Interactive Transcript
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All right, it is now 12:00,
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and we are going to get started.
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So, I just wanted to say hello and welcome to the 7th of
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many live stream noon conferences hosted by MRI Online.
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In response to the changes happening around the world
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right now and the shutting down of in-person events,
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we have decided to provide free daily noon conferences
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to all radiologists worldwide.
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Today we are joined by Dr. Stephen J. Pomeranz.
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He is the founder of MRI Online,
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CEO and medical director of ProScan Imaging.
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He has authored numerous medical textbooks in MRI,
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authored numerous MRI texts,
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including the MRI Total Body Atlas.
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He is an avid conference lecturer,
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chairs fellowship training programs
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in MR and advanced imaging.
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A reminder that there will be time at the
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end of this hour for a Q&A session.
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Please use the Q&A feature to ask these questions and
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we'll get to as many as we can before our time is up.
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That being said, thank you so much for joining us today.
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Dr. P, I will let you take it from here.
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Dr. Pomeranz: Welcome to everybody around the world.
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Hope you're all doing well.
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Today, we're going to talk about
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critical concepts in spine imaging.
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And I'm going to predominantly stay away from disc disease,
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which is a commonly understood subject and
1:10
one that we will cover at a later date.
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Although there will be some description and discussion
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of this matter as it relates to contact or collision events.
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These are my faculty disclosures.
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I have nothing else to declare.
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And I'd like to begin with my first case,
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which is a
1:33
middle-aged individual with back pain.
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And I'm going to scroll on the left,
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a T1 spin echo image.
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In the center, a T2 spin echo image.
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And on the far right,
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I've got a fat suppression proton density image.
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And these three images demonstrate a cardinal MR finding
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in an entity that you should all recognize,
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and that is discovertebral osteomyelitis.
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Now, there are several highlighted abnormalities that make
2:08
this diagnosis and is pathognomonic
2:11
and diagnostic on MRI alone.
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First, on the T1-weighted image,
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we have completely lost the normal endplate.
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I'm going to draw the normal endplate for you,
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or I'm going to highlight it for you
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with a few little tick marks here.
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And the endplate is this very subtle...
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Actually, I'm going to draw it with my little arrow here,
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this very subtle area of low signal intensity right
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there, between the vertebral body and the disc.
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Now, this line is composed of both the cortex and the
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osteochondral endplate. So it's a summation of both.
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And look at how it is completely destroyed on the
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T2 weighted image and completely destroyed
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on the proton density fat suppression image.
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In its wake is an area of diffuse inflammation,
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increased signal in the disc space,
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and an area of prespinous soft tissue inflammation.
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This pattern of endplate destruction.
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And I'm going to scroll a little bit so you get a better feel for it.
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It's typical and diagnostic of discovertebral osteomyelitis
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and allows it to be differentiated from
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microinstability, sterile spondylitis.
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Now, let's go back to our PowerPoint and talk about Discitis.
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I want to focus on three key issues.
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One, understanding the pattern of endplate effacement.
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Regardless of whether the patient
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has had an operation or not,
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this effacement of the endplate is still diagnostic of
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an infectious Discitis and is best appreciated on
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the T1 and the fat-suppressed proton density image.
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Issue number two.
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Discitis is an MRI neuroclinician, neuroimaging diagnosis.
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It is not a diagnosis that you should necessarily
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be making by aspirating the disc space,
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by relying on the sedimentation rate,
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or by relying on the white count. In other words,
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this is an imaging diagnosis.
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And finally,
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what are the constellation of signs for Discitis
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and how to slam the door open,
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making the diagnosis,
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or closed,
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shutting down the diagnosis
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in a patient who has endplate swelling,
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but one of those two diagnoses.
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Now, there are three key findings that allow you to
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differentiate inflammation at the disc endplate complex
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that is infectious versus mechanical or noninfectious.
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The first,
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increased signal in the disc space
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without a vacuum phenomenon favors infectious Discitis.
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Vacuum phenomenon, on the other hand,
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favors sterile spondylotic mechanical disease.
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Number two.
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As already shown,
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endplate destruction or erasure of the end plate
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is typical of discitis versus swelling or edema,
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but still, sharply defined low-endplate signal that is
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marginated by reactive fat in the vertebral body.
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Reactive fat is an excellent sign around the disc endplate
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complex that you are not dealing with an infection.
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Number three.
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Disproportionately long elongated and high signal intensity
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on water-weighted imaging,
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pre and paraspinous masses that does not represent a SPIR
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or fibrous tissue, or a ligament.
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This is another supportive sign of infectious discitis.
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And I'll add one more to that.
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The amount of edema in the vertebral body.
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More than 50% of the vertebral body edematous or even
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holo vertebral edema is typical of infection,
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whereas laminar or linear small volume edema is typical of
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noninfectious mechanical spondylitis.
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Clinically, any patient with inordinate pain that is so severe that
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even bumping the patient or the patient coughing,
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so-called 'Tuss of back pain'
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is typical of infectious discitis.
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Aspiration.
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Sometimes performed in situations
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where you have a walled-off abscess
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is positive only 15% of the time.
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So culture positivity is not going to
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be found in 85% of aspirations.
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So we empirically treat with antibiotics
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based on the MR findings.
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Only occasionally will you feel the need
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to drain a walled-off abscess
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in patients who are immunosuppressed,
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such as diabetics and patients with renal insufficiency.
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Check for air or gas.
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Gas in the soft tissues, bad infection.
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Air in the disc space or air in the facet,
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good, so-called vacuum phenomenon.
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So where the air or gas is located really matters.
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Fourth point.
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MR has a very poor correlation temporarily with
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the clinical improvement of the patient.
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In fact, the patient may get better,
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but the MR may not show improvement
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for six to nine months or more.
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So MR is not necessarily used to ascertain
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the efficacy of antibiotic treatment.
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Perhaps most challenging for the more advanced
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practitioners of you out there
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is the postoperative spine.
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You would think that when someone has a cage placement
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and a fusion that you would get inordinate amounts of
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edema at the disc endplate complex, but in fact,
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you don't.
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And any endplate and what I call non-marginated
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vertebral edema, which I'm going to show you,
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should be viewed with suspicion, even around cages.
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Let's take this case.
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Sagittal T1-weighted image on the left.
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Sagittal T2-weighted image on the right.
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The cages are obvious as oblong areas of low signal intensity.
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But look at the vertebral signal.
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Look at a normal vertebra, the T2-weighted image,
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not as valuable
9:00
for T2 imaging is not that water-sensitive.
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But compare L3 with the subtle loss of vertebral signal,
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the entire vertebra, holo vertebral edema
9:11
should absolutely not be present, even with this cage.
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And look at the loss of the endplate
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low signal intensity stripe,
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and it's even more severe and worse at L5.
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Yes, the simple T1-weighted image,
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any scanner can do it,
9:30
tells the story of non-marginated edema with loss of
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the disc endplate complex or linear low signal stripe,
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both at L4-5 and L3-4
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in a patient who has sustained
9:47
a postoperative infection.
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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
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and sterile reactive endplate change
10:04
from infectious destructive aggressive
10:08
discovertebral osteomyelitis.
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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.
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It does show enhancement of this prespinous mass,
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which was present on the non-contrast portion of the study.
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It shows enhancement of the disc,
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it shows enhancement of the vertebral bodies,
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but so what? It adds nothing to the diagnosis.
10:34
Let's take a look at
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noninfectious discospondylitis.
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The first thing you should note
10:43
is the listhesis present at L4 on L5,
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on the Sagittal T1 and proton density
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fat suppression image.
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The very presence of listhesis should make you
10:55
suspicious that these changes are mechanical.
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Now, at first glance,
11:00
you might assume that the disc endplate
11:04
complex is effaced or erased.
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But when you look at the water-weighted image,
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you actually can still see it on the right.
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And above it is a linear area of edema.
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The rest of the vertebral body is relatively low in signal.
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And even around that low signal intensity area,
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is a high signal-intensity area of fat.
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Fat marginating this area of low signal on T1
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is a very strong sign as opposed to a fadeaway.
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In musculoskeletal MRI,
11:39
we call this a narrow zone of transition abnormality,
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whereas in our postoperative patient,
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you saw a wide zone of transition edema.
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This is a critical differentiator of infection
11:54
from mechanical inflammation.
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And in this case,
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we do have mechanical inflammation.
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So we do have a high signal intensity disc.
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So the disc signal, in this case,
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doesn't necessarily help us, but everything else does.
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And at the bottom,
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you have a summation of all of the findings that support
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the diagnosis, not of infectious discitis,
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but of sterile mechanical discospondylitis.
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Sometimes in patients like that, we'll actually do
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standing lateral flexion and extension views, to see just
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how unstable they are.
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Here's the T2 weighted image.
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You saw the T1 and the proton density fat suppression.
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Look how bland appearing the T2 weighted image is.
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On the T2 weighted image,
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the disc is not so bright anymore, is it?
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There's no disc abscess.
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There's no real disc swelling on the T2.
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We do see the low signal intensity of the endplate.
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And the vertebral edema that we saw an infectious discitis
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is not visible on the T2 weighted image.
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Although, T2 signal intensity of the vertebral bodies
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is a very variable finding,
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it's less reliable than the pattern of edema on
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the proton density, fat suppression, SPIR, STIR,
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SPAIR or special images, which are required
13:21
in the assessment of the spine,
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especially when you're looking for discovertebral osteomyelitis.
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So T2 alone with T1 is not sufficient.
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Here's a dramatic example.
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At the L3-L4 level,
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we have completely lost the disc endplate complex.
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We have holo vertebral edema at L3 and L4.
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We have soft tissue masses anteriorly and posteriorly.
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We see the normal disc endplate complexes
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at more proximal levels,
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low signal intensity as a stripe all
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the way from anterior to posterior,
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even at this level where a small node exists.
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Now, let's go to the T2 weighted image.
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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.
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But the pattern of disc anatomy,
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endplate anatomy and disc signal is,
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you saw a T2 weighted image in a
14:32
mechanical spondylitic case that
14:34
was low in the disc space.
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But now you see this puffy area of signal alteration
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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.
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This is the typical pattern that one sees in chronic
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discovertebral osteomyelitis on the T2 spin echo image,
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even though fat suppression is on board.
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Now, let's turn to the all-important proton density
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fat suppression, SPIR, SPAIR, or Special image.
15:16
It's an edema party. It's an edema explosion.
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Look at the center of that disc space.
15:24
This is all inflammatory material.
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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.
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The disc is completely destroyed.
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You're not seeing an endplate here.
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You're seeing what's left of the cortex-to-cortex.
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The disc and endplate are now completely gone.
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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.
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We've given you some cardinal signs to differentiate it
16:06
from sterile mechanical spondylitis.
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Let's move on, shall we?
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I'd like to turn our attention to example number two.
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So now I have three sagittal images.
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A sagittal T1,
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a sagittal T2,
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and a sagittal proton density fat suppression image
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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,
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both sports that involve hyperextension activities.
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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.
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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
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Keep looking.
17:22
I'm going to scroll from right to left,
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and you should see a change in the signal intensity at one level.
17:30
And that is L4 right there.
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Now, let's see if I can get my pen working here.
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Take a run at it.
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I'm going to draw it for you.
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And here we go. Right there.
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Nice high signal intensity
17:55
throughout the pedicle laminal complex.
17:58
Let's take that even one step further.
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Right there, where my pointer is,
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does everyone see the crack?
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I'll bet you do.
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Not so easy to see on the T2-weighted image.
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Not as easy to see on the T1-weighted image,
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but present.
18:18
Excuse me.
18:19
Present involving the upper cortical surface
18:23
of the L4 lamina pedicle complex.
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What are the two most common causes of back pain
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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.
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This is Spondylolysis Syndrome.
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Now let's see if I can tactfully get out of my drawing tool
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and do some clearing here.
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And now let's bring down a couple of other images.
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Let's bring down our axial. Let's scroll the axial.
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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.
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I'm going to blow it up for you.
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Everybody see the crack right there?
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There it is.
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It's horizontal.
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Now let's go back to our facet. The facet is arc-shaped.
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Facet.
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Crack.
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Horizontal crack with sclerosis,
20:02
facet arcuate shaped with cartilage intervening.
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Now, let's return to our PowerPoint.
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Let's talk about spondylolysis.
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I'm trying to feed you information that you can't
20:19
necessarily get out of the book.
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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.
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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.
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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
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59:29
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59:33
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59:36
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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
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59:50
Thank you so much and have a great day.
59:53
Pleasure.
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