0:01

Hello and welcome to Noon Conference, hosted by MRI Online

0:06

Noon Conference connects the global radiology community

0:08

through free live educational webinars that are accessible

0:12

for all and is an opportunity

0:13

to learn alongside top radiologists from around the world.

0:16

You can access a recording of today's conference

0:19

and previous noon conferences

0:20

by creating a free MRI online account.

0:24

Today we are honored to welcome Dr.

0:25

Joshua Nickerson back to the noom Conference stage

0:28

for a lectured entitled SWI Imaging Practical Applications.

0:33

Dr. Nickerson is a professor

0:34

of radiology at OHSU in Portland, Oregon, where he serves

0:38

as the Division Chief of Neuroradiology

0:40

and Vice Chair of Academic Affairs.

0:42

He's also the editor-in-Chief of Neuro Graphics,

0:45

and holds a variety of positions

0:46

with the A-S-N-R-A-B-R-A-U-R

0:49

and A PDR at the end of his lecture.

0:52

Please join him in a q

0:53

and a session where he will answer questions you may have

0:55

on today's topic.

0:57

Also, feel free to throw any questions you want answered

1:00

immediately into the chat, and Dr.

1:01

Nickerson will do his best to reply.

1:04

Please remember to use the q

1:06

and a feature to submit questions so we can get to as many

1:09

as we can before our time is up.

1:11

And with that, we are ready to begin today's lecture. Dr.

1:13

Nickerson, please take it from here.

1:17

Thanks everybody for, for joining us this morning.

1:19

It's really, uh, nice to be working with modality again

1:22

and, uh, hopefully we will get something good

1:24

outta this conference this morning.

1:26

So, as you mentioned, uh, my name is Joshua Nickerson.

1:28

I'm, uh, a radiologist at OHSU in Portland.

1:30

This is the hospital that I work at.

1:32

I have the, uh, the pleasure of commuting to work sometimes,

1:34

sometimes by aerial tram.

1:36

You see those, uh, those little pods carry us up from the

1:39

waterfront up to my hospital

1:40

and drop you in the ninth floor.

1:41

And radiology is just one step above that.

1:45

So I thought today we would talk about susceptibility

1:47

weighted imaging, which is a topic

1:49

that I am particularly passionate about.

1:51

Uh, it's definitely one of my favorite MRI sequences,

1:53

and I think lots of folks are very familiar

1:56

with SWI in the setting of trauma.

1:59

Uh, and we will talk about trauma,

2:00

but I was hoping to show you maybe some other ways

2:02

that SWI can be really useful clinically, uh,

2:05

beyond just trauma imaging and,

2:07

and maybe some you've seen,

2:08

maybe some that might be new to you.

2:09

Uh, as I mentioned, as, as was mentioned in the beginning,

2:12

I have little chat window open.

2:14

Uh, I also have the q and a panel open.

2:16

Um, if you have a question that you think is timely

2:19

to the subject we're talking about at that moment,

2:21

feel free free to put it in the chat.

2:23

I'll try to keep an eye on that.

2:24

Um, if you have a question that you'd rather cover at the

2:26

end of the conference, just put it in the q

2:28

and a panel, the the separate one, and,

2:30

and at the end, hopefully we'll have time to go

2:31

through a few of those things.

2:34

So one thing I wanna do, uh,

2:36

which might be a little different from some

2:37

of these conferences, is I have a few poll everywhere

2:41

questions embedded in the talk today.

2:43

And, and I will, you know, full disclosure, I have to say,

2:46

uh, I was at the University of Vermont for many years

2:48

before I was in Oregon, and I have yet

2:49

to actually pay the fee to change my username.

2:52

So it's still UVM Neuro, but if you have a, uh, a smartphone

2:56

or you have laptop open, feel free

2:58

to pop open this browser address poll ev.com, uvm neuro,

3:03

and uh, it will take the first 25 or 30 of you who log in

3:07

because I also have the free, uh, the free version.

3:10

It'll only let me have so many.

3:12

So you can be the representatives of the group, um,

3:14

and other people, you can chat stuff into the

3:16

chat if you don't quite get in.

3:17

But this will be a fun way to kind of keep you entertained

3:19

and keep you interactive with the, uh, with the program.

3:23

So, uh, and this will show on the slides too when we get

3:25

to them, so you don't have to to rush right now.

3:28

So, but let's see if it's working.

3:29

So, uh, how many of you, I'm curious

3:32

before we start the presentation, how many

3:33

of you are using SWI and how are you using it?

3:37

So if you have access to that address,

3:39

I see a few responses coming in, that's great.

3:42

Um, do you not use it at your institution?

3:44

Do you only use it when you specifically

3:47

get a request for it?

3:48

Um, and how do you do it in comparison to GRE?

3:51

So some places still do both.

3:53

Some people do SWI only, uh, some people still do GRE only.

3:58

All right, so I've got a few responses

4:01

and let's see what tho those 10 folks have said.

4:03

I don't wanna take up lots of time here. Alright, good.

4:06

That's great. So it looks like a little over half

4:08

of you are actually only using SWI and that is fantastic.

4:12

Um, that is what I was hoping the response would be.

4:15

There's no right answer here, uh,

4:17

but I just kind of wanted to, to see what folks were doing.

4:21

So a little bit about the history

4:22

of susceptibility weighted imaging.

4:23

It's been around for a while.

4:25

Uh, it's, uh, traditionally when we would do MRI, prior

4:28

to the advent of this technique, we would look

4:30

for the phase, uh, information to be discarded,

4:32

and we would really be looking for

4:33

the magnitude information.

4:35

But by isolating the phase data, that's

4:37

how you can actually get at SWI.

4:39

And that was done all the way back in 1997.

4:41

So it's not like this is new,

4:42

but it's taken a really long time for this to really, uh,

4:46

make its way into routine clinical practice.

4:48

So if you combine those two, you can get that SWI image

4:52

susceptibility, probably most of you are aware,

4:55

is simply defined as anything

4:56

that interacts with a magnetic field.

4:58

So, uh, some things interact very strongly

5:01

with a magnetic field.

5:02

Some things yet react, uh, more weak.

5:04

But any local thing

5:05

that disrupts the local magnetic field will cause

5:08

what we call susceptibility artifact.

5:10

And, uh, that will differ depending on the tissues that

5:13

that material is in.

5:15

And so deoxyhemoglobin is the one we think about frequently

5:18

in the setting of venography.

5:19

It turns out that SWI actually was initially developed, uh,

5:22

back in the nineties as a technique for venography,

5:25

but we found very quickly that it's really good for looking

5:27

for other things other than deoxygenated blood,

5:30

like hemosiderin, which is of course the one we look

5:32

for in the setting of previous trauma,

5:33

but also ferritin, um,

5:35

and also in certain velas in states calcium.

5:37

So we'll talk a little bit about more about that,

5:40

uh, in a little bit further.

5:42

So, uh, a little bit of physics for those of you

5:45

who like physics and chemistry, um,

5:46

these are the different classifications of materials

5:49

that can interact with a magnetic field.

5:51

So we are not really looking

5:53

for diametric DME substances in, uh, SOWI.

5:56

These are things that have very weak interactions

5:58

with the magnetic field because they don't have any

6:00

unaired electrons.

6:02

Uh, paramagnetic substances have some interactions.

6:05

So these are, uh, substances

6:06

that have some unpaired electrons,

6:08

which will align with magnetic field.

6:09

And then Pharaoh magnetic are obviously, hence the, uh,

6:12

the Greek flx Pharaoh, uh, are things

6:15

that interact very strongly with a magnetic field.

6:17

Things like iron that have a lot of unaired electrons, uh,

6:20

which will interact with a magnetic field.

6:24

Uh, a little bit about how these will be performed best.

6:27

So the better, the stronger the field strength,

6:30

the better SWWI typically is going to be,

6:32

the more pronounced the susceptibility artifact will be in a

6:35

str in a high magnetic field.

6:37

Um, the te can be shorter.

6:38

You're gonna have increased signal

6:39

to noise if you have a higher field strength magnet.

6:42

Uh, this used to be a fairly long sequence.

6:45

Um, now if you use parallel imaging,

6:47

you can do an SWI acquisition in around four minutes.

6:50

And now if you add to that AI, uh, algorithms

6:54

for further shortening your acquisition,

6:56

you can get these down quite a bit lower.

6:58

That was one of the major limitations initially with SWI, is

7:02

that it can be fairly emotion sensitive.

7:04

And so when the sequences were longer, uh, we tended

7:06

to get a lot of motion artifact.

7:08

But now with, uh, addition of more, uh, techniques,

7:11

we can get these down to even in some cases people are

7:14

pushing acceleration factors in ai, uh, reconstructions down

7:17

around the one minute mark.

7:18

So, um, more to come on that,

7:20

but certainly the time thing has been overcome

7:22

for the most part, uh, the T one differences decrease.

7:25

But as we increase in field strength,

7:27

you will see increase in susceptibility, which I mentioned.

7:32

So one of the things, one of the barriers to implementation

7:34

of SWI when this came along is that people, uh,

7:37

didn't like the fact that you couldn't really differentiate

7:39

very well between a lot of brain structures.

7:41

The gray white differentiation was poor,

7:43

sometimes even it was hard to tell where the margin

7:45

of the ventricle was in relation

7:47

to the adjacent of white matter.

7:49

Um, but I would argue that

7:51

that's not why you include this sequence

7:53

in your protocols, right?

7:54

You have all kinds of other, uh, sequences

7:56

to look at brain structure and brain white differentiation.

7:59

The whole reason that we used to do gradient imaging was not

8:02

so we could look at brain structures.

8:03

It was just to look for things

8:04

that result in susceptibility artifact.

8:07

And so since SWI is substantially more sensitive

8:10

to the presence of things

8:11

that cause susceptibility artifact, uh,

8:14

that's why we've switched over for the most part.

8:16

So again, use your other sequences, correlate it

8:19

with your SWI link them if you have to, um, to figure out

8:22

where to localize things, but the sequence

8:24

isn't for doing those other things.

8:26

You also can use the phase data if you want

8:29

to differentiate calcium from blood.

8:31

So I mentioned in certain valence states,

8:32

calcium ions can also cause susceptibility artifact, uh,

8:37

that requires you to know exactly how your vendor,

8:40

uh, performs the rest.

8:42

WI, so I'm not gonna go into a great deal of detail here.

8:45

There are what are called left-handed systems

8:47

and right-handed systems.

8:49

And you can look at the phase map

8:50

and compare it to the SWI image

8:52

and see if an item is bright on the phase map,

8:55

but dark in SWI, it may be calcium,

8:57

it may be iron depending on your system.

9:01

So you can either look that up

9:02

and that data is all available, uh, on the internet.

9:04

The other way you can do that for sort

9:06

of more practically is find something

9:08

that you know is calcified.

9:09

So a lot of folks will say, find some choroid, find, uh,

9:12

some pineal region calcification.

9:15

See what that looks like on the phase map.

9:16

If it's bright, uh, in the pineal gland,

9:18

then likely calcium is bright on your machine.

9:21

If it's dark, then it's likely dark on your machine.

9:23

And that's probably a little bit, uh, faster

9:25

and easier way to use the phase map if you need

9:28

to differentiate calcium from blood,

9:29

although frankly, that doesn't come up clinically all

9:32

that often, but it is nice to know that it does exist.

9:37

So these are some of the clinical applications we're going

9:39

to go through, as I mentioned.

9:40

We'll, we'll talk a little bit about traumatic brain injury,

9:42

but then, uh, we will go through all

9:43

of these other potential, uh, uses of SWI over the course

9:47

of the next 45 minutes, half hour or so.

9:51

So here is case number one.

9:54

I like to present conferences in a case format.

9:56

I think, you know, that's what we all like

9:58

to look at as radiologists.

9:59

We have a TT weighted image on the left

10:01

and an SWI image on the right.

10:04

And, uh, and the image on the left in in panel A,

10:07

you can see that, you know,

10:08

there's no mass effect, there's no shift.

10:10

Ventricles look pretty normal.

10:12

There is a small amount

10:13

of T two hyperintensity in the subcortical parietal lobe on

10:16

the left, but for the most part,

10:18

we really don't see a whole lot else.

10:19

If you squint your eyes, you might imagine

10:21

that there's also a little bit

10:22

of T two hyperintensity in the posterior body

10:24

of the corpus callosum, but at roughly the same level,

10:27

you see that there is substantially, uh,

10:30

worse looking image on the SWI.

10:32

So not only do we see a bit of susceptibility artifact in

10:35

that region of T two signal change,

10:36

but we see several other foci, uh, in the anterior, uh,

10:40

frontal lobes sort of following those

10:41

white matter fiber pathways.

10:43

And we see quite a lot of susceptibility artifact, uh,

10:46

throughout the body and splenium of the corpus callosum.

10:49

So this is gonna bring us to our next question.

10:53

So you of course, I'm not gonna just ask you

10:55

what is the diagnosis here?

10:57

Hopefully all of you, uh,

10:58

have looked at enough brain imaging to know

11:00

that this is going to be a case of diffuse axonal injury

11:03

or axonal sheer injury.

11:05

But let's take it, uh, another step further.

11:07

So if you have your ability to answer the question,

11:10

how would you grade the DAI here

11:12

and do you grade DAI in your reports?

11:16

The ability to grade DAI is helpful.

11:18

Uh, and ly you are really facilitates, uh, the ability

11:21

to do that accurately.

11:23

See if few responses coming in, again,

11:25

I won't spend too long waiting.

11:27

Oh, I see one went away. People have changed their mind.

11:29

It's good. Alright, let's see

11:33

how people respond.

11:37

Great. So, uh, that's excellent.

11:39

So about two thirds of you are correct.

11:41

This is, uh, at least grade two.

11:43

And that's always amusing when the,

11:45

when the answers start to change.

11:46

When I, when I say what the answer is, uh, DAI is graded,

11:50

um, one through three.

11:52

So I threw four in there just to be difficult.

11:54

Uh, but it's based on

11:56

how peripheral versus deep the hemorrhages are,

11:59

and it has prognostic implications.

12:01

So if you have, uh, hemorrhages that are limited to sort

12:04

of the subcortical regions,

12:05

that would be a grade one injury.

12:06

Those patients tend to do better.

12:08

If you have involvement of the corpus callosum,

12:11

now you're talking about a patient with grade three

12:13

or grade two injury.

12:14

And once you start to see injury in the deep structures like

12:17

the midbrain and the pons,

12:18

now we're talking about a grade three injury.

12:20

And as you might expect, based on the importance

12:22

of those locations, the patients

12:24

with grade three DAI tend to do the worst.

12:27

So it does have prognostic significance.

12:29

And having this technique, which is substantially more

12:32

sensitive to the presence of those small hemorrhages really

12:34

can help you predict, uh, how the patient is going to do.

12:38

Alright. So, uh,

12:39

CT obviously remains the primary initial imaging modality

12:42

just because it's fast and easy to get out of the er.

12:46

But, uh, you know, the, the hallmark

12:48

of DAI in the literature prior to the advent of SWI was

12:53

clinical presentation out of proportion to the degree

12:55

of imaging findings because CT can be quite insensitive

12:58

to the presence of those really small hemorrhages.

13:01

Uh, in fact, you, we really don't see them quite frequently.

13:03

And then you get the SWI

13:05

and that shows you all of those little, uh, sheer injuries.

13:08

Uh, in comparison, head to head

13:09

with G-R-E-S-W-I has been shown to be anywhere between three

13:12

and six times more sensitive to the presence of hemorrhages.

13:16

Um, and so that does actually correspond also

13:19

with neurological psychological outcomes.

13:21

If you're wondering why, uh, I I'm interested in this topic,

13:25

I will tell you, this is how I know g uh, SWO has been

13:27

around for a very long time.

13:29

When I was a medical student, which was now, uh,

13:32

quite a long time ago,

13:33

my summer project one year was working with Dr.

13:35

Karen Tong, uh, who published some

13:37

of the first papers in MRI on SWI counting, uh, innumerable

13:42

susceptibility weighted, uh, lesions

13:44

and comparing them to SWI.

13:46

So I can tell you with great certainty that in fact, uh,

13:49

SWI is more sensitive than GRE.

13:51

And, uh, we did publish a paper in that group, uh,

13:54

looking at the neuropsychological outcomes.

13:56

And so, you know, some people say, well,

13:59

what's it matter if they have 50 versus a hundred

14:01

or 10 versus 50?

14:03

It does. Uh, it turns out that, um,

14:05

even those very small additional hemorrhages do have

14:09

prognostic implications for how patients will do.

14:12

And so, um, you know, I've never liked that argument

14:14

that yes, it's very, very sensitive,

14:16

but we don't know what those additional little

14:17

tiny hemorrhages mean.

14:19

Our job as imagers is to do the best job we can

14:23

of depicting what's happening.

14:24

And if we have a technique that shows more,

14:26

then we should be using that technique.

14:28

And that's, that's sort of my,

14:30

my hill I will die on for SWI.

14:33

So here's another, uh, example from one

14:35

of those papers back in the day comparing, uh,

14:38

looking at SWI at its ability to depict the number

14:40

of hemorrhages here, you can see just a few small

14:42

hemorrhages on the T two weighted imaging imaging.

14:44

But again, we see several additional

14:46

foci throughout the parenchyma.

14:48

Uh, and this was a study done in children

14:50

who had suffered a traumatic brain injury.

14:54

Alright, that's all I'm gonna say about trauma.

14:56

Uh, I think that you all probably understand

14:58

the utility in trauma.

14:59

Let's look at another case.

15:01

So here we have a diffusion weighted image in a,

15:04

I'm not showing you the a DC map

15:05

because there's nothing abnormal on the diffusion, uh,

15:08

imaging on the B 1000.

15:10

I'm giving you a cerebral blood volume map on, uh, image

15:15

B, uh, I'm sorry, cerebral blood flow map.

15:18

And then I'm giving you a susceptibility weighted, uh,

15:21

MIP in image C.

15:23

What do we, what do we think is going on here?

15:25

So this is an interesting case

15:26

because, uh, this patient was on the table.

15:29

I remember, uh,

15:30

and for whatever reason the technologist happened

15:33

to call me to check the images.

15:35

And, uh, we didn't do the profusion at the time.

15:37

Um, they were gonna get contrast anyway.

15:39

But I looked at the SWI

15:40

and I thought that's really interesting.

15:42

There's this very, uh, interesting asymmetry where all

15:45

of the veins, as I mentioned,

15:47

the technique was originally developed for venography, uh,

15:50

are really prominent throughout this cerebral hemisphere.

15:53

A lot of them in the MCA territory in particular,

15:55

but probably some, uh, in the, you know,

15:57

parietal region as well.

15:59

Uh, and so when I saw that

16:00

and the diffusion looked normal,

16:01

I thought, oh, this is interesting.

16:02

I wonder if this patient has something like migraine

16:04

headaches, which can be all, uh, associated with, uh,

16:07

elevated cerebral blood flow

16:09

and volume in the setting of vasodilation.

16:11

So we, we gave the contrast, we did the profusion,

16:13

and we actually saw that the flow was down in this region.

16:17

So what do you think could be going on here?

16:19

Well, this is a patient who actually had a dissection, uh,

16:23

in their carotid artery, which was unexpected.

16:26

And so being able to see the veins is helpful in that

16:29

the cerebrovascular reactivity is such

16:32

that these veins have dilated,

16:33

the vessels have dilated maximally to try

16:35

to maintain blood flow.

16:37

And so even though flow is a little bit down, it's not

16:39

to the point where there's stroke yet,

16:40

but this is all area that sort of, this is the

16:44

swis, uh, equivalent.

16:45

Uh, when we see elevated cerebral blood volume in the

16:48

setting of an area that's oli gmic,

16:50

and you get that, uh, that sort

16:52

of paradoxical increase in cerebral blood volume,

16:54

even though the flow is a little bit down.

16:56

So this was, uh, an unexpected case that led us

16:59

to the diagnosis of the person's carotid dissection at the,

17:02

uh, in the neck and the skull base.

17:05

So SWI can also be useful in the setting of stroke to look

17:08

for early hemorrhagic conversion.

17:10

So obviously, uh, it is extremely sensitive

17:12

to the presence of hemorrhage.

17:14

And as I mentioned in this case, you can see, uh,

17:16

increased draining veins volume due to, uh, deoxyhemoglobin.

17:21

This also can be really useful in the setting

17:22

of looking for embolism.

17:24

So I'll show you a case here of that.

17:26

So I think lots of us have, uh, had the experience

17:29

where we are reading a, a study

17:31

of a patient comes into the ED

17:32

and gets a CTA to work up stroke,

17:35

and we don't see any proximal occlusions in the,

17:38

in the circle of Willis, but maybe there's

17:39

some motion who knows what.

17:41

And then the patient gets an MRI

17:43

and you see that there is a small stroke,

17:46

but you still never saw necessarily,

17:47

you know, where that clot is.

17:49

And so you go back and you follow those vessels out

17:51

to those branch points where the, where the stroke occurs.

17:54

And sometimes you can find a small

17:55

occlusion, sometimes you don't.

17:57

But I think what can be really interesting is sometimes on

18:00

the SWI, you can actually get

18:01

a hint of where you wanna look.

18:03

So for example, this is a patient who has, uh, a clot sort

18:06

of around the region of the MCA bifurcation.

18:08

And you know, it's pretty obvious on the MRA as well,

18:11

but it's not always this obvious.

18:12

And so sometimes I've seen cases where you see a focus

18:15

of blooming because there is a, a clot

18:17

with the oxyhemoglobin in it fairly distal like in an M

18:20

three or even sometimes an M four branch.

18:22

And then if you go back and you look at the CTA

18:25

and you can hone in your search on that very specific spot

18:29

that you can correlate with the SWI, you will be able

18:31

to find that occluded vessel in that thrombus.

18:34

So this patient obviously has, uh,

18:36

the same finding in the area of emia.

18:38

You see that really pronounced, uh,

18:40

venous engorgement throughout the MCA territory as a result

18:43

of this proximal occlusion Because of that cerebrovascular

18:46

reactivity, I,

18:50

I saw a comment in the chat

18:52

about Aria, we'll talk about that.

18:53

Uh, at the end. I'm gonna save your comment about

18:56

Aria for, for the end.

18:57

Uh, but we will talk about cerebral amyloid angiopathy,

19:00

which is certainly related to, uh, the aria question, right?

19:03

So cerebral amyloid, uh, angiopathy is the result

19:06

of deposition of amyloid in the small, uh,

19:08

intracranial vessels.

19:10

Technically, it is still only diagnosed

19:12

by biopsy or autopsy.

19:14

Um, there are the modified Boston criteria for, uh,

19:18

diagnosis based on imaging, uh,

19:19

for presumptive diagnosis based on imaging.

19:22

Uh, but these patients are at risk for developing small, uh,

19:25

micro hemorrhages, usually in the periphery of the brain.

19:28

Uh, they can also have low bar hemorrhage,

19:30

they can have repetitive subarachnoid hemorrhage as a result

19:33

of these small peripheral hemorrhages.

19:35

And, uh, those can also be, uh, easy to detect with SWI

19:38

and up to about 25% of them according to the literature,

19:41

can be missed on gradient imaging.

19:43

And so that brings us

19:45

to your question eventually about aria.

19:47

We'll, we'll come back to that. So here is a very classic

19:50

appearance of cerebral amyloid angiopathy on

19:54

susceptibility weighted imaging.

19:55

And this, again, this is a relatively recent case.

19:58

So even with the newer techniques, you see

20:00

that the gray white differentiation is not great,

20:02

but you can read through the image to see

20:04

that this patient has a fair bit

20:06

of non-specific chronic white matter change in the

20:08

periventricular regions.

20:09

They do have some volume loss.

20:10

So it, it is an older patient, uh, with a little bit

20:13

of ventricular magaly, but we also see all

20:15

of these peripherally located foci

20:17

of susceptibility artifact.

20:19

And in a few spots, you might imagine

20:21

that there's even a little bit of superficial cirrhosis,

20:24

for example, uh, at the level of the left frontal lobe on

20:27

that image at the far left.

20:30

But you also notice that the deep structures really are not

20:33

involved, and that's a pretty typical, uh,

20:35

differentiating feature from another en

20:37

entity we'll talk about in a moment.

20:38

So when you see this peripheral pattern, um, think

20:41

that this could very well be a patient

20:43

with cerebral amyloid angiopathy,

20:45

especially if you see superficial cirrhosis.

20:47

Um, and these patients are at risk

20:49

of developing big low bar hemorrhages as well.

20:51

So a lot of times what happens is the patient will come into

20:54

the ed, get a head ct,

20:55

and they have a peripheral low bar hemorrhage,

20:58

and then they'll get a CTA, which is,

21:00

at least at our institution, everybody gets a CTA

21:02

where they come into the ER

21:03

with anything related to the head.

21:04

And we don't see, we don't see anything,

21:06

we don't see any vascular malformations or aneurysm.

21:09

And then when the patient gets the MRI, we see all

21:11

of these additional foci

21:13

of hemosiderin deposition in the per of the braining.

21:15

We say this was almost certainly, uh,

21:17

a low bar hemorrhage related

21:18

to underlying cerebral amyloid angiopathy.

21:23

Let's talk a little bit about neurodegeneration.

21:26

So, uh, patients

21:27

that have diseases like a pantothenic kinase associated

21:31

degeneration, uh,

21:32

which is the prototypical iron deposition disorder,

21:35

obviously you can see this very clearly on SWI

21:37

because of the ferromagnetic properties of iron.

21:40

So here's a patient with T one imaging that's showing kind

21:43

of indistinct T one hyperintensity in the globus palates,

21:46

which is exceptionally non-specific, right?

21:48

That could be calcium, um,

21:49

that could even be copper in the

21:51

setting of Wilson's disease.

21:52

There are other entities that will give you T one

21:54

hyperintense signal like this.

21:56

But when we look at the SWI, um, if image,

21:59

we see marked susceptibility artifact corresponding

22:02

to the globus palus primarily, uh, bilaterally.

22:05

And this is a patient with that iron deposition disorder.

22:07

You can also see iron deposition, uh,

22:10

in Parkinson's disease, uh, looking for the swallow tail

22:12

or loss of the swallow tail.

22:14

You can see it occasionally in Huntington's disease,

22:16

Alzheimer's, um, a LS we'll talk about later as well.

22:20

So here's another question to keep you awake,

22:24

see if you're paying attention, see if any

22:27

of you are old enough to remember this song

22:36

or any of these bands for that matter.

22:41

Good, good. Very nice.

22:45

So at least, at least more than half of you are

22:49

probably at least as old as me, which is excellent.

22:51

So that is correct. Uh, this is a recording by the band, uh,

22:56

survivor from the rocky movies, I believe.

22:59

And, and the reason I bring that up is

23:00

because this is called, this has been called the Eye

23:02

of the Tiger Sign,

23:04

this iron deposition in the Globes palus in the setting

23:06

of pantothenic kinase associated neurodegeneration.

23:10

I'm not too sure where, how

23:12

that looks like the eye of a tiger.

23:14

I have not seen a lot of tigers in my lifetime,

23:16

but I would not say that

23:17

that would be the first thing I would name this.

23:19

But when you look at that, nah, it doesn't work for me.

23:24

Let's talk about multiple sclerosis,

23:25

because this is a really interesting, uh, application

23:28

for susceptibility weighted imaging that has, um,

23:30

really caught on in the fairly recent past.

23:34

So it turns out that in multiple sclerosis, as probably some

23:37

of you know, the inflammation tends to be periannular.

23:40

And that is actually different from a lot

23:42

of the other things that give you the, the sort

23:45

of non-specific chronic white matter changes

23:47

that we see every day on scans most epidemiologically

23:51

associated with things like hypertension

23:53

or hypercholesterolemia, those actually tend to occur

23:55

between the, uh, veins in the spaces in between.

23:59

And so what folks have done

24:01

is if they have started combining using the SWI image

24:05

and the flare image

24:06

or what's sometimes termed a flare star image,

24:09

and what we're looking for is what's called

24:11

the central vessel sign.

24:13

So in patients who have those, those T two hyperintensities,

24:16

a lot of times you're left giving

24:17

this big long differential.

24:18

But if you can see a vessel coursing through the middle

24:21

of one of those T two hyperintensities in the appropriate

24:24

clinical setting that may be more specific

24:27

for the possibility that the patient has demyelinating

24:29

disease, um, these, uh, the theory is

24:32

that the inflammation causes iron deposition along the

24:35

margins of the, uh, the vessels

24:38

and it, you know, may be underestimated with just flare.

24:41

So this is something that's really kind

24:43

of coming along in the last two years,

24:44

and I believe that there are a few vendors now

24:46

who are offering flare star as, uh, as a sequence out

24:49

of the box on machines.

24:51

Although, uh, most institutions including ours,

24:53

it's something that we still have to

24:54

sort of do as an add-on.

24:55

It's not part of our routine protocols.

24:57

But here's another example of a case

24:59

of a nice flare star image, I think in both images,

25:02

if you look in the lower, uh, in the parietal lobe, sort

25:05

of in the, uh, in the left,

25:06

you can see T two hyperintensities

25:08

that very cl very clearly have a vein

25:10

coursing right through the middle of them.

25:12

Um, and if you look, get a chance

25:13

to look at these in patients who have, like I say,

25:15

hypertension or other causes

25:17

of non-specific white matter change, they tend not to have,

25:20

uh, vessels coursing through them.

25:21

So it can be, can be pretty helpful if that's something

25:23

that you're considering including in your differential.

25:28

Let's talk a little bit about vascular malformations.

25:31

So you might imagine SWI would be very useful in looking

25:34

at vascular abnormalities.

25:35

We'll talk about cavernous malformations first.

25:37

That's sort of the classic, um,

25:39

cavernous malformations make up, you know, between 10, 20%.

25:42

They're fairly common. We see them every day.

25:44

Uh, in fact, the prevalence worldwide is felt to be

25:47

around half a percent.

25:48

So that's a huge number of people

25:50

that have a cavernous malformation.

25:52

Remember, these are slow flow lesions.

25:54

So if you're doing an angiogram

25:55

and you're, you know, not standing on the pedal

25:57

for long enough, uh, you will not see anything.

25:59

So they're angiographically occult

26:01

and they're just a collection of abnormal

26:03

capillary cavities.

26:04

Uh, they do have a propensity for hemorrhage,

26:06

which is why they have that classic popcorn appearance.

26:09

So over time, they will have slow, uh, hemorrhages,

26:11

which result in hemosiderin deposition.

26:14

And here's sort of they all, once you've seen one,

26:16

they often look kind of the same.

26:17

So on T one imaging,

26:19

they often have blood products within them, uh,

26:21

because it tends to break down fairly slowly.

26:23

So you may see some intrinsic T one hyperintensity,

26:26

this one is about as popcorny as I guess they get.

26:29

I would say that's a pretty good representation of

26:31

what a piece of popcorn might look like.

26:33

And then the really characteristic finding is this rim

26:36

of hemosiderin deposition.

26:37

And just like anywhere else

26:38

where you have hemosiderin deposition,

26:40

if you see it on T two, you're going

26:41

to see it much more dramatically on SWI.

26:44

And so, again, this one may not be a diagnostic dilemma.

26:47

I think most folks would look at this, uh, primary lesion

26:50

and say, yes, that looks like a classic

26:51

cavernous malformation.

26:52

And because they tend to sort

26:54

of slowly hemorrhage over time, they tend not

26:56

to have a bunch of edema around them or mass effect.

26:59

Uh, but on SWI, you may see additional lesions.

27:02

So sometimes these patients have familial cerno ptosis

27:05

syndromes, or perhaps they have, uh,

27:07

radiation induced injuries,

27:08

and you're gonna see, uh, have more sensitivity

27:10

to the presence of additional lesions.

27:13

Oh, I forgot. I haven't been scroll,

27:14

I haven't been scrolling down on the chat.

27:16

I apologize for those of you who've put things in the chat.

27:19

I saw somebody mention hemiplegic

27:21

migraine for that profusion case.

27:22

That's awesome. That's exactly what I thought too.

27:24

We were both wrong, but it, it, it's a great thought.

27:26

Uh, alright, let's, uh, let's keep going a little bit.

27:32

So here's, here's another, uh, example

27:34

of a vascular malformation,

27:35

but this one looks a little different, right?

27:37

So on our T one weighted mature, I would say this is normal.

27:41

I see nothing, uh, in the area.

27:43

On our T one post contrast imaging, we have, uh,

27:47

a little bit of a blush of contrast in sort of the region

27:50

of the, uh, pars of peris of the inferior frontal lobe,

27:53

most likely right adjacent to the, the, uh, insula.

27:58

And we see a corresponding area of T two hyper intent

28:00

or of susceptibility artifact on the SWI.

28:03

But what do you notice? It's different here

28:04

on the flare as well.

28:05

We see v virtually nothing in that location.

28:08

So really the abnormality here is limited

28:10

to just the post contrast imaging

28:13

and the susceptibility weighted imaging.

28:15

And prior, again, prior to the advent of SWI,

28:18

this entity was defined from an imaging perspective

28:21

by the statement

28:22

that it was only evident on our post contrast imaging

28:25

and would be normal on all additional pulse sequences.

28:27

And so if that phrase sounds familiar to you,

28:30

you probably know that this is going

28:31

to be a capillary telangiectasia.

28:33

But again, I'm not going to ask you just where,

28:35

what is a cap, you know, whether

28:36

or not it's a capillary and dicta.

28:38

So where are these most common?

28:40

We see these all the time, and technically they can

28:42

occur anywhere in the brain.

28:43

This is a chance for you to try to, you know,

28:46

push the limits of the software.

28:47

So you, so actually just touch your screen

28:49

where you think is the most likely, uh,

28:51

or most frequent location for a cavernous mouth from

28:54

or for a, uh, capillary till education.

28:56

And then we'll see where people vote.

29:04

We'll see, I've got at least 10 or so people playing along.

29:07

If you have just joined us and you try to log in

29:09

and it doesn't let you, I apologize.

29:11

Uh, it's limited in number.

29:13

So let's see where people have voted here.

29:16

Excellent, excellent. I see some folks

29:18

labeling words, that's fine too.

29:20

So it is the ponds, in fact.

29:21

Um, these are most frequently seen in sort

29:23

of the central ponds,

29:25

but I don't think you should limit your differential if you,

29:27

if you see something beyond like excellent,

29:29

somebody labeled PAs, love it.

29:31

Uh, you can have these anywhere in

29:33

the brain, just like this case.

29:35

And what we see very frequently is, uh, without the SWI

29:39

or even with it, sometimes patients will come in

29:41

with a reported history of having a, a brain tumor,

29:45

or they may be getting worked up

29:47

for metastatic disease from a primary elsewhere,

29:49

and somebody will see an enhancing lesion

29:51

and they'll say, I, you can't exclude

29:53

that this is a metastatic lesion.

29:55

I would argue that if you see this classic appearance of,

29:59

uh, smudgy enhancement corresponding susceptibility,

30:03

that's limited just to that area

30:06

and no signal abnormality on T two.

30:08

Uh, no edema, no even discernible hint

30:12

of a T two signal abnormality.

30:14

I would be definitive, even if the person has a systemic,

30:16

uh, primary, and I would say this is a capillary

30:19

telangiectasia and it is an incidental finding,

30:21

and it is not a metastatic lesion.

30:23

Uh, but we see this sort of, uh,

30:25

hedge done quite frequently.

30:28

Uh, let's talk a little bit about

30:30

developmental venous anomalies.

30:31

So these are extremely common.

30:32

They're the most common, in fact, 60%

30:34

of all vascular malformations.

30:36

Uh, there is a statistical association with corresponding,

30:40

uh, cavernous malformation.

30:41

So you've probably seen that before as well.

30:43

Um, for the most part, these are congenital venous variants.

30:47

Um, and they, uh, we mentioned the capillary TE as well.

30:51

So once you've seen a few devis, you've sort

30:53

of seen them all.

30:54

Uh, they can be big and gnarly

30:56

and involve whole portions of lobes or the cerebellum,

31:00

or they can be small and subtle.

31:02

These, again, you're really only gonna see on your post

31:04

contrast imaging as an area of an abnormal venous drainage.

31:08

But remember, these are draining normal brain parenchyma.

31:10

So these are entirely incidental. Do not touch lesions.

31:13

So if you were to, if someone were

31:15

to foolishly embolize A DVA, uh, you're gonna cause a stroke

31:18

because they're unlike an A VM, they're draining, uh,

31:21

draining normal brain parenchyma.

31:23

And they can, again, like I said,

31:24

they can look very interesting.

31:25

They tend to be very conspicuous on the SWI sequence.

31:28

So even if you don't have a post contrast image, if you see,

31:32

for example, this image on the far left, you,

31:34

you're gonna know that's a developmental venous anomaly.

31:36

It doesn't require any further workup.

31:38

Um, they tend to have no significant signal abnormality

31:42

around them on your T two or flare imaging.

31:44

Uh, because again, they're just draining normal brain

31:46

parenchyma sometimes when they're really big.

31:49

I, I must admit, even though the textbooks say there

31:51

shouldn't be T two signal around them, um,

31:53

I think sometimes you do see a little bit.

31:55

Um, and I think if everything else is classically just A

31:58

DVA, I will still leave it as that.

32:01

Um, so that could be a gray zone if,

32:02

if it's a fairly large DVA.

32:06

All right, let's go on to our next unknown case.

32:10

So here we have a post contrast in a

32:13

and a susceptibility weighted MIP

32:15

with some extremely helpful arrows, uh, in C And

32:19

what do we notice about this patient?

32:21

Well, they have a gross asymmetry, right?

32:23

So the, uh,

32:25

left cerebral hemisphere looks quite a bit smaller than the

32:27

right, and so that's, yeah,

32:29

somebody's already all over this in the,

32:30

uh, in the chat, correct?

32:32

Uh, and we also noticed

32:33

that they have this diffuse peel enhancement throughout the,

32:37

that affected cerebral hemisphere.

32:39

And then when we look at our SWI, we see extensive sort

32:43

of GY reform,

32:44

but in this case, very bulky susceptibility,

32:46

weighted a susceptibility artifact

32:48

throughout the affected hemisphere.

32:49

So of course, this is Sturge Weber syndrome, um,

32:52

and that case it was not subtle, right?

32:53

Nobody's gonna miss that, uh,

32:55

and say that that's something else.

32:57

Uh, it's relatively rare.

32:58

Um, and it is the result

33:00

of this leptin meningeal venous malformation.

33:02

So these patients get the chronic venous stasis

33:05

and they get the eventual mineralization as a result

33:08

of the chronic venous hypoxia, which leads

33:11

to chronic atrophy, um,

33:12

and eventually calcification, which we can see on ct.

33:15

And obviously it's gonna be even more evident on SWI.

33:19

So again, here's another case, uh, where we see

33:22

that dense calcification throughout the

33:24

affected cerebral hemisphere.

33:25

We see that peel venous malformation on the post contrast

33:29

imaging and the susceptibility.

33:30

This is fairly old SWI case,

33:32

but very easily shows you all those areas

33:34

of abnormal mineralization.

33:36

Notice also in this case that they have another sort

33:39

of interesting corollary,

33:40

which is this choroid is enlarged

33:42

in the image on the center.

33:44

So remember that, uh, you know, if you like trivia, uh,

33:47

structures and or entities which result in, uh, volume loss,

33:51

hemispheric volume loss, you will often see, uh,

33:54

ipsilateral enlargement of additional structures,

33:57

the whole Monroe Kelly doctrine and taking up the space.

34:00

So if you have loss of volume in one cerebral hemisphere,

34:04

you may see enlarged choroid,

34:06

you may see enlarged frontal sinus, you may see, uh,

34:08

over pneumatized, mastoid air cells, pneumatized,

34:12

OID process, everything sort of to take up the space.

34:14

And if you like eponyms, remember that syndrome goes

34:17

by the epi of d**e, Davidoff Maison syndrome

34:20

that overgrowth ips laterally to, uh, volume loss.

34:24

So here's a more subtle case,

34:25

and I think this is where SWI sort of shows

34:27

that it can shine in Incy Sturge Weber syndrome.

34:31

So this was a very young patient, uh, this patient was,

34:34

I wanna say only two or three years old,

34:36

and they had seizures and they came in and got an MRI.

34:40

And I will tell you that on the, the ct, uh,

34:43

we did see a little bit of calcification in the, uh,

34:47

posterior temporal

34:48

and occipital region on the right,

34:50

which you can see on the image, uh, to your left

34:52

where the cortical susceptibility artifact

34:54

is sort of gyre formm.

34:56

And so this patient did end up

34:58

with a diagnosis of surge Weber syndrome.

34:59

But what else do you notice? You also notice that, uh,

35:02

they have some abnormal signal in the

35:04

contralateral hemisphere.

35:06

They have some enlarged, uh,

35:07

deep per medullary veins in the, uh, left frontal region.

35:11

And this patient actually ends up having bilateral sturge

35:14

Weber, which is fairly unusual.

35:16

It can happen. We usually think of it as more of a, a, uh,

35:19

unilateral process.

35:20

But unfortunately, this patient had involvement

35:22

of the frontal lobe as well, which had not manifested itself

35:25

on any of the other pulse sequences or on the ct.

35:28

And so if you, if we had not done the SWI, uh,

35:31

we would've thought their disease was simply limited

35:33

to the posterior aspects of the right cerebral hemisphere.

35:36

But here we see both involved.

35:39

Alright, let's look at another case,

35:42

moving on to a different entity.

35:44

So here we have a, uh, patient T one.

35:47

You can see another helpful arrow sign

35:49

with some T one hyperintense material in the region of,

35:52

well, I won't say it, but you all know what it is.

35:55

Uh, and on the SWI, we see some foci

35:58

of focal susceptibility artifact.

36:00

And on the T two weighted imaging, we see

36:02

what clearly looks like a stroke

36:04

involving the temporal lobe.

36:06

So this is a case of infarct,

36:09

and you tell me here's a true false,

36:11

you've got you all smart.

36:12

You don't, it's not 50 50.

36:14

I think you all are, you know the answer here,

36:16

but give you a chance to answer anyway.

36:19

Do Venus infarcts have a greater propensity

36:22

or hemorrhagic transformation than arterial infarcts?

36:25

This would definitely not be an accepted,

36:27

acceptable board question.

36:28

Not enough options. And I gave you the answer when I gave

36:31

you the image probably so we'll take a look.

36:34

And indeed the answer is true.

36:36

So venous infarcts are more likely to cause hemorrhage, um,

36:41

than arterial infarcts.

36:42

Which actually, if you just think about the pathophysiology

36:44

kind of makes sense to me intuitively in

36:47

that when you have an arterial infarct,

36:48

there's no blood flow into the area of dead tissue.

36:51

When you have a venous infarct,

36:53

there's still blood flow coming in from the

36:54

arterial side and it can't get out.

36:56

And so, uh, at least that's

36:57

how I think about it in my brain.

36:59

I'm sure that it's actually more complicated than that,

37:01

but I'm, I'm a simple guy

37:02

and that's, that's how I think of it.

37:03

And remember it lots of risk factors for venous thrombus.

37:06

That's what this patient had. Uh, malignancy is a big one.

37:10

Oral contraceptives, uh,

37:11

but also just that dehydration pregnancy protein CNS

37:15

deficiencies, there's a long list.

37:17

Um, oral contraceptives used to be sort of the one

37:19

that always would show up on board exams,

37:21

but I think more often now we see venous thrombus in the

37:25

setting of malignancy as much as anything else.

37:27

And this can be really pretty easily picked up, uh,

37:30

in the setting of SWI

37:31

because of the, uh, deoxyhemoglobin in the clot.

37:34

But use your other sequences to find that

37:36

where SWI shines is looking for

37:37

that hemorrhagic transformation.

37:39

Um, so as this patient had some foci

37:41

of hemorrhage within their in farts, here's another case

37:46

of a separate patient

37:48

with a venous sinus thrombosis involving

37:50

the transverse sinus.

37:51

And you can see on the angio,

37:52

they also have thrombus involving fairly large portions

37:55

of the superior sagittal sinus, uh,

37:57

at least the posterior aspects of that.

37:59

And they have quite a lot of he of infarct.

38:01

And on the SWI, you can see lots of small foci of, uh,

38:05

hemorrhagic transformation throughout the cerebral

38:07

hemisphere that would be drained, uh, by that sinus

38:10

and by this, uh, by the, this being impeded by the, uh,

38:13

venous sinus thrombus.

38:17

Alright, let's do a little bit of a trickier one.

38:20

So here is case number six for today.

38:23

And again, this is a pediatric patient, uh,

38:25

and I remember the exact age,

38:26

but they were under the age of 10 anyway, so

38:29

that should tell you these ventricles are too big.

38:33

And on the CT we also see some hyper density along the

38:36

margin of the atrium of the left lateral ventricle,

38:39

but the rest of it looks pretty unremarkable.

38:41

Other than the loss of volume on the SWI,

38:45

we see quite a few foci of abnormal susceptibility artifact.

38:48

A few do look like they are per ventricular,

38:51

so maybe corresponding to that area of mineralization,

38:53

but a few are also in the deep grade nuclei.

38:56

And so what might this be?

38:59

So this is an example of torch, uh, in fact.

39:03

So this was a patient good?

39:05

Yes, somebody I see that it's all over that, uh,

39:07

there are several infections that can cause, uh, deposition

39:09

of calcium or other mineralization.

39:11

Um, neurotic psychosis is probably the prototypical one.

39:15

The patients who have had neuro cystic psychosis in the long

39:18

past may have small foci of calcification, uh, in the areas

39:22

of affected parasites

39:24

that have been long since dead and calcified.

39:26

Um, but of course you probably are all aware of the sort

39:28

of multiphasic nature of that disease.

39:30

Again, this is one place where sometimes you can use the,

39:34

uh, the phase map to determine calcium versus blood.

39:37

CNS malaria is a really interesting, uh, application of SWI.

39:41

There have been a few cases published of looking at

39:43

that entity with, uh, with this technique.

39:45

I'll show you that. So here is, uh, a case

39:49

that we published years ago.

39:50

Uh, and I like this case

39:52

because it's a really, if, if you need a poster child

39:55

for SWI being better than gradient,

39:57

it just sounds like the majority of you don't, based on

39:59

how you're using the technique, this is it.

40:02

Right? So this was a, a patient who had been in, uh,

40:05

an endemic area and had not been taking their anti malaria

40:09

prophylaxis, and they came in with cyclic fevers

40:12

and all the things you would expect.

40:14

And I would argue that the T two image here is normal.

40:18

The middle image is your gradient sequence,

40:20

and you know, yes, is there maybe one tiny focus

40:23

of susceptibility in the occipital lobe on the left?

40:25

If you squint, yes, there's one,

40:27

but for the most part it looks pretty much unremarkable.

40:30

But the SWI is anything but unremarkable, right?

40:33

You see, I hate the word innumerable

40:35

because most of the time I would say you can count

40:37

everything, but in this case, I think it's appropriate.

40:39

This patient has innumerable foci

40:41

of susceptibility artifacts scattered

40:42

throughout their parenchyma.

40:44

And so this is the look of cerebral malaria.

40:47

And if you talk to a neuropathologist for a patient

40:49

who succumbs to this entity, if they get an autopsy, this is

40:52

what they see at brain cutting.

40:54

They just see innumerable tiny foci

40:56

of hemorrhage scattered all throughout the parenchyma.

40:58

Now, the good news for this patient is, uh,

41:00

remarkably she made a complete recovery once she got put on,

41:04

uh, anti-malarial medications,

41:06

and despite the severity of what we see here, uh,

41:09

she went back to work and, and did fine.

41:11

So, um, sometimes the imaging doesn't always correlate

41:14

with the clinical picture, but certainly this was a fairly

41:16

dramatic example of how SWI can be helpful.

41:20

Uh, we include SWIS as ours part of our routine protocol.

41:24

So, you know, we do see it in the setting of tumors.

41:26

I will say it's probably not the workhorse in tumors

41:28

that some other sequences can be,

41:30

but certainly if a patient has intratumoral hemorrhage, um,

41:34

this can be helpful in determining that.

41:36

Uh, you can sometimes see neovascular associated

41:39

with a tumor in the setting of extra veins

41:41

or prominent veins.

41:42

Draining an area can be helpful

41:44

for looking at the relationship to adjacent vessels.

41:46

So if they're planning a surgery, it can be helpful to see,

41:49

uh, where are the veins surrounding the tumor?

41:51

What, how that might, uh, I improve their approach

41:54

to minimize morbidity and then radiation induced changes.

41:57

So, um, patients

41:59

who have especially had whole brain radiation,

42:01

this is a patient who had whole brain radiation as a child

42:04

for a medulloblastoma and are now in their thirties.

42:06

Um, the process of the radiation that the proposed mechanism

42:11

for this is that you get vascular injury

42:14

as a result of the radiation.

42:15

And through the reparative process, patients can develop,

42:19

uh, capillary telangiectasia

42:20

and cavernous malformations, which I, I, I have had looked

42:23

that up because I, I always sort

42:24

of annoyed me when people said it was

42:26

an acquired malformation.

42:27

Those two words don't go together in my brain.

42:29

Like I think of malformation as, uh, a congenital thing,

42:33

and I think of these as acquired as the result of radiation.

42:37

But, um, it is the result of the, uh, of the, uh,

42:42

reparative process of the vessels.

42:46

So a couple of, uh, at least one bonus case here at the end.

42:50

So this is a, I've given,

42:51

you know, the history helps, right?

42:53

Uh, this is a 65-year-old who comes in

42:55

with upper motor neuron symptoms

42:58

and the flare, I'm showing you the top

43:01

for a very specific reason, right?

43:02

The flare is, is normal, I would say.

43:04

Um, and,

43:06

but what we see on the SWI is this fairly gyro form area

43:10

of susceptibility artifact,

43:11

a little more prominent on the left than the right.

43:14

And it's very much limited to a single gyrus.

43:17

In fact, it's limited to the precentral gyrus.

43:20

So yes, you're, I see the folks in the

43:21

chat are all over this.

43:23

Um, but I think what's interesting about this case is he did

43:26

go on to develop other signs of a LS

43:28

and was eventually diagnosed with that entity,

43:30

but we think of a LS usually as causing some degree

43:33

of volume loss and T two signal change in the

43:36

precentral gyrus on flare.

43:38

But SWI can be abnormal first,

43:41

and this was an example of that.

43:42

So this was the only thing about his scan was abnormal, uh,

43:45

and I think they clinically were worried about it, right?

43:47

That's why when they put this history,

43:48

that's what they're looking for.

43:50

Uh, but this was confirmatory so fairly uncommon.

43:53

But if you're interested, there's the motor band sign,

43:55

which was referenced, uh, by Dr.

43:57

Sahu in the chat. Very, uh, very good, uh,

43:59

published back in 2015.

44:02

So that is it. We have a little bit of time right at eight,

44:05

at 9 45 my time, 1245 on the East Coast.

44:09

Uh, let, let me look through some of the chat here

44:12

and see if there are any things.

44:15

So I guess I'll just go in order.

44:16

So why are, why have ma, so a question from Dr. Solomon.

44:19

Uh, why have manufacturers been

44:22

so slow in making QSM available?

44:24

That's a great question. So, uh, my, hmm,

44:27

this is my gonna be my, uh, I'm not on the, I'm,

44:31

I'm not on the payroll of any of the companies,

44:32

so I can say whatever I want, I guess.

44:34

I think because they don't think

44:35

there's money in it, frankly.

44:37

Um, you know, it's the same as we were struggling, uh,

44:41

literally just yesterday with processing a functional MRI,

44:44

and we were, I was talking with one of our fellows about,

44:46

you know, why are there so few vendors

44:49

making good post-processing software for functional imaging?

44:53

And I think it's because they look at the return on that.

44:56

And I think with QSM, you know, it, it took a long time

44:59

for SWI to really become, uh,

45:02

a prevalent part of people's protocols.

45:04

And I think they're probably looking at QSM

45:06

and saying, you know, are people going to pay for this?

45:09

Uh, does it add enough value

45:11

to your average radiologist over SWI?

45:14

That's just my, my guess.

45:16

I, I don't, I don't have the inside info.

45:18

I'm not on any of the, any of those advisory boards, sadly,

45:23

uh, regarding SWI versus grading for aria.

45:26

Um, that's a great question, right?

45:28

So, uh, I am, I have asked that question of several folks

45:33

of why in the world was gradient used as the, uh,

45:38

technique of choice when determining whether

45:40

or not a patient has aria h Uh,

45:42

and so for those of you who are, who are not maybe familiar

45:45

with this conversation, with the advent

45:48

of the anti amyloid medications, the patients are at risk

45:51

of developing two different complications

45:53

from an imaging perspective.

45:54

One Aria E, which is an edema like pattern in one aria h

45:58

and in the setting of which is hemorrhage.

46:00

And in the setting of the development of those,

46:01

they may stop the drug

46:03

and the criteria are, you know, imaging based, right?

46:06

But they use gradient to determine whether

46:07

or not the person had developed hemorrhage rather than SWI,

46:12

you know, again, maybe it's philosophical,

46:13

maybe they didn't wanna know quite as well

46:15

as they can with SWI.

46:17

But what I have heard, and again, I'm not on the panel,

46:19

but what I have heard is then the next, uh, rendition

46:22

of the criteria for Aria SWI will be part of the criteria.

46:26

So let's hope that that turns out to be true,

46:28

because I agree with you, I was incensed at the idea

46:30

of having to add gradient back to our protocol just

46:34

so we could do the appropriate ARIA screening.

46:38

Uh, let's see how to differentiate cavernous angioma, uh,

46:44

from HGE in the brainstem without SW

46:51

I'm, I'm trying to remember what you would,

46:52

what HGE is referencing in this setting.

46:55

Uh, maybe chatted to me at the bottom too.

47:00

I'll come back to that. Oh, wait, here's the chats.

47:06

Uh, I'll come back to that.

47:08

How do you differentiate between slow flow in an, uh,

47:10

in duro venous sinuses from thrombus?

47:12

That's a great question. Um,

47:14

and I wish I could tell you that SWI is the answer

47:16

to the question, but I don't think it is.

47:18

Um, so I tell our trainees to

47:23

always get every sequence you can when you're trying

47:27

to differentiate a, a venous sinus thrombus,

47:29

especially if you can't give contrast, right?

47:31

So that's where this gets really challenging is we have

47:34

patients who come, I mentioned pregnancy

47:35

is a risk factor, right?

47:36

For, uh, for venous sinus thrombus.

47:39

And we're not gonna give contrast gadolinium anyway in the

47:42

setting of, of a pregnant patient.

47:43

So use all your sequences.

47:46

Um, diffusion can be helpful, right?

47:48

So oftentimes, uh, acute clot will be bright on diffusion.

47:51

Use your T two and your T one together.

47:54

Sometimes it will be hard though.

47:56

I think sometimes if you have slow flow from some other

47:58

cause, uh, you may see differential signal, particularly,

48:01

I mean, this comes up all the time in the transverse sinus.

48:03

Um, if you are doing a time, a non-contrast, time of flight

48:08

or phase contrast flow, uh, study acquire multiple planes,

48:13

I will have our technologists actually acquire an oblique

48:16

sagittal plane rather than a plane purely in the, in the,

48:19

uh, orthogonal to the sinus so that you are not having,

48:22

having in plain flow problems.

48:24

That can sometimes be really helpful too.

48:27

But it can be tricky. And, you know, worst case scenario,

48:30

you have to give contrast in the setting of ct.

48:32

If you can give Mr. Contrast, um,

48:34

there are some papers out there now suggesting

48:36

that probably if you have really high quality 3D post

48:39

contrast, uh, gradient based sequences,

48:42

that's probably even better than our

48:43

traditional MRV sequences.

48:45

And I would say that's true at my institution,

48:47

that if I have a contrast study,

48:48

that's the first thing I look at.

48:49

And thrombus tends to be really, uh, quite apparent

48:53

to differentiate calcium from hemorrhage

48:55

with, uh, phase image.

48:56

Again, like I said, it really kind

48:58

of depends on your vendor, so you have to know what kind

49:00

of study you have.

49:02

But from a practical perspective,

49:03

I would say find a calcified structure.

49:05

Uh, and I like the pineal gland,

49:07

but you can also use choroid and see what it looks like

49:10

and then compare that to the thing you're interrogating.

49:12

And if it looks the same on the

49:14

phase map, then it's probably calcium.

49:15

And if it looks the opposite, then it's probably hemorrhage.

49:19

Uh, let's see. Can we replace T two star?

49:22

Uh, I would say yes.

49:25

Uh, I have, we have, we've definitely gotten rid

49:27

of gradient, uh, on our protocols.

49:30

Uh oh, okay. Oh, there's the answer to Dr.

49:32

Solomon's question. Um, hemorrhage versus, uh, cat telling.

49:37

So I would say, um, in the acute setting the,

49:40

a hemorrhage in the pons should have a diva around it.

49:43

And so that kind of comes back to the original definitions

49:45

of a, of cap capillary lanasia

49:47

of not seeing any signal abnormality

49:49

on the additional sequences.

49:51

So even if it was an old hemorrhage, um, even if it was, uh,

49:54

a hypertensive hemorrhage from 10 years ago, almost always,

49:57

if you look at your flare sequence,

49:58

you're gonna see some T two signal abnormality in the pons.

50:02

I think if I didn't see any T two signal abnormality, um,

50:06

and I only saw the gradient finding

50:08

and the enhancement, uh, then I would say that that's a,

50:10

a icta, I wouldn't necessarily bring

50:12

in hemorrhage as a possibility.

50:15

Uh, let's see. Keep going here. What's next in the list?

50:19

How do you explain the presence

50:20

of venous engorgement on SDI?

50:22

So if you're referring to that, to that, uh, dissection case

50:25

or, but to any of the stroke cases, what you're seeing is

50:28

that sort of cerebrovascular reactivity.

50:30

So remember if you think of, like, if you think about

50:32

how we used to look at profusion imaging in the setting

50:34

of stroke, when a person has, uh, blood flow is down

50:38

to an area because of cerebrovascular reactivity, the blood,

50:42

the blood vessel is distal to the stenosis

50:44

or the occlusion, we're gonna maximally dilate

50:46

because they're basically, the way I again think

50:48

of it is they're just trying to extract as much oxygen

50:50

as they can and trying to keep the blood in

50:52

their territory as long as they can.

50:53

And so the veins will get engorged.

50:55

Um, and it's that sort of cerebrovascular reactivity

50:58

that causes us to see, uh,

51:00

the more prominent veins in the territory at risk.

51:05

All right. Uh, good.

51:08

So I think that might be all

51:10

of the questions in the q and a piece.

51:14

And let me just quickly look at the chat here.

51:16

I think we're almost out. Well, we're doing okay.

51:19

Lipoma strikingly black on SWI. That's interesting.

51:25

Um, usually, you know,

51:28

SWI is not always fat sat, uh,

51:31

but it depends on your technique, right?

51:33

So you some SWI sequences do use fat saturation,

51:36

and if yours does, uh, that may be why you saw that

51:39

as looking like a lipoma.

51:40

I'm just going back to look at some

51:41

of these other, um, yeah.

51:44

So if you have homogeneous fat suppression, it may not be

51:47

that there was susceptibility artifact.

51:48

It may be that you were seeing, uh,

51:50

fat suppression in the sequence.

51:54

All right, I'm gonna stop sharing my screen

51:56

and, uh, it's been a pleasure.

51:58

I'm gonna kick it back to Ashley and Jackie with modality.

52:00

Thank you all really for joining me this morning.

52:03

Hopefully you, uh, got something out of that.

52:05

Hopefully you are all converts to the utility of SWI,

52:09

regardless of the indication for your study

52:10

and that you will look at it a little, uh, more critically,

52:14

although I'm sure you already all do it

52:15

sound like you know what you're doing.

52:16

But it's been a pleasure and I hope you all

52:17

have a great rest of your day.

52:19

Dr. Nickerson, thank you so much. That was excellent.

52:22

Had a lot of fun. Thank you so much

52:24

for everyone asking all those questions.

52:26

Appreciate you, uh, taking the time to answer those.

52:29

Um, you can access the recording of today's conference

52:32

and all our previous noom conferences

52:33

by creating a free MRI online account.

52:36

And we will also email out a link to the replay later today.

52:40

Be sure to join us next week on Thursday,

52:42

September 5th at 12:00 PM Eastern,

52:44

where Dr. Grace Mitchell will deliver a lectured entitled

52:48

pediatric ultrasound cases vascular anomalies.

52:52

You can register for that@mrionline.com.

52:54

Follow us on social media

52:55

for updates on future NOOM conferences.

52:58

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