L5 in a patient

21:56

with spondylolysis syndrome,

21:59

but as yet no listhesis.

22:03

There are three subtypes of anterolisthesis

22:07

you're going to encounter.

22:09

Traumatic.

22:10

In other words, a single acute traumatic event

22:13

that is not what we call a stress-type form of anterolisthesis.

22:19

These patients often have fractures or ligamentous

22:22

injuries, which you have to search for.

22:24

Now, I bring this up for a very important reason.

22:27

If you have a traumatic listhesis in the neck or in the

22:31

thoracic region, you must get an MRI before reducing it.

22:35

Before you put the head in tongs and distract the neck,

22:39

you need an MRI for the following reason.

22:46

back in place, what if you have a disc extrusion?

22:49

You now push the disc extrusion into the cord and you

22:53

can paralyze the patient.

22:55

MR in the cervical thoracic region

22:58

in a traumatic listhesis is required

23:01

for this very reason.

23:04

The next type of anterolisthesis is

23:07

apophyseal related listhesis.

23:10

Related to swollen distended facets.

23:16

This should prompt a lateral standing flexion and

23:19

extension view to see just how unstable the patient is.

23:23

On the axial MRI,

23:25

there are two signs that will help you.

23:28

One, the facets will appear wide and distended,

23:32

and they'll appear bright.

23:34

I refer to this as the distended facet sign.

23:39

And two, the patient will have not foraminal stenosis,

23:43

but central canal stenosis in this type of listhesis.

23:49

And then we go to spondylolysis-related listhesis,

23:52

also known as spondylolisthesis.

23:55

These patients have that horizontal defect

24:00

that I showed you and foraminal stenosis,

24:04

but the center of the canal is spared and may even

24:07

appear widened or stretched from anterior to posterior.

24:12

Now, let's talk about the stages of stress injury

24:16

that occur not, in the back alone,

24:20

but also in the tibia

24:21

and just about everywhere else in the body.

24:24

Let's have a look.

24:25

And I'm going to do a little drawing here.

24:27

Assuming my drawing tool works.

24:29

Let me give it a try.

24:33

Give me 1 second to load it up here.

24:36

This is a little new for me.

24:39

Sorry.

24:40

Let me take one more shot at it.

24:48

Well, it's not going to function for me,

24:50

but there are four stages of stress injury.

24:53

Stage one, edema.

24:56

Stage two,

24:58

a crack in the bone in the medullary bone.

25:03

Stage three,

25:04

it involves or transgresses one cortex.

25:07

And stage four,

25:09

both cortices are involved. Is this important?

25:12

It is important because patients that are in stage four

25:16

are much more likely to slip if you let them continue with sport.

25:21

The treatment for this disorder,

25:24

which is an overuse stress phenomenon in

25:27

individuals that have longer pedicles,

25:30

is rest, and the rest periods are longer with higher

25:34

grades of abnormality.

25:36

Let's have a look.

25:39

The sagittal T1-weighted image at the L4 level

25:43

shows the lamina pedicle complex. And right there,

25:49

a vertical line goes right into the cortex.

25:52

So it involves one cortical surface

25:55

and some of the medullary bone.

25:57

On the water-weighted image,

25:59

the edema is highlighted and obvious when you

26:03

compare the L5 and L3 levels.

26:06

A dark piggy,

26:08

a dark piggy and a white piggy with a vertical line in it

26:11

as a very small early stress fracture that is

26:17

incomplete, involving the superior cortical surface,

26:20

so-called grade 2 to 3 spondylolysis syndrome.

26:26

Here's one that's more complete.

26:28

This is a sagittal T2-weighted image.

26:31

Now, I said that proton density fat suppression

26:34

imaging is essential, and it is.

26:37

But the T2-weighted image may make it a little

26:39

easier to see the actual line, not the edema.

26:42

So for pure detection, especially in the early stages,

26:46

you've got to have the PD fat suppression,

26:49

but the T2 can add some information.

26:52

And in this case,

26:53

you see a line going all the way from superior cortical

26:56

surface to inferior cortical surface in this patient

27:00

with stage 4 spondylolysis syndrome.

27:03

And here again, is our arc-shaped facet, which is normal,

27:08

highlighted by our green arrow.

27:10

And with our squiggly white arrow is our transverse

27:14

low signal intensity spondylolysis fracture,

27:17

surrounded by sclerosis.

27:20

Spondylolysis,

27:20

horizontal facet arc-shaped.

27:24

So the end is up on this diagnosis.

27:28

Let's stop radiating teenagers, adolescents,

27:31

and young patients and start using the proper

27:35

examination to diagnose spondylolysis,

27:38

which is MRI with T1 and heavy water weighting.

27:43

Let's turn now to example number three,

27:46

and this time I'm going to display the abnormality initially

27:51

as a video.

27:53

We're going to talk about contact

27:55

impact and collision injuries.

27:57

But I want to focus on, first, contact

28:00

impact as it relates to sport.

28:03

And then I'll transition to more high velocity collision

28:07

injuries as might occur with an NBA.

28:10

Although I will admit, in patients,

28:14

in individuals who are playing professional sport,

28:17

two men that weigh 150 kilos or more colliding with each

28:22

other is the equivalent of a 30-mile-an-hour car collision.

28:26

But let's have a look and see what happened here.

28:29

My beloved Cincinnati Bengals are playing

28:32

the Cleveland Browns, two Ohio teams,

28:36

and one of our players is coming in to hit their player.

28:41

And you can see the head to shoulder contact.

28:44

It doesn't really look like much,

28:47

but understanding the mechanism

28:48

of injury is so important.

28:51

And I ask you,

28:52

is this a hyperextension injury

28:53

or a hyperflexion injury?

28:55

And I think most of you would say hyperflexion.

28:59

Watch one more time in slow motion,

29:02

which would make you think about flexion teardrop,

29:06

burst fractures, compression fractures.

29:09

So, let's tackle these three issues in contact sport

29:14

before we go on to high-velocity collision events.

29:19

Ligaments, stingers, and hyperacute blood.

29:24

Let's make a few definitions.

29:27

First definition: What's a cord concussion?

29:31

And this gentleman sustained one.

29:34

Transient loss of motor

29:36

and/or sensory function for less than 30 minutes

29:40

unassociated with an MR abnormality

29:43

on standard imaging.

29:45

In other words,

29:46

a normal MRI is part of the definition

29:50

of a clinical cord concussion.

29:54

Fortunately, as you'll see,

29:55

this gentleman recovered neurologic function

29:58

fully in less than 30 minutes,

30:01

although his injury was substantial.

30:05

A stinger.

30:07

A stinger is a root concussion.

30:10

It's characterized by transient burning in a dermatome

30:13

at the time of contact.

30:16

It's a peripheral nerve injury.

30:18

The nerve itself is normal unless you use

30:21

specialized imaging such as MR Neurography.

30:25

But there are indirect signs that

30:27

you will need to evaluate.

30:31

Let's begin with ligaments of the neck.

30:33

Here's our young man in his early 20s.

30:38

This was one of his first games playing,

30:40

and he's a 250-pound man,

30:44

about 110 kilos or so.

30:47

This is a sagittal T2-weighted image in our open

30:50

MRI in the stadium.

30:51

He went right into the MRI,

30:53

and it's pretty good image quality considering open MRI,

30:57

acutely injured individual with a large, thick neck.

31:02

And it shows the posterior longitudinal ligament.

31:05

Take a look at it.

31:09

It's contiguous, but stretched out a bit.

31:11

And the anterior longitudinal ligament gone.

31:14

There's no black line that should normally

31:17

be present right there, as there is here.

31:20

That black line is missing.

31:22

The anterior longitudinal ligament is ruptured.

31:24

A burst fracture has occurred in the anterior

31:28

half of the C6 vertebral body.

31:31

And he also had some posterior soft tissue injuries

31:35

that are beyond the scope of our discussion today.

31:39

Here's the sagittal T1-weighted image.

31:41

There is the burst.

31:43

There is the broken floppy ligament.

31:47

And here is another image showing a tear in the anterior

31:50

longitudinal ligament in this individual who sustained

31:55

a hyperflexion impact injury that led eventually to a

32:01

fusion and graft.

32:03

It ended his career, unfortunately,

32:05

and he became a very successful broadcaster.

32:09

So, ligaments, the soft tissues are a strength of MRI,

32:13

and not just the anterior longitudinal ligament,

32:16

the posterior longitudinal ligament,

32:18

the ligamentum flavum, the interspinous ligaments,

32:21

the supraspinous ligaments.

32:23

We're going to show you some examples

32:25

of those a little bit later on.

32:27

Let's turn our attention now to stingers in the neck.

32:31

This can occur in any contact sport,

32:34

especially sports where people lead with their head.

32:37

American football,

32:39

rugby,

32:41

Australian rules football.

32:45

The incidence of spondylosis in patients with stingers

32:48

is higher than those without, even in teenagers.

32:53

Give me an 18-year-old with a stinger

32:55

and I'll show you premature degenerative disease.

32:59

The re-stinger rate in collision athletes

33:02

is astounding.

33:03

It's 80%.

33:05

MRI and CT are combined to evaluate stingers for

33:10

detailed evaluation of foraminal opening size.

33:13

And MR is used for assessment of soft disc disease.

33:19

So together, they give you soft and hard assessments.

33:24

Hard bone assessment, CT.

33:26

Soft disc assessment,

33:27

and ligamentous assessment, MRI.

33:31

If the patient has a disc, central stenosis,

33:35

or foraminal stenosis and a stinger,

33:38

and the stinger has recurred more than twice,

33:41

that patient is a candidate for intervention,

33:44

foraminotomy or even disc space fusion.

33:50

One measurement technique,

33:51

and I'm not a big measuring guy,

33:53

because it takes a lot of time and can be inefficient,

33:56

is the Torg-Pavlov ratio.

33:58

And we use this in athletes.

34:00

It's the ratio of the vertebral body at its midpoint

34:04

to the ratio of the canal.

34:07

Or said another way,

34:09

the blue interval divided by the white interval.

34:13

Now normally, this should be greater than 1.2.

34:17

1.0 - 1.2 is mild.

34:19

And you can see as it decreases...

34:22

So as this space gets smaller

34:24

and this space gets bigger,

34:26

the Torg-Pavlov ratio goes down.

34:30

Patients with 0.7 or below have a very high stinger rate.

34:34

The people with a ratio of blue to white

34:37

of 0.6 or less, should not participate in contact sport.

34:43

There are other techniques that come out of Korea

34:47

to assess the stinger and cord concussion risk,

34:50

but those are beyond the scope of our discussion today.

34:54

And I'm just going to share with you today

34:56

the commonly employed Torg-Pavlov ratio.

35:00

Here's an example of a professional athlete who has,

35:04

what's known as Speartackler's Neck.

35:07

He leads with his head,

35:09

premature extensive degenerative disc disease and spondylosis.

35:13

And look how the CT myelogram, which, by the way,

35:16

we no longer use.

35:17

We use MR myelography,

35:19

combined with non-contrast CT,

35:22

but in this case, an older one,

35:24

showing the extent of foraminal stenosis,

35:28

which is incredibly severe on the right

35:30

and moderate to severe on the left,

35:33

with the facement of the cord and thecal sac in this MR

35:37

myelogram. But CT for the skeleton,

35:39

MR for the soft tissues.

35:41

Here's another one.

35:42

This is a famous American who played the position of

35:47

linebacker, which is a defensive position.

35:49

A large man,

35:50

a little bit over 120 kilo, and he had already had,

35:55

playing at the professional level, two fusions.

35:58

And it's done very well.

36:00

He played for three years with these fusions.

36:03

And now he presents, not with a cord concussion,

36:06

but with a stinger.

36:07

And there is his soft disc extrusion seen on

36:11

the T1 and on the center T2 weighted image.

36:16

So MR for the soft abnormalities,

36:19

CT for the bony abnormalities,

36:22

to assess central stenosis, acquired discs,

36:26

and foraminal stenosis in the young

36:29

vigorous athlete who has stingers.

36:33

The next subject I want to cover is hyperacute blood.

36:38

Hyperacute blood, I lumped in with sport,

36:41

but it can occur from a number of conditions.

36:45

The reason that I'm talking about hyperacute blood in

36:48

a spine talk is because you're never going to see

36:52

hyperacute blood in the brain or in the body.

36:55

And the reason is,

36:56

they're not on the MRI scanner fast enough.

36:59

When you bleed in the brain,

37:01

the bleed may be silent.

37:03

In fact, it may be silent for 6 hours, 12 hours, a day,

37:08

sometimes chronic subdural weeks on end.

37:11

But in the spine,

37:13

just the smallest amount of blood can

37:16

produce neurologic compromise.

37:17

And you've only got 3 hours to

37:19

get to that cord and save it.

37:22

So that patient is going to be on the table really quickly.

37:26

That's why it's appropriate to talk about hyperacute

37:28

blood from any cause in a spine talk that is

37:34

focused on unique scenarios.

37:36

Like this one.

37:38

This is from our Total Body Atlas, and...

37:41

Sorry.

37:41

This is from our Craniospinal book from 1990.

37:44

But it still holds up the evolution of blood.

37:49

Blood on T1 imaging goes from black to white,

37:55

from the acute to the chronic phase,

37:57

over about 3 to 14 days.

38:03

Now, what about hyperacute blood?

38:05

Hyperacute blood is less than 3 hours old.

38:08

Hyperacute blood may look like protonaceous fluid.

38:11

It can be dark or gray.

38:15

So it doesn't really look like blood.

38:17

In fact, it's hard to recognize blood

38:20

until you see methemoglobin

38:22

staining on the T1 weighted image,

38:24

which is displayed here at about four days.

38:28

That's why we have T2 weighted imaging.

38:31

Let's see what happens to blood on the T2-weighted image.

38:36

Let's just talk acute to chronic for a minute.

38:39

Acute blood, let's say blood that's three days old,

38:42

two days old, maybe even a day old,

38:45

will have some black signal intensity on the T2-weighted image

38:50

because of the intact red cells harboring deoxyhemoglobin

38:54

and methemoglobin, intracellularly,

38:57

it produces preferential T2 shortening.

39:00

This is the cardinal finding that one sees in acute blood,

39:04

and eventually it matures to white and may or may

39:08

not be surrounded by siderotic low signal intensity material.

39:12

But what about hyperacute blood?

39:14

Blood that's less than 3 hours old?

39:17

It looks like water.

39:20

Now, if we go back to our T1-weighted image for a minute,

39:23

intermediate to low on T1, high on T2,

39:27

you're not going to recognize it as blood.

39:30

Now, what if you get to the patient at about hour three?

39:34

The blood has to go from white to black at some point, right?

39:39

So what if the blood is now going

39:42

through a shade of gray?

39:46

Then it'll be gray to dark on T1 and gray on T2

39:52

if you catch it in this transition period.

39:55

And so, it may look like a mass.

39:59

It won't have the characteristics you've

40:01

come to know and love related to blood.

40:05

This is such an important trick

40:07

because if you think it's a mass,

40:09

you may not rush the patient to

40:11

the operating room in time.

40:13

Let's have a look.

40:15

This young woman, the sister of a famed,

40:19

well-respected orthopedic surgeon,

40:21

calls her brother in the middle of the night

40:24

and tells him, with her husband on the phone,

40:26

that she can't move her arms and legs.

40:28

So this wasn't a sport case,

40:30

but it illustrates hyperacute blood.

40:33

On the axial T1 weighted image,

40:35

the signal intensity is gray.

40:37

The cord is over here,

40:40

pushed to the viewer's right, the patient's left.

40:45

What is the signal intensity on the T2-weighted image?

40:50

This is the proton density image,

40:52

which we don't use so much anymore.

40:53

But look at the T2-weighted image,

40:56

the signal intensity is gray.

40:59

You are just reaching that threshold where you are going

41:02

from the hyperacute phase to the acute phase.

41:05

And on the T2-weighted image,

41:07

you're passing through this gray phase.

41:10

So if you were not an expert,

41:12

if you weren't on your game,

41:14

you might have called this a meningioma or a mass,

41:17

or a lesion, but not fresh blood, which it is,

41:21

and it got evacuated immediately.

41:24

And today, she is asymptomatic with no neurologic sequelae.

41:30

She was pregnant at the time.

41:31

And this is spontaneous epidural hematoma of pregnancy.

41:35

But this is what hyperacute blood will look

41:37

like from any collision type of event.

41:43

Let's compare hyperacute blood with acute blood.

41:48

There's a T1-weighted image,

41:51

acute blood,

41:52

low in signal intensity on T1,

41:55

just like the diagram.

41:57

On T2,

41:58

because there's intracellular deoxy and methemoglobin,

42:02

low signal intensity.

42:05

Dark signal,

42:07

acute blood,

42:08

subdural,

42:10

time for an evacuation.

42:13

Compare that with chronic blood.

42:15

Chronic blood is bright on T1 and bright on T2.

42:20

That one is easy.

42:24

Now let's talk about collision

42:26

higher impact injuries.

42:28

Although many of these sport injuries are pretty

42:30

high impact, as we alluded to earlier.

42:32

Let's tackle these three issues.

42:34

Traumatic discs,

42:36

whiplash, and as time allots,

42:38

cerebrospinal fluid leaks from dural tears.

42:43

Let's start out with traumatic discs.

42:48

Traumatic discs have a much greater

42:50

likelihood of bleeding.

42:53

Traumatic discs often extrude into the longitudinal ligament,

42:58

into their layers along with blood.

43:02

This acute blood,

43:03

if imaged in the first three to seven days after

43:07

the motor vehicle accident or event,

43:09

will be, as you saw in our subdural,

43:13

dark on T2.

43:16

Now, there are other signals that may be dark on a spine MRI,

43:22

including fast flow in veins,

43:25

fast flow in vessels and arteries,

43:27

calcification.

43:28

Air in an HNP.

43:31

Bleeding in the posterior longitudinal ligament.

43:34

Bleeding in the disc itself acutely

43:37

and calcified disc fragments.

43:40

Calcification of a disc fragment

43:42

may take four to six months,

43:44

as you'll get asked this question a lot

43:47

by the medical legal community.

43:48

But the presence of blood in a disc related to a motor

43:53

vehicle accident, or other high-velocity trauma,

43:55

has medical, but also medical-legal implications.

44:00

Here's a T2 and a heavily fat-suppressed,

44:03

water-weighted image on the right.

44:05

There's your disc extrusion subligamentous imposition.

44:09

It's better seen here on the right.

44:11

It's elliptical in shape,

44:13

but it's dark in signal intensity,

44:15

demonstrating its time course of three-day-old

44:19

blood in a patient who sustained an MVA.

44:24

Darkened signal intensity representing acute hemorrhage.

44:28

If you're unsure about whether you're

44:30

looking at calcification,

44:31

there's no crime in getting one limited level CT.

44:34

And this may support a medical legal scenario,

44:37

but also a clinical scenario.

44:39

But most of the time,

44:41

with the swelling that's present in the history

44:43

as well as the patient's neurologic status,

44:46

you should be able to glean that this

44:48

is blood and not calcification.

44:51

Whiplash.

44:53

Whiplash used to be a clinical term.

44:58

A sore neck,

45:00

a stiff neck,

45:01

decreased range of motion after a velocity

45:05

event or a deceleration event.

45:10

I use this pattern of posterior-to-anterior search in Whiplash.

45:15

I look for subcutaneous fat tears,

45:18

supraspinous ligament tears, interspinous ligament,

45:21

ligamentum flavum, anterior longitudinal ligament,

45:24

posterior longitudinal ligament, the disc, the cord,

45:28

the dura, and the skeletal pattern of injury,

45:32

to determine what I'm dealing with.

45:36

Here are three heavily water-weighted images.

45:39

And yes, the patient has sustained compression injuries

45:42

in the upper thoracic region,

45:45

illustrating that this was a high-velocity impact event.

45:49

But look at the other findings that include injury

45:54

and tearing of the subcutaneous fat,

45:57

a rent in the supraspinous ligament.

46:00

Right there.

46:01

And areas of interspinous ligament injury.

46:04

Right there.

46:06

Whiplash now has a soft tissue correlate on MRI,

46:11

but it must be evaluated using heavily

46:14

water-weighted sequences.

46:16

Once again, the proton density, fat suppression,

46:19

SPIR, STIR, SPAIR, or special.

46:24

The last subject I want to cover are dural tears.

46:29

Dural tears may sometimes be associated with

46:32

cord herniations through the dural tears,

46:34

but we're not going to cover that today.

46:37

We're going to cover a dural tear with leaking of the

46:41

cerebrospinal fluid through the tear

46:43

as it occurred anteriorly.

46:47

Here it is in the sagittal projection.

46:49

If you just glance at this image, first take,

46:54

you won't see anything wrong.

46:56

You've got the cord,

46:58

you've got the posterior intradural space,

47:00

and you've got the anterior intradural space.

47:03

Well, wrong.

47:05

That's the anterior intradural space.

47:07

This is all extradural fluid that has leaked out.

47:12

This is a patient with a pseudomeningocele,

47:15

and these often occur as a manifestation of a high

47:20

velocity traumatic event.

47:21

Here's another one.

47:22

Cord intrathecal anterior space,

47:27

intrathecal posterior space,

47:29

extrathecal extradural collection from a tiny little

47:34

leak with an associated traumatic disc extrusion.

47:38

And here it is on the CT myelogram.

47:41

There's the tiny little rent right there.

47:43

The CSF has extruded

47:45

or leaked out into the anterior extradural space.

47:49

This is extrathecal.

47:50

This is intrathecal.

47:53

That is the cord.

47:54

That is intrathecal.

47:56

And there's also blood in the posterior intrathecal space.

48:01

And yet here's another one.

48:03

This one has leaked out anteriorly and crept out

48:06

to the viewer's right, the patient's left.

48:09

And the patient has sustained a cord injury

48:13

with siderotic hypointensity in the

48:15

anterior aspect of the cord.

48:18

So you should be suspicious of a leak,

48:20

whether it's traumatic or surgical.

48:23

And sometimes, surgeons can produce the leak by tearing

48:27

the dura when the collection is eccentric,

48:30

especially when it surrounds the cord or extends anteriorly.

48:35

When the epidural veins,

48:37

which distend to fill the low pressure

48:39

of the intrathecal space are conspicuous.

48:44

When the cord retracts towards the collection,

48:47

when there's mass effect or pressure due to a ball valve

48:51

phenomenon, when there are orthostatic headaches,

48:54

the patient lies down, they feel good.

48:57

They get up

48:58

and they have the most excruciating

49:00

bifrontal superorbital headache.

49:03

When the cerebellar tonsils are sagging,

49:07

when the optic chiasm is sagging in the brain on the

49:11

sagittal cervical spine MRI,

49:13

if these happen to be seen,

49:14

and if you can catch the pituitary on a cervical MRI,

49:18

it will be large,

49:20

as the patient has intracranial hypotension.

49:25

So before I summarize,

49:27

I'm going to do a little wardrobe change here

49:29

because Dave Yousem did once.

49:30

And you know, I'm a copycat.

49:32

And I'm putting on my father's World War II hat

49:37

from the 351st Bomb Group.

49:40

He was also a member of the 10th Mountain Division,

49:43

the greatest generation.

49:44

He gave his life for this country.

49:46

And let's summarize.

49:48

Discitis.

49:50

We talked about the signs,

49:52

especially destruction of the endplate.

49:56

It's an imaging neuroclinician neuroimaging diagnosis,

50:00

not a laboratory diagnosis,

50:02

most of the time.

50:04

Spondylolysis, read it.

50:07

Get the right sequences.

50:09

Proton density fat suppression,

50:11

stage it,

50:13

and please, don't radiate it.

50:16

Contact sport.

50:17

You saw ligamentous injuries,

50:19

including the anterior longitudinal ligament.

50:23

You learned about cord concussions.

50:25

You learned about root concussions known as stingers.

50:29

And we took a moment to talk about this pitfall of

50:33

hyperacute blood that can be misconstrued for a mass.

50:37

And then we finished with a flurry, talking about

50:40

collision types of events at high velocity with

50:44

traumatic discs that bleed the many faces of Whiplash

50:48

and CSF leaks and their signs.

50:51

I'll take any questions.

50:53

Thanks for your attention and regards to all

50:56

of you around the world who are listening.

51:00

Thank you. Dr. P.

51:01

Let's get up your questions for you.

51:08

Now, I can read these to you,

51:10

or can you see your question-and-answer

51:11

panel down at the bottom?

51:13

I can try, but I cannot see it.

51:16

Okay, I'll just read them off to you.

51:20

Dr. Pomeranz, what do you mean disc endplate complex?

51:24

What structures are included in this?

51:27

Okay, let's see if I can get my drawing tool to work.

51:38

Okay, so let's draw a vertebral body,

51:43

and let's draw one next to it.

51:46

And then in between the vertebral body,

51:47

we're going to have a disc.

51:52

So let's make our disc blue.

51:54

Here we go.

51:56

Now, making up the disc endplate complex,

51:59

because we can't separate these out,

52:01

except with extremely high resolution,

52:04

are three layers.

52:06

And those three layers are going to include,

52:09

they're going to include the annulus fibrosis,

52:11

which I'm going to make in yellow.

52:13

So it's going to be dark around the periphery of the disc.

52:16

So the annulus is included in that.

52:20

Then just above that,

52:22

we're going to have the osteochondral endplate in green.

52:29

And then beyond that,

52:30

we have the cortex of the vertebra, which is in red.

52:34

So you're actually looking at three structures there.

52:36

That's why I call it a complex.

52:38

The annulus, the osteocartilaginous endplate,

52:42

and the cortex.

52:43

All of these are destroyed with that puffy exploding

52:47

disc sign that I showed you in my example,

52:51

in multiple examples of disco vertebral osteomyelitis.

52:56

Next question.

52:58

What is the slice thickness recommended in

53:01

sagittal images to detect spondylolysis?

53:07

Well, I don't have a specific thickness.

53:10

I prefer to have three-millimeter cuts.

53:13

But if you've got quality contrast resolution,

53:17

in other words,

53:18

a great quality STIR and a great quality T1,

53:22

which you can do at any field strength,

53:24

5 mm will get the job done.

53:27

So the answer is 5 mm,

53:29

but I prefer three.

53:30

And on some of my high field systems,

53:33

I often use T2 isotropic fast spin echo

53:38

with 1.2-millimeter slices.

53:40

But this is not a requirement by any stretch

53:43

of the imagination.

53:44

Five is the number.

53:48

This one simply says,

53:49

"Infection versus charcot spine."

53:52

I don't know if you have any commentary on that.

53:54

Yes, infection versus charcot spine.

53:57

Well, first, people with charcot spine

54:00

will have a reason for their charcot spine.

54:03

They don't just have it and show up with it.

54:05

So there's usually a clinical tip-off.

54:07

But unfortunately,

54:08

people with charcot spine also get infected.

54:11

So I'm going to use this same diagram and I'm going to

54:15

draw something that may be conceptually

54:17

a little difficult to conceive.

54:20

But when somebody has a charcot anything,

54:23

whether it's a foot or a spine, it's a very etched,

54:26

jagged edge to the charcot interface.

54:30

Whereas when somebody has an infection,

54:34

it is kind of an ill-defined sort of fade away pattern

54:38

of edema where you completely lose the edges,

54:41

you lose the signal intensity of even fragmented,

54:45

fractured cortices.

54:46

So this jagged appearance charcot,

54:50

this erasure fading appearance infection,

54:53

and sometimes they coexist when you

54:56

have charcot with an infection.

54:58

I just had such a case in one of my former

55:01

attendings about a year and a half ago.

55:03

So it's an excellent question.

55:05

Next.

55:07

How do you differentiate between dyscitis osteomyelitis

55:10

and mets or focal tumors, such as plasma cytoma?

55:17

Well, that one is pretty easy.

55:19

You know, somebody that has a discitis

55:23

is going to have disc disease.

55:25

I mean, you rarely get

55:28

hematogenous involvement of the vertebral

55:31

body without involving the disc.

55:33

So the disc is involved in disc vertebral osteomyelitis.

55:37

I have only seen one case in my entire 35 year

55:41

career of a metastasis to a disc space.

55:45

So involvement of the disc combined with destruction

55:48

of the end plate like we showed you.

55:50

Now, in somebody with a met,

55:52

even if the met is right up against the endplate,

55:55

it'll usually be rather focal and confined to that area,

55:58

which is usually the posterior one third of

56:01

the vertebral body and/or the pedicle.

56:03

So it has a focality to it.

56:06

Now, it may be a mass with edema around it,

56:09

but you'll usually be able to see the mass in the middle

56:12

and then you'll be able to see the edema surrounding the mass.

56:15

And that edema will fade away,

56:17

but there will be a mass around it.

56:19

So the answer is focality for a metastasis.

56:22

Metastases don't involve disc spaces.

56:25

It's extremely rare.

56:27

And you'll often be able to spot

56:29

a mass in the middle column,

56:31

which is the posterior one-third of vertebral body,

56:34

or in the adjacent pedicle,

56:36

which is where metastases go.

56:38

Discospondylitis can go anywhere,

56:40

but it tends to like the middle and front,

56:43

whereas metastases like the posterior one-third back here.

56:50

Is DWI helpful for evaluating blood in the spine?

56:55

Is DWI helpful for evaluating blood in the spine?

57:00

Yes, it is.

57:02

And the reason is there's a lot of pulsation

57:04

that occurs in the spine,

57:06

and that pulsation leads to low signal

57:09

intensity on T2 imaging.

57:11

So if you're trying to...

57:12

if you're equivocating or trying to decide

57:15

between blood and a pulsation phenomenon,

57:17

the presence of diffusion restriction supports

57:20

the diagnosis of blood.

57:22

Also, diffusion restriction occurs in an abscess.

57:25

Remember that.

57:26

And sometimes an abscess can have low signal intensity

57:30

on T2 because it contains neutrophils,

57:33

and neutrophils contain peroxidases,

57:36

and peroxidases are paramagnetic.

57:38

So just because it's dark,

57:40

you're not off the hook in differentiating

57:42

blood from an abscess.

57:45

Let's try and get through two

57:47

more here in the time left.

57:50

Do you advise substituting routine STIR with

57:54

PDFS, sagittals in the acute trauma setting?

57:59

Do I advocate using STIR as opposed to PD fat suppression?

58:06

You know, as long as you have a high-quality

58:10

fat suppression, I don't mind if it's a spectroscopic type

58:13

like SPAIR, SPIR, or special,

58:16

or non-spectroscopic type like STIR,

58:19

which is used at lower field,

58:21

as long as you get quality fat suppression.

58:24

Often in those cases, time is of the essence.

58:27

The patients are uncomfortable.

58:29

So if you can expediently perform a STIR faster

58:33

and that's all you've got in your scanner,

58:35

that's going to get the job done.

58:40

Okay, last one here,

58:42

and I'm sorry to everyone that we

58:43

couldn't get to these questions.

58:46

There are so many coming in.

58:47

But the last question,

58:49

For CSF leaks is IV contrast

58:52

of any value in diagnosing?

58:54

For CSF leaks,

58:57

I mean, I suppose it could be of some value

59:00

in a weird scenario,

59:01

but the answer to that question is an overriding no.

59:04

Most of the time,

59:05

these are traumatic or they are post-operative

59:08

or perioperative.

59:14

Okay. Thank you so much, Dr. Pomeranz.

59:16

I'm going to let Ashley take us out.

59:18

Thank you all.

59:19

As we bring this to a close, I want to say thank you,

59:21

Dr. Pomeranz, for your time today.

59:23

And thanks to all of you for joining us and

59:25

participating in our noon conferences.

59:26

A reminder that this conference will be made available

59:29

on-demand within the next 24 hours at mrionline.com.

59:33

Please join us tomorrow, April 1st at 12:00 p.m,

59:36

Eastern Standard Time.

59:38

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59:43

Oh, that is not correct. She'll be with us tomorrow.

59:46

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59:48

to be notified of reminders and updates.

59:50

Thank you so much and have a great day.

59:53

Pleasure.