Myelopathy: From Spinal Cord Signal to Diagnosis, Dr. Francis Deng (10-23-25)
HIDEInteractive Transcript
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Hello and welcome to Noon Conference, hosted by Modality
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Noon Conference connects the global radiology community
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through free live educational webinars that are accessible
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for all and is an opportunity
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to learn alongside top radiologists from around the world.
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Today we are honored to welcome Dr. Francis Dang
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for a lecture entitled Myelopathy from Spinal Cord Signal To
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Diagnosis, Dr.
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Dane completed his radiology residency
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and neuroradiology fellowship at Massachusetts General
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Hospital and is currently a diagnostic neuroradiologist
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and assistant professor of radiology
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and radiological science at Johns Hopkins University.
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He's received multiple teaching awards from medical
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students, radiology residents, and neuroradiology fellows,
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and was a runner up for the Ant Mini Most Effective
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Radiology Educator in 2024.
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At the end of the lecture, please join him in a q
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and a session where he will address questions
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you may have on today's topic.
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Please remember to use that q
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and a feature to submit your questions so we can get to
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as many as we can before our time is up.
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With that, we're ready to begin today's lecture, Dr.
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Dang, please take it from here.
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Thank you so much. So it's my pleasure to present
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to you about myelopathy
1:10
and specifically how to come
1:12
to a specific diagnosis when you can.
1:14
Very often these patients are undifferentiated when they
1:17
present, and I'm gonna show you a few, uh, pearls
1:20
that will allow you to narrow the differential diagnosis.
1:24
So, first of all, let's begin with discussing
1:27
what is a myelopathy.
1:29
A myelopathy from a clinical standpoint, is any disorder
1:32
that is attributed to spinal cord pathology
1:36
and clinically how it presents is motory
1:38
and sensory signs and symptoms.
1:40
Um, they usually, uh, they have to spare the head
1:44
and face, uh, because the spinal cord subserves only the
1:47
torso and the extremities and, and not the head and,
1:50
and, uh, and face.
1:51
So the symptoms, uh, that would be isolated
1:54
to the lower part of the body would potentially be something
1:57
that refers to the spinal cord.
2:00
Usually the symptoms are bilateral
2:03
and, uh, affect the body below a certain level.
2:06
So if you have a problem that affects only
2:09
above a certain level, that is less likely to refer
2:13
to the spinal cord is sometimes you can have myopathies
2:16
that are unilateral, and those are somewhat more difficult
2:20
and challenging to localize based on your neurologic exam.
2:24
And so what I mean by motor and sensory symptoms
2:26
and signs are weakness of the lower extremities and
2:30
or upper extremities, um,
2:32
and long tracked signs, which
2:34
in neurological parlance refers to such signs
2:37
as hyperreflexia spasticity
2:40
and babinski skin, which is when you stroke the sole
2:43
of the foot and there are outgoing toes.
2:46
In addition, you would have a sensory level, which refers
2:48
to reduced sensation below a certain level of the body.
2:52
And, uh, very commonly you can also have bladder symptoms.
2:55
And the bladder symptoms
2:56
that occur when you have spinal cord dysfunction are
3:00
urinary retention with overflow incontinence.
3:03
And that's because you no longer have volunteer control of,
3:06
uh, bladder emptying.
3:08
And so the bladder empties only by a, uh, automatic reflex,
3:12
uh, within the, within the, the, the neurons
3:15
that supply the bladder itself.
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So you have urinary retention
3:18
and then, uh, people have incontinence due
3:20
to overflow incontinence.
3:23
So what is the imaging
3:25
that should be obtained if you have a patient
3:27
that is suspected to have a myelopathy?
3:30
The American College of Radiology has put out
3:33
appropriateness criteria for myelopathy,
3:35
and they divide it into two different scenarios depending on
3:38
whether the symptoms were acute
3:39
and onset versus subacute and chronic and onset.
3:41
But the table between the two are actually the same.
3:44
And so let's take a look at this table right here that says,
3:46
usually appropriate is MRI of the spine of the area
3:50
of interest without and with contrast
3:51
or MRI of the spine of the area
3:53
of interest without IV contrast.
3:55
So breaking down, breaking down those two
3:58
in, uh, a little bit.
3:59
So they're saying spine of the area of interest.
4:01
Well, that depends on if you're able on neurologic exam
4:04
to localize the spinal cord dysfunction
4:07
to a particular level, then you could,
4:09
uh, focus on that level.
4:10
But more and more in practice in recent years,
4:12
we're seeing people, uh, from the clinical side asking
4:17
for total spine imaging
4:18
because number one, they're not confident of their ability
4:22
to localize to a specific level.
4:24
And number two, there are situations where
4:27
you localize a lesion to the thoracic level,
4:29
but the actual pathology is in the cervical level.
4:33
Uh, you just, you know, had milder
4:35
symptoms affecting the upper extremity, so you didn't think
4:38
that the lesion would be in the
4:39
cervical level, for instance.
4:40
And so more and more there's a, a, a more of a trend
4:43
to image more and more of the spine.
4:45
The general rule of thumb is if you localize it
4:47
to a certain level, you want to image
4:48
that level plus the level of above it.
4:50
Um, because the spinal cord ends in most individuals
4:54
around the L one two level, it is not necessary
4:57
to image the lumbar spine.
4:59
So as long as you're sure your thoracic spine field
5:02
of view includes the tip of the conus
5:05
and that your neurologic exam is consistent with kind
5:08
of a upper motor neuron dysfunction referable
5:11
to the spinal cord and not to the cauda equina per se.
5:15
So if you're confident that you have a myelopathy,
5:17
a cervical and thoracic spine, MRI without ima, uh,
5:21
without contrast or without
5:23
and with contrast would be appropriate.
5:25
Now, listed under here
5:26
as may be appropriate would be CT based imaging, and that's
5:30
because CT is relatively limited in the breadth of diagnoses
5:34
that it can identify
5:35
and we'll talk about that in a little bit.
5:37
But the a CR has listed under here, CT myography
5:40
of the spine area of interest,
5:41
and that would allow you to identify areas
5:43
of compression of the spinal cord.
5:45
And then CT spine of the area of interest without contrast
5:48
or with IV contrast is again limited in its ability
5:51
to define all the pathologies that
5:53
that could affect the cord.
5:54
It has, uh, very little ability to define,
5:56
define intrinsic lesions of the cord itself,
5:58
but could define, uh, you know, vertebral lesions
6:02
that are affecting the cord.
6:03
Usually not appropriate within these include MR angiography
6:07
of the spine, even if you suspect a vascular lesion causing
6:11
a myelopathy, usually it is not appropriate as part
6:14
of the initial evaluation
6:16
and should only be obtained on, um, you know,
6:18
a second order evaluation.
6:20
Once you have reasons to suspect a,
6:22
a certain vascular lesion like a dural arterial venous
6:25
fistula, and you're planning a spinal angiogram,
6:27
might you consider Mr.
6:28
Angiography, uh, um, uh, of the area of interest?
6:33
So how do we approach myelopathy?
6:35
So I would say that, uh,
6:36
step one is actually getting the history
6:39
and I think it, uh, behooves radiologists to try
6:42
to obtain from chart review
6:45
or conferring with the referring clinician
6:47
or the treating clinician.
6:49
The history as to the nature of the patient's symptoms,
6:53
it is not enough to read an MR of the spine
6:56
with the only history being, you know,
6:57
evaluated for core compression.
6:59
I want to know what are the nature
7:01
of the patient's symptoms.
7:02
And mo most importantly, I wanna know the tempo of the onset
7:05
of the patient's symptoms because step one here is
7:08
that if the patient has hyperacute onset symptoms,
7:11
meaning from onset to peak deficits less than 12 hours,
7:16
then the top of my differential should be a spinal
7:20
cord infarct.
7:21
Okay, the diagnostic criteria suggested proposed
7:26
for diagnosing acute spinal cord infarct
7:30
includes very prominently the clinical history of an onset
7:33
to the nadir of their severe sensory motor deficits
7:37
of 12 hours or less.
7:40
On imaging, you can see intramedullary T two
7:44
hyperintensities within the cord.
7:46
Here we can see a very subtle T two hyperintensity
7:49
and the ventral aspect of the cord of the cervical spine.
7:52
This is a patient who, um,
7:55
had acute hyperacute onset sensory motor deficits
7:59
on axial images.
8:00
A classic sign that has been described is this snake eye
8:03
sign where you have ventral, uh, cord ventral, um,
8:08
uh, you know, anterior horn T two hyperintensities.
8:11
That creates a two dot of a, uh, two dots
8:14
of T two hyperintensity in the ventral cord
8:17
that suggests a gray matter predominant injury, uh, due to,
8:21
you know, lack of blood supply to the anterior spinal artery
8:24
and the most, um, you know, oxygen
8:27
and, uh, blood supply sensitive parts
8:29
of the cord are injured.
8:30
In this case, on the sagittal image would appear
8:33
as a pencil like hyperintensity, and it can be very subtle.
8:37
If you had a artifact degraded exam,
8:38
this would be very easy to miss.
8:40
So it's very important to also review your axle images for
8:44
cord signal abnormalities such as this.
8:48
Very often the history is not provided upfront
8:51
or the referring clinicians did not, you know,
8:53
have a high enough suspicion for a cord infarct,
8:56
and the patient will have to return for additional imaging
8:59
to include a DWI.
9:00
That's because most centers do not include A DWI
9:03
of the spinal cord as part of
9:05
of spinal MRI routine protocols.
9:08
If you had the history
9:10
or the clinical state of clinical suspicion
9:12
for a cord infarct, we should obtain a DWI of that portion
9:16
of the spinal cord to evaluate for diffusion restriction.
9:21
Additional signs that have been identified in addition, um,
9:25
include arterial dissection, uh,
9:27
or occlusion adjacent to a lesion such as
9:29
of the vertebral arteries.
9:30
If you're referring to the cervical spine,
9:33
you may see lack of a flow void.
9:35
Uh, you may see, uh, you know, uh,
9:37
two separated flow voids indicating a dissection flap.
9:40
Sometimes you can see a vertebral body signal abnormality
9:43
that actually represents a vertebral body infarct.
9:45
Uh, but those are relatively less common in my
9:47
experience in this case.
9:50
A DWI was obtained two days after the first MRI,
9:53
and what we see here is an area
9:55
of hyperintensity on this DWI high B value tracing image
9:58
representative of Accord infarct, explaining
10:01
that signal abnormality.
10:04
Now, I wanna make a note here that the timing
10:06
of imaging when it comes to accord infarct matters
10:10
very often in the hyperacute period
10:12
that is within the first day, often upon first presentation,
10:15
the spinal imaging will be nearly normal.
10:17
You'll be very hard pressed
10:19
to call any signal abnormality in this
10:20
cord on, in this case.
10:22
In this case, uh, it was a child who fell down some stairs,
10:26
um, and they had a paraplegia afterwards.
10:30
Uh, uh, I believe here on the, uh,
10:33
on the initial scan on the axial images,
10:36
there were some faint signal abnormalities.
10:38
And that, uh, because of the high level
10:39
of suspicion from the referring clinician's part,
10:41
the patient was brought back for additional imaging
10:44
to include A DWI.
10:45
And this was obtained on day three after the accident.
10:49
And what we see here is progression, uh,
10:51
or new newly apparent signal abnormality in the cord on this
10:55
stir image, uh, T two hyperintensity within the cord.
10:59
And on DWI.
11:00
Here we see areas of high signal intensity representing
11:03
diffusion restriction.
11:04
And so this would be compatible with cord infarct.
11:08
Now, it's also important to note that later on,
11:10
as in the evolution of cerebral infarcts,
11:14
cord infarct will also develop blood
11:16
brain barrier breakdown.
11:18
And in the late acute
11:19
to subacute phase will develop contrast enhancement.
11:22
And so you can imagine a scenario where a patient, uh,
11:26
had these, um, cord deficits
11:29
and was only image at a subacute period,
11:31
and they have all this contrast enhancement.
11:33
You may mistake this into thinking this is an inflammatory
11:36
process because of the contrast enhancement.
11:38
However, the clinical history is very important about the,
11:42
uh, length of time from onset to the peak
11:46
of their spinal cord deficits.
11:49
This would be compatible in the subacute period
11:51
with a cord infarct.
11:53
So again, so we see very little signal abnormality
11:56
after a little bit, we see core T two hyperintensity
11:58
diffusion restriction that is most apparent.
12:00
And then eventually we have continued swelling
12:03
and blood break, blood, uh,
12:05
blood cord barrier breakdown resulting
12:08
in contrast enhancement.
12:09
And that is possible, and that should resolve
12:11
after a few weeks, and the swelling will reduce.
12:15
So what if you can't get MRI?
12:16
This is not, uh, an infrequent occurrence in, you know, uh,
12:20
current radiology practice
12:21
because of a proliferation
12:23
of cardiac devices that are electronic.
12:26
And so, uh, you have to be, uh, you know, uh, either stuck
12:30
with CT or there may be a delay in obtaining a,
12:33
a device enabled, uh, MRI, um, due to the safety precautions
12:38
that have to be undertaken with certain MRI devices, uh,
12:41
with certain cardiac devices rather.
12:43
So this was a, a 84-year-old who had a pacemaker,
12:47
and, uh, that pacemaker was not compatible with MRI,
12:50
who had sudden onset paraplegia and a sensory level as well.
12:54
And a non-contrast CT was obtained,
12:57
and a very sharp-eyed reader, uh,
13:00
caught a hyper density within the spinal canal here
13:04
and is, you know, probably not well projecting,
13:06
but I'll, I'll say that probably an average reader would not
13:10
have caught this, but very, uh, a very astute reader, uh,
13:13
did raise the possibility
13:14
of an intraspinal hematoma in this case.
13:17
Well, uh, they were not confident of this,
13:19
and so the neurosurgeons, uh, asked
13:21
for additional evaluation
13:23
before, uh, they would take them
13:26
for operative intervention in order to, you know, uh,
13:29
reduce the likelihood of a, of a, a, a kind
13:32
of a unnecessary, uh, operation.
13:35
Um, what CT without contrast is good for in the evaluation
13:39
of a acute onset myelopathy is to evaluate
13:43
for any bony compression of the cord.
13:45
And so in the trauma setting, you're looking
13:47
for a burst fracture with retropulsion
13:49
of the posterior cortex of the vertebral body
13:52
that would be compressing the cord.
13:53
Uh, you would certainly be evaluating
13:55
for any translational injury
13:57
that could be transecting the cord.
13:59
Uh, you would also be evaluating for ossification
14:01
of the posterior longitudinal ligament.
14:03
OPLL creates spinal canal stenosis
14:06
that then upon even trivial trauma can cause cord
14:09
compression and cord contusion.
14:11
Um, and, and a
14:12
and a less common, uh, finding is ossification
14:14
of the ligament and flam typically in the thoracic spine,
14:17
which can also contribute to a spinal canal, stenosis
14:20
and cord compression, um, uh, with myelopathy induced
14:24
after even trivial trauma without a, a spinal fracture.
14:28
Uh, the next step in imaging for patients
14:30
who cannot get MRI is a CT myography.
14:33
And so that's obtained by, uh, uh, doing a lumbar puncture,
14:36
instilling, uh, intrathecal I contrast,
14:39
and then positioning the patient tilting the bed in a way
14:42
to run that contrast up the spinal canal
14:45
to see if there's any lesion that is, uh, uh, kind
14:50
of occluding or narrowing the thecal sac.
14:53
In this case, uh, with the suspected intraspinal hematoma,
14:57
uh, CT myelogram was performed,
14:59
and you can see that the contrast does not run
15:02
above a certain level in the mid-thoracic spine.
15:05
And the way that it was configured on axial images was there
15:08
was this suggestion that this was a subdural hematoma.
15:12
So, what CT myelogram is good for evaluating
15:14
that a non-contrast CT is not good at evaluating
15:17
or, uh, any soft tissue
15:19
or fluid collections that are compressing the cord.
15:21
And this would include abscess a hematoma, uh,
15:24
and potentially epidural tumor as well in a patient who has,
15:28
you know, vertebral metastases
15:29
that may be extending into the epidural space.
15:32
So say you've, uh, excluded a hyperacute onset, um, you,
15:36
you've crossed off a spinal cord infarct, uh,
15:39
or any, um, you know, epidural metastatic disease
15:42
or hematoma, uh,
15:44
and the patient is presenting with a myelopathy
15:46
that is more acute, subacute, or chronic.
15:49
So acute in the myelopathy setting means, um, from onset
15:52
to peak symptoms of less than three weeks.
15:54
Subacute is, you know, slightly longer than that,
15:57
and chronic is, um, many months.
15:59
So step two is, um, uh,
16:02
considering whether the myelopathy is due to compression,
16:05
and that is actually probably the most common cause
16:08
of myelopathy in adults and,
16:10
and usually occurring in patients
16:12
who are older than 55 years of age.
16:14
And so when we interpret any imaging for the indication
16:17
of myelopathy, that is probably the first consideration
16:20
that you're gonna think about, and you're gonna evaluate
16:23
and try to exclude, um,
16:25
provided you, you know, did not have the
16:27
provided history of a hyperacute onset and so forth.
16:29
Most patients are gonna have an acute onset
16:31
and they're undergoing imaging, uh, or a subacute onset,
16:33
and they're undergoing imaging for,
16:35
you know, uh, myelopathy.
16:36
The first thing you want to look for is cord compression.
16:39
And so in this case, this is a very typical case
16:41
of cervical spondylosis, meaning multilevel dys bulges,
16:44
enfolding of the ligament of flam, uh, you know,
16:47
potentially superimposed on congenital stenosis
16:49
of the cervical spinal canal, causing indentations
16:52
of the cord IE compressions of the cord.
16:54
And in the center of the cord,
16:56
you can also see elevated T two signal.
16:58
So this is consistent with a myelopathy
17:01
that was explaining this patient's symptoms,
17:03
which were bilateral upper extremity weakness
17:05
and paresthesias.
17:08
This is a case, uh, of, uh, a patient
17:11
who also had myelopathic signs and symptoms.
17:14
They had imbalance, a feeling
17:15
of their legs giving out from them.
17:17
They also had bilateral hand numbness
17:19
and, uh, on imaging contrast was administered.
17:23
I'll say that contrast is not required, uh,
17:27
for this evaluation,
17:28
but when obtained, sometimes you can see a band
17:31
of contrast enhancement at the level
17:32
of greatest compression or right below it.
17:34
And this is known as the pancake sign.
17:36
And this is relatively specific for spondylotic myelopathy,
17:40
as in you get a band
17:41
of contrast enhancement on the sagal image on the axial
17:44
image is kind of more diffused throughout the level.
17:47
And this is due to cord compression.
17:50
And this is really helpful in cases where you're not sure
17:53
that the degree of compression
17:54
that you see on T two weighted images is really enough
17:57
to cause the signal abnormality in the cord.
17:59
Here, for instance, I can still see a sliver
18:02
of CSF signal ventral, uh, to the cord and,
18:04
and the ligament of flam here is, you know,
18:07
mostly effacing the CSF on the dorsal side.
18:10
But, you know, I, if given this alone,
18:12
I wouldn't be confident that compression was the
18:14
only etiology here.
18:15
But once I see the pancake sign, I could be more confident
18:18
that this degree of stenosis
18:19
and may any motion that may be occurring that we're not able
18:22
to image, um, you know, during normal flexion extension
18:25
of the neck, could be contributing
18:27
to a cord compression picture here.
18:29
And that would be causing spondylotic, uh,
18:31
spondylotic myelopathy.
18:33
Now, as I said, contrast is not required
18:35
for spondylosis assessment.
18:37
So if, uh, a patient just has neck pain, radiculopathy,
18:40
whatever you don't need to protocol at with contrast.
18:43
Um, but if performed because a patient has myelopathy not
18:46
otherwise specified, and the clinical suspicion was
18:48
for inflammatory causes, then contrast is typically given.
18:53
In this case, uh,
18:54
patient already had an A CDF anterior cervical discectomy
18:57
infusion for prior cork compression.
18:59
By clearly it had not, um,
19:01
completely decompressed the spinal canal.
19:04
There is still some degree of spinal stenosis here
19:06
with ligament and flam thickening and,
19:08
and overall congenital spinal canal stenosis.
19:11
And what we saw in this patient here
19:12
who had myelopathic symptoms is, um,
19:15
a longitudinally extensive T two signal hyperintensity,
19:18
as well as a large region of contrast enhancement.
19:22
And so you have to wonder whether it's coincidental
19:24
that it's at the level
19:25
of cord compression at the operated levels
19:28
or due to an inflammatory cause.
19:31
Um, but in this case,
19:32
because there is any cord compression, our presumption is
19:35
that that needs to be ruled out
19:36
before considering other causes.
19:38
Compressive myelopathy being common,
19:40
common things being common,
19:42
that would be the target to treat.
19:43
Uh, and that is the kind of thinking
19:45
that spinal surgeons undergo.
19:47
And so this case, uh,
19:48
underwent surgical decompression from posteriorly
19:51
to take off that lamina
19:52
and, um, give that, uh,
19:54
posterior dural sac more room to breathe.
19:56
So there is now res restoration of the CSF, uh,
19:59
signal ventral and dorsal to the cord.
20:02
The T two signal abnormality decreased,
20:05
and the contrast enhancement resolved confirming the
20:08
diagnosis was spondylotic myelopathy IE due
20:11
to compression of the spinal cord.
20:13
And so that contrast enhancement can happen, uh, due
20:17
to compression of the cord.
20:18
And that's the teaching point here.
20:20
Sometimes compressive myelopathy can be subtle and tricky
20:23
because it's not an obvious compression of the cord.
20:27
And there are other subtle signs in, in more rare conditions
20:30
that you should consider if you see intrinsic cord signal
20:33
abnormality in a deformity to the cord as well.
20:37
So this is a scalpel sign, uh,
20:39
where you see a dorsal cord indentation that is kind of, um,
20:43
uh, asymmetric like this, kind
20:45
of like the knife blade on a scalpel.
20:48
And in the cord substance we see T two hyperintensity, um,
20:52
uh, kind of like a developing snx,
20:54
but it's, it's a pretty stark, um,
20:56
T two signal abnormality in the cord right above
20:59
where we see this narrowing of the cord due
21:01
to a dorsal scalpel sign.
21:03
And this is due to a dorsal thoracic arachnoid web.
21:07
This is a thickening of the arachnoid mater
21:10
that causes a constriction of the dorsal side
21:14
of the thoracic cord.
21:16
And, uh, this patient was symptomatic.
21:18
They had like paresthesias, they have feeling of imbalance,
21:20
feeling of their legs giving out as, as well
21:22
as on clinical exam hyperreflexia.
21:25
And so that was consistent with the myelopathy.
21:27
They underwent imaging and found this, uh, arachnoid web.
21:31
They underwent surgery to release that arachnoid web, um,
21:34
and, and the patient's symptoms, uh, improved, right?
21:38
Another condition that is very subtle is, uh,
21:41
that can cause compressive myelopathy is hi a YAMA disease.
21:45
So, hi, a Yama disease is a rare condition
21:49
that was originally described in, um,
21:52
adolescent young adults, uh, Asian males predominantly
21:55
who had bilateral upper extremity, uh, weakness
21:58
and potentially sensory signs.
22:00
Um, and that was found to be due to this abnormality
22:05
where the posterior dura
22:07
of the thecal sac comes off from the lamina, swings forward
22:11
with flexion of the neck, and then compresses the cord.
22:14
And so that's called a flexion induced
22:16
posterior drill detachment.
22:17
There's detachment of the thecal sac from the lamina
22:21
and the epidural space, engorges with, you know,
22:24
the epidural venous plexus
22:26
and contributes to, uh, anterior displacement
22:29
of the cord and compression of the cord.
22:31
And over time, repetitive injuries
22:33
to the cord causes a myelopathy.
22:36
Now, I'm not showing you a case of classic hi,
22:39
Yama disease is relatively rare.
22:41
I've only seen two cases in my career.
22:43
This is another case, uh, out of my institution that is a,
22:47
has been described as a hi yama,
22:48
like disease happening in the thoracic spine.
22:51
This patient was a 23-year-old male who presented
22:54
with lower extremity weakness that was concerning
22:56
for a myelopathy
22:57
and underwent imaging of the thoracic spine.
22:59
And typically that is done on MRI
23:01
in the neutral position, right?
23:02
You're lying, uh, flat in the bore.
23:05
And what was noted here were a prominent, um,
23:08
epidural flow voids.
23:10
And that could be one of two things.
23:11
Number one, you have just engorgement
23:13
of the epidural venous plexus.
23:15
Number two, you could have a vascular anomaly such
23:17
as a dural arterial venous fistula
23:19
or something like that, um, that is causing engorgement
23:22
of these veins, uh,
23:23
because of the suspicion for a hi yama like disease.
23:27
The patient underwent a repeat MRI in the flexion position.
23:31
So the technologists were instructing the patient, uh,
23:34
to image themselves, uh, with, with their neck flexed.
23:37
And sure enough, this caused greater engorgement
23:40
of that epidural space.
23:41
You can see this line that represents the posterior, uh,
23:44
part that puts your wall
23:45
of the thecal sac coming anteriorly,
23:47
decreasing the space available for the cord
23:50
and kind of compressing the cord
23:51
because of this engorgement of the, uh, uh,
23:53
epidural venous plexus
23:55
and kind of, um, you know, lymphatic channels in there.
23:58
Uh, whatever is causing, uh, this, uh, high signal with kind
24:02
of serpentine flow voids here, uh,
24:05
because the dura is now no longer attached to the, um,
24:09
osteo ligament structures of the posterior elements, right?
24:12
And so this is here yama,
24:13
like disease in the thoracic spine,
24:15
causing this patient's myelopathy.
24:18
Now, um, one, uh, final entity I want
24:21
to make sure everyone is aware of, uh,
24:23
as CRO causing a a compressive myelopathy is a,
24:27
is an acute analog
24:28
to the hir yama like disease case that I just showed.
24:31
And this is due to a de novo fluid collection in the
24:35
epidural space, and like huma,
24:37
and here, yama like disease, this causes dural displacement
24:40
and you have fluid signal in the epidural space.
24:42
But in addition, you would have, um, a fluid signal outside
24:47
of the epidural space in the
24:48
paraspinal soft tissues as well.
24:50
Uh, and so this was a case of a spinal epidural abscess.
24:53
This was a, a young adult injection drug user
24:56
who developed progressive proximal upper
24:58
and then lower extremity weakness and numbness.
25:00
And that was concerning for a myelopathy.
25:02
And they underwent a total spine MRI, uh,
25:04
initially without contrast.
25:06
And, um, and the diagnosis may be difficult for you
25:11
to reach without contrast
25:13
because, you know, you may be thinking,
25:14
oh, I'm looking for an abscess.
25:16
I'm looking for a room enhancing fluid collection rate.
25:18
Um, I want to put forward
25:20
that you can make this diagnosis very confidently on a
25:23
non-contrast exam alone,
25:24
when you see this anterior displacement
25:27
of the posterior dural sac,
25:28
and you can see on fat suppressed
25:30
or stir, uh, you know, uh, T two fat s sat
25:32
or stir images of the spine
25:34
that you can see this abnormal fluid signal in the epidural
25:38
space, um, separating the posterior elements from the
25:41
posterior dural sac
25:42
that represents an abnormal fluid collection in the setting
25:45
of someone who has risk factors like injection drug use.
25:48
This would be highly suspicious for an epidural abscess.
25:52
This was longitudinally extensive,
25:53
extended all the way from C two down all the way into
25:56
the lumbosacral spine.
25:58
And the key to look
25:59
for on these sagal fat suppressed images is this thick,
26:03
dark line that represents the dura, right?
26:05
You should not have this thick, dark line, uh, just, uh,
26:09
as a, as a normal structure related to the cord.
26:12
This is the, uh, the dura
26:14
of the thecal sac being displaced anteriorly.
26:16
So make sure to look for that, uh, both on sagittal
26:20
and axial views
26:21
of the spinal cord on these total spine screening.
26:24
Uh, studies for patients who have risk factors
26:27
for developing a spontaneous spinal epidural abscess, mainly
26:30
inject drug users, but also, you know, patients
26:33
who are immunocompromised and may have bacteremia
26:35
and so forth, spinal epidural abscess.
26:39
So say you've evaluated for spinal cord compression,
26:42
you've rule out spinal cord compression,
26:44
your job is not done.
26:45
We have to consider other etiologies myelopathy next.
26:48
And so the category that I want
26:50
to next consider are subacute or chronic myopathies.
26:54
And within the categories of subacute
26:56
and chronic myelopathy is several
26:57
of them have particular imaging features that allow you
26:59
to narrow your differential diagnosis.
27:02
So step three in my diagnostic algorithm here is, uh,
27:06
does the patient have a subacute
27:07
or chronic myelopathy based on clinical history?
27:10
And I'm gonna look for particular imaging features.
27:13
The first set of imaging features I'm gonna look
27:15
for are signs of a duro arterial venous fistula.
27:18
The main sign to look for are engorged per medullary veins.
27:23
So, uh, this can be subtle sometimes.
27:26
Um, but I'm gonna, I'm gonna show you, uh,
27:29
a a couple of images here.
27:30
Uh, first in the zoomed out view, just to show you
27:33
that there are a few, uh,
27:35
T two hyperintense do dots here at the ventral aspect
27:37
of the conus that represent, um, abnormal flow voids.
27:42
And then on a zoomed up view here, we can see this busyness,
27:45
uh, around the coquina and,
27:47
and around the conus meis
27:49
that represents these abnormal flow voids.
27:52
Um, uh, in addition,
27:54
we can see there's chord signal abnormality,
27:56
like longitudinally extensive throughout the thoracic cord.
28:00
And so that's sign number one
28:01
that you have a radiographic, uh, myelopathy.
28:04
That's the intramedullary T two Hyperintensity Number two,
28:07
the specific sign is per medullary flow voids.
28:10
And these can be around the cord and around the conus.
28:12
It can also be around the CAU aquina.
28:14
And when around the cau kaa, it gives a busy appearance.
28:17
Um, people have described this in the literature.
28:19
It's ka a EQU disorder, like there's a disorderly appearance
28:23
to the ka equina.
28:24
It's not a smooth flowing horse hair appearance.
28:27
In addition, another classic sign
28:29
that has been described in the literature, um,
28:31
in a classic Adrian r article by Bob Grossman and,
28:34
and others, uh, is a peripheral core T two hypo intensity
28:38
that refers to this starkly dark appearance on axial T two
28:41
weighted images at the periphery of the cord.
28:43
And the central part
28:45
of the cord is the abnormal T two hyperintensity,
28:48
but the periphery is not just spared cord,
28:50
it's actually kind of relatively dark,
28:52
darker than you expect it to.
28:54
There are various hypotheses put forth
28:56
what this T two hypo intensity represents,
28:59
but the, I, uh, the, the thought is that this is due
29:02
to chronic venous congestion.
29:04
So remember that dur venous fistula creates a myelopathy
29:07
because it causes chronic venous hypertension.
29:10
And so the blood supply
29:12
to the cord can't drain out the venous side as well.
29:15
And this causes congestion,
29:17
and this causes backup in the capillaries.
29:18
This causes edema in the cord.
29:20
Uh, you can also have dilation
29:22
of capillaries maybe at the periphery,
29:24
maybe at hemosiderin deposition.
29:25
So people are suggesting that that is
29:27
what causes a peripheral core tial hypo intensity.
29:30
So if you see a longitudinally extensive subacute, uh,
29:34
myelopathy, uh,
29:36
with a peripheral core T two hypo intensity look really hard
29:39
for these perminary flow voids that can raise the suspicion
29:42
for a dural arterial venous fistula.
29:44
And the next step of evaluation
29:45
to recommend is really a spinal angiogram, uh,
29:50
because that offers the, um, resolution,
29:53
the spatial resolution to identify, uh, uh,
29:55
fistula connections, uh, allows the temporal resolution
29:59
to isolate the venous phase
30:00
and identifying any venous, uh, drainage as well
30:03
as abnormal, uh, arterial, uh, facialist connections.
30:07
And, uh, you know, most importantly allows you to kind
30:09
of isolate each spinal artery to, you know, kind of identify
30:13
what is the level and the source of
30:14
that fistulas connection.
30:16
Um, some people do suggest getting Mr Angiography
30:19
as a precursor to spinal angiogram,
30:21
but I find that it is mainly helpful when positive
30:25
to guide the spinal angiogram.
30:27
And it never obviates the need for a spinal angiogram, uh,
30:30
catheter angiogram because that is more
30:32
sensitive and specific.
30:33
Um, Mr angiography
30:35
of the spine is technically challenging in order
30:37
to have sufficient spatial resolution,
30:39
also temporal resolution to identify the, you know,
30:42
ideal arterial phase
30:43
and the, um, art arterial source
30:45
of any abnormal vessels within the spinal canal.
30:48
And so I, I find that generally it's, it, it's,
30:50
it's not supremely helpful
30:51
and not a mandatory part
30:52
of the evaluation if you do suggest a presence
30:56
of a dural arterial venous fistula.
30:58
Another specific sign to look for in the cases of subacute
31:02
and chronic myopathies is a dorsal column, inverted V sign.
31:06
This refers to on axle T two weighted images,
31:09
you have T two hyperintensity of the dorsal columns,
31:11
which creates an inverted V appearance here on sagal images.
31:16
This can be very subtle
31:17
because it kind of blends in, uh, kind of tapers out, uh,
31:21
with the CSF in the adjacent, uh,
31:23
in the adjacent, uh, CSF space.
31:25
And I'll tell you, this case was subtle enough
31:27
that the original reader had missed it.
31:29
Um, this was not suspected clinically, uh,
31:31
but then upon, you know, further evaluation
31:34
as this is actually discovered on peer review, um,
31:36
that there wasn't, uh, dorsal column, inverted v sign, the,
31:40
the, the, um, high clinical, uh, kind
31:44
of high radiologic suspicion
31:46
for subacute combined degeneration was raised
31:48
and communicated to referring clinicians who then said, oh,
31:50
well, um, I guess that does make sense
31:53
with the patient's clinical presentation
31:54
that did have a large amount of weight loss recently failure
31:57
to thrive for unclear reasons.
31:59
Uh, why don't we do the laboratory workup
32:01
for vitamin B12 deficiency?
32:03
Their vitamin B12 actually returned within the normal range,
32:06
but actually, uh, you know, the clinician should remember
32:09
that vitamin B12, uh,
32:10
level testing is not entirely sensitive
32:13
for the diagnosis of B12 deficiency.
32:15
You also have to check, um, homocysteine,
32:17
methylmalonic acid, which were abnormal in this case,
32:20
and allowed them to establish
32:21
the diagnosis of B12 deficiency.
32:23
In this case, it was due to pernicious anemia.
32:26
Upon further testing, there were antibodies
32:27
to intrinsic factor, uh, which account for the, uh,
32:32
diagnosis of pernicious anemia, um,
32:33
B12 deficiency causing subacute combined degeneration,
32:36
this patient who had myelopathic symptoms referable
32:38
to the dorsal columns.
32:41
Uh, one final set of, uh, uh, of findings
32:44
and entities to consider, especially if you have a subacute
32:47
to chronic myelopathy.
32:49
Um, this is a, uh, this category of subacute
32:51
and chronic myelopathy is, is difficult
32:53
because the patients often present within the acute phase,
32:56
and you're considering the acute etiologies first,
32:58
and they have to have good clinical follow up
33:01
and then repeat imaging to see if the abnormalities improve
33:04
or that they're, or, or they're persistent
33:06
or they're, you know, progressive in order
33:08
to consider this final kind of category, uh,
33:11
which is neoplasm.
33:13
So neoplasm can simulate, you know, acute myopathies
33:16
and myelitis in, in various manners
33:18
because, uh, if it's a diffusely infiltrating glial tumor,
33:22
uh, the only abnormality may be, uh, kind
33:26
of a ill-defined T two hyperintensity of the cord.
33:29
And, uh, and the reason to suspect a neoplasm is if you see
33:33
that it is, uh, persistent
33:36
or progressing despite treatment for the other etiologies
33:39
that have been considered, including inflammatory causes.
33:41
So they've received steroids,
33:43
but upon repeat imaging, a month
33:45
or two later, you still have the persistent
33:47
and essentially static signal abnormality, uh,
33:49
in the spinal cord,
33:51
and it has a expand style appearance,
33:54
then neoplasm has to be considered.
33:56
And most commonly you'll have, uh, kind of glial series, um,
34:00
tumors, uh, astrocytomas, um, appendamoma is potentially,
34:04
um, uh, in this case, uh, there was no contrast enhancement,
34:08
uh, which would, you know,
34:09
make appendamoma a little less likely, consider ace cytomas.
34:13
In this case it was biopsied, uh, eventually.
34:15
And the diagnosis pathologically was diffuse midline glioma,
34:18
H three K 27 altered, which is a histone modification
34:22
that is, uh, diagnostic of this particular entity
34:24
of diffuse midline glioma.
34:25
Diffuse midline glioma must commonly affects the brainstem,
34:28
but it can also affect, um, you know,
34:31
other midline structures, uh, including the thalami as well
34:34
as the spinal cord that has been described in adults.
34:39
So if none of the above apply, we've ruled out compression,
34:42
we've considered hyperacute etiologies,
34:44
we've considered subacute and chronic etiologies,
34:46
then you're dealing with the biggest bucket,
34:48
which is acute onset myopathies,
34:51
and you might be doing with the myelitis.
34:52
So this is where I want to go into the discussion of
34:55
what is a myelitis.
34:56
So, um, the traditional term has been transverse myelitis,
35:00
and that was always a term that was relatively confusing
35:02
for me because the, uh, radiologic appearance
35:05
of these transverse myelitis is not always like a,
35:08
a transverse section of the cord.
35:10
This is a clinical term.
35:12
Uh, but first I want to talk about what is myelitis.
35:14
And myelitis is a myelopathy that is due to inflammation.
35:16
And so patients will have, um, uh, you know,
35:19
classic transverse of myelitis
35:20
as you infect the entire
35:22
level of the cord at a certain level.
35:23
So you have bilateral symptoms that are either sensory
35:25
or motor or autonomic dysfunction.
35:27
I mentioned weakness or sensory deficit
35:30
or bladder, uh, uh, lack of bladder control.
35:33
That's a, uh, attributed to the spinal cord.
35:36
The correlate that we see on imaging is T two
35:38
hyperintense signal change.
35:40
And the suggestion
35:41
that there's an inflammatory component would be either
35:44
by the presence of contrast enhancement on MRI,
35:47
or if you don't have contrast enhancement,
35:49
you can still suggest it is myelitis based on CSF analysis.
35:54
So you would see Cleo cytosis meaning elevated white count
35:58
or elevated IgG index, suggesting that there is, you know,
36:01
de novo synthesis of immunoglobulins within the thecal sac.
36:05
And of course, you have to exclude other things
36:07
that we've already discussed, like compression.
36:09
So, uh, this bucket of transverse myelitis is clinically
36:13
and radiologically heterogeneous
36:15
because they don't always involve the entire
36:17
transverse section of the cord.
36:18
Um, there have been recent suggestions
36:21
that we should revisit the p nomenclature,
36:23
drop the transverse part, call it a myelitis.
36:24
I think that makes a lot more sense than me.
36:26
A myelitis is inflammatory myelopathy.
36:29
So say you may be dealing with a myelitis
36:31
and you have a patient with acute onset myelopathy,
36:34
and you've identified some chord signal abnormality with
36:37
or without contrast enhancement you may be doing,
36:40
dealing with a myelitis.
36:42
The first step in evaluation of these is
36:45
determining whether the abnormality is short
36:47
or longitudinal extensive,
36:48
and that should be in your impression in the description
36:51
of these chord signal abnormalities.
36:53
So the classic cause of a short lesion causing a, a myelitis
36:58
or a, you know, inflammatory myopathy is multiple sclerosis.
37:02
So multiple sclerosis, what is defined
37:04
by short lesion less than three vertebral bodies in length.
37:06
You have a short T two hyperintensity here in the mid
37:10
cervical cord associated
37:12
with contrast enhancements
37:13
suggesting inflammatory component.
37:15
Uh, uh, this by itself would not be sufficient
37:19
to diagnose someone with, with, um, with multiple sclerosis,
37:23
but you have to refer to the, um, McDonald criteria,
37:27
which were recently revised and released.
37:29
The 2024 McDonald criteria were recently published,
37:33
you know, in, uh, September
37:35
or October of 2025 in the Lancet.
37:38
So refer to those and what criteria you need to meet.
37:42
Uh, at a minimum, you need imaging of the brain and,
37:44
and optic nerves, as well as whatever you image
37:47
for, for the myelitis.
37:49
Um, and, um, potentially, you know,
37:51
a clinical evaluation for other causes.
37:54
Other causes of short lesions include, um,
37:58
atypical cases of neuromyelitis optica spectrum disorder,
38:02
or myelin oligodendrocyte glycoprotein associated disease.
38:05
And so I'm gonna call these N-M-O-S-D and MAD from now on.
38:09
So most cases of N-M-O-S-D
38:10
and moga D have longin like extensive lesions,
38:12
but a minority, maybe less than 20%
38:15
of them will have short lesions as well.
38:17
And so that's important to
38:19
consider in the differential diagnosis.
38:20
If you see an isolated short, uh, you know, uh,
38:23
myelitis lesion, uh,
38:25
that is still within the differential diagnosis,
38:27
it's you cannot automatically establish multiple sclerosis.
38:30
In addition, sarcoidosis can cause, uh, short lesions
38:34
and then, uh, a very large category
38:36
of idiopathic, uh, myelitis.
38:38
So the, the entity known as idiopathic transverse myelitis
38:42
or idiopathic myelitis very often will have isolated,
38:46
uh, short lesions.
38:47
And, uh, and, and that's what the diagnosis
38:50
of exclusion would be for this patient if they had not met
38:53
the criteria for multiple sclerosis.
38:56
So let's talk about longitudinally extensive lesions.
38:58
So longin extensive lesions refers to lesions
39:00
that expand more than three vertebral bodies in length.
39:03
And so, um, very commonly you'll have idiopathic myelitis.
39:06
And this one is a case
39:08
of N-M-O-S-T neuromyelitis optica Spectrum Disorder.
39:11
Uh, so this is a longitudinal
39:13
extensive T two hyperintensity.
39:14
We see it spanning three vertebral body levels.
39:17
Uh, there was, uh, some areas of contrast
39:20
and enhancement within this lesion,
39:21
and this is what it, uh, the lesion looks like
39:23
on an axial image.
39:25
Uh, this appearance is not specific to N-M-O-S-T.
39:28
I'm just showing you one example
39:29
of a relatively non-specific myelitis within longitudinally
39:33
extensive lesion here.
39:35
Uh, that on further, you know, clinical workup with, uh,
39:38
auto antibody testing proved
39:40
to be aquaporin four antibody sm, that's N-M-O-S-D,
39:44
other etiologies in the differential diagnosis
39:46
of longitudinally extensive transverse myelitis
39:49
or longitudinal extensive myelitis lesions are mo a d.
39:52
So, uh, myelin oligodendrocyte,
39:54
glycoprotein associated disease aem,
39:57
acute disseminated encephalomyelitis sarcoidosis infectious
40:01
or para infectious myelitis, as well
40:03
as per neoplastic syndromes.
40:04
So if you had a patient with cancer
40:06
and you saw this, you might suggest you introduced to the,
40:10
uh, differential diagnosis of paraneoplastic myelopathy.
40:13
So say you're dealing with the long
40:15
two link extensive myelitis.
40:16
What are specific additional imaging features
40:18
that you should look for that could narrow your differential
40:21
diagnosis down even further?
40:22
So one, one imaging feature
40:24
that has been described is called the bright spotty lesion.
40:27
This has been described in association with N-M-O-S-D.
40:30
The bright spotty lesion refers to, um,
40:33
a T two hyperintensity that is very bright, uh,
40:36
and it is about as bright as the CSF signal surrounding it.
40:40
I will say that in clinical practice, I have found this
40:42
to be a challenging one to call with certainty, uh,
40:45
because, uh, number one, axial images,
40:48
you often have flow voids
40:49
that are messing up your signal in the CSF on axial images,
40:53
on the sagal images, uh, it kind of depends on, you know,
40:56
how much artifact you have related to, you know,
40:58
respiratory motion and so forth
40:59
that a superimposed upon the spinal canal.
41:02
Uh, this was the closest I could find in my database
41:05
of a bright spotty lesion of a part of this longin link,
41:08
extensive T two hyperintensity that was especially bright.
41:11
And on some images it appeared as bright
41:13
as the CSF surrounding it.
41:14
And there was a very, very faint patchy enhancement
41:17
associated with part of this LONGIN link extensive, uh,
41:20
T two hyperintense lesion here.
41:22
And this one did turn out to be on antibody uh,
41:25
antibody testing to be aquaporin four positive.
41:28
So that's N-M-O-S-D.
41:30
Another pattern to look out for is central gray,
41:33
restricted T two hyperintensities,
41:35
and that should raise the differential primarily of mo a d
41:38
and acute flacid myelitis.
41:40
So I'll go through these one by one.
41:42
So, uh, this was a case
41:43
of mo ad myelin oligo droy glycoprotein associated disease
41:47
with the so-called H sign, which just means
41:49
that the T two hyperintensity is restricted
41:51
to the gray matter of the cord, which on axle images appears
41:54
as an H 'cause there's the ventral horn, uh,
41:57
on this side is connected, um, in the center,
41:59
and then there are posterior horns as well.
42:01
So it looks kind of like an H um,
42:03
you wouldn't really be able to tell
42:05
that on the satchel image alone.
42:06
So it's very important to true review the kind
42:08
of transverse configuration on an axial image in order
42:12
to identify this h sign.
42:13
And this is, uh, somewhat not completely specific, uh,
42:17
for MAD disease.
42:19
And this one did, uh, turn out to be mo a d upon, um,
42:23
serum auto antibody testing for the, uh, MOG antibody.
42:29
Uh, this was another case of central gray restricted, uh,
42:32
trans, uh, kind of myelitis.
42:34
Um, this patient presented with acute, um, uh, lucidity
42:39
flacid paralysis of the extremities
42:42
and what we see here in the cervical cord.
42:44
And then the, uh, kind of cervical thoracic junction is, uh,
42:49
kind of an H butterfly shaped appearance
42:52
of T two hyperintensity.
42:53
So this is gonna be predominantly affecting the ventral
42:56
horns a little bit, the posterior horns
42:58
and kind of crossing in the middle here.
43:00
Um, and this is an entity called Acute flas and myelitis.
43:05
Uh, and that was proven upon, uh, infectious disease workup
43:09
that identified West Nile virus, um, uh, on, uh, PCR.
43:14
Um, and what that looks like on sagal images, this like, uh,
43:19
uh, linear marker
43:21
of T two hyperintensity longitudinally
43:24
extensive in the cord.
43:25
Uh, but the configuration here of, uh, you know,
43:29
ventral horn predominant involvement, um, and, and,
43:32
and diffuse gray matter involvement should raise the
43:34
possibility of, uh, acute flas
43:36
and myelitis in the appropriate clinical setting.
43:38
So when you see a central gray restricted disease, um,
43:43
you need to test for MAD, uh, you need to test
43:46
for infectious etiologies of acute flas and myelitis.
43:49
Now, in this country, the, um, sporadic outbreaks
43:52
of antivirus, different types
43:53
of antivirus have been associated
43:55
with acute flas and myelitis.
43:56
And that is the, probably the predominant, uh, cause
43:59
that has been associated with this entity of a FM, uh,
44:03
happens in children as well as adults.
44:05
Um, and, uh, you know, during, uh, kind of mosquito season,
44:09
you should also consider, uh, west Nile virus.
44:11
Um, and, and that has been, uh, described, uh, as a cause
44:15
of acute flas and myelitis as well as,
44:16
but antivirus is probably the predominant cause.
44:19
And, and that needs to be considered in the, uh,
44:21
infectious disease testing.
44:24
So another pattern to consider within the categories
44:27
of acute, uh, myelitis are, uh, having enhancement
44:31
that seems to be sub peal and or lepto meningeal, uh,
44:35
because that should raise the possibility of sarcoidosis.
44:39
So this patient had longitudinally extensive, uh,
44:42
T two hyperintensity, um, with patchy areas
44:45
of contrast enhancement.
44:46
And so, uh, the configuration
44:48
of this contrast enhancement is important to notice
44:50
that this area is intramedullary.
44:52
Um, this is kind of traversing the entire cord,
44:55
but then there's also this linear enhancement that is in
44:58
between these two lesions that is on the dorsal aspect
45:01
of the cord alone.
45:02
And that should, uh, you know, be described
45:05
as either subpial or lepto meningeal.
45:08
Uh, sapi, you know, refers to stuff on the dorsal aspect
45:12
of the core, typically,
45:13
but can be infiltrating even deeper in contiguity with
45:16
that contrast enhancement.
45:18
And when you see this, uh, type of contrast enhancement, um,
45:21
the evaluation for sarcoidosis should be recommended.
45:23
That includes chest imaging, uh,
45:26
or if you're, you know, uh, at a rich institution,
45:29
you would go for a full body FDG pet.
45:32
In this case, the patient underwent that FDG pet,
45:35
and you can see FDG avid lymphadenopathy within the
45:38
mediastinum that would be highly suggestive
45:40
of sarcoidosis in this case.
45:43
Um, and, and one of these nodes were biopsy
45:45
that showed non necrotizing granuloma is consistent with,
45:49
um, sarcoidosis.
45:51
Um, this is a another case,
45:53
a longitudinally extensive myelitis with this is
45:57
what I would call classic kind of subpial appearance
45:59
of contrast enhancement.
46:00
Um, at an outside institution, this was actually interpreted
46:03
as appendamoma, but this, uh,
46:05
on reinterpretation our institution, um,
46:08
this dorsal speal appearance was more suggestive of,
46:13
of sarcoidosis.
46:14
And appropriate evaluation was performed,
46:16
which included a chest ct,
46:18
which identified this para tracheal SubCal lymphadenopathy.
46:22
And one of these was biopsied with granulomas consistent
46:25
with the clinical diagnosis of sarcoidosis.
46:28
So this is neuro sarcoidosis of the cord.
46:30
Um, there are various different phenotypes,
46:32
sarcoidosis being known as the great Mimicker has various,
46:35
uh, morphologies to note, um, the plurality of cases,
46:40
uh, reviewed at our institution of, uh,
46:44
neurosarcoidosis related myelopathy.
46:46
Um, the plurality had longitudinally extensive myelitis.
46:49
Um, uh, a smaller
46:51
fraction had short tumor effective myelitis.
46:54
Some patients had, uh, spinal meningitis
46:56
or meningo radiculitis appearance,
46:59
where you see contrast enhancement
47:01
of the intradural spinal nerve roots.
47:03
And an even smaller proportion had a appearance
47:05
of anterior myelitis that were associated with areas
47:08
of disc, um, degeneration.
47:11
So areas of mechanical friction related to dis protrusions
47:15
or extrusions or dis bulges on the ventral side
47:18
of the core can induce focal inflammation in patients
47:21
who have neurosarcoidosis.
47:22
And you can have, uh, areas
47:23
of contrast enhancement due to those levels.
47:26
The enhancement patterns I mentioned,
47:27
the dorsal subpial enhancement account
47:30
for the majority at our institution,
47:32
and then a minority have meningo, uh, meningeal
47:34
or radicular enhancement, uh, ventral subpial enhancement,
47:37
or, uh, a few cases where non enhancing as well.
47:40
So in this case, we could see two different lesions in this
47:42
case with a, a sarcoidosis associated myelopathy.
47:45
The top one has this dorsal subpial contrast enhancement,
47:48
but the bottom one does not have any
47:49
enhancement at this time.
47:52
Uh, moving on to, uh, kind of more common, uh, etiologies
47:56
for, uh, acute myelitis would be the
48:00
demyelinating disorders.
48:01
And these are typically associated
48:02
with multifocal CNS lesions.
48:05
And if a patient presents with clinical myelopathy
48:07
and you only did thoracic, uh,
48:09
or cervical spine imaging alone, uh, if you identify lesions
48:13
that would be suspicious for a multifocal disease,
48:16
then the next step in evaluation would be imaging the rest
48:19
of the central nervous system, which includes the brain and
48:21
or the optic nerves.
48:22
So this patient presented with a myelopathy.
48:25
We saw, uh, we saw earlier with the bright spotty lesion
48:27
and the longin extensive, um,
48:29
T two hyperintensity in the upper cervical cord.
48:31
Um, around the same time they also had visual complaints
48:34
and underwent, uh, optic, uh,
48:36
and, uh, brain imaging,
48:37
which identified a posterior optic neuritis.
48:39
There's contrast enhancement of the intracranial portion
48:42
of the left optic nerve here.
48:44
And, um, around this time, uh,
48:46
antibody testing return positive
48:47
for aquaporin four antibodies.
48:49
So that was neuromyelitis optica spectrum disorder.
48:53
Uh, this is a different patient who, um, again, had a, a, a,
48:57
uh, myelitis picture here with these T two hyperintensities,
49:00
either two separate lesions
49:01
or one longitudinal extensive lesion
49:03
with contrast enhancement.
49:04
And around the same time, uh, they also had optic neuritis.
49:08
Uh, here's the intra orbital portion
49:10
of the left optic nerve.
49:11
Uh, contrast enhancing.
49:13
The challenge with these is that the, uh, the onset of, uh,
49:17
spinal cord lesions and, you know, brain
49:20
and optic nerve lesion are not always synchronous.
49:22
They're, uh, often, you know, offset.
49:25
And so there may be a period
49:26
of time there's diagnostic uncertainty
49:27
because you don't have symptoms
49:30
or you don't have, you know,
49:31
radiographic lesions in the other site that allow you
49:33
to make a confident diagnosis.
49:34
But if you see the constellation
49:36
of the two at the same time,
49:38
or in serial succession,
49:40
you can strongly suggest the diagnosis if it has not
49:42
already been tested for.
49:44
And that's important because not all cases of, uh,
49:48
N-M-O-S-D are sero positive.
49:50
There, there is an entity of, uh, kind
49:52
of sero negative N-M-O-S-D.
49:54
So the imaging features do figure into that diagnosis.
49:59
Here's another case of a, a young patient, a 13-year-old
50:02
where, um, MAD is more common, uh, of a patient
50:06
who presented with optic neuritis.
50:08
And, uh, this patient didn't present with myelopathy per se,
50:11
but they, they had optic neuritis, so they had the rest
50:13
of their central nervous system evaluated.
50:16
And what we saw was a focal small T two INE
50:20
lesion in the conus.
50:21
And the presence of conus lesions is, um,
50:25
somewhat well described in the entity OFM ad.
50:28
And so the radiologists were the first
50:30
to suggest the diagnosis OFM a d,
50:32
although this was tested for at the same time,
50:34
it didn't result for some time later
50:35
because it takes a while for
50:37
some of these tests to come back.
50:38
And the final diagnosis was confirmed.
50:40
Anti MOG antibody positive mog a d Um,
50:44
this is a case I already showed
50:46
before of a, of a short lesion of the cervical spinal cord.
50:49
And upon further imaging of the brain, uh,
50:52
we saw multiple white matter hyperintensity, some
50:55
of them immediately adjacent
50:56
to the lateral ventricular margin,
50:58
radiating outward like Dawson's fingers.
50:59
So these are paraventricular lesions,
51:01
and that helped satisfy the McDonald criteria
51:04
for dissemination in space.
51:06
You have spinal cord and para ventricular lesions.
51:08
In addition to satisfy the criteria for, um, the rest
51:12
of the McDonald criteria, you either have dissemination in
51:15
time, which means a presence of an enhancing lesion,
51:19
IE in the cord here, and a non enhancing lesion,
51:21
which these were in the brain
51:22
that would satisfy dissemination time.
51:24
In addition, the patient underwent lumbar puncture testing
51:27
for oligoclonal bands, which are positive,
51:29
which can substitute for the presence
51:31
of dissemination in time in the, uh,
51:33
latest McDonald criteria.
51:35
So those allow you to satisfy the McDonald criteria
51:37
and give the diagnosis of multiple sclerosis in this case.
51:41
So finally, I wanna say if you're dealing with a myelitis,
51:44
uh, with a non-specific appearance, you don't have any
51:46
of these specific features, maybe have, you know,
51:48
some sites affected and not others, um, then, uh,
51:51
what happens is you kind of have to say, uh,
51:54
correlate, correlate clinically.
51:56
And the differential diagnosis, again includes some
51:58
of the entities we've talked about,
52:00
including central nervous system,
52:02
isolated inflammatory diseases, has multiple sclerosis.
52:04
Um, in the kind of acute mono basic, uh, presentation,
52:08
it would be aem acute dissemination, uh,
52:10
acute disseminated encephalomyelitis,
52:12
especially like a post-infectious phenomenon.
52:14
Uh, you have N-M-O-S-D and MO a d.
52:17
You can have, uh, myelitis
52:19
and associated with systemic inflammatory diseases such
52:21
as sarcoidosis, sjogren, and lupus,
52:23
and kind of a, a, a serological evaluation
52:26
and a radiological evaluation
52:28
for sarcoidosis would be warranted.
52:30
In some cases, it's a infectious
52:32
or apparent infectious phenomenon.
52:34
And so I mentioned enterovirus
52:36
and West Nile would be causes of acute FLA and myelitis.
52:39
There are also rare cases of herpes, HIV myelopathy,
52:43
HTLV, uh, myelopathy, syphilis, uh,
52:46
which causes like tabes DOS and Lyme disease
52:49
and causing encephalomyelitis as well.
52:51
Uh, peroneal plastic syndrome is possible.
52:53
Perineum plastic myelopathy is associated
52:56
with various auto antibodies, um, such
52:58
as most commonly associated with small cell lung cancer.
53:01
So, um, anti who CRMP antibodies.
53:04
There's a whole panel that the referring clinicians can send
53:06
off to test for these auto antibodies, if
53:08
that is in the differential diagnosis.
53:09
And then finally, if as a diagnosis of exclusion,
53:12
we have idiopathic myelitis.
53:14
So, um, so o other than MRI of the spine, you know what I,
53:19
I hate the phrase clinically correlate,
53:20
and if I have an idea of
53:21
what the appropriate next steps should be, I'll try
53:23
to suggest it and tailor my differential diagnosis,
53:26
my discussion with the referring clinicians,
53:28
or at least in my report accordingly.
53:30
So again, so what does clinically
53:32
correlate actually mean specific?
53:34
Well, it means referring to the chart history,
53:38
and you can do some of this as a radiologist.
53:40
I think it behooves radiologists
53:42
before you come down to a conclusion about
53:44
what the final diagnosis is.
53:46
You try to, uh, put the pieces together as best
53:49
as you can based on a chart review.
53:51
Um, we're not responsible just for looking at the images.
53:54
We're kind of responsible
53:55
for interpreting the images in the context of the patient
53:57
as understood and represented in the
53:59
electronic medical record.
54:01
And so the history that would be relevant here for a,
54:03
you know, otherwise non-specific myelitis would be,
54:06
do they have a history of cancer, rheumatologic disease
54:09
or infectious, uh, signs and symptoms?
54:11
Um, do they have additional imaging either prior
54:14
or, you know, ordered, uh, MRI of the brain
54:17
and orbits, uh, without
54:18
and with contrast, um, can they get a lumbar puncture
54:22
to correlate specifically for infectious causes with,
54:24
you know, CSF cell count, uh, protein IgG index
54:27
for autoinflammatory disorders, oligoclonal bands, again
54:30
for, you know, MS and, uh, and,
54:32
and similar AUTOINFLAMMATORY disorders.
54:34
Uh, can they get blood testing, uh, for MOG Aquaporin four
54:38
and N-M-O-S-D, uh, rheumatic disorders, uh, with a NA RO
54:42
and law, um, infections.
54:45
Um, in this case, this is a patient
54:46
who had a non-specific myelitis.
54:49
Um, they had, uh, Sjogren's syndrome, um, positive, uh,
54:53
either RO or law antibodies.
54:56
And, uh, can additional imaging be performed?
54:59
Well, you know, it is definitely in our place
55:01
to suggest additional imaging if we think it is appropriate.
55:04
So if we see a lesion of, uh,
55:07
longin extensive transverse myelitis
55:09
with dorsal cell peel enhancement,
55:11
I'm gonna recommend additional chest imaging
55:13
that can be obtained with CT of the chest
55:15
or, uh, even FDG pet of the whole body,
55:18
or is the thighs to evaluate for evidence
55:20
of systemic sarcoidosis.
55:22
Uh, and that can direct further biopsy
55:24
that would be not invasive to the central nervous system
55:27
that would be more readily accessible by, you know,
55:29
endoscopic bronchoscopy and so forth.
55:31
And then finally, you know, in this, in the purview of our,
55:34
you know, referring neurologists
55:36
to sometimes treat these lesions, uh, empirically
55:39
with IV steroids or plasma exchange under the theory
55:42
that is some kind of inflammatory disorder
55:44
that may be steroid responsive.
55:45
And you kind of see what happens after that.
55:47
And, um, if there's not a specific diagnosis to be obtained,
55:50
then it's just idiopathic myelitis.
55:53
So here's my summary approach to myelopathy
55:55
that I've given in this talk so far.
55:57
The first step is to obtain the history
55:59
and determine what is the onset, uh, of the symptoms from,
56:03
uh, onset of symptoms to the nadir of their, you know,
56:07
sensory motor deficits or autonomic dysfunction, so forth.
56:10
In the hyperacute setting, you,
56:12
you would be considering cord infarct,
56:14
and if you knew that history, try
56:15
to protocol your MRI with DWI.
56:17
Another entity to consider is spinal hemorrhage,
56:20
as we saw in our case with the interval, uh, hemorrhage,
56:23
that was a case of somebody who was anticoagulated
56:25
and that was the final diagnosis for their hyperacute onset,
56:28
uh, myelopathy, uh,
56:30
which leads into the second large category
56:32
of disorders causing myelopathy, which is compression.
56:35
You have to rule out compression on any spinal imaging, uh,
56:38
with a patient with myelopathy.
56:40
And the most common cause is spondylosis
56:42
or cervical spondylosis.
56:43
So arthritis degenerative changes,
56:45
whatever you wanna call it, spondylosis.
56:47
But after ruling that out, um, if you have, you know, kind
56:50
of thoracic abnormalities you have
56:51
to consider other more subtle, uh, etiologies
56:54
that I've seen often miss.
56:56
So those are arachnoid web, uh, huma disease
56:59
for the cervical thoracic junction,
57:00
or here yama like disease for the mid, uh, thoracic spine
57:04
that I showed, uh, in my case.
57:06
And as well as longitudinally kind of, uh, uh, diffuse, uh,
57:10
epidural abscesses in injection drug users as well
57:14
as spontaneous, you know, epidural hematomas
57:16
or, um, epidural tumor in a patient
57:19
who has vertebral metastasis.
57:21
If a patient has subacute
57:22
or chronic myelopathy, look
57:24
for specific signs like flow voids
57:25
that would suggest an AV fistula look
57:27
for in the inverted V sign
57:28
that would suggest subacute combined degeneration,
57:30
IEP 12 deficiency
57:31
or nitrous oxide abuse, or something like that.
57:33
Look for, um, expansile and chronically progressing
57:37
or persistent lesions despite steroid therapy
57:39
that would raise the possibility
57:40
of diffusely infiltrating glioma like a diffuse midline
57:44
glioma or asto cytoma.
57:46
Um, that should be, uh, kept on the back burner in the back
57:49
of your mind in the differential diagnosis
57:52
with a large bucket of IQ myelitis, you want to distinguish
57:54
between short and longitudinal extensive lesions.
57:56
The classic short lesion, the entity is multiple sclerosis,
57:59
but, uh, one short lesion alone is not
58:01
enough to make that diagnosis.
58:03
Referred to the McDonald criteria,
58:04
longitudinal extensive lesions, you look
58:05
for a bright spotty lesion indicating N-M-O-S-D central gray
58:09
restricted lesions, uh, indicating a mo a d
58:11
or acute flacid myelitis to infection, a dorsal sub appeal
58:14
or lepto ngel enhancement that suggests sarcoidosis
58:17
or multifocal CNS disease like MS A-D-N-M-O-S-D or mog a d.
58:21
Finally, there is a large component of clinical correlation
58:24
that is required for these in terms of LP blood testing, um,
58:27
you know, potentially systemic imaging that, uh,
58:29
could contribute that you have to keep in the back of mind
58:32
as you know, part of the diagnostic workup,
58:35
an arsenal that you can recommend.
58:37
So that's all I have, and I'm happy to take any questions.
58:40
Thank you so much for that very comprehensive lecture, Dr.
58:44
Ding, we've got a couple questions in that Q
58:46
and A box if you wanna pop that open
58:48
and see what you wanna answer.
58:52
Yeah, sure. Okay. So the first question was,
58:53
how can I differentiate between an arachnoid web
58:56
or an arachnoid cyst in the dorsal
58:58
compartment posterior to the cord?
58:59
Okay, so that, that is a common question.
59:01
Um, when we see a expansion of the CSF signal, uh, dorsal
59:06
to the cord and thoracic spine, um, the difference, uh,
59:09
between arachnoid web and cyst is that the erect
59:12
cyst is kind of, uh, walled off.
59:14
Um, and whereas OID Web, it's kind of a band
59:16
that's constricting the cord, um, uh, it is difficult
59:19
to distinguish sometimes, um, uh,
59:22
what the difference is in between the two.
59:25
Um, some clues that you can see on MRI is, if you could see,
59:28
uh, CSF flow artifacts within that space, um, that suggests
59:33
that CSF is still flowing up
59:34
and down, that is more typical of interact with web.
59:36
Whereas within an OID cyst, the CSF is relatively stagnant.
59:40
So you're not gonna see flow related artifact, uh, within
59:43
that CSF space.
59:44
Um, if there's any uncertainty, the test
59:47
to do would be a contrast.
59:49
Um, you know, CT myelogram, you inject the contrast,
59:52
and if that CSF space does not fill with, uh, you know,
59:55
your ated intrathecal contrast, then that would be OID web.
60:00
Um, if it does fill with contrast, then that is, you know,
60:03
contiguous with the rest of the subarachnoid space, and
60:05
therefore that is arachnoid, uh, web, uh, so sorry if it,
60:09
if it does not fill, that's arachnoid cyst.
60:11
If it does, that space does fill, then it's arachnoid web.
60:17
Um, next thing is, next question is,
60:20
do you do flexion extension imaging?
60:21
In other cases, what sequences do you run?
60:24
So we don't commonly have flexion extension imaging
60:27
as part of our MR protocol.
60:28
Really the only time to do it in, in, um,
60:32
our cases is if there's kind of a suspicion for here,
60:35
YAMA disease based on clinical suspicion based on the
60:39
patient's demographics of being, you know, young adult male,
60:42
maybe of Asian ancestry, um, where they have kind
60:46
of mono maleic, uh, a my atrophy, which is the classic term,
60:49
uh, describing hir yama disease.
60:52
Um, or, uh, you can see, uh, imaging abnormalities
60:55
that might suggest the diagnosis, like you see,
60:57
like subtle widening of the dorsal CSF space
60:59
or engorgement of the epidural venous plexus,
61:02
as we did in our case that prompted the flexion extension,
61:05
uh, or really just flexion and neutral imaging.
61:09
Um, and, uh, and you, you would just do, um, the
61:13
sagal T two weighted images in those cases.
61:16
'cause all you're looking for is anterior displacement of
61:19
that posterior, uh, thecal sac.
61:23
Uh, next question is, um,
61:26
how much symptomatology do you think can be contributing,
61:29
uh, contributed to mild cord flattening in the setting
61:33
of minimal to mild spinal canal narrowing
61:37
as a question better, better answered by a spine surgeon?
61:39
Um, and, and that answer will, will differ, uh,
61:42
dramatically depending on how, um,
61:45
willing a spine surgeon is to operate
61:47
for a particular symptomatology.
61:48
It does require a lot of clinical correlation.
61:50
I would think very little if you're describing as minimal
61:54
to mild spinal canal narrowing.
61:56
I, I would, you know, de-emphasize that in my reports,
61:58
not even mention it in the impression, um, uh,
62:02
and, uh, uh, if it's moderate
62:05
or severe, then I, I would think it's, uh,
62:08
potentially symptomatic
62:09
and, uh, would pull that to the impression in a patient
62:12
who has symptoms of myelopathy.
62:14
Um, the next question is, what's the difference
62:16
between the peripheral cord hypo intensity
62:17
and the low signal from chronic hemorrhage
62:20
induced cirrhosis?
62:21
Um, so that, that question is referring to the findings of,
62:26
uh, congestive, uh,
62:28
myelopathy in dural arterial venous fistula cases with, uh,
62:31
peripheral core T two hypo intensity.
62:33
How is that different from low signal
62:35
and chronic hemorrhage induced cirrhosis?
62:36
So, um, the, the, the clinical context is different.
62:40
Um, and, you know, the patients
62:42
with chronic hemorrhage induced, uh,
62:44
cirrhosis have had prior, uh, surgery of the spine
62:47
or prior trauma related to or,
62:49
or a vascular lesion that, um, uh, has bled, uh, you know,
62:54
some, some prior known episode of subarachnoid hemorrhage.
62:57
Um, uh, to be honest,
62:58
I don't know the clear question to that.
63:00
It's like such a uncommon ent,
63:02
both these are such uncommon entities.
63:04
I haven't really thought to that degree, how,
63:06
how would I distinguish the two?
63:08
They're merely observations that have
63:10
to fit within the larger constellation of findings for you
63:12
to come down on this particular diagnosis.
63:15
And the next question was acute myelopathy syndrome.
63:18
Uh, myelopathy symptoms, left sided contralateral loss
63:21
of pain sensation
63:23
with abnormal upper thoracic spinal cord unilateral, uh,
63:27
there's a, there's a lot here in this question.
63:30
Um, would you consider unilateral cord infarction
63:33
and what would be on the differential diagnosis?
63:36
Um, it seems to be referring to a specific patient case
63:39
that, um, is a little bit difficult
63:41
for me to parse right now.
63:43
Um, so as a, I would say as a general statement,
63:46
unilateral myopathies are possible, uh,
63:48
it wouldn't be called what is
63:49
classically transverse myelitis.
63:51
You can have injuries to one part of the cord
63:53
that spares the other half of the cord.
63:55
And so demyelinating diseases like MS lesions very commonly
63:58
affect, you know, one part of the cord.
64:00
And so you have unilateral symptoms, uh, you know,
64:04
trauma causing a brown sakara syndrome affects
64:06
one half of the cord.
64:07
So you have, you know, ipsilateral symptoms in,
64:10
in one modality and contralateral symptoms
64:12
and another modality based on the site
64:14
of de accusation of those tracks, right?
64:16
And so any, any of these entities that I've, uh,
64:19
listed here, um, that, uh, would cause a, a focal rather,
64:23
rather than transversely diffuse, uh, abnormality, uh, uh,
64:27
like, um, like a demyelinating disease would be
64:31
in the differential diagnosis.
64:33
Um, next question is,
64:35
how would you differentiate subpial enhancement
64:37
for subdural or epidural?
64:38
So that's really hard. So that, uh,
64:40
if you have good high resolution axial, uh,
64:42
T one post contrast images, you can see, you know,
64:44
the distinction between what's the chord
64:47
and what is the dura.
64:48
So if you can see any CSF space separating the two,
64:51
then you can make that distinction.
64:53
Um, uh, subpial enhancement can be ventral.
64:57
Yes, subpial enhancement can be ventral.
64:58
It just so happens that in sarcoidosis,
65:00
the subdue enhancement is, uh,
65:01
is more commonly dorsal than it is ventral.
65:03
And when, when ventral is very often associated
65:06
with mechanical irritation from protruding discs.
65:10
Uh, any role for phase contrast in erect wipe incy I
65:13
that I do not have any contra, uh, any, um, experience
65:17
with using face contrast in the spine.
65:20
Uh, what is the difference between SAH subdural
65:23
or epidural hge e of the spine?
65:27
Uh, hemorrhage, right, so hemorrhage, so, um,
65:30
epidural hemorrhage will displace the,
65:32
the T two hypo intense border.
65:34
That is the dural sac.
65:37
Uh, subdural hemorrhage would be within the confines
65:40
of the dural sac, um, and focal
65:43
and confluent, whereas subarachnoid hemorrhage would kind
65:45
of layer around everywhere.
65:50
Um, next question is, in cases of hir Yama disease,
65:53
is the underlying cause related to lack of adherence of dura
65:55
to the dorsal spine ligaments?
65:57
I think so. Um, if that's the case, why would you refer
66:00
to the case you presented as hi huma, like disease
66:03
as posing, as opposed to calling it hirata disease?
66:05
That's, that's really just a, a,
66:06
a historical nomenclature here.
66:08
YAMA disease was described in respect to the cervical spine,
66:11
lower cervical spine causing upper extremity symptoms.
66:14
Uh, huma like disease was subsequently described
66:17
as a similar, um, radiological manifestation
66:20
of posterior dur detachment,
66:22
but causing, uh, thoracic spinal cord abnormality.
66:25
And so the symptoms were referable
66:27
to the lower extremities instead of the upper extremities.
66:29
So the syndrome of, of the originally described here,
66:31
YAMA disease was, uh, cervical cord,
66:33
upper extremity symptoms.
66:35
Here, YAMA like disease is the same pathophysiology,
66:38
but for the thoracic cord causing lower extremity symptoms.
66:41
And then the final question is any reference to detect
66:44
or define cord atrophy?
66:45
Sometimes it's hard in patients with HTLV infection.
66:49
Uh, that is, uh, a great question.
66:51
I don't know the answer to that question.
66:52
Like what it, when do you call chord atrophy?
66:55
Because some, some of these entities can cause chord atrophy
66:58
with very minimal signal abnormality.
67:00
And then, um, uh,
67:01
because the cord is such a small structure, we don't have,
67:04
uh, you know, great confidence in calling, you know,
67:06
what is normal versus atrophic chord.
67:08
That's, uh, that's really a matter of judgment
67:10
and having seen enough chords to kind
67:12
of build a mental database of what is the normal range
67:14
of chord size,
67:17
but certainly if it is focal atrophy, that
67:19
that is a little bit easier to tell.
67:21
Right? Um, chord gets, uh, narrowing and gets wider.
67:25
Again, as you go down the,
67:26
the chord should very smoothly taper down in caliber
67:30
as you're going inferiorly.
67:31
Um, but for diffuse atrophy, like in cases of HIV
67:35
and HTLV, uh, with, without, you know,
67:38
clear focal Corsi abnormality, that is really difficult.
67:42
And so that would be really driven by the clinical suspicion
67:45
for that particular entity.
67:49
Wow, Dr. Dang, I think you got through 'em all.
67:52
Great. Awesome. Thanks so much.
67:55
Thank you. Thank you so much for this lecture
67:57
and for everyone else for participating
68:00
and asking such great questions.
68:02
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68:15
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Thanks again for learning with us, and have a great day.
Francis Deng, MD
Assistant Professor of Radiology and Radiological Science
Johns Hopkins University School of Medicine
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