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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

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learn alongside top radiologists from around the world.

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Today, we are honored to welcome Dr.

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Siddhartha Gattamangu for a lecture entitled Imaging of Meningeal

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Pathology. Dr. Gattamangu completed his radiology

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residency at Nizams Institute of Medical Sciences and went on to complete

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fellowship training in neuroradiology and nuclear medicine at University of

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Alabama in Birmingham. He previously worked at the Birmingham VA

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Medical Center, where he served as residency site director and is currently an

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associate professor in the Department of Radiology at UAB and serves as

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fellowship director of the neuroradiology program.

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At the end of his lecture, please join him in a Q&A session where he will address

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questions that you may have on today's topic.

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Please remember to use that Q&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 are ready to begin today's lecture. Dr.

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Gattamangu, please take it from here.

1:03

Thank you, Ashley.

1:05

Today, I will be talking on imaging of

1:09

meningeal pathology.

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I have no disclosures. And

1:15

so I'll give a brief outline

1:19

about on this presentation. We will start with

1:22

anatomy of the meninges and techniques to

1:26

identify meningeal pathology.

1:28

We will focus on the differential diagnosis of different

1:32

patterns of meningeal enhancement.

1:34

As you all know, what is pachymeningeal,

1:38

leptomeningeal, and within the focus of

1:41

pachymeningeal, focal meningeal enhancement, and some diagnostic

1:45

traps when we see

1:49

meningeal enhancement or meningeal pathology.

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So I'm going to start with

1:56

the anatomy. And as you all know,

1:59

we're just going to have a review of the anatomy.

2:02

And

2:03

this is the calvarium, and

2:07

attached to the inner margins of the calvarium, you see the dura

2:11

mater. And the dura mater, as you all know, has an outer and inner

2:15

layer. And the outer and inner layer actually

2:18

separate at certain areas just to enclose

2:22

the dural venous sinuses. And the dural venous sinuses are

2:26

obviously outpouched, or there's an outpouching within the dural venous

2:30

sinuses right here, which are the arachnoid granulations.

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Now, the arachnoid matter is much thinner layer,

2:37

which also parallels the calvarium, but it actually also parallels

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the inner

2:42

dural layer. The outer dural layer remains confined to the

2:46

margins of the periosteum, but the inner dural layer, along with the arachnoid,

2:50

actually will go into the

2:53

fissura and form the tentorial leaflets and the

2:57

falx.

2:58

And inner to the arachnoid matter

3:02

is what we call as the fourth layer, which we'll not be discussing, but

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recently, a fourth layer has been discovered in the meninges.

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And this fourth layer is called the subarachnoid lymphatic-like membrane, and these

3:13

are nothing but those tiny septations or partitions which you

3:17

see in the subarachnoid space, which is below the arachnoid.

3:21

And this is not visible on imaging, but it has now

3:25

been known to play a pivotal role in the glial

3:28

lymphatic system, which is actually

3:33

faulty in many neurodegenerative conditions and neuroinflammatory conditions.

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And lastly, the innermost layer is the pia mater, which is closely invested

3:41

along the surface of the brain.

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So the

3:46

pachymeninges are considered to be

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the dura arachnoid. So that is the

3:54

pachymeninges.

3:56

Whereas the leptomeninges are considered to be the

3:59

pia mater and the subarachnoid space.

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So that is the leptomeninges. The subarachnoid space and the pia mater are

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considered to be leptomeninges, whereas the pachymeninges are

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the outer inner layers of dura, along with the

4:13

arachnoid. Now, there's some confusion over here.

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When we talk about pachymeninges, sometimes they refer only to the dura

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mater.

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And when it comes to leptomeninges, its lepto is more thin or leaf-like, and they

4:24

consider that to be the pia mater and the arachnoid.

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So the arachnoid is kind of a controversy which side it goes.

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But when it comes to meningeal enhancement, when we talk about

4:34

meningeal enhancement, it is the dura arachnoid.

4:36

We're talking about the dura and the arachnoid together.

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And when we come to leptomeningeal enhancement, we're talking about

4:43

enhancement of the pia mater and the subarachnoid space.

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So let's look at this image. And

4:52

for example,

4:54

normally you can see some degree of pachymeningeal

4:58

enhancement, and this is

5:00

some normal pachymeningeal enhancement you actually will normally see,

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and it's actually common to see some degree of pachymeningeal

5:08

enhancement.

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So

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just outlining what are the dural layers.

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So, this is the,

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what is the outer dural layer, and the outer dural layer parallels the

5:21

calvarium or the periosteum. And this is the

5:25

inner dural layer, which forms reflection. It goes into the falx.

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And this is the thinner arachnoid membrane, which is paralleling

5:34

the inner dural layer.

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And this wavy membrane is the pia mater.

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So what is normal versus abnormal meningeal enhancement?

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And that's sometimes tricky, and it is important to know that normal

5:48

meningeal enhancement is best seen when you actually do thinner slices,

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especially when you do 3D T1 thin slices.

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And usually it is discontinuous and linear.

5:59

Sometimes it can be continuous.You see it better on the coronal

6:03

views. And remember that it's only the pachymeninges, which is

6:07

the dual layers, which enhance. The arachnoid and the pia

6:11

mater do not normally enhance.

6:15

So some technical parameters. Again, you can see

6:18

pachymeningeal enhancement normally with CT and post-contrast

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MRI. The higher the magnet strength, the 3D

6:26

acquisition, and the thinner slices, the more likely you're going to see

6:30

normal meningeal enhancement. I have had better success with gradient

6:33

echo images as opposed to spin-echo images.

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Gradient echo images, which you see on the far right, actually

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show pachymeningeal enhancement much better

6:45

than spin-echo images.

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Now, role of contrast-enhanced FLAIR.

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I want to be upfront that we are currently not

6:55

doing contrast-enhanced FLAIR in our institute, but we are actually

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going to adopt that pretty quickly.

7:01

We're going to implement that

7:05

for all our tumor protocol patients

7:09

in the next six months. And

7:12

contrast-enhanced FLAIR is much more sensitive

7:16

to both pachymeningeal and leptomeningeal enhancement,

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and its sensitivity has a higher negative

7:23

predictive value and also increases the confidence to

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diagnose meningeal pathology. The

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reason why is when you do a T1

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post-contrast, sometimes vascular enhancement

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can mimic leptomeningeal enhancement, and

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the vascular enhancement is actually not seen in

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FLAIR post-contrast. So it actually increases your

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specificity and confidence to identify

7:55

meningeal enhancement. It is also sensitive to look at in concentration.

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The recommendation is actually do this study

8:02

sequence four to five minutes after post-contrast.

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So if you give contrast, start with your T1 post-contrast

8:10

and while terminating the study, do the post-contrast

8:13

FLAIR just prior to termination.

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So let's go and look at some cases. So we have a case over here.

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On a CT, this patient seems to have some

8:26

subdural effusion. And on this FLAIR, and this is not

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a post-contrast, it's a pre-contrast FLAIR,

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we see a bright signal in the central space.

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So it looks like a subdural effusion or like a subacute

8:40

subdural hematoma. However, on the post-contrast, there is diffuse

8:43

pachymeningeal enhancement. So this can look like a subdural

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effusion on pre-contrast FLAIR and

8:51

CT. However, now we know this is diffuse

8:54

pachymeningeal enhancement. So

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if you look on the SAS tool image, you can see the

9:02

call mark findings of intracranial hypertension where you have an

9:06

enlarged sella, decreased suprasellar cistern,

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mamillary peduncle angle being narrow.

9:12

So this is the classic

9:14

spontaneous intracranial hypertension.

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Again, this patient has a very high BONES score, and one of the

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major indices of a BONES score is pachymeningeal enhancement, venous

9:25

engorgement, and suprasellar cistern, which is small.

9:28

So these findings prove that this patient actually has intracranial

9:32

hypertension, which is one of the most common causes of

9:36

pachymeningeal enhancement.

9:39

So smooth pachymeningeal enhancement.

9:41

So let's divide pachymeningeal enhancement into

9:45

smooth and nodular.

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The most common cause of smooth pachymeningeal enhancement remains

9:51

intracranial hypertension, as you see over here.

9:54

It is resulting from CSF loss.

9:58

Usually, the CSF loss in idiopathic, or I shouldn't use the term idiopathic, it's

10:02

spontaneous intracranial hypertension, is actually a CSF leak

10:06

in the lower thoracic spine.

10:08

And the CSF loss results in

10:12

meningeal hyperemia and thickening, and there is smooth dural thickening that's

10:15

sometimes associated with a subdural effusion.

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The combination of a subdural effusion and pachymeningeal thickening

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raises the BONES index and also raises the

10:27

likelihood that this is due to intracranial hypertension.

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However, smooth pachymeningeal thickening can also be seen in other conditions, and

10:34

this is the patient with leukemia, this patient had acute

10:38

lymphoblastic leukemia. Again, looks very similar, so you

10:42

want to look for the engorged venous sinuses.

10:45

You want to look for other findings to suggest

10:48

intracranial hypertension. But this was a case of

10:51

leukemia.

10:53

So moving on to smooth pachymeningeal thickening.

10:58

This is a patient who has,

11:00

again, very smooth pachymeningeal thickening.

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However, it's noted by its predominance on one side,

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which is atypical for intracranial hypertension.

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If you look on the coronal T2, notice how the pachymeningeal thickening is dark.

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And typically when you see that, you think of a fibrous condition, a condition

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which results in fibrosis and resulting in

11:20

due to dark signal, and that is seen in granulomatous conditions.

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And if you look at the coronal post-contrast, there

11:28

is this central hypointensity within the pachymeningeal thickening.

11:31

I know it's not that very conspicuous, but

11:34

these are the central hypointensity, and that creates the Eiffel by night sign,

11:39

which has been described in granulomatous polyangiitis.

11:42

And granulomatous polyangiitis is one of the ANCA.

11:46

It is one of the subtypes of antineutrophil cytoplasmic

11:49

antibody diseases, and we know that there are three subtypes.

11:53

One is granulomatous polyangiitis, the other one is microscopic

11:56

polyangiitis, another one is

12:00

granulomatosis with eosinophilic syndrome.

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AndIt is typically granulomatous polyangiitis

12:07

which actually causes

12:10

the pachymeningeal enhancement in the T2 dark signal.

12:14

Now, smooth pachymeningeal enhancement can also be caused by other

12:18

conditions and this, again,

12:21

very non-specific pachymeningeal enhancement, but there is actually a venous

12:25

sinus thrombosis. And venous sinus thrombosis can also

12:29

cause hyperemia of the overlying pachymeninges and cause

12:33

smooth pachymeningeal enhancement.

12:35

So whenever there is smooth pachymeningeal enhancement, you look for venous

12:38

engorgement, but you also want to look for a venous sinus thrombosis, and you may

12:42

want to do an MR venogram if you're also very suspicious.

12:45

But that is one cause of smooth pachymeningeal enhancement.

12:52

So

12:53

now let's go to the other subtype of pachymeningeal

12:57

thickening, which is irregular and nodular.

13:01

And while this is a patient with intracranial hypotension in which

13:05

there is smooth pachymeningeal enhancement, but later

13:08

on, this patient developed superimposed nodularity.

13:11

For example, there's one nodule here overlying the left frontal lobe and

13:15

a poorly enhancing nodule overlying the left parietal lobe.

13:19

And this patient actually developed dural metastases.

13:22

So this is a patient with underlying intracranial hypotension who developed

13:26

focal nodularity in the dura,

13:29

and this is characteristic of dural metastasis typically seen in prostate and

13:33

breast cancer.

13:34

And

13:36

so that's one cause of nodular pachymeningeal thickening.

13:40

As we move on, this is a patient who has diffuse pachymeningeal thickening, but

13:44

there is some nodularity and again, very fibrous

13:48

T2 dark signal. We talked about this occurring in granulomatous

13:51

polyangiitis, but it can occur in other granulomatous conditions.

13:55

And by far the most common granulomatous condition, which

13:58

involves the dura in the Western world, in particular the United

14:02

States, is neurosarcoidosis. And that is

14:06

something you always want to

14:10

suggest that in a differential whenever you see nodular irregular

14:14

pachymeningeal thickenings. Apart

14:18

from pachymeningeal thickening, patients with neurosarcoid can also have cranial

14:21

nerve and leptomeningeal involvement.

14:23

And actually, leptomeningeal involvement is actually more common than

14:27

pachymeningeal involvement in neurosarcoid.

14:29

So the other inflammatory conditions such as SLE, rheumatoid,

14:34

granulomatous polyangiitis, they typically cause a

14:37

pachymeningeal enhancement or pachymeningeal pathology, whereas

14:40

neurosarcoid is one of the inflammatory or unknown conditions

14:44

which actually causes

14:47

involvement of both pachymeningeal and

14:50

leptomeningeal disease with T2 hyperintense thickened dura.

14:57

So other causes. For example, this is another patient who has

15:01

extensive pachymeningeal disease, and it is smooth at certain

15:05

locations, but then it develops nodularity.

15:07

It also develops significant nodularity and mass-like thickening

15:11

involves the cavernous sinus skull base.

15:14

And this was a path proven case of Rosai-Dorfman disease,

15:18

which is a sinus histiocytosis with massive lymphadenopathy.

15:22

It involves lymph nodes, but it can involve other areas of soft tissue.

15:26

It can involve the paranasal sinuses, it can involve the deep soft tissues of neck,

15:30

but when it involves intracranial compartment, it usually mimics a

15:34

meningioma. It's like focal, solitary or

15:37

multiple dural-based masses, typically along the skull base.

15:41

And this was a case of Rosai-Dorfman disease.

15:45

It's not very common, but something...

15:48

One of the histiocytosis syndromes which actually can

15:52

cause focal dural mass-like thickening.

15:56

Now, if you look at the osseous changes, because the dura is

15:59

intimately associated, intimately connected to the

16:03

bone, and it's very close. So this is a patient who actually

16:07

has dural thickening, which is heterogeneous.

16:09

The dural thickening extends into the orbit, causing proptosis, and there's

16:13

also some bony expansion with soft tissue

16:17

in the temporalis muscle. And if you look on the corresponding CT, there is

16:20

extensive dural hyperostosis, and this is a straightforward case of an

16:24

N-plaque meningioma. So whenever there is bony changes, you don't want to think of

16:28

inflammatory conditions. You really want to think about an N-plaque meningioma.

16:33

You have to remember this subtype of meningioma.

16:35

Usually, most meningiomas are focal dural based, but sometimes

16:39

meningiomas can be diffuse, linear and cause bony changes, and

16:43

that's an N-plaque meningioma. The differential for this is bone

16:47

sarcomas. Especially in younger children age group, you need to think of

16:50

osteosarcomas, fibrosarcomas or metastatic neuroblastoma.

16:54

So if it's actually someone who's below two years of age, so metastatic

16:58

neuroblastoma. So remember, primary bone diseases

17:02

can result in secondary infiltrative

17:05

dural

17:08

thickening. We can also see this sometimes in metastatic disease.

17:13

Now let's move on to focal dural masses.

17:16

And

17:17

I just want to talk about the dural tail.

17:20

The dural tail, which you see in meningioma.

17:23

This case on my right side is an invasive meningioma

17:27

that it's embedded the adjacent frontal bone.

17:31

Notice how the enhancement pattern is very similar to the extra-axial component.

17:34

You have a hyperenhancing dural tail.

17:37

When the dural tail is biopsied, in most situations, it

17:41

is a reactive thickening containing no tumor cells.

17:45

And the dural tail is usually more hyperenhancing compared to

17:49

the tumor itself. Now, the dural tail is not typical

17:53

for meningiomas. You can also see the dural tail in

17:56

patients with

17:58

lymphoma or any other extra-axial lesions, or even in

18:03

tumors which infiltrate the cortical gyrus.

18:07

And this is a B-cell lymphoma with dural tail.

18:11

It taps again a finding of dural tail is atapers

18:15

away from the lesion, becomes more thinner as you go more farther

18:19

or further from the primary lesion.

18:23

So focal dural masses, we always think of lymphoma, but there are many

18:27

conditions which may mimic a meningioma.

18:29

I just want you all to be aware of that.

18:31

For example, breast metastasis or prostate metastasis

18:35

can present as a dural mass.

18:38

A solitary fibrous tumor, AKA hemangiopericytoma, can look

18:42

very similar to a meningioma.

18:46

GBM, multicentric GBM, primary GBM, especially

18:50

when GBM is multicentric in different locations, can secondarily

18:54

involve the dura. This is a patient with multicentric glioblastoma.

18:58

And lastly, also lymphoma can present as solitary or

19:02

multifocal dural-based masses, and

19:05

the only way we can know the exact diagnosis is the

19:09

presence of a known malignancy, like breast cancer, prostate cancer would

19:13

suggest that these are dural-based mets.

19:15

Otherwise, we require biopsy to confirm the

19:19

diagnosis.

19:22

So now let's move on to the second part of the topic, which is

19:26

leptomeningeal enhancement.

19:31

So

19:32

again, as we discussed, leptomeningeal enhancement is enhancement in the

19:36

subarachnoid space and pia mater.

19:38

It's

19:40

enhancement of the pia mater or subarachnoid space.

19:44

Or you can also say in the subarachnoid lymphatic system, or

19:48

the subarachnoid lymphatic space

19:51

system also.

19:54

One of the most common causes is infection.

19:57

So we talked a lot about pachymeningeal enhancement, and while certain

20:00

infections like TB and fungus can cause

20:04

pachymeningeal enhancement, most often infection

20:08

involves the leptomeningeal space.

20:11

And

20:12

this is a case with very diffuse cortical

20:16

subarachnoid space enhancement, and this is a bacterial meningitis.

20:20

On my right, I have a more basal

20:23

subarachnoid space enhancement involving the basal cisterns.

20:27

And the enhancement is also very modular and not

20:31

smooth like the one on the left side.

20:33

And this was a case of coccidioidomycosis, which is

20:37

very prevalent, especially in the southeast where I am located in

20:41

southeast United States. It is an irregular and nodular

20:45

basal leptomeningeal enhancement.

20:50

I want to reiterate again that the arachnoid matter is a very

20:53

avascular area. It does not enhance usually, normally or in pathological

20:56

conditions. So when you're talking about pachymeningeal enhancement, it is the dura

21:00

which is enhancing. When you're talking about leptomeningeal enhancement, it's the

21:03

subarachnoid space and the pia mater which is enhancing.

21:08

Typically, for diagnosing a leptomeningeal disease, you

21:11

do a lumbar puncture. For pachymeningeal disease,

21:15

the diagnosis needs to be known by biopsy, you do a dural

21:19

biopsy

21:20

or a meningeal biopsy.

21:23

Now, continuing on nodular leptomeningeal enhancement,

21:27

neurosarcoidosis can be thin linear or nodular.

21:31

I've seen different, the same neurosarcoidosis doing everything.

21:35

It can cause both thin and nodular enhancement.

21:40

Then we have leptomeningeal carcinomatosis from systemic

21:43

malignancies, which can cause thin and nodular enhancement, as in this case

21:47

with lung disease, lung cancer. And on my

21:51

extreme right is a patient with a spine pleocytic astrocytoma who had

21:55

upstream, I wouldn't say drop metastasis, but

21:58

upstream metastasis into the leptomeningeal spaces of the posterior

22:02

fossa. Quite a rare case. We typically see a

22:06

posterior fossa pleocytic astrocytoma,

22:09

but this was a case of spine astrocytoma, pleocytic astrocytoma, which

22:13

caused leptomeningeal disease in the posterior fossa.

22:16

That can be spontaneous or can occur after surgery due to spillage

22:20

of tumor.

22:23

Now, what are the accompaniments of leptomeningeal enhancement?

22:27

So

22:28

the leptomeningeal or the subarachnoid space is contiguous with the

22:32

ventricles and is also contiguous with the cranial

22:36

nerves, which traverse the subarachnoid space.

22:40

So on my left, we have this patient who has leptomeningeal

22:44

enhancement but also has

22:47

ependymal enhancement. And on my right, we have this patient

22:51

with bilateral fifth nerve enhancement.

22:54

So cranial nerve enhancement is frequently seen when patients have

22:57

extensive leptomeningeal disease.

22:59

I've seen that in patients with neurosarcoid who have a high instance of

23:03

facial nerve palsy, and even tuberculosis or

23:07

any

23:09

granulomatous leptomeningeal enhancement or

23:12

any leptomeningeal enhancement which frequently resides in the

23:16

skull-based cisterns can cause cranial nerve enhancement.

23:22

So what are the complications of leptomeningitis?

23:25

So there are two main complications which you need to be aware of.

23:29

One is the presence of hydrocephalus, because these leptomeningeal exudates

23:33

block the CSF outflow, so it can cause a communicating

23:37

obstructive hydrocephalus. And I've seen it very fairly

23:41

common in tuberculosis meningitis

23:43

or fungal meningitis, cryptococcal meningitis.

23:47

Another one is

23:49

infarcts, which are usually around the

23:53

distribution of the perforator arteries of the anterior cerebral arteries and

23:57

the middle cerebral arteries. It is actually, infarcts are

24:01

very commonly seen in patients who actually have a

24:04

streptococcal meningitis in children.

24:08

But I've seen them in different types of bacterial and fungal

24:11

and TB meningitis. But in children, it has been well described in

24:15

patients with streptococcal

24:17

meningitis.So

24:21

this is another patient who had some degree of

24:25

leptomeningeal enhancement in the left temporal

24:29

and parietal lobe. And this patient also gets an MR venogram, which shows

24:33

that the superior sagittal sinus and the transverse sinus are occluded, or the

24:37

left transverse sinus and superior sagittal sinus are occluded due to deep venous

24:41

sinus thrombosis. And in the presence of deep venous sinus thrombosis, as we

24:45

discussed, you can get a pachymeningeal enhancement, but you also can get

24:49

hyperemia or congestion in the draining veins because of obstruction, and

24:53

that can mimic leptomeningeal enhancement.

24:55

And this is why contrast enhanced FLAIR is very useful.

24:58

It actually omits signal from congested vessels, and it

25:02

actually depicts pure leptomeningeal enhancement.

25:07

Propofol for sedation in children can also cause leptomeningeal enhancement.

25:10

I don't know the exact mechanism, and I'm not sure if post-contrast

25:14

FLAIR can actually alleviate this problem.

25:17

But that has been described, especially in children who receive anesthetics for an

25:20

MRI. Be aware of propofol, which can cause

25:23

vascular engorgement mimicking leptomeningeal enhancement.

25:29

So what are some other

25:33

differentials for leptomeningeal enhancement, meaning conditions which can mimic

25:36

leptomeningeal enhancement? Gyriform enhancement.

25:39

So gyriform enhancement is not considered to be in the meninges.

25:43

It's in the cortical gyri. And this is a patient with gyriform

25:47

enhancement, and I don't know exactly what the cause is.

25:49

But gyriform enhancement can be seen in patients with strokes, it can be seen

25:53

in patients with encephalitis. So those are some

25:57

conditions. And again, as we discussed, normal vessels,

26:02

vascular enhancement can be misinterpreted as a leptomeningeal enhancement,

26:06

and that is where contrast FLAIR can be useful.

26:10

So

26:12

another cause of gyriform enhancement can be

26:15

post-reversible encephalopathy.

26:19

So this was an interesting case who actually had a squamous

26:23

cell cancer of the skin who... and this patient actually

26:27

had

26:28

erosion of the skin and ulceration and had

26:32

very thick dural enhancement. So many times,

26:36

when tumors erode the table or erode the

26:40

calvarium, there is dural enhancement, and it's important to distinguish what

26:43

is reactive

26:45

dural enhancement from true malignant infiltration.

26:49

Whenever there is a focal nodular dural enhancement, we call that tumor

26:52

infiltration. And if the dural thickening is more than five millimeters, we

26:56

call it dural invasion. If there is just smooth pachymeningeal

27:00

enhancement like this adjoining a tumor which has eroded the

27:04

calvarium, we usually call it reactive.

27:06

So this is probably a reactive

27:08

dural enhancement. But this area is much more than five millimeter thick, and that

27:12

is probably nodular. This nodular pachymeningeal

27:16

enhancement is likely tumor. So this patient actually had

27:19

biopsy-proven squamous cell cancer involving dura. This was resected.

27:23

This patient got a graft, and he comes back later after the

27:26

graft with edema in the right parietal region

27:30

with very irregular

27:33

nodular leptomeningeal enhancement.

27:36

And even MR perfusion shows some degree of

27:40

increased perfusion right here in the leptomeningeal enhancement.

27:44

So

27:45

this question is actually key for several reasons.

27:50

In this case, if you look carefully, the venous sinus or the superior

27:54

sinus is thrombosed, and that can potentially cause edema

27:58

and congestion of the vessels. And this patient was also

28:02

on immunotherapy. And patients who are on

28:06

immunotherapy can actually show leptomeningeal congestion, and the

28:10

time period is so variable, it can start immediately from one week and can last for

28:14

several weeks. So we were not sure if this patient was getting

28:17

leptomeningeal enhancement from immunotherapy, venous sinus thrombosis.

28:21

However, when they cultured

28:23

this area,

28:24

all Pseudomonas was grown and this patient was put on long-term antibiotics.

28:27

So this patient was actually presumed to have infection

28:31

from the surgery. And this was considered to be a

28:35

leptomeningitis from surgery. So you need to think of alternative

28:39

conditions

28:41

when you actually have leptomeningeal enhancement, immunotherapy, and

28:45

infection, even when you have a patient with known skin

28:49

malignancy.

28:51

What are some other atypical meningeal enhancements?

28:54

So this is a patient with subdural empyema, and I just want to show the rare

28:58

enhancement of the arachnoid membrane. So this is the subdural empyema.

29:02

And on the outer margin of the subdural space are the dura.

29:04

So this is the enhancement dural margin, and this enhancement is of the

29:09

arachnoid membrane, so the arachnoid margin.

29:12

So you have both leptomeningeal and pachymeningeal enhancement.

29:15

And

29:16

again,

29:18

we don't actually, as I discussed, the arachnoid matter

29:22

is part of the...

29:24

the arachnoid matter is considered lepto because it is thin.

29:28

But when we talk about pachymeningeal enhancement, we actually talk about dura

29:31

arachnoid. So it's a bit confusing, but I really want to showcase this as a

29:35

case with both arachnoid matter enhancement and dural

29:38

enhancement.

29:41

So to summarize, what are the cause of pachymeningeal enhancement?

29:45

Intracranial hypotension remains the most common cause.

29:48

Look for venous engorgement. Look for enlarged pituitary

29:52

gland. Look for the bone score. Post-operative, which we have not discussed, but is

29:55

self-explanatory.

29:57

Inflammatory conditions apart from neurosarcoid, IgG4 related Granulomatous

30:01

with polyangiitis, rheumatoid, SLE, all cause pachymeningeal enhancement.

30:06

Prostate and

30:09

breast mets, lymphoma, leukemia, certain infections such as TB and

30:13

fungal and dural venous sinus thrombosis.

30:16

Leptomeningeal enhancement, on the other hand, is predominantly caused by

30:18

infections, systemic malignancies, where it is known as leptomeningeal

30:22

carcinomatosis, lymphoma and leukemia, neurosarcoid, which

30:26

can fit into both categoriesAnd always remember

30:29

immunotherapy.

30:31

You can get pseudoleptomeningeal enhancement in patients with dural venous sinus

30:35

thrombosis and anesthetic medications.

30:39

So that concludes my lecture. So I'm

30:43

ready to answer any questions you all have.

30:51

Thank you so much for that lecture.

30:53

We are open for questions.

30:57

We've got one in that Q&A box right now. I'll go ahead and read it to you.

31:01

Can you distinguish the pachymeningeal thickening

31:05

of IG4 disease from other causes?

31:09

Yeah. So,

31:10

not really.

31:12

IG4 related will look very similar to neurosarcoid and

31:16

granulomatous with polyangiitis.

31:19

The only thing is it doesn't really cause much leptomeningeal enhancement, but the

31:22

pachymeningeal enhancement will appear very similar to

31:26

granulomatous with polyangiitis and

31:29

neurosarcoid.

31:35

Does lung cancer cause smooth pachymeningeal enhancement in one hemisphere?

31:40

I have never seen that.

31:43

Lung cancer typically is known to cause leptomeningeal

31:46

enhancement. Again, we do have very rare,

31:50

bizarre cases which don't follow the rules.

31:53

But

31:54

when you have smooth pachymeningeal enhancement, even if the patient has no lung

31:57

cancer, that's not typically what we

32:01

think as a first cause. I have, on the other hand, actually seen breast cancer

32:05

actually cause smooth pachymeningeal enhancement rather than nodular.

32:09

I do have one case of breast cancer with smooth pachymeningeal enhancement.

32:12

So I've seen that with breast, but not lung.

32:18

How to DD from thickening of the tentorium.

32:23

So

32:25

the differential diagnosis with thickening of the tentorium, again, it

32:29

all depends whether it's accompanied by diffuse pachymeningeal thickening

32:32

elsewhere. If it is accompanied by diffuse pachymeningeal thickening

32:36

elsewhere, I would first think of intracranial hypotension.

32:40

However, if the thickening is focally in the tentorium,

32:44

then my differential diagnosis would be dural Mets lymphoma

32:48

or neurosarcoid or other granulomatous conditions.

32:54

Is leptomeningeal enhancement in children due to supplemental oxygen and

32:58

anesthesia or propofol itself?

33:01

So yeah, that's a great question. So, I don't think supplemental

33:05

oxygen actually causes leptomeningeal enhancement.

33:07

It usually is a flare phenomenon, and we've seen

33:11

that, and I don't really have much experience with kids, but I've seen that so

33:15

common in adults when patients are on supplemental oxygen.

33:18

They actually have flare hyperintense signal, but they lack the

33:22

leptomeningeal enhancement. So the answer to that question is it's probably due

33:26

to propofol, not due to supplemental oxygen.

33:33

Which cortical primary tumor infiltrates meninges?

33:37

Yeah. So GBM, when it infiltrates the meningeal cortex,

33:41

is the most common tumor which can

33:45

actually cause meningeal or thickening and cause a dural tail.

33:49

So I've seen that with GBM and metastasis.

33:52

When they infiltrate the cortex, they cause

33:55

dural tail. When GBM is confined to the deep white

33:59

matter, you won't expect to see a dural tail.

34:03

But when the GBM involves the cortex, yes, you can see a dural tail.

34:07

The same thing is true for metastasis.

34:12

What about post-lumbar puncture meningeal thickening?

34:17

Yeah. So,

34:19

post lumbar puncture causes, again, a smooth,

34:23

what do you say, the pachymeningeal thickening.

34:25

It can mimic intracranial hypotension.

34:29

I don't think I have actually seen a very high bone score.

34:32

But yes, it can cause a smooth pachymeningeal enhancement,

34:37

mimicking

34:38

other conditions. So it's very, very important to know if the patients have had

34:42

a prior history of lumbar puncture.

34:45

I typically ask my fellow clinicians to perform a

34:49

lumbar puncture after they get the MRI and if they're

34:53

suspecting any inflammatory condition or any

34:58

condition which they want further diagnosis.

35:01

We first do an MRI and then do a lumbar puncture, because lumbar puncture

35:05

can cause a diffuse pachymeningeal enhancement from a

35:08

temporary CSF leak.

35:12

If hyperdensity is seen in tentorium or falx in trauma cases, is it

35:15

subdural or subarachnoid?

35:18

Oh, that is actually subdural. And that's a good

35:22

question because sometimes you see a focal area of hyperdensity in the

35:26

intermsic fissure, and when it's so focal, it's actually very

35:30

difficult to actually tell if that focal

35:33

hyperdensity adjacent to the falx is subarachnoid or subdural.

35:37

But the more linear and the more

35:40

sulci it traverses, it is subdural.

35:42

So the answer is, if it is a long segment, it is definitely

35:46

subdural. But if the focal hyperdensity is very

35:50

short along the tentorium or along the

35:54

falx, you cannot actually say whether it's subdural or subarachnoid, and we usually

35:58

tend to call it subdural most of the time.

36:03

Okay. We'll do a couple more. What is the minimum protocol details, slice

36:06

thickness, and other settings in the evaluation of cranial meninges?

36:10

Yes. So we have

36:14

a very universal protocol where

36:18

our post-contrastOur T1 postcontrast on our

36:22

FLAIR both. We are not doing a postcontrast FLAIR,

36:25

but in future, we are going to replace our precontrast FLAIR with a postcontrast

36:29

FLAIR.

36:31

Ideally, I would like to have both, but because we want to minimize our

36:35

scan times, we are going to replace the precontrast FLAIR with a postcontrast

36:38

FLAIR. The slice thickness is we do a one millimeter slice thickness,

36:42

and that increases your sensitivity for identifying meningeal disease.

36:47

Our T2 weighted sequences, because those are less sensitive for diagnosing

36:51

meningeal pathology, we actually retain them at four to five

36:54

millimeter thin slices. We do a

36:58

routine DWI, which has limited utility in

37:03

leptomeningeal disease or pachymeningeal disease.

37:06

SWI is great to look for leptomeningeal siderosis,

37:09

and

37:12

we incorporate that in all our

37:15

sequences.

37:17

But the most important sequences for meningeal pathology remains

37:21

FLAIR and T1, which we do at one millimeter 3D slices, and these are

37:25

isotropic 3D slices, which we reformat in multiple orthogonal

37:28

planes.

37:31

Okay. And- What is the best MRI sequence to evaluate the

37:35

cause of leptomeningeal thinking?

37:38

B.

37:39

I would say it's a postcontrast FLAIR.

37:41

If you want to single out one, it's a postcontrast FLAIR.

37:45

So it is. Okay. I think we got

37:49

them all.

37:50

I think we got all the questions. Thank you so much for your lecture and for

37:54

staying on to answer those questions. We really appreciate it.

37:57

And I think,

37:59

just reading out some more.

38:01

So in suspected meningeal pathology, do you always perform postcontrast FLAIR

38:04

sequences? Do you also acquire postcontrast T1, or

38:08

do you sometimes omit them, and why?

38:11

So the answer to that is,

38:15

it is best to do both. And

38:19

you want to do both postcontrast T1 and postcontrast FLAIR.

38:21

The reason why you want to do a postcontrast T1 also is because

38:26

you want to look for parenchymal enhancement also.

38:29

And I think,

38:30

so you want to look for other areas which enhance.

38:33

So,

38:34

you want to do a postcontrast T1 to look for brain enhancement and postcontrast

38:38

FLAIR to look for meningeal enhancement.

38:40

And so inversion recovery sequences,

38:44

we don't do that. I know it's very great to look for demyelination.

38:49

My best experience with inversion recovery is to look for

38:53

areas of demyelination in the brain in multiple sclerosis, but I really don't know

38:56

if that's particularly useful for looking for meningeal pathology.

39:00

And the last question I see is, which one is more involved in AIDS,

39:04

lepto or pachymeningeal enhancement?

39:09

So if you're in

39:12

AIDS, the most common

39:14

meningeal disease is Cryptococcus, which typically causes leptomeningitis.

39:18

So the answer to that is leptomeningeal enhancement.

39:21

Any more-

39:21

Fantastic.

39:23

Yeah.

39:23

Thank you so much.

39:24

Thank you. Thank you, everyone. Thanks for joining. Have a great day.

39:28

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39:33

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39:45

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