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Hello and welcome to Case Crunch Rapid case review

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for the core exam hosted by modality.

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In this rapid fire format,

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faculty will show key images along

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with a multiple choice question,

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and you'll respond with your best answer via

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the live polling feature.

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After a quick answer explanation, it's onto the next case.

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You'll be able to access the recording

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of today's case review

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and previous case reviews

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by creating a free account using the

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link provided in the chat.

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Today we're honored to welcome Dr. Francis Dang

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for a neuro brain Imaging Board prep case review.

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Dr. Dang is a board certified radiologist

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who completed his radiology residency

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and neuroradiology fellowship at

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Massachusetts General Hospital.

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He's on the neuroradiology faculty at

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Johns Hopkins University.

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If you've got questions, please remember to use that q

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and a feature to submit those.

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And with that, we are ready to begin today's board review.

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Dr. Dang, please take it from here.

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All right, welcome everybody.

0:56

I am so glad to see

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so many attendees in the webinar right now.

1:01

So over the course of this hour,

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we're gonna do rapid fire questions on brain imaging,

1:06

and hopefully the topics will be high yield

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for your core studying.

1:11

Now I want to get a sense for who the audience is.

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Uh, I think a poll will launch right now

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and let me know if you're a resident setting for the core

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or an attending physician or

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otherwise somebody else just here for the cases

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or some other category not captured by these options.

1:31

Alright, 71% are residents here setting for the core.

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All right, so let's get started.

1:38

Case number one is a 45-year-old

1:40

with breast cancer initial staging.

1:43

I'm showing you one single image.

1:46

Where is the brain metastasis in this image?

1:48

Is it the postcentral gyrus, the precentral gyrus,

1:52

the superior frontal gyrus, or the superior parietal lole?

2:02

And that's all the time we have.

2:04

So it looks like 38% of you got the answer correct,

2:07

which is postcentral gyrus.

2:08

Now, it is important to know your central sulcus localizing

2:12

signs in order to distinguish things

2:14

that are in the frontal lobe from the parietal lobe

2:16

as the peric salsi, uh,

2:18

or the peric gyri are very important, eloquent territory

2:23

for functional purposes.

2:24

Now, uh, a couple of signs

2:26

that can help you identify the precentral gyrus is look

2:29

for this inverted omega sign that, uh,

2:31

signifies the hand knob of the precentral gyrus.

2:34

In some patients, it's uh, kind of two humps, um, uh,

2:38

in an epsilon shape.

2:39

The postcentral gyrus is always bifid medially around this,

2:43

uh, little sulcus, which is the pars ali

2:46

of the cingulate sulcus,

2:48

or also known as the marginal ramus of the cingulate sulcus.

2:51

And that forms this kind of bracket, um, across the, um,

2:56

interhemispheric fissure.

2:58

And so our brain metastasis here is looking at the medial

3:01

portion of the postcentral gyrus,

3:03

and that is the correct answer here.

3:06

Case two is a 60-year-old with intracranial lesion

3:09

that was detected on whole body MRI.

3:11

Further characterization is obtained

3:13

with this dedicated brain MRI protocol.

3:16

Where is the mass?

3:18

Is it the aqueduct of Sylvia, the freeman of Luka,

3:21

the Freeman of Maja D or the Freeman of Monroe?

3:28

And may be missing some choices from this question.

3:37

All right, um, uh, it looks like a, uh, the

3:42

c and D were left off the answer choices,

3:44

but the answer is C frame of Mai.

3:48

Um, notice the enhancing lesion here at the midline, uh,

3:53

inferior fourth ventricle.

3:54

And this is the median aperture of the fourth ventricle,

3:56

also known as the frame of mai Great case.

4:00

Three is a 30-year-old person who fell

4:03

and struck their head,

4:04

and they're presenting with vomiting syncope

4:06

and right ear bleeding.

4:08

Take a look at these images.

4:10

What compartment is the hemorrhage?

4:12

Is it epidural, intraparenchymal, subarachnoid or subdural?

4:23

94% of you got the answer correct, which is epidural.

4:26

So epidural hematomas, as you all know,

4:29

are usually bi convex in shape.

4:31

They're len deformed, they're lemon shaped.

4:33

They cause more focal mass effect

4:35

because they're bound

4:37

by the dural attachments near the sutures.

4:40

And so they have this bi convex, uh, shape

4:43

that is pretty typical.

4:44

And I try to be tricky by showing a coronal image where part

4:47

of it is not quite as by convex.

4:49

But the context clues here was

4:51

that the patient's bleeding out their ear.

4:53

And how does blood from the

4:55

intracranial compartment come out to the ear?

4:56

It has to be in the epidural space, go through dehi sense

4:59

of the teman tip knee

5:01

and go through a tepa membrane

5:03

perforation to come out the ear.

5:05

And that's what happened in this case.

5:08

Case four is an 80-year-old with, um, a a one day history

5:13

of, um, some decreased level of consciousness that occurred

5:18

after having a catheter,

5:19

a transcatheter aortic valve replacement.

5:22

Take a look at these two images.

5:25

What vessel is occluded is the,

5:27

the anterior inferior cerebellar artery,

5:29

the posterior cerebral artery,

5:31

the posterior inferior cerebellar artery,

5:34

or the superior cerebellar artery.

5:42

Okay, it looks like most people got the answer correct,

5:44

which is the superior cerebral artery, 53% of you.

5:48

Now, the key here is to recognize that this area

5:51

of hypodensity is in the right superior server hemisphere,

5:54

which is obviously by its name, the territory of the SCA.

5:58

You could also see on this coronal max intensity projection,

6:02

CTA, that uh, you have lost a ification

6:06

of the right SCA normally on CTAs.

6:09

You should be able to see both posterior cerebral arteries

6:12

and superior cerebral arteries in a double T kind

6:16

of, uh, look.

6:17

This is the logo of Texas tech

6:19

and very variably in patient to patient.

6:22

You may or may not see the iica or the pica.

6:26

Now, um, the SC should be visible on, um, really all CTAs

6:30

or MRIs unless you have an occlusion, uh,

6:32

of either those branches

6:34

or the parent artery, which is the basal artery.

6:36

So look for that double T.

6:38

And in addition to supplying the superior cerebellum,

6:41

the SCS do also supply the upper pon

6:43

and the ponto mu cephalic junction.

6:45

So look for hypodensities there as well.

6:49

Case fives is a 60-year-old with imbalance

6:51

and a memory issue.

6:54

Where is the obstruction?

6:56

Is it cerebral aqueduct, the framing of Monro,

6:58

the fourth ventricular outlet or the lili quis membrane?

7:07

65% got the answer correct.

7:10

So you notice that on this sagal kiss image we have dilated

7:13

lateral and third ventricles.

7:14

We have anterior bow in the, of the, uh, laminate terminis.

7:19

And then we have this dilation of the proximal part

7:21

of the cerebral aqueduct.

7:23

And then this focal narrowing very tight stenosis.

7:25

So this is aqueduct stenosis

7:28

and, um, in kids aqueduct stenosis is the most common cause

7:32

of congenital obstructive hydrocephalus,

7:34

but in this situation, it was an adult

7:37

and aqueduct stenosis can also be acquired in adulthood such

7:40

as after infection or hemorrhage.

7:47

If you have any questions about the questions,

7:50

put them in the q and a

7:51

and we'll try to address them as they come up.

7:54

K six is a 70-year-old with altered mental status.

7:57

What is the likely cause? Is it cerebral edema?

8:00

Qre one deformity pseudotumor cerebra or spinal CSF leak?

8:11

And 82% got the correct answer, which is cerebral edema.

8:14

Now this is the typical appearance on a sagal image,

8:16

which is a little bit atypical way of depicting it.

8:19

Diffuse cerebral edema,

8:20

which appears this great white differentiation loss,

8:23

CSF space effacement and downward brain herniation.

8:26

So we see a complete effacement of the basal cisterns.

8:29

We see displacement of the cerebellar tonsils down

8:32

through frame and magnum.

8:34

We see this calcification, which is a pineal calcification,

8:37

um, inferiorly displacement,

8:38

it's usual position down into the middle

8:40

of the posterior fossa.

8:41

And this sharp angulation of, uh, the vein of galin, uh,

8:45

with the straight sinus over here.

8:48

Uh, so this is due to massive downward, um,

8:50

central herniation and, um,

8:53

and effacement of the CSF spaces in the posterior fossa.

8:59

K seven is the 50-year-old who woke with aphasia.

9:02

They were last seen well before bed 12 hours ago.

9:05

Take a look at these two images

9:07

and answer the question, what is the best

9:09

next step in management?

9:10

Is it an EEG electroencephalogram, IV to 10 connected place

9:15

lumbar puncture or a neurosurgical consult?

9:21

I'll go back to the clinical presentation

9:23

and mention that they awoke

9:26

with aphasia in their lasting well 12 hours ago,

9:34

and the correct answer chosen by half

9:36

of you was IV 10 place.

9:38

So the clinical scenario here is that, uh, by

9:42

standard criteria, they would be outside of the TPA

9:45

or ECT place window.

9:47

Uh, but they awoke meaning their last, uh, awoke

9:50

with the deficits, meaning their last known well is unknown.

9:53

It could have been an hour ago,

9:54

it could have been 12 hours ago.

9:56

And under the criteria, under the wake up trial, uh,

9:59

so-called DWI flare mismatch is when you have a DWI positive

10:04

lesion, but flare negative lesion that suggests

10:08

these patients are just a few hours out from their stroke

10:12

onset and they may benefit from thrombolysis even though

10:15

they're on, uh, time of onset was technically unknown.

10:19

So describing the fact that you have an infarct here

10:23

of the lateral aspects of the precentral gyrus

10:26

that is not significantly hyperintense on flare makes them

10:31

eligible for getting IV thrombolysis.

10:35

Dr. Daniel has a couple questions for cases

10:38

that we just covered, if you wanna

10:40

Sure. A

10:41

question on case six was why is there

10:43

hyperintensity off the tentorium?

10:45

So in cases of diffuser edema,

10:49

the brain is hypo dense,

10:51

and that gives an appearance of relative hyper density

10:55

of the vascular structures,

10:57

including the veins which are congested.

10:59

And that gives you, um, on the sagal image a kind

11:02

of appearance of hyper density of the dural venous sinuses.

11:05

Uh, and sometimes, uh, on axial images, you see engorgement

11:09

of cerebral veins in the seine fissures and basal cisterns,

11:13

and that gives you a pseudo

11:14

subarachnoid hemorrhage appearance.

11:16

This is kind of the, um, sagal counterpart

11:19

where you see hyper density of the, of the venous sinuses

11:22

that contain, you know, um, normal hematocrit.

11:25

Um, uh, but it, you know, that normal blood, uh, density is,

11:30

um, just so much more distinct than the brain, which is emus

11:33

and low density case six.

11:36

Can, uh, can this be the appearance

11:38

of intracranial hypotension was a question.

11:40

So, um, this, uh, brain sagging

11:44

by itself is an appearance of intracranial hypotension,

11:48

which is why there is the distractor D

11:49

but is not the correct answer in this case

11:51

because there's such massive brain sagging

11:55

and swelling of the entire brain,

11:57

and you cannot see any gray white distinction on any part

12:01

of the brain that is imaged here.

12:03

So, um, if you just had brain sagging

12:07

and you had pituitary engorgement

12:09

and you had, you know, venous sinus engorgement,

12:12

but you could still make out the gray white differentiation,

12:16

then intracranial hypotension would be a proper answer.

12:19

But in this case, there's an empty cell,

12:22

there's no gray white differentiation,

12:24

and there's brain sagging.

12:25

This is diffusive real edema.

12:29

So moving on to case eight,

12:31

A 75-year-old is present presenting

12:33

with amnestic mild cognitive impairment.

12:36

What is the most likely diagnosis?

12:38

Is it cerebral amyloid angiopathy, diffuse axonal injury,

12:42

familial cerebral cavernous malformations

12:44

or hypertensive small vessel disease?

12:53

Okay, and 87% of you got the answer correct,

12:55

which is cerebral amyloid angiopathy.

12:57

The mi uh, the main finding here is multiple

13:01

cerebral microbleeds in a peripheral location,

13:04

which is called a strictly low bar

13:07

or a cortical subcortical location.

13:09

There are no micro hemorrhages in the deep gray

13:12

nuclei that are imaged here.

13:14

And having that finding of multiple strictly low bar

13:19

hemorrhages is one

13:21

of the diagnostic criteria in the Boston 2.0 criteria for

13:26

probable cerebral amyloid angiopathy.

13:27

Okay, the imaging hallmark of CAA is having

13:31

multiple strictly low bar hemorrhagic lesions,

13:33

and that may be microbleeds macro hemorrhages,

13:36

superficial cirrhosis, or subarachnoid hemorrhages.

13:39

Now, there are all, there are some non hemorrhagic features

13:42

that are in the criteria, but those are less prominent, uh,

13:45

and less common case.

13:49

Nine is a 55-year-old with Horner syndrome.

13:53

Take a look at these two images. What is the diagnosis?

13:57

Is it carotid dissection, jugular, paraganglioma, petre,

14:01

apex, cholesteatoma, or wallenberg syndrome?

14:11

And the majority of you got the answer correct is

14:13

carotid dissection.

14:14

So the crescent sign

14:15

of an internal carotid artery dissection indicates

14:19

intramural hematoma within the vessel

14:21

that on routine brain imaging can be seen.

14:24

If you get an axial T one image,

14:27

this one is just a routine in axial T one without contrast.

14:31

You can see this hyperintensity, it doesn't stand out

14:33

so much because we didn't do any fat sat on this.

14:35

This is a routine brain sequence,

14:38

and you can often see it on DWI

14:40

because in the subacute phase when you have met hemoglobin

14:43

and it's T one hyperintense, you'll also have, um,

14:46

DWI hyperintensity, which appears

14:49

as this similar crescent shape at the bottom

14:52

of your routine brain DWI sequence.

14:54

So that should clue you in, uh,

14:56

when the history is Horner syndrome,

14:58

that you have a carotid dissection as the culprit

15:04

case 10 is a 60-year-old with left-sided weakness.

15:07

I have three images.

15:13

What is the stroke etiology?

15:17

Is it atheros plaque, carotid dissection,

15:19

CRD web or paraganglioma?

15:23

The, the prior image just showed a, a right

15:26

hemispheric infarct,

15:32

okay?

15:33

And the correct answer is CRD web, 74%

15:35

of you got the answer correct.

15:36

So the finding here is this, um, linear, uh,

15:41

luminal filling defect at the origin

15:43

of the cervical internal carotid artery,

15:45

which on a sagittal maximal intensity projection image

15:48

appears very shelf like it's linear.

15:50

It's not rotund like in atheros plaque,

15:53

it's not calcified like in atheros plaque,

15:56

and it's not in the distal cervical ica

15:58

like a crowded dissection.

15:59

So this is a typical appearance of a crowded web,

16:01

which is thrombogenic

16:03

because it creates this, um, kind of turbulent flow just,

16:07

um, posterior to this crowded web.

16:09

And, and that can, uh, form aus for, uh, thrombogenesis,

16:13

which then embolize to the, uh,

16:15

you know, anterior circulation.

16:17

So, uh, crowded web, important to recognize even if, uh,

16:21

this shelf of tissue doesn't cause, you know,

16:24

traditional stenosis by NASA criteria,

16:27

this is still thrombogenic

16:28

and important to flag for the, uh, STR neurologist.

16:35

So case 11 is, uh, 30 5-year-old

16:38

with hemoglobin SC disease and altered mental status.

16:47

What is the diagnosis?

16:48

Is it acute hemorrhagic encephalomyelitis,

16:51

metastatic calcification, fat embolism, or septic emboli?

17:02

Okay, we have a little bit of a spread here.

17:04

Okay, so 38% of you said, um, uh, a

17:07

and 36% of you said fat embolism.

17:09

The correct answer is fat embolism on the dwi.

17:12

I, we see diffusion restriction in the pleenum

17:14

of the corpus clom, but the really striking finding is on

17:16

the SWI as profuse microbleeds

17:20

throughout the cerebral white matter.

17:21

You can see them really everywhere, um,

17:23

with the predilection for the paraventricular white matter,

17:25

but also going all the way into

17:27

the subcortical white matter.

17:29

So this is a typical appearance of a cerebral fat embolism

17:32

or a part of the fat embolism syndrome,

17:35

and that can occur in the setting of trauma,

17:37

long bone trauma, um, especially, um,

17:40

surgeries like liposuction, as well as, uh,

17:42

sickle cell crises, especially hemoglobin SC

17:45

and hemoglobin S beta thalassemia disease where you have,

17:50

um, kind of low level chronic, uh, bone infarctions

17:53

that somehow liberate, um, fat particles into the vassi

17:57

that are then metabolized in the lungs into free fatty

18:00

acids, which have a, uh, kind

18:02

of a chemo toxic effect on the endothelium.

18:04

And results in this, uh, micro hemorrhage pattern

18:08

on SWI has been described that the profusion

18:10

of microbleeds kind of outlines all the sibal white matter

18:13

and gives a walnut kernel appearance.

18:15

And sometimes on DWI, you have scattered, uh,

18:18

punctate infarcts

18:19

that are described as the starfield pattern.

18:22

In our case, we didn't have that many, uh, DWI, uh, foci.

18:26

And so it didn't really meet the criteria

18:28

of a starfield pattern, but

18:29

that has been described classically.

18:32

Now it's not acute hemorrhagic encephalomyelitis, which, um,

18:35

a plurality you chose

18:36

because that is a hemorrhagic version of aem, uh,

18:39

which occurs in children, you know,

18:41

in the post infectious kind of setting, um,

18:44

you'd have demyelinating lesions that then hemorrhage, um,

18:47

and it, uh, it,

18:49

it wouldn't be like perfuse micro hemorrhages like this

18:55

case 12 is a 30-year-old woman with headache.

19:01

What is the most likely etiology of hemorrhage?

19:04

Is it brain arteriovenous malformation, cardio embolism,

19:07

cerebral sinal venous thrombosis,

19:09

or reversible cerebral vasal constriction syndrome?

19:18

Okay, and 79% of you got the answer correct. Great.

19:21

So the answer is cerebral sino venous thrombosis.

19:24

What we see on Theron CT image is a

19:27

small jux cortical hemorrhage.

19:29

This has been described as the cashew nut sign,

19:32

which suggests cortical venous thrombosis.

19:34

So we're gonna look for direct evidence

19:36

of cortical venous thrombosis.

19:38

We see hyperdense vessels over the cerebral convexes as well

19:41

as in the superior sagittal sinus.

19:43

It is relatively dense compared to the brain parenchyma.

19:46

Um, the surrounding, uh, brain parenchyma, uh,

19:49

around this hemorrhage is also relatively hypodense

19:51

that's due to venous congestion and edema.

19:54

And so if you see a small juxta cortical hemorrhage at the

19:57

depth of a sulcus just like this, as well

20:00

as hyperdense vessels,

20:01

think cerebral sinal venous thrombosis.

20:06

Case 13 is a 55-year-old man with several hours

20:09

of forgetfulness.

20:11

If his wife noticed when he was unable to recall

20:14

that they had sex this morning,

20:17

what is the most likely diagnosis is an anterior choroidal

20:20

artery infarct, non convulsive status epilepticus,

20:24

opioid associated amnestic syndrome,

20:26

or transient global amnesia.

20:34

All right, A plurality view 41% got the correct answer,

20:38

which is transient global amnesia.

20:39

The imaging findings are on DWI,

20:43

tiny hyperintense foci.

20:45

You may have one

20:47

or few, um, in the hippo campi.

20:51

And here we see three, uh,

20:53

one in the right hippocampal head and two in the left.

20:56

And that is the imaging hallmark

20:57

of transient global amnesia.

20:59

Now, some of the other choices that some

21:00

of y'all chose are not correct,

21:02

opioid associated amnestic syndrome is total bilateral

21:06

diffusion, uh, restriction of the hippo campi.

21:08

So the entire length

21:10

of bilateral hippo campi would be diffusion restricting, um,

21:13

anterior cordal artery infarct would, um, be unilateral

21:17

and cause diffusion restricting, uh, um, you know, tissue

21:20

outside of just the hippo campi, um, you know,

21:22

some somewhere, uh, else I would show you, um,

21:25

extra hippocampal territory that is diffusion restricting

21:29

and non convulsive status epilepticus.

21:32

So that can cause hippocampal diffusion, uh, restriction.

21:35

But, um, it would be, uh, you know, um, complete

21:39

and, uh, linear and not punctate, uh,

21:41

like we see in transient global amnesia.

21:46

Okay, so the next case is a 30 5-year-old with headache

21:50

and icoria and right-sided ptosis.

21:55

I have a single image for you.

21:56

What is the most likely cause?

21:57

Is it aneurysm herniation ischemia or neoplasm?

22:07

So 39% of you got the correct answer, which is aneurysm,

22:11

but a plurality view chose neoplasm, which is 42%.

22:15

So on the single image that I gave you, I tried

22:17

to make this a little bit difficult.

22:19

So, uh, on the single T two weighted image,

22:21

we can see these, uh,

22:23

lines which represent the third cranial nerves, um,

22:26

traversing the, um, super cell cistern and

22:29

before they dive into the ca sinuses,

22:32

and here we see a rounded, uh, flow void, um, right where

22:36

that third cranial nerve is entering.

22:38

Now you had to take the clinical context into account.

22:41

Um, somebody has a pupil involving third

22:44

cranial nerve palsy.

22:45

The most, uh, dreaded cause, uh, is a aneurysm

22:49

that is compressing the nerve from the outside.

22:51

So not only affecting the, um, uh, extraocular muscles,

22:56

but also involving the pupillary muscle.

22:59

And, um, and

23:01

because the, you know, fibers

23:02

that ated the pupillary muscle, uh, the periphery

23:04

of the nerve, so that would implicate a extrinsic

23:07

compression causing third nerve palsy as opposed

23:09

to an intrinsic lesion IE microvascular ischemia.

23:12

So when it comes to things

23:14

that compress the third cranial nerve, the, uh, as I said,

23:18

the dreaded one is aneurysm

23:20

because these are actively enlarging

23:22

and may blow, uh, the most common location of

23:25

that is the posterior communicating artery IE the ICA origin

23:29

of the posterior communicating artery

23:31

because this is right where the cranial nerve enters

23:33

the cavern sinus.

23:34

So here's just some images on the subsequent MR Angiogram

23:38

depicting that aneurysm.

23:39

And here's a coronal max intensity projection, uh,

23:42

depicting that aneurysm.

23:44

So if you're given a scan with the history of a,

23:48

of a pupil involving third nerve palsy, look very hard

23:51

for any evidence of an aneurysm.

23:56

The next case is a 30-year-old with an episode

23:58

of right gaze deviation followed by chronic body movements.

24:03

So I have a stack of T 2 8 8 images here.

24:05

What is the most likely diagnosis?

24:07

Is it a brain arterial venous malformation,

24:09

cavernous malformation, developmental venous anomaly,

24:13

or a dural arterial venous fistula?

24:21

Okay, 57% if you've got the answer correct,

24:23

which is brain arterial venous malformation.

24:25

So brain A VM most commonly appears as a compact NIUs,

24:30

which is a nest of intraparenchymal vessels

24:33

that are abnormal, right?

24:35

And so on the T two weighted image I showed you,

24:38

flow void essentially

24:39

that were located within the parenchyma here in the middle

24:41

frontal gyrus, and there's some, uh,

24:44

surrounding parenchymal signal abnormalities,

24:46

T two, uh, hyperintensity.

24:49

And, um, this is what typical brain AVMs look like.

24:52

Um, this is what they look like on time of flight, Mr.

24:54

Angiography, this is

24:55

what they look like on digital subtraction angiogram.

24:58

We have that NIUs, um, in the brain parenchyma

25:01

and early, uh, contrast filling of these draining veins

25:05

that drain into, um, cortical veins and dural sinuses.

25:09

And then on arterial spin labeling, um,

25:12

because there's not a normal capillary bed

25:14

to trap all those labeled spins, um,

25:17

you'll just have a collection of high signal intensity, uh,

25:20

within that, um, arterial venous malformation as well

25:23

as the veins that drain it.

25:25

So here we see abnormal high signal in the superior sagal

25:29

sinus, uh, because part

25:30

of this a VM drains into superior sagal sinus

25:34

because of shunting.

25:35

So the next case is a 30-year-old with seizures.

25:38

So I'm showing you four MR images.

25:41

What is the most likely pathology?

25:43

Is it astrocytoma IDH mutant cortical tuber,

25:46

focal cortical dysplasia glioblastoma or IDH wild?

25:50

Uh, or or yeah, or glioblastoma? I DH wild type.

25:58

Okay, the correct answer that was chosen by a plurality

26:01

of you is astrocytoma IDH mutant.

26:03

So this is a, a young adult who is presenting

26:06

with a expansile looking lesion

26:09

that shows the T two flare mismatch sign

26:11

where it is very bright on T two,

26:13

but the center part of it drops in signal intensity on flare

26:17

and is not contrast enhancing,

26:18

and it's not really diffusion restricting.

26:20

And so this is a typical appearance

26:22

of an astrocytoma IDH mutant.

26:24

So the T two flare mismatched sign, um, uh,

26:27

if you're presented with a lesion

26:28

that you think is a diffuse glioma,

26:29

the T two flare mismatched sign is, um, relatively specific

26:33

for astrocytoma as opposed to oligo dendri glioma.

26:37

And if you're presented in a patient who is younger,

26:39

younger than say age 40 is probably more likely

26:43

that they have an IDH mutant tumor than an IDH wild type

26:46

tumor getting a lot

26:50

of questions in the chat.

26:53

So I may defer answering them

26:58

until the end, actually, uh,

26:59

because looks like there are a lot.

27:02

K 17 is a 7-year-old with headache

27:04

and bilateral optic disc edema.

27:09

What is the most likely pathology?

27:10

Is it diffuse midline glioma, H three K 27 altered

27:15

medulloblastoma pilocytic as, uh, astrocytoma

27:18

or posterior fossa?

27:20

Appendamoma,

27:27

okay.

27:27

All right. So the correct answer here is pilocytic

27:30

astrocytoma, and the key here is to recognize

27:33

that on the a DC you have very high A DC, okay?

27:37

So medulloblastoma is a small round blue cell tumor.

27:40

It should have relatively low A DC and,

27:42

and, uh, you know, unfortunately a majority

27:44

of you pick medulloblastoma,

27:46

but it's not the correct answer here,

27:48

primarily based on the findings on the A DC.

27:50

So this is a, a diagram taken from an article in scientific

27:54

reports reporting kind of the distribution of a DC values,

27:58

um, drawn within regions of interest of, uh,

28:01

pediatric posterior FOSS tumors.

28:03

It is high yield to know for the boards

28:04

that the most common primary brain tumors

28:08

of the posterior fossa in children are medulloblastoma,

28:11

appendamoma and pilocytic astrocytoma.

28:14

And these can be somewhat distinguished by their, uh,

28:17

location as well as their, uh, diffusion, uh, properties.

28:21

Pilocytic astrocytoma I think of as microcystic, it's kind

28:24

of in the name pilocytic sounds like cystic.

28:27

And those have high a DC value somewhere in the range

28:31

of 1500 to 2000 times 10

28:34

to the minus six millimeter square per second.

28:37

Whereas medulloblastoma is a very highly cellular tumor

28:40

to a small round blue cell tumor.

28:42

And these are gonna restrict diffusion to a degree similar

28:45

to that of surrounding brain parenchyma

28:47

or even, uh, more restricting than that.

28:50

And then in poma is somewhere in between.

28:53

Um, but um, sometimes may be distinguished by the fact

28:57

that it is in the ventricle

28:58

and extruding through the ventricle.

29:00

So if you are faced with a child, uh,

29:02

with a cerebellar lesion that has enhancing components

29:06

and it has cystic components

29:08

and it has really high diffusivity,

29:10

think pilocytic astrocytoma

29:14

case 1850 5-year-old with headache, dizziness

29:17

and gait difficulty.

29:19

So an adult. Now, what is the likely pathology?

29:23

Is it he angio blasts, stoma, neuro psychosis,

29:27

pilocytic astrocytoma or pleomorphic ex anthro astrocytoma?

29:37

Okay, 85% of you got the answer correct,

29:39

which is heman osteoblast in adults

29:42

and you have a posterior fossa, uh, cerebellar mass.

29:46

Think, uh, one of two things.

29:48

Is it metastasis or gio blasts?

29:50

Stoma, I didn't give you metastasis

29:52

and choices, so I made it easy for you.

29:54

It is likely Gio Blas stoma.

29:56

What are the features of Gio Oblasts?

29:58

This is the classic appearance with a cyst

30:01

with a mural nodule that is solidly enhancing,

30:04

and this nodule is very vascular.

30:06

You can see a flow void going to it.

30:09

This is enlarged training vein.

30:10

These are very highly vascular tumors.

30:12

Sometimes hematomas are solid, um,

30:15

and don't have cystic component,

30:16

and sometimes they have cystic component

30:19

and it falls under your differential of, um, cyst

30:22

with neural nodule, uh, differential diagnosis.

30:26

The other choices here are, um, uh, not right

30:28

because cy astrocytoma happens in kids polymorphs,

30:32

antho astrocytoma happens in the sial compartment

30:35

and neurosis psychosis doesn't really have this

30:37

large enhancing component.

30:38

That's hypervascular case 19 is a

30:43

45-year-old with seizure.

30:47

What is the likely pathology?

30:48

I'm giving you CT images and T one post contrast

30:52

and T two weight images.

30:53

Is it central neuro cytoma, choroid plexus,

30:55

papillo meningioma, or subependymal giant cell astrocytoma?

31:04

So since I'm deferring questions to the end,

31:07

it would be helpful it when you type your questions to

31:11

indicate which case they are talking about.

31:13

So when I come to them at the end,

31:14

I can go back to the correct case.

31:16

Um, the correct answer here, uh, is meningioma,

31:20

which only 15% of you chose.

31:22

Okay? So the, uh,

31:25

the reason it's not choroid plexus Papillo is that is a,

31:28

a disease of children primarily,

31:30

and we're here dealing with an adult, um,

31:33

meningiomas have an in adults

31:35

and they can be intraventricular.

31:37

And, um, even in that location,

31:39

they have the typical appearances of a, uh,

31:43

dural based meningioma, uh, where, uh,

31:46

there's calcifications, there's, you know,

31:48

maybe slightly higher density than normal brain.

31:50

It's homogeneously enhancing

31:52

and, um, they're clearly extra axial tumors in

31:54

that you can see like a CSF cleft around this tumor.

31:58

And it's, um, the calcified mineralized components are low

32:01

signal intensity on T two weighted imaging.

32:03

Um, the, this is the most common site

32:06

of an intraventricular meningioma.

32:08

It's the in the atrium of the lateral ventricle.

32:10

The other choices that some of you also chose were,

32:12

you know, not really right,

32:13

because of location of sub abend giant cell astrocytoma,

32:17

which is a Sega, that is also a, um, disease of children

32:21

with tumor sclerosis.

32:22

And that happens at the Freeman of Monroe

32:24

and not in the, um, atrium of the lateral ventricle.

32:27

A central neuro cytoma is also a tumor

32:30

that primarily occurs in the Freeman of Monroe region, um,

32:33

arising from the septum halluc

32:35

and not in the atrium of the lateral ventricle.

32:37

So if you see an adult

32:39

with a homogeneously enhancing calcified mass in the atrium,

32:42

lateral ventricle than meningioma, first

32:46

case 20 is a 75-year-old with two days

32:49

of a neurologic change.

32:51

We have a non-con head CT

32:52

and a CT angiogram maximal intensity projection.

32:56

What is the most likely clinical deficit in this patient?

32:59

Is it cognitive impairment, right sided hemiparesis

33:03

left hemi oia or right hemis spatial neglect?

33:13

So the correct answer here is cognitive impairment,

33:16

which only 9% of you chose.

33:19

Um, the findings here are this hypodensity in the left

33:23

anterior thalamus, which corresponded on a later DWI

33:26

to diffusion restriction.

33:28

And on the CTA that I showed earlier, there was a cutoff

33:32

of the left PCA.

33:33

Now, the reason it's not left hemi noia,

33:35

because that's the wrong laterality.

33:37

If you have a, uh, a left sided PCA deficit,

33:41

you're gonna have a right hemopsia hoon hemopsia.

33:45

Uh, and I was trying to get you to think

33:48

what deficits could be attributed

33:50

to an anterior thalamic infarct.

33:52

Okay? And this is a good time to review the functional

33:56

and vascular anatomy of the thalamus.

33:58

So the thalamus can be divided into four quadrants.

34:02

The medial quadrant is supplied by branches of P one,

34:06

including if you have the anatomic variant,

34:08

the artery perron.

34:09

And this is responsible for arousal memory.

34:11

And so patients who have, uh, medial thalamic infarcts, uh,

34:15

like a artery perron infarct, or just like a top of the base

34:17

or infarct, they have reduced levels of consciousness.

34:21

Now, patients who have anterior thalamic infarcts,

34:23

like our patient present with impaired language

34:26

and memory, especially if this is in the dominant

34:28

hemisphere, which is the left in most individuals,

34:31

and this is due to an occlusion of the, um, P one, uh,

34:35

or the posterior communicating artery, um,

34:39

which supplies the anterior thalamus.

34:42

This is the relay station

34:43

for everything in your ipsilateral kind of frontal lobe,

34:46

which includes your, um, language centers and, um,

34:49

and also, you know, kind of relays for memory as well.

34:52

So anterior thalamus is a site for causing, um, language

34:57

and memory difficulties.

34:58

The lateral thalamus includes the ventral lateral nucleus,

35:01

the ventral posterior medial, uh,

35:04

and ventral posterior lateral nuclei, which subserve sensory

35:08

and motor functions.

35:09

And I remember this because this is right, uh, adjacent

35:11

to the posterior limb of internal capsule, which subserves,

35:14

uh, many of the same functions.

35:16

And so occlusions

35:17

of the PCA P two will infarct the lateral thalamus

35:20

and result in sensory motor deficits.

35:22

And then less well described are posterior thalamic lesions.

35:24

Um, usually, uh, uh, occlusions of,

35:27

of the posterior choroidal arteries, which are branches

35:29

of P two, will affect the posterior thalamus as well

35:31

as the lateral gen nucleus.

35:33

And that causes a visual deficit independent

35:36

of any infarction of the occipital lobe, of course.

35:39

So there's a, a concept known as strategic infarct locations

35:43

where, um, if you have, uh, large

35:45

or a little infarct, um, that can, um,

35:48

vary reliably cause cognitive impairment or other deficits.

35:52

So, uh, when we're talking about small subcortical infarct,

35:55

what location is most strategic in causing post stroke

35:59

cognitive impairment is the left anterior ery thalamus.

36:01

So here, right in the left anterior ery thalamus is, um, uh,

36:05

a high probability of causing

36:07

post stroke cognitive impairment.

36:08

This is based on a voxel by voxel meta-analysis

36:11

that was published, uh, in lance

36:13

and neurology of a bunch of, uh, stroke studies.

36:15

So the left anterior thalamus is a strategic site

36:17

for causing vascular dementia.

36:19

So look for infarcts

36:21

and raccoons in that location on your dementia

36:24

studies case.

36:27

20 ones a 65-year-old with right cranial nerve three palsy.

36:34

Okay, what is the likely cause?

36:36

Is it cardio embolic infarct, diffuse large B-cell lymphoma,

36:40

glio, uh, glio, mitosis, cerebri or multiple sclerosis?

36:52

Okay, good. A plurality if you got the correct answer,

36:54

which is diffuse large B-cell lymphoma.

36:56

But there's a really big spread in the answers.

36:58

The key findings on the CT here is this hyperdense lesion,

37:02

the right cerebral peon call region, um,

37:05

extending into the mid, uh, you know, kind of the,

37:07

the midbrain mentum really.

37:09

And this is contrast enhancing homogeneously

37:11

and it's bright on DWI

37:13

and diffusion restricting, um, uh, is confirmed on the A DC.

37:16

And so when you faced with lesions like this, um,

37:19

this is typical of in, um, CNS lymphoma,

37:23

the most common histology

37:24

of which is diffuse large B-cell lymphoma.

37:27

Now, why is it not glio mitosis cerebri?

37:30

Um, so glio mitosis doesn't restrict diffusion, um,

37:32

to the degree that lymphoma does.

37:35

Um, and it's also not gonna be

37:38

hyperdense on non-contrast ct, uh,

37:41

multiple sclerosis is not gonna be hyperdense on ct

37:44

and it's, um, more likely to gonna have, um,

37:47

a complete ring, um, uh,

37:49

or a kind of nodular contrast enhancement, not this,

37:52

uh, kind of wispy.

37:53

Um, and, and solid, uh, infiltrative enhancement

37:57

and cardio embolic infarcts, um, are not gonna be

38:00

as expansile mass like, like we have here.

38:03

Um, uh, those are gonna be, you know, small and,

38:06

and territorial kind of lesions.

38:09

So CNS lymphoma, think about that.

38:11

When you have a paral infiltrative lesion, that's expansile,

38:14

especially if it has all the markers of hyper cellularity,

38:17

like hyper density on non-con ct, as well

38:21

as marked diffusion restriction.

38:23

And, um, and, um,

38:25

and other features that are clues are having, um, uh,

38:29

a solid contrast enhancement

38:30

and a paraventricular predilection, uh, which, uh, you know,

38:34

some of our lesions were.

38:35

So this one was, uh, by the left lateral ventricle,

38:38

and you can see that it was, uh, quite diffusion.

38:40

Restricting case

38:45

22 is a 65-year-old with altered mental status

38:48

for a few weeks after having a cyto reductive surgery

38:51

for gastric cancer with peritoneal carcinomatosis.

38:56

What is the likely diagnosis?

38:57

Is it dural venous sinus thrombosis, leptin meningeal,

39:01

carcinomatosis status epilepticus or wees encephalopathy?

39:12

Majority of you got the answer correct,

39:14

which is lept menal carcinomatosis.

39:15

So the key finding here are sheets

39:17

of enhancement on the surface of the brain

39:19

and cranial nerves.

39:20

We can see enhancement through, um, the surface

39:23

of the cerebellar folia, uh, on the s the medial surface

39:27

of the exci lobes and the parietal lobes.

39:30

Um, on other images we can see that as well.

39:32

Um, the key is that there are sheets of enhancement,

39:35

meaning you can see them on consecutive slices as opposed

39:37

to vessels which course in and out on a single slice.

39:41

And you can also see contrast enhancement

39:42

of the trigeminal nerves in the pre, um, in the cer uh,

39:46

cbell pontin naval cisterns here.

39:48

Um, and this represents leptin, nal carcinomatosis,

39:51

which most of you got correct?

39:52

So I won't belabor it.

39:54

The next case is a 25-year-old female with headache.

39:59

What is the pathology? Is it a dermoid cyst?

40:02

Lipoma meningioma or teratoma?

40:10

Okay, the answer is lipoma, which a majority

40:13

of you chose 56%, got the answer right.

40:16

So intracranial lipomas are, um, uh,

40:19

abnormal differentiation of the mens priva.

40:23

And, um, these are most commonly located in

40:26

midline locations.

40:27

The peric collosal cistern, the quad trigeminal cistern,

40:30

the super cell cistern,

40:31

and less commonly the rebell pontin angle cistern.

40:34

And so this is a case of quad trigeminal cistern lipoma.

40:36

You can see that it's homogeneously T one hyperintense fat

40:40

signal intensity, and this is the typical location

40:42

of quadrical cistern lipoma.

40:43

So that's the correct answer.

40:45

Um, a dermoid cyst would be more heterogeneous.

40:48

It may have some lipid, but it's not gonna be bulk fat.

40:51

Um, and it's gonna have a lot of like epidermal, um,

40:53

you know, keratinized, uh, debris, uh,

40:56

with this gonna have a more heterogeneous appearance.

40:59

Um, um, Alan Cytoma, um, uh, i i is gonna,

41:04

um, be T one hyperintense as well,

41:05

but not quite as, uh, bright as this, you know, bulk fat.

41:08

And the teratoma is a kind of a pineal region tumor, um,

41:12

uh, germ cell tumor.

41:14

And, um, it,

41:15

it also is not gonna have just fat signal intensity is gonna

41:18

have other stuff as well.

41:21

24, uh, uh, case 24 is a 30 5-year-old with a headache.

41:27

What is the pathology is an arachnoid cyst,

41:29

epidermoid cyst meningioma or schwannoma.

41:39

So the correct answer is epidermic cysts,

41:41

the vast majority you got this correct.

41:42

So the key findings here is a diffusion restricting lesion

41:46

in the cerebral ponty ankle that is not contrast enhancing.

41:50

And so it's not a meningioma, um,

41:52

it's diffusion restricting, so it's not an arachnoid cyst

41:55

and, um, it's not contrast enhancing.

41:57

So it's not stroma either.

41:58

So, okay, so diffusion,

42:00

restricting non-contrast enhancing lesion, the CP angle,

42:03

it's gonna be epidermoid cyst

42:07

case 25, a 40-year-old with dizziness and division changes.

42:14

What is the most likely diagnosis?

42:15

Is it methanol poisoning, posterior reversible

42:17

and encephalopathy syndrome,

42:19

solvent abuse or thymine deficiency?

42:28

All right, the vast majority,

42:29

you've got this answer correct.

42:30

So this is waris encephalopathy, which is thymine deficiency

42:33

or vitamin B one deficiency.

42:35

And the classic imaging appearance is T two flare

42:40

and sometimes DWI hyperintensity of three locations,

42:44

the medial thalami, um, the, um,

42:48

periaqueductal region of the midbrain, as well

42:51

as the mammary bodies.

42:52

Okay? So, uh, these locations are classic

42:56

for warkin encephalopathy,

42:57

and you can be the hero by suggesting the diagnosis if the

43:00

clinicians were not expecting it already.

43:06

Case 26, 40-year-old with altered mental status.

43:11

I'm showing you flare, D, WI

43:12

and T one pre contrast, what is the diagnosis?

43:16

Is it diabetic tripathy, hepatic encephalopathy,

43:20

hypoxic ischemic brain injury,

43:22

or West Nile virus encephalitis?

43:31

So, uh, as I was saying the, the answer here, um, uh,

43:37

I, I think it was a tie between B

43:38

and C among the respondents.

43:41

And now if you just had the, um, uh,

43:45

the T two flare

43:46

and DWI, uh, you know, c might be a reasonable response.

43:51

Um, but in the setting of having chronic liver disease

43:55

and, um, the clinical context is not like they had a cardiac

43:58

arrest, um,

44:00

the more likely diagnosis is hepatic encephalopathy.

44:02

Now, hepatic encephalopathy creates cortical diffusion

44:06

restriction, um, most classically

44:08

with the predominance involving the cingulate gyre

44:11

as well as the insula.

44:13

Whereas hypoxic ischemic brain injury, um,

44:16

can involve those areas, but is really more

44:18

diffuse than that.

44:19

Um, and uh, another clue is

44:22

that in hepatic encephalopathy there's sparing

44:24

of the occipital lobes

44:25

and the peric um, cortex, whereas those are, um,

44:29

often involved in hypoxic ischemic brain injury.

44:32

So taking into all the context clues here of a background

44:36

of chronic liver disease,

44:37

given the global palai T one hyperintensity

44:40

and the predilection for cingulate

44:42

and insula, the best answer here is acute

44:44

hepatic encephalopathy.

44:50

The next case is a 25-year-old

44:52

with uncontrolled nausea and vomiting.

44:56

What antibodies are likely present in this patient?

44:59

Is it anti aquaporin four,

45:01

anti myelin oligodendrocyte glycoprotein,

45:05

anti N methyl D aspartate receptor,

45:08

or antiphospholipid?

45:16

All right. And the majority of you chose the correct answer,

45:18

which is anti aquaporin four.

45:20

So the findings here are a T two hyperintensity without

45:23

contrast enhancement often, uh, in the dorsal medulla,

45:27

which is, uh, an area known as the area post rema,

45:30

which is kind of the brain's chemo receptors

45:32

and is responsible for causing nausea, vomiting,

45:35

as well as hiccups.

45:37

And, um, the core clinical features of N-M-O-S-D,

45:41

which is neuromyelitis optica spectrum disorder, are

45:45

as the name suggests, um, uh, optic neuritis

45:49

as well as longitudinally extensive transverse myelitis.

45:53

But the, um, uh,

45:55

a third core clinical feature is area post Remus syndrome,

45:58

which is manifest by intractable nausea

46:01

and vomiting, um, and sometimes hiccups.

46:03

And then there are other core clinical features as well

46:06

that involve brainstem dysfunction or,

46:08

or cerebral dysfunction or thalamic dysfunction.

46:11

Um, but the, the classic distinct ones are gonna be, um,

46:15

optic neuritis, uh, transverse myelitis,

46:18

and then area postma, which is,

46:20

you know, not built into the name.

46:21

You just have to remember that association.

46:23

And so it's associated with this T two hyperintensity

46:25

of the dorsal medulla.

46:27

And, um, these are most commonly caused by

46:30

or associated with aquaporin four antibodies.

46:35

Case 28 is a 50-year-old woman with right eye blurriness.

46:43

What is the likely diagnosis? Is it Bette's disease?

46:47

Multiple sclerosis, progressive multifocal leuk

46:50

encephalopathy, or Sach syndrome?

46:59

Okay. And the majority, you chose the correct answer,

47:02

which is multiple sclerosis.

47:04

The findings here are T two hyperintensity

47:07

of the optic nerve, the para ventricular white matter here

47:11

and here there's an inflator lesion here at the, um,

47:15

pons, the midbrain junction.

47:17

And if you look closely,

47:18

there's another lesion here in the spinal cord.

47:21

And, um, there are also lesions here involving the

47:24

sub portable U fibers.

47:25

These are known as juxta cortical lesions,

47:28

and they can involve the overlying cortex as well.

47:30

So that'd be intracortical.

47:31

So this is a juxta cortical lesion, periventricular

47:35

infratentorial, spinal cord and optic nerve.

47:37

These are the typical sites

47:38

that are considered key topographies

47:41

in the McDonald criteria.

47:42

Optic nerve was not traditionally in the McDonald criteria,

47:45

but in the 2024 revision to the McDonald criteria that are

47:50

yet to be formalized in a peer review setting, uh,

47:53

they're gonna add optic nerve into

47:55

one of the key topography.

47:56

It's well known that optic neuritis is well associated

47:59

with multiple sclerosis, but it had not up

48:01

to this point be considered, um, one of the sites

48:03

for the purpose of initial diagnosis of multiple sclerosis.

48:07

But this is a typical appearance

48:09

of multiple sclerosis when you have, um,

48:11

dissemination in space of multiple demyelinating lesions.

48:16

And, um, features that are specific for MS

48:20

are these kinds of, um, lesions

48:22

that in the paraventricular white matter

48:23

that radiate away from the margin

48:25

of the ventricle in a perpendicular manner

48:28

because they surround veins.

48:31

Uh, there's a periannular distribution,

48:33

if you looked at it on a sagittal,

48:35

it would look like fingers.

48:36

Those are dawson's fingers.

48:38

And now if you have multiple of these sites involved,

48:41

you can confidently make a diagnosis of multiple sclerosis,

48:44

even if you don't see contrast enhancement.

48:47

Um, if you have extensive such lesions

48:50

with a clinical history that is suggestive,

48:52

then you can make the diagnosis of of multiple sclerosis.

48:55

Why is it not ssec syndrome?

48:57

A lot of people chose Ssec syndrome.

48:58

So those present with, um, snowball like, um, demyelinating,

49:03

uh, lesions of the corpus close.

49:05

Some you can have, uh, re uh, you know, retinal issues

49:08

and, um, cochlear issues causing, uh,

49:11

sensor neural hearing loss.

49:12

Um, but that is, you know, the, the appearance

49:15

of those lesions is not like that.

49:17

Uh, multiple sclerosis,

49:18

which again involve multiple of these sites.

49:23

Case 29 is a 65-year-old with lethargy history

49:27

of recent ear infection.

49:31

What diagnosis is present is an invasive o mycosis,

49:36

spontaneous intracranial, hypotension, subdural and emia

49:39

or venous infarction.

49:47

Okay? And the correct answer was chosen by a plurality

49:49

of view, which is subdural and emia.

49:51

On the CT image, we see a focus of pneumo ephalus here.

49:56

Um, it's not clear by the CT image where exactly this is,

49:59

but um, if you scroll back

50:00

and forth, you would know this is somewhere

50:02

along the tentorium.

50:05

And on subsequent MRI,

50:06

we see this curvilinear DWI hyperintensity along the

50:09

tentorium or on the under surface of the occipital lobe.

50:14

And you have to correlate that with the coronal T

50:16

one post contrast image.

50:17

There's this space here of non enhancing fluid in

50:20

between the brain and the left temporal leaflet.

50:23

In the left tentorial leaflet is thickened

50:25

and hyper enhancing.

50:27

So what does this represent?

50:28

What is a flu collection in the subdural space

50:32

that is diffusion restricting has pneumo ephalus in the

50:35

context of an ear infection that is a subdural and emia.

50:39

Now, um, why is it not some of the other choices?

50:43

Um, spontaneous intracranial hypotension would create

50:46

subdural flu collections,

50:47

but it, those would not necessarily diffusion restrict,

50:51

and I would show you sagging of the brain.

50:53

It would not cause neo ephalus is it, um, venous infarction.

50:56

You may have thought venous infarction if you thought this

50:59

diffusion restricting, um, stuff was in the brain.

51:03

But, um, you'd have to correlate

51:04

with the T one post contrast image to see

51:07

that this is outside the brain.

51:08

So this is subdural flu collection,

51:10

and so it's not related to, uh, venous infarction per se.

51:14

So forms of focal intracranial infection

51:17

with separation are brain abscess, subdural and paa

51:20

and epidural abscess.

51:21

So recognizing what the appearance of subdural

51:24

and emia is, it's basically a subdural flu collection

51:28

with diffusion restriction is very important.

51:32

Now we have the last case case, 30 60-year-old with months

51:35

of functional decline with difficulty walking.

51:40

What is the likely diagnosis?

51:42

Is it baso artery occlusion,

51:44

hypertrophic olive area degeneration,

51:47

Erwin leuk encephalopathy, or multiple system atrophy?

51:57

Great, 72% of you got the correct answer,

51:59

which is multiple system atrophy.

52:01

The key findings on this T two flare image are this

52:04

cruciform hyperintensity known as the hot cross bun sign.

52:08

This represents degeneration of the pontine median nuclei

52:12

and the ponto cerebellar tracks going

52:14

across the ponds like this.

52:16

There's also cerebellar atrophy.

52:18

You can see widening of the cerebellar fissures.

52:20

You can see atrophy, the middle cerebellar peduncles

52:23

and associated T two hyperintensity.

52:26

Um, and these are known

52:27

as the MCP signs when you have T two hyperintensity of the

52:32

cps in addition to the hot cross bun signs.

52:34

These are all signs that have been described

52:36

with multiple system atrophy.

52:38

So this is a multi-system, um, problem patients present

52:42

with autonomic dysfunction, motor problems like kind

52:44

of Parkinsonism type of things, um, uh, as well as,

52:49

uh, parametal symptoms.

52:51

And the imaging findings are cerebellar atrophy,

52:54

pontine atrophy, MCP atrophy,

52:57

and you can see T two hyperintensity in these regions

52:59

as well as the pons

53:01

and the typical hot cross bond sign, which we publish

53:04

as a case report in clinical imaging recently.

53:07

Okay, so at this point, um, thank you for participating

53:11

and I'm gonna take an opportunity to answer some questions

53:13

that you guys put in the q and a.

53:17

So, um, just going back, next question was,

53:22

do you expect the fourth ventricle to also be dilated in,

53:24

in cases of aqueduct stenosis?

53:26

No, you don't expect the cases at the fourth ventrical

53:29

to be dilated because the, uh, stenosis causes a buildup

53:33

of CSF upstream of it,

53:34

and so downstream, um, will be normal in size.

53:39

Uh, the next question is, what would be the best

53:40

approximation to ventricular dilation in CT

53:45

with the angles be comparable?

53:46

With MRI angulation this, I'm not sure

53:51

what exactly that is saying.

53:53

Um, the, uh,

53:57

you can see the ventricles quite well on CT

54:00

and, um, that would correlate exactly to

54:02

what you see on MRR, but just, you know, slightly hazier,

54:05

uh, when it comes to the, the walls of the third ventricle,

54:08

but you can see the lateral ventricles quite well

54:10

and the fourth ventricle quite well.

54:12

Um, somebody asked about the sub

54:14

subarachnoid hemorrhage sign.

54:16

So that is a sign of, uh, diffuser edema

54:20

where you have relative hyper density of, um,

54:24

venous structures that are coursing the, uh, basal cisterns

54:28

and sci and so forth that gives the, um,

54:31

mimicking appearance of subarachnoid hemorrhage.

54:33

But it's actually not subarachnoid

54:34

hemorrhage, it's venous congestion.

54:35

And the surrounding brain is just so edematous that, uh,

54:38

it, it is very low density.

54:40

So everything that is normal blood, uh, looks high density

54:43

and that gives the appearance of subarachnoid hemorrhage,

54:45

but it's not subarachnoid hemorrhage.

54:48

Can I point out Luka and Monroe on the sagal?

54:51

So f frame of Luka is not seen on the sagal image.

54:54

F of Luka would have to be seen on a para sagal image

54:56

where an axle image, because they point out laterally frame

54:59

of Luka is the lateral apertures of the fourth ventricle.

55:02

So it cannot be seen on a mid sagal image.

55:05

The framing of Monroe, um, is, um, right here.

55:09

Um, you know, again, the framing

55:11

of Monroe is just slightly off of the mid sagal image, so

55:13

that would be the connection between the lateral ventricle

55:16

and the third ventricle and just, uh, right in,

55:18

uh, this situation.

55:19

So there's some partial volume averaging effects of some,

55:23

you know, cord plexus here across pyramid of Monroe,

55:25

but that's where it would be.

55:29

Um, I had a question about in the CAA case,

55:33

what is the reason for a single dropout in the Baal ganglia?

55:36

So this is very common with age people get mineralization

55:39

of the global palatine and

55:40

that causes signal dropout on SWI in the global palate,

55:43

that's just due to deposition of some minerals.

55:46

May or may not be seen on ct.

55:48

Often it's not, but iron deposition in the global

55:50

palate occurs with age.

55:52

That happens a lot.

55:53

And these are not to be considered micro hemorrhages.

55:57

Um, someone had a question.

55:59

What was the triangular hypodensity abutting the s uh,

56:03

ss in the cortical venous thrombosis case?

56:05

Does anyone remember what case that was?

56:08

Cortical venous thrombosis. This one.

56:11

Okay, what is the hypodensity?

56:13

This hypodensity triangular hypodensity

56:16

that is normal CSF space, that is the subarachnoid space.

56:23

The next question was can we use a flare

56:25

and DWI sign for stroke for prognostication?

56:28

So they're talking about, um, what case was this?

56:34

DWI flare mismatch sign,

56:35

perhaps this case, right?

56:40

Can we use this for stroke prognostication?

56:42

I don't know that people have described this

56:44

for prognostication.

56:46

All DWI flare mismatch tells you is the relative

56:48

age of this infarct.

56:50

When you have a hyperacute infarct,

56:51

you're gonna see diffusion restriction first,

56:54

and then once you develop more and more, um, ionic edema

56:58

and eventually vasogenic edema, then you're gonna develop

57:01

flare hyperintensity, right?

57:03

That doesn't happen for several hours in most patients.

57:06

And so that's why this was used as the imaging criteria

57:09

for eligibility in the wake up trial, right?

57:11

If you can identify patients that are fla, uh,

57:14

DWI hyperintense,

57:16

but flare negative, that suggests

57:18

that you're within a couple hours of stroke onset

57:21

and there's still may be some, um, reversibly damaged tissue

57:26

that can be salvaged if you recanalize the, um,

57:30

thrombo arteries here.

57:31

The idea is that, you know, even though this is diffusion

57:35

restricting, um, you know, there may be tissue

57:37

that is still not infarcted, you know, within this region

57:40

or just around this region

57:42

that is not irreversibly infarcted

57:44

that could be saved if you apply thrombolysis soon enough.

57:50

Next question was how will a cortical tuber present?

57:54

Now, which question was a cortical tuber? A distractor?

57:58

Remind me here. Cortical tuber was a cortical tuber

58:03

will present in children with a history of tuber sclerosis

58:06

as a small area

58:08

of T two flare hyperintensity involving the cortex

58:12

and subcortical white matter in a wet shaped fashion,

58:15

usually smaller than this and maybe half the size

58:18

or a third the size of this lesion.

58:21

And you may see a radial band in the white matter,

58:25

like a T two hypertense band in the white matter

58:26

that goes towards the ventricle.

58:28

Those are cortical tubers. Uh, question 19.

58:33

Somebody had a question for case 19.

58:35

If this were a child, would you say papillo? Um, um, yes.

58:40

So if this were a child,

58:41

papilloma would be a much better option in the

58:45

differential diagnosis.

58:46

So, uh, cord plexus papillomas can occur, um,

58:50

in the lateral ventricle as well as in the fourth ventricle.

58:54

Um, they typically have a more fron like appearance,

58:57

like a cauliflower, uh, floret or a broccoli floret.

59:01

And instead of this is more like large loation

59:04

that you see in meningiomas, um, cor plex of paps, uh,

59:09

have a much more papillary architecture

59:12

and they don't really have this kind of, um, uh,

59:17

calcification pattern that is more typical of,

59:19

of meningiomas.

59:20

These kind have a, a starburst calcification pattern in

59:23

meningiomas, um, uh, due to kind of the architecture

59:27

that's kind of reading outward from the initial

59:29

neoplastic titis.

59:33

Um, someone asked for question 22,

59:37

what's the relationship of bariatric surgery

59:40

to carcinomatosis?

59:41

They did not have bariatric surgery.

59:43

They had cyto reductive surgery,

59:44

meaning they had peritoneal carcinomatosis

59:47

and they went in labaro, um, you know, uh, with a laparotomy

59:51

to, um, reduce the burden of tumor in the peritoneal cavity.

60:01

Question 21.

60:02

Somebody had a question that, uh, does

60:04

diffuse large B-cell lymphoma

60:06

or primary CNS lymphoma

60:09

normally have multiple intracranial lesions?

60:11

Yes. So I would say more often than not primary CNS lymphoma

60:15

manifests with multiple lesions, not a solitary lesion.

60:18

Yes. For question 24, someone asks,

60:23

why does it have flare bright lesion for epidermoid cyst?

60:28

So, uh, epidermoid cyst is a collection

60:31

of keratin debris due to skin where it shouldn't be,

60:36

and that is in the intracranial cavity.

60:37

And the cyst represents a collection

60:40

of basically wet keratin

60:42

and, uh, they're like sheets of keratin

60:46

and there's fluid in between these sheets.

60:48

And so you can have some areas

60:50

that are not gonna suppress totally on flare just

60:54

because of the debris

60:55

and the, you know, protein, you know, stuff there, uh,

60:59

interferes with the normal signal characteristics

61:02

of the CCSF in which it is bathing.

61:05

So it is possible that sometimes you don't have a,

61:08

a complete flare signal suppression within

61:11

an epidermoid cyst.

61:12

They're not like, they're not like arachnoid cysts,

61:14

which are pure CSF,

61:15

and those should absolutely suppress on

61:18

flare or case 26.

61:22

Somebody asks, is CJDA good choice?

61:27

So, um, CJD would be a choice

61:31

here if you did not have the context clue of, uh, background

61:36

of chronic liver disease based on the T one weighted images.

61:40

CJD yes would have diffusion restriction of cortex as well

61:45

as of basal ganglia.

61:48

Um, I would not favor, uh, favor CJD in this case

61:51

because usually it is not this bright on flare.

61:54

Um, usually the finding is limited to DWI, um,

61:58

unless you have like a really FMT case,

62:00

but I really haven't seen that.

62:02

Usually the, the findings are limited to DWI

62:05

and they're very subtle even though the patient is,

62:08

you know, very rapidly progressing, um, in terms

62:11

of their dimension functional status.

62:14

And then finally last question, question, uh, case 29

62:19

is the dural vein thrombus two.

62:23

Okay, so, um, this one turned out to be arachni granulation.

62:28

You wouldn't know that based on a single image.

62:30

If I scrolled back and forth, you would see

62:32

that this was nodular and not rope like.

62:35

And so it was not a venous thrombosis.

62:37

This was, um, uh, just for me

62:40

to trick you guys into saying it was venous thrombosis, um,

62:44

uh, or venous infarction.

62:46

Uh, but this was, this nodule filling defect was just merely

62:50

a arachnoid granulation.

62:51

These are very common at this location as well.

62:54

All right, thank you guys so much.

62:57

I think I've answered all the questions.

63:00

I think you got 'em all. Great.

63:02

Appreciate you being here

63:04

and thank you so much for everyone else for participating

63:07

and asking such great, great questions.

63:09

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63:12

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63:15

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63:17

Mahesh, who will lead us in our

63:18

final case crunch of the year.

63:20

And he'll be doing a review of high yield topics pertaining

63:23

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63:25

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63:27

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63:29

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63:32

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