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Hello, and welcome to Noon Conference hosted by Modality.

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Noon Conference connects the global radiology community through free live

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educational webinars that are accessible for all and is an opportunity to learn

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alongside top radiologists from around the world.

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Today, we are honored to welcome Dr.

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Taylor Pomerantz for a lecture entitled "CNS Tumor Mimics in the Brain and

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Spine."

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Dr. Pomerantz completed her radiology residency at the University of Pennsylvania,

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where she also served as chief resident from 2021 to 2022.

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She completed a fellowship in neuroradiology at the University of Utah and is on

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staff at ProScan Imaging full-time, sub-specializing in neuroradiology.

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She also serves as an adjunct professor at the University of Utah in the division

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of neuroradiology. At the end of the lecture, please join her in a

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Q&A session where she will address questions you may have on today's topic.

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Please remember to use the Q&A feature to submit your questions so we can get to as

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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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Pomerantz, please take it from here.

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Okay, great. All right. So this is going to be actually a

1:04

case-based presentation. We are going to look at

1:08

some tumor mimics in the brain and spine, start in the spine and

1:12

work our way up to the head. This is going to be mostly an

1:15

MR-based

1:17

case review.

1:20

And all these cases are from our community practice, probably over the last

1:24

six months at ProScan. We're an MR shop, and we read across all

1:28

50 states. So, these are cases that we see out in the community.

1:31

They're not just academic cases.

1:36

Okay. Nothing to disclose. Okay?

1:40

So again, reviewing tumor mimics, we're really going to try and focus

1:44

on

1:46

mimics that have characteristic imaging features that are going to help you keep

1:50

patients out of the OR that don't belong there and also expedite

1:54

the appropriate workup and therapy for these patients.

1:59

So we're going to jump right in and we're going to start with

2:01

an entity that everybody should know.

2:04

If you're reading spine and you've not seen this before, you're going to see it.

2:09

We see this very frequently in our practice.

2:11

So this is a 77-year-old gentleman with right-sided

2:15

low back pain.

2:17

Every trainee I've worked with that has not seen this before,

2:20

100% of the time calls these mets, okay?

2:23

We've got T1 STIR and contrast

2:26

enhanced sagittal sequences through the lumbar spine, and we can see

2:31

we've got contiguous target-like lesions in consecutive

2:35

vertebral bodies,

2:37

right on STIR with contrast enhancement.

2:41

We'll make note of the preserved fatty marrow in

2:45

the central aspect of the lesion on T1.

2:47

And we'll also make note that this patient has some Modic 1

2:51

edema changes at the L4, L5 level.

2:57

This is a classic imaging appearance for post-Intracept or

3:01

ablation related changes.

3:04

We've seen a huge spike in volume of this type of procedure,

3:08

and subsequently, a lot of MRs that look like this in the outpatient

3:12

setting. Intracept is approved for vertebrogenic low back

3:16

pain for patients with Modic 1 or 2

3:19

changes from levels L3 to S1, and it

3:23

involves ablation of the basivertebral nerve. Okay?

3:27

We see target-like lesions that enhance, and the other clue that

3:31

should tip you off is the adjacent Modic

3:34

changes.

3:38

Our next case is a 57-year-old gentleman with

3:41

left-sided low back pain and a history of an

3:45

L2 pathologic fracture.

3:49

Again, we've got sagittal T1, T2, and STIR sequences through the lumbar

3:53

spine.

3:55

We can see at the L2 vertebral body level, there is a

3:59

diffusely enlarged vertebral body and not captured on the

4:03

single slice image, also diffuse enlargement of the spinous process.

4:08

There is heterogeneous T1 and T2 signal

4:12

in the L2 vertebral body, a tiny

4:16

curvilinear hypointensity along the posterior corner with some

4:19

associated edema. So that may represent a little

4:23

subcortical or microtrabecular fracture.

4:28

Here is a companion case for this entity on CT and contrast

4:32

enhanced MR. Again,

4:34

diffusely enlarged vertebral body and spinous process,

4:39

has a mixed lytic and sclerotic appearance with

4:42

hypertrabeculation,

4:44

enhances in the active phase of disease.

4:47

And notably, one clue is the straightening

4:50

of the normally expected concave margin along the

4:54

anterior aspect of the vertebral body.

4:59

This patient has Paget's disease of the spine, also known as osteitis

5:02

deformans. This is a metabolic disorder characterized by

5:06

excessive and disorganized bone remodeling, most

5:10

frequently seen in the pelvis, then the spine.

5:13

Can be complicated by pathologic fracture and notably in

5:17

the cervical spine, cord ischemia, either from shunting or compression,

5:22

myelopathy, and radiculopathy.

5:25

Keep in mind, 1% of these lesions have sarcomatous

5:29

transformation.

5:34

On CT, similar to MR, we see an expanded

5:38

square vertebrae with coarsened trabecula, or

5:42

some of you may be familiar with the term picture frame vertebrae.

5:47

Mixed lytic and sclerotic appearance we see in the active or mixed

5:50

phase of the disease,

5:53

can subsequently progress to an ivory vertebrae or

5:56

diffusely sclerotic vertebral

5:59

bodyThe patients will have elevated alk

6:03

phos and typically normal calcium and phosphorus.

6:06

The differential, particularly for ivory vertebrae or

6:10

diffusely sclerotic, would be blastic mets and lymphoma.

6:14

Typically, in lymphoma, we are not going to see a

6:17

fusiformly enlarged vertebral body different than

6:22

a typical expansile lesion that we would talk about.

6:27

So what do we do with a patient like this?

6:29

We ship him off to endocrine and we are done with him?

6:31

Well, the patient definitely needs an endocrine referral, but what is left to

6:35

do on our end? Well,

6:39

patients with Paget vertebrae are subject to dynamic and

6:42

load-dependent spinal deformity.

6:45

Patients need to be followed with standing full spine radiographs.

6:49

I think this is a lesser-known

6:51

complication of Paget vertebrae, and it's our responsibility as the

6:55

radiologist to make sure that they get appropriate follow-up in this regard.

7:04

Our next case, this is a favorite case of mine from this year.

7:07

This is a 54-year-old patient with

7:10

chronic back pain,

7:13

a 54-year-old female. This patient bounced

7:16

around our community for many years with lots

7:20

of imaging. So we'll start on the left here.

7:23

We've got sagittal sequences, T1, T2, and

7:27

contrast through the thoracic spine.

7:30

On T1 sequences, we can see there's ill-defined

7:34

low T1 marrow signal with associated

7:38

stir or T2 hyperintensity and enhancement, and

7:42

it really seems to be centered along the ventral aspect of

7:46

the vertebral bodies.

7:48

Some of these lesions have a hemispherical appearance.

7:52

We can see the image on the far right, the arrow

7:56

denoting similar appearing lesion involving the

7:59

majority of the sternum. Okay? This patient

8:03

presents for the first time in an outpatient imaging center or

8:07

hospital.

8:08

Nine times out of 10, I think people are going to call this

8:12

sclerotic mets and recommend the patient

8:16

get a mammogram, and everyone is probably thinking of breast cancer,

8:19

especially with this sternal involvement.

8:25

This is what the patient looks like on CT, densely

8:28

sclerotic, little end plate erosions.

8:32

Notably, does not have any bridging syndesmophytes.

8:37

I will tell you, her imaging was grossly stable over a

8:41

five-year period.

8:44

Multiple diagnoses of mets and

8:47

smoldering discitis with multiple negative

8:51

biopsies and a completely negative rheumatologic

8:55

workup. The patient was referred for

8:58

nuclear medicine imaging given the suspected diagnosis of

9:03

cancer.

9:05

Minimal to no uptake in the vertebral body

9:09

lesions,

9:10

which is reassuring, but intense uptake at the

9:14

sternoclavicular joint, an imaging finding that is

9:18

pathognomonic for this entity and also known as the bull's

9:21

head sign.

9:25

What else do we want to know about this patient?

9:30

We want to know if this patient has a history of a pustular rash.

9:34

The top images are in fact from our patient, and while she does not

9:38

have the typical palmar plantar

9:41

distribution of this expected rash,

9:45

she does have a typical pustular rash that we see

9:49

with this disease. And it's important to note this can

9:53

occur at any time in the disease course.

9:56

This rash was probably two years before her imaging presentation.

10:01

This is a case of SAPHO,

10:04

synovitis, acne, pustulosis, hyperostosis, and

10:07

osteitis. Okay? This is an inflammatory arthropathy

10:11

typically seen in adults between the ages of 30 and 50.

10:15

Many of these patients have extremely delayed

10:19

diagnosis due to repeated

10:22

misdiagnosis on imaging of either cancer or

10:26

smoldering infection.

10:29

On imaging, we see findings that are

10:33

typical of active or prior enthesitis

10:37

involving the anterior vertebral body corners

10:41

with erosions, the bull's head sign on nuclear medicine

10:44

imaging, and marked sclerosis on

10:48

CT,

10:50

MR imaging characteristics that are quite similar to

10:53

malignancy.

10:56

This is a diagnosis of exclusion

10:59

and a radiologic diagnosis. This is

11:03

a diagnosis that is almost always made by the radiologist

11:08

who must put all the pieces together.

11:11

These patients will be referred to rheumatology when there is a

11:14

suspected inflammatory arthropathy based off imaging if

11:18

you are able to pick up this enthesitis pattern.

11:22

But then they often will have a completely normal workup and will

11:26

be sent on their way and will not be pipelined

11:30

into proper therapy unless they arrive with a

11:34

presumed diagnosis or suspected diagnosis of

11:38

SAPHO.

11:39

Okay? And that is how we can help change the patient's management.

11:44

Treatment is first-line bisphosphonate therapy.

11:48

And if there is first-line treatment failure,

11:51

subsequent methotrexate, biologics,

11:55

and other disease-modifying

11:57

agents.Now

12:02

we're going to move on to some cord lesions.

12:05

So this is a 73-year-old gentleman with pain and

12:09

myelopathy.

12:12

This is a case we actually see pretty frequently in our practice because we

12:15

read a lot of spine, and occasionally we see it get sent

12:19

to us for surveillance imaging of a tumor.

12:23

So we've got sagittal T1, T2 sequences

12:27

through the thoracic spine. We can see there is expansile

12:31

T2 hyperintense intramedullary signal in the thoracic cord,

12:35

and just below that signal,

12:38

some dorsal kinking or some of you may recognize it

12:42

as a scalpel sign along the dorsal thoracic cord.

12:48

On axial sequences,

12:51

we typically will see ventral displacement of the thoracic cord and

12:55

flattening of the dorsal margin.

12:58

This is the expansile intramedullary signal cranial to that.

13:06

Here's another companion case, a 40-year-old with radiculopathy.

13:09

Very similar findings. Expansile intramedullary signal in the

13:13

thoracic cord with some dorsal kinking.

13:17

Not as prominent on the sagittal sequence, but you can see here on the axial

13:21

ventral displacement a flattening.

13:24

This patient actually is starting to develop a thoracic cord

13:27

syrinx.

13:29

And then here again, here is a more dramatic kind of a scalpel

13:33

sign.

13:38

This is presyringomyelia edema, in this particular example, due to

13:42

a thoracic arachnoid web.

13:45

And we're specifically talking about the intramedullary signal here.

13:48

So sequela of altered CSF flow,

13:53

on MR, expansile-appearing stir bright cord

13:57

lesion intramedullary,

13:59

no enhancement.

14:01

And in the setting of a web, we see a

14:05

typical scalpel sign or ventral cord displacement with

14:08

flattening or kinking of the dorsal cord.

14:11

Can also be seen in the setting of dorsal cyst,

14:15

which will sometimes have a more obtuse margin, or you may actually see a

14:19

rim of the cyst or a loss of CSF pulsation artifact

14:23

dorsally or a cord herniation, which has a much more acute

14:27

or C-shaped angle.

14:32

Moving on to our next case. This is a 36-year-old

14:36

gentleman who had an ACDF six months ago

14:39

and presented for left radicular symptoms and

14:43

is now being subsequently followed for a possible

14:47

diagnosis of MS.

14:50

So we've got sagittal sequences, T2 and contrast

14:53

enhanced through the cervical spine.

14:55

We can see, at around the level of his ACDF,

14:59

a spindle-shaped, non-expansile,

15:03

T2 and stir hyperintense intramedullary

15:06

cord signal.

15:08

And right at the center of that,

15:11

a more thin, flat or pancake-like

15:15

area of enhancement.

15:19

This is what his preoperative imaging looked like.

15:21

So he has your

15:24

typical most favored nation, C5-C6

15:28

spondylosis with a retrolisthesis and a disc herniation

15:31

compressing the cord, contributing to either a compressive

15:35

myelopathy or myomalacia.

15:40

Here's another companion case, a 64-year-old gentleman with

15:44

weakness and tingling. This was being followed as a spinal

15:48

tumor and very similar imaging

15:52

findings. Signal alteration near the fusion level with,

15:56

again, at the central aspect, very thin, flat

16:00

area of contrast enhancement. And

16:04

notably, on the axial sequences, circumferential

16:08

white matter enhancement, very short segment at that level, with sparing of the

16:11

gray matter.

16:13

This is an entity called pancake-like gadolinium enhancement.

16:17

We've already covered the imaging characteristics.

16:19

It typically spans one vertebral body and is most

16:23

commonly located immediately below the point of maximal

16:27

stenosis, which we know in most patients is at the

16:30

C5-C6 level.

16:33

Again, circumferential white matter enhancement with gray matter sparing and a

16:37

very flat pancake-like appearance on the sagittal sequences.

16:41

You can actually see this both preoperatively or

16:44

pre-decompression and postoperatively

16:47

post-decompression. We almost never see it preoperatively

16:51

because preoperative degenerative spinal imaging is

16:55

almost never ordered with contrast.

17:00

So this is an enhancement pattern of spondylotic myelopathy and

17:04

is thought to be due to disruption, focal disruption of the

17:08

blood-brain barrier.

17:11

It can persist beyond one year. That's normal.

17:15

The important thing to note, though, is these patients should have no

17:19

progression, either clinically or on imaging.

17:23

And if that is not the case, you need to back up, go back

17:27

to broader differential that includes things like demyelinating

17:30

disorders and neoplastic processes.

17:37

Move on to another cord lesion here.

17:39

So this is a

17:41

44-year-old young woman with balance and numbness issues and

17:45

incontinence, was also being followed for a

17:49

suspected tumor in the spinal canal

17:53

when she came to us. Okay. We've got sagittal

17:56

T2 and contrast enhanced sequences through the

18:00

cervical and thoracic spineOkay?

18:03

And this is a funky looking lesion. Okay?

18:07

You open this case and first thing you're saying is, "What the heck is going on

18:11

here?" Okay? We've got very lobulated

18:15

T2 hyperintensity in the canal just on the single

18:19

sagittal slice sequence. It's not

18:22

definitively clear what compartment this is in, whether it's

18:25

intramedullary or subarachnoid or subdural.

18:30

But notably, on the contrast sequence, there's no enhancement

18:33

here, and it does appear to be pretty dark on the

18:37

T1 fluid signal.

18:44

Here are some cine clips to give you a

18:48

more complete picture of this lesion.

18:53

Again,

18:54

long segment, very lobulated, scalloping

18:59

lesion in the canal and on axial.

19:06

We're going to see there is marked deformity of

19:10

the cervical and thoracic cord at

19:14

multiple levels, long segment.

19:17

On these, these are 3D T2 drive sequences, and on these

19:21

particular sequences, it looks like there is a differential in

19:25

the signal between the

19:29

dominant component of the lesion and the adjacent surrounding CSF at other

19:33

levels. Okay.

19:36

We've all seen and are quite familiar with adhesive

19:39

arachnoiditis of the lumbar spine. Okay?

19:42

This is a textbook example of adhesive

19:46

arachnoiditis in the cervical and thoracic spine.

19:50

These are extensive adhesions and

19:53

loculated CSF.

19:57

We see this in the setting of prior trauma, infection, particularly

20:01

TB or pyogenic infection,

20:03

patients who have had prior surgery and prior intraspinal hemorrhage.

20:10

They can present with pain and progressive myelopathy.

20:13

And on MR, we see these lobulated areas

20:17

of cystic dilation of the subarachnoid space with

20:21

cord deformity and compression, can be present with or without a

20:25

syrinx and can present with septal enhancement,

20:29

both infectious and non-infectious.

20:31

But if you see septal enhancement, the next thing you need to do is get a

20:35

travel history and make sure the patient doesn't have TB.

20:43

We're going to move on to a 73-year-old woman with

20:47

left arm weakness who presented to the emergency department.

20:52

We have sagittal T2 and contrast enhanced sequences,

20:56

and we can see there is a very ugly

21:00

intramedullary cord lesion here.

21:02

So very expansile, T2 hyperintense,

21:07

long segment,

21:10

cord signal abnormality extending from the cervicomedullary

21:14

junction down to the cervicothoracic junction,

21:18

avid enhancement on post-contrast sequences.

21:22

And I will point out one really

21:26

key finding that hopefully will also catch your eye

21:30

and is one of the clues to this particular case.

21:34

This nodular area of leptomeningeal enhancement in the

21:38

posterior fossa.

21:41

And that is going to trigger us to go searching for

21:46

the pathognomonic finding of this entity in the spine that

21:50

is going to

21:51

send you down a different direction than biopsy.

21:56

These are some axial scrollable sequences.

21:58

Again, we can see very expansile,

22:02

hyperintense intramedullary signal,

22:06

cystic dilation of the central canal,

22:09

avid post-contrast enhancement.

22:12

And then again, we see one little nodular leptomeningeal enhancing

22:16

lesion there.

22:17

So what are we going looking for? We're windowing down,

22:21

we are scrolling slowly,

22:24

and we are looking for this.

22:28

This is the same patient

22:33

properly windowed at the right slice.

22:36

This is the Rebel Alliance sign for all you "Star Trek" fans out

22:40

there.

22:43

And this is really a hallmark imaging feature

22:47

of

22:49

this entity. I'm going to spoiler alert it for you.

22:53

Neurosarcoidosis. Okay?

22:55

The next thing we are doing is not biopsying the cord.

22:59

We are going on a search for systemic sarcoidosis to

23:03

find a non-CNS target. Okay? This is this

23:06

patient's chest CT, recommended chest CT, and she has the classic

23:10

Garland triad of right paratracheal and hilar

23:14

adenopathy. She underwent transbronchial biopsy

23:18

with the pathology, as you would expect, of non-caseating

23:21

granulomas.

23:25

So neurosarcoidosis. Here is another

23:28

very textbook example of the Rebel Alliance sign in another

23:32

patient that we saw in our practice with neurosarcoidosis.

23:37

We are looking for supportive signs of neurosarcoidosis to try and

23:41

avoid a CNS target biopsy, and those

23:45

would include a chest CT, transbronchial biopsy,

23:49

occasionally PET-CT to look for active extra CNS

23:53

disease, but good luck getting that approved on any inpatient.

23:58

And then, of course, the serum laboratory workup, serum ACE.

24:01

I will tell you, though, neurosarcoidosis isolated in five to

24:05

15% of cases andSerum lab

24:08

workup is rather nonspecific and only positive in about

24:13

50% of cases. And in my experience so far, it has been

24:16

positive in zero cases.

24:19

These patients should undergo full neuro axis imaging with contrast

24:23

and CSF analysis, which will show the typical lymphocytic

24:26

pleocytosis. As a granulomatous disease, you must

24:30

exclude TB as an alternative diagnosis.

24:36

So this is the 2018 Neurosarcoidosis Consortium consensus

24:40

that was established to help standardize the clinical criteria,

24:43

diagnostic

24:45

certainty for neurosarcoidosis.

24:47

In this particular patient, we are looking at a case of probable

24:51

neurosarcoidosis because we have pathologic confirmation of

24:55

systemic granulomatous disease outside of the CNS and a clinical

24:59

presentation that is consistent with neurosarcoidosis.

25:06

Okay, now we're going to move up into the brain.

25:09

So this is a 25-year-old African

25:13

American male who presented with left-sided

25:16

weakness, progressive.

25:19

We've got T2 and FLAIR hyperintense

25:23

sequences of the brain. We can see there's very expansile

25:28

isogenic edema centered in the right thalamus and

25:31

gangliocapsular structures and extending down into

25:35

the right midbrain

25:38

and brainstem.

25:42

On diffusion,

25:44

there is no restricted diffusion, and we are bright on the ADC

25:48

map.

25:54

On the left is a pre-contrast T1 sequence, and on the right,

25:58

we are scrolling through

26:02

a very ill-defined nodular,

26:06

almost stellate-appearing pattern of

26:09

enhancement.

26:12

We're going to make note of the significant mass effect, ventricular

26:16

effacement, and some midline shift in this lesion.

26:22

Okay, what are we dealing with? So these should be some of the things

26:26

that are running through your mind.

26:28

We likely already ticked off some of them just based on imaging

26:32

appearance alone. But in a case like this, the first thing

26:36

that we should be asking ourselves is

26:39

priors.

26:41

Before we do that, though, I want to point out one

26:45

area that should always be part of your search pattern,

26:49

especially if you think you are dealing with something that may be partially a

26:52

leptomeningeal process, and that is the

26:56

IACs. Okay? This patient has nodular leptomeningeal

26:59

enhancement of the bilateral internal auditory canals,

27:03

and this is going to come up again.

27:06

So priors. Okay? In a case like this, priors can tell

27:10

you everything.

27:13

Patient didn't have priors at the hospital he presented to, but we were able to

27:16

scrape around priors from various places in the community.

27:20

He'd been imaged at several places over the past

27:24

four years,

27:25

dating all the way back to 2021. And we can see he has this very

27:29

interesting waxing and waning

27:33

flare signal abnormality involving the

27:36

gangliocapsular structures and the midbrain.

27:41

He was supposedly intermittently treated on and off with steroids during

27:45

this period. And then in May, prior to the

27:49

images I just showed you, his hospital presentation, this is what his

27:53

imaging looked like. So just very faint, linear,

27:56

nonspecific flare signal in the posterior limb of the

28:00

internal capsule.

28:02

But he did have this finding back in May.

28:04

This was really the isolated finding, nodular leptomeningeal enhancement

28:08

of the IACs.

28:10

In addition to sarcoid, you should, of course, be thinking of Lyme disease in a

28:13

young patient like this, especially in Ohio or the East Coast.

28:18

So he was put on steroids a week later.

28:21

Granted, this is a severely motion degraded image, but

28:26

the enhancement is completely resolved, okay, but our

28:30

edema and mass effect is not. So

28:33

what are we dealing with? Is this lymphoma? Is this vanishing lymphoma?

28:38

Well,

28:40

typically with vanishing lymphoma, everything goes bye-bye. Right?

28:44

The enhancement, the mass effect, the edema, and that's not the case here.

28:47

Right? So far, all we've really lost is the enhancing component of the

28:51

lesion.

28:53

Okay? This is a case of possible neurosarcoidosis.

29:00

Oh, we've already covered some of the diagnostic

29:04

criteria. I will tell you in this patient,

29:07

a systemic search for a non-CNS

29:12

target was not found.

29:14

He did have a lymphocytic pleocytosis in his CSF

29:18

and was discharged with a presumed neurosarcoidosis

29:22

diagnosis,

29:25

and

29:26

referred to neuroimmunology. Behcet's would be the

29:30

other

29:32

main consideration here.

29:35

Again,

29:36

then we're starting to get more into a little bit of demographic information that

29:40

may lean you.

29:42

Okay,

29:43

we're going to move on to another young patient. This is a 29-year-old female.

29:48

It's got T2 and FLAIR sequences of the brain.

29:52

Same location,

29:54

slightly different appearing lesion, though.

29:56

Okay, we've got a relatively circumscribed T2

30:00

dark lesion centered in the right thalamus and

30:04

gangliocapsular structures. It looks like there may be a little capsule

30:08

around it and a T2 dark rim.

30:11

A lot of surrounding isogenic edema and some mass effect with partial

30:15

effacement of the third

30:16

ventricleOops.

30:21

Again,

30:23

expansile FLAIR signal extending down into the midbrain

30:27

and right cerebral peduncle.

30:31

And what does it look like on contrast and diffusion?

30:33

It's going to look pretty different than our last case.

30:36

This is a solitary ring-enhancing lesion.

30:42

And on diffusion, which may be the most important

30:46

sequence here in conjunction with our T2 sequence, there

30:50

is rim-like restricted diffusion.

30:56

Again, this might be a differential that you're

30:59

working through as you

31:03

are processing this case. And I'm going to bring you back again

31:07

to the T2 signal and the diffusion on this

31:11

case.

31:13

But before we move further, let's

31:16

remind ourselves what's dark on T2.

31:18

Acute blood product, mineralization or

31:22

calcs.

31:23

Very, very hypercellular lymphoma can sometimes be very

31:27

dark on T2 and have a phenomenon called T2 blackout, where there is

31:31

no diffusion signal, will still be dark on ADC.

31:36

Fibrotic lesions, and then, of course, fungal and granulomatous processes.

31:40

And then when we're dealing with more of a rim-like T2 hypointensity,

31:45

evolving, particularly subacute hematomas, abscess,

31:49

both pyogenic and fungal. And then,

31:52

less frequently seen, tumefactive demyelination, where we have that

31:56

iron-laden macrophages along the lesion

32:00

edge.

32:02

So this is an example of CNS fungal disease, dimorphic fungus,

32:07

histoblastomycosis.

32:10

This can present really variable imaging appearance with

32:14

either meningeal or ring enhancement, can be

32:18

complicated by infarcts, vasculitis,

32:21

hydrocephalus, mycotic aneurysms.

32:26

As in this particular case,

32:29

for a

32:30

fungal abscess, a T2 dark rim.

32:36

The hallmark or characteristic feature

32:39

that we can sometimes look for but do not always see are

32:43

intracavitary projections, which I'm going to show you on the next slide.

32:47

And we should be thinking along this line, fungal, granulomatous,

32:52

and lymphoma.

32:55

This is an example from the literature,

32:58

from a paper on typical MR features of fungal brain abscess.

33:02

And these are the intracavitary projections.

33:05

These lobulated nodular projections that are protruding

33:09

into the abscess cavity. This is a diffusion

33:13

sequence with restricted diffusion.

33:20

Now we're going to move on to a 72-year-old female

33:23

presented to the ER with left arm weakness.

33:26

She's HIV positive with a very low CD4 count of 50.

33:31

She's got some senescent age-related changes in the brain, but I want to

33:35

draw your attention to what's happening in the descending right

33:38

corticospinal tract here.

33:41

This is a

33:42

importantly non-expansile

33:45

T2 and FLAIR hyperintense lesion

33:49

extending down into the right cerebral peduncle.

33:53

Let's see what it looks like on some other sequences.

33:57

So these are all very important imaging characteristics of this entity.

34:01

Number one,

34:03

no enhancement.

34:06

Number two, dark on T1

34:11

and has, again, rim

34:15

of restricted diffusion.

34:21

So let's come back and remind ourselves when we see rim-like restricted diffusion,

34:25

what should we be thinking? Fungal abscess,

34:29

demyelination with leading edge phenomenon,

34:32

sometimes subacute hematoma, and some centrally necrotic

34:36

neoplasms.

34:40

This patient, of course, with a history of HIV, you must

34:43

consider PML,

34:46

especially in a case with these imaging features.

34:50

So this is not the classic

34:54

biparietal white matter lesions, but this is

34:58

another typical presentation. So this is progressive

35:02

multifocal leukoencephalopathy.

35:04

This is a demyelinating disease caused by the JC

35:08

virus. It's diagnosed with CSF analysis.

35:12

We see it in

35:14

severely immunocompromised patients.

35:17

HIV is a typical population, also reported in patients with

35:21

MS on Tysabri therapy.

35:24

On MR, asymmetric and supratentorial white

35:28

matter abnormality.

35:31

Often have thalamic involvement, like in our case.

35:35

Non-expansile, no mass effect, no

35:38

enhancement,

35:40

dark on T1 and rim-like or

35:43

peripheral and patchy diffusion signal abnormality.

35:47

The other hallmark feature of PML is

35:51

involvement of the subcortical U fibers, which is not

35:55

what is going on here. This is a nice example from the

35:58

literature. I believe this is from StatDX.

36:01

I'm sorry, I don't have my annotation here.

36:04

Which very nicely demonstrates preserved

36:07

subcortical U fibers. We can see there is vasogenic white matter edema that

36:11

extends all the way up to, but does not involve this thin

36:15

gray stripe here, which represents the subcortical U

36:19

fibers. And in PML, we will lose that.

36:22

That will be

36:23

goneThis

36:28

is our last case here. So this is

36:32

a 45-year-old gentleman with headaches and

36:36

blurry vision.

36:38

So we can see

36:41

in the left frontal

36:44

area, precentral gyrus, we are

36:49

looking at a bubbly

36:52

T2 flare hyperintense, kind of cystic

36:56

cortical, subcortical lesion without mass effect

37:00

or any surrounding vasogenic edema.

37:09

On diffusion, it's very bright.

37:12

This lesion is also very bright on ADC, though not well

37:16

depicted in this particular example or single slice

37:20

image.

37:25

This is a very nice example of

37:29

MVNT or multinodular vacillating

37:32

neuronal tumor.

37:35

On MR, this will be clustered T2 and flare

37:39

hyperintense and bubbly appearing lesions that involve the deep cortical

37:43

ribbon and the superficial white matter.

37:45

There's typically sparing of the superficial gray matter.

37:50

These are often U-shaped. They have no mass effect,

37:54

no enhancement, and are bright on both diffusion

37:58

and ADC maps. Okay? Looks very

38:02

much like a DNAD. So what can we use to

38:06

distinguish the two? Well, MVNT is

38:10

typically bright on flare, and DNAD

38:13

typically has the central flare

38:17

suppression with the flare rim sign.

38:21

Other things to consider in a patient like this, particularly

38:25

if there is a history of seizure, would be focal cortical dysplasia,

38:29

and then less so, perivascular spaces can sometimes have

38:33

a similar imaging appearance.

38:38

So MVNT or multinodular vacillating neuronal tumor.

38:42

This is a distinct tumor that was recognized in

38:45

2021,

38:47

WHO Grade 1 tumor. Okay? These

38:50

lesions are clinically indolent, stable for

38:54

years, and unless it is a

38:57

proven epilepsy focus, these are do

39:01

not touch lesions. Many providers will not even follow

39:05

them if they have the pathognomonic imaging appearance on

39:09

MR.

39:13

So that's our last case. This is a quick,

39:17

but by no means comprehensive,

39:22

table of some of the tumor mimics. Many of

39:26

these we did cover today.

39:30

And

39:31

in conclusion, remember, fungus is among

39:35

us. Okay?

39:38

The main point I want to make about that is, especially in

39:42

this world of teleradiology, where every

39:46

practice is a teleradiology practice now.

39:49

You are working in a setting where you may have trained in one

39:53

part of the country and now find yourself reading imaging studies

39:57

for

39:58

an area of the country or a patient population that you have never served

40:02

before. And it's really important to understand what

40:06

the endemic diseases are for

40:09

the regions that you're reading for, and also what

40:13

the local immigrant populations are and what the endemic diseases

40:17

are for those patients.

40:21

Someone who has trained in New York and is suddenly reading

40:25

for a neurology group in Arizona, you're going to see

40:28

cocci meningitis. So you need to be familiar with what it looks

40:32

like on imaging, and it needs to be on your radar.

40:36

Again, look for some of these very pathognomonic

40:40

features on imaging that can help you make a diagnosis,

40:44

get the patient on the right management pathway, and keep them out of

40:48

the OR.

40:49

And when that's not enough, go back to your toolbox.

40:53

We didn't really cover this. This is for another lecture.

40:55

But perfusion imaging,

40:58

MR spectroscopy can still be helpful in

41:02

certain cases, even though

41:05

it's really not used very fruitful anymore.

41:08

And then, of course, CSF analysis and in some examples which we

41:12

didn't cover today because they are pretty frequently seen,

41:16

evolving hematomas and infarcts.

41:19

A short interval follow-up MR in three to seven days

41:23

can give you all of the information that you need and keep you out of trouble.

41:27

And with that, we'll stop there, and I think we saved plenty of time for questions.

41:31

But, this is my email. Please feel free to reach out to me, and I

41:35

will give it back to Ashley.

41:37

Yeah. Thank you so much, Dr. Pomrenze. That was awesome.

41:40

We've got one question in the Q&A box right now.

41:43

I don't know if you can pop it open and if you want me to read it to you.

41:47

How do I, Q&A?

41:48

It might be at the top of your...

41:50

Yes. Okay. So this is a great question. Okay.

41:53

Lymphoma with dark signal. Okay? So there

41:57

is a phenomenon called T2 blackout with

42:01

lymphoma. Okay? When lymphoma is so

42:05

hypercellular, it can appear very, very dark on

42:08

T2,

42:10

such that it actually blacks out the diffusion signal.

42:13

So you will have a very T2 hypointense lesion

42:18

with avid enhancement and no restricted diffusion.

42:21

Okay?

42:23

It will still be very dark on ADC. Okay?

42:26

So, I think ADC map is one of the

42:30

most underutilized sequences in neuroimaging.

42:33

It gives you so much information, and it does not

42:36

lie.But

42:41

yes. So that is the T2 blackout phenomenon

42:45

with lymphoma. So when

42:47

lymphoma is so hypercellular,

42:50

and very dark on T2, you may not see the true restricted diffusion

42:54

that you would expect. The other thing that can happen with lymphoma

42:58

is once a patient is on treatment or if they've been treated with

43:01

steroids, it can alter the signal characteristics, and

43:05

you may no longer see the expected restricted diffusion on follow-up

43:09

imaging.

43:11

And with the way patients kind of bounce around, end up in

43:14

hospitals-

43:15

Yeah

43:15

... get put on steroids. We had a case just like that recently in our

43:19

hospital in February.

43:22

When you see a lesion and you're not sure what you're dealing with, it's important

43:25

to find out where the patient's been, what they've been

43:29

on in the interval,

43:32

because it can change the way that you interpret the imaging.

43:36

The diagnosis of the T2 hypointense signal cases

43:39

again. So that was a

43:43

fungal abscess, fungal CNS disease.

43:45

I believe that was blastomycosis.

43:50

And the diagnosis of the first case, vertebral infarct,

43:54

secondary ablation. I don't know if I'd really

43:58

call them infarcts. That's a good question.

44:01

I have to get back to you on that one.

44:06

The diagnosis, so it's intercept. Yeah.

44:08

It's ablation of the vein.

44:14

Sorry. Not the vein, the nerve. The basivertebral nerve

44:18

root.

44:21

Okay. I think

44:24

you got them all.

44:25

All right.

44:26

No one else has any questions?

44:28

Well, thank you so much for being here, Dr. Pomeranz. Really appreciate it.

44:30

Yeah. Great to be with you all. Yeah.

44:32

Feel free to email me if anything else pops up or you want to share some

44:35

interesting cases.

44:37

Awesome. And thank you for everyone else for participating in today's noon

44:40

conference.

44:42

You can access the recording of it and all our previous noon conferences

44:46

by creating a free account. We'll also email a link to the replay later today.

44:51

Be sure to join us next week on Thursday, May 7th at 12:00 PM Eastern,

44:55

where Dr. Anup Shetty will deliver a lecture entitled "Approach to

44:59

Runoff Lower Extremity CTA." You can register for that at

45:02

medallia.com and follow us on social media for updates on future noon

45:06

conferences. Thanks again for learning with us, and have a great day.