0:02

Hello, and welcome to Noon Conference, hosted by Modality

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Noon Conference connects the global radiology community

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through free live educational webinars that are accessible

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to learn alongside top radiologists from around the world.

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You can access the recording of today's conference

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and previous noon conferences by creating a free account.

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Today we are honored to welcome Dr.

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Mylan Ho for a lecture entitled, A Practical Approach

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to Neonatal Brain Imaging.

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Dr. Ho is an accomplished neuroradiology physician,

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scientist, and leader specializing in the full

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scope of advanced imaging.

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She leads multiple national

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and international initiatives

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for data science at Precision Health and serves on national

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and international society committees

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and editorial boards dedicated to advancing imaging and ai.

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At the end of the lecture, please join her in a q

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and a session where she'll address questions you

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may have on today's topic.

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Please remember to use that q

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and a feature to submit your questions so we can get to

0:57

as many as we can before our time is up.

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With that, we are ready to be in today's lecture. Dr.

1:02

Ho, please take it from here.

1:05

All right, so we're gonna spend, uh,

1:07

this noon hour talking about, uh, practical approach

1:11

to neonatal brain imaging.

1:12

And I think this is very important

1:14

because I am trained in both adult

1:16

and pediatric neuroradiology.

1:17

But, uh, what you see is

1:19

that you either have a very specialized practice

1:22

of freestanding children's hospital,

1:23

or, uh, you have an adult hospital with, you know, a,

1:26

a smaller, uh, kind

1:28

of associated children's hospital, maybe a nicu.

1:30

And so you get some of these, uh, babies that are

1:34

born in occasionally will get imaging,

1:36

and even if they are later to be transferred

1:38

to a more specialized center,

1:40

you do end up being responsible for interpreting them.

1:42

So I wanted to provide, just based on my career, some

1:45

of the key insights

1:47

and hopefully make it, uh, simpler for everyone

1:49

to understand from a mechanistic standpoint.

1:53

Okay. So today we will review the general principles

1:55

for neonatal clinical care and imaging.

1:58

I will show classic examples

1:59

of preterm and term brain injury.

2:01

That's what you, let's see, in all the textbooks.

2:03

So I'll try to make it, um,

2:04

a little bit more straightforward, mechanistically.

2:07

And then we're gonna mention a number of special diagnoses

2:10

that have characteristic imaging features,

2:12

things you don't wanna miss, uh, that do have more unique,

2:15

uh, features that can actually help you

2:18

understand the diagnosis.

2:20

Okay, so let's start with basic principles.

2:23

So from an epidemiological standpoint, uh,

2:26

in the United States and developed countries, about 10% of,

2:29

um, babies are born preterm.

2:32

Now, there are varying levels of prematurity, uh,

2:35

but approximately one in 10, uh, babies.

2:38

And then one in three out

2:39

of every thousand live births suffers from

2:42

hypoxic ischemic injury.

2:43

So this could be difficult delivery,

2:45

placental abruption, uh, and so forth.

2:48

And, uh, in undeveloped countries, the incidence is,

2:51

is higher, it's around 11% preterm and up to 30, uh,

2:56

or more per thousand life births.

2:59

So these conditions have a high morbidity in

3:02

mortality, uh, for a couple reasons.

3:03

Uh, the primary insult essentially hits

3:07

what we call the selectively vulnerable structure.

3:09

So essentially in these early, uh, phases

3:12

of neonatal development,

3:14

there are certain immature structures

3:16

or maturing structures that are developing.

3:18

And so if you have a hypoxic and

3:21

or ischemic insult, those will be selectively hit, right?

3:24

So you'll see these imaging patterns that are unique

3:27

to the neonate and not seen in older children or adults.

3:31

Um, and maybe even more importantly for prognosis,

3:34

there are, uh, secondary

3:36

and tertiary delayed injuries, um,

3:39

that essentially are metabolic,

3:40

inflammatory cascades induced by the primary insult.

3:43

And the tertiary effects on neurodevelopment can actually

3:46

persist for months or even years at school age or adulthood.

3:50

We can see, for example, impact of, um, extreme

3:53

or very preterm birth.

3:56

So the outcomes, there's this term called cerebral palsy

3:59

or cp, it's kind of a bucket, you know,

4:01

waste bucket, uh, diagnosis.

4:03

And so, uh, it can mean many different things, right?

4:06

And it's not always, uh, it,

4:08

although it's clinically diagnosed, uh, it on imaging,

4:10

it can actually reflect many different things.

4:12

So in terms of the clinical definition,

4:15

they are disturbances of movement and or posture.

4:18

Uh, there are different subtypes.

4:19

The spastic, uh, which is stiffer, uh, usually associated

4:23

with, um, more white matter injury.

4:25

The diskinetic is, uh, abnormal uncontrolled motions,

4:28

and those that are typically more gray matter injury.

4:31

And then ataxic, uh, imbalance,

4:33

which is often cerebellar injury.

4:34

And obviously you can have mixed subtypes,

4:37

but when you look at imaging, there's all sorts

4:39

of preterm term birth injury.

4:40

Genetic diagnoses actually is now up to a quarter

4:43

of them unsuspected, genetic malformation.

4:45

So again, it's a, it's a very loose term

4:48

that's used clinically

4:49

and really can lead to a lot

4:51

of different imaging manifestations.

4:54

And then importantly,

4:55

and we still don't understand this completely,

4:56

but you know, how do we intervene and,

4:58

and optimize these outcomes, right?

5:00

So obviously modifying risk, any risk for preterm birth,

5:03

any risks in terms of the extended or difficult delivery.

5:06

And then neuroprotection, can we modify, um,

5:10

and decrease the burden of delayed injury, right?

5:13

The secondary and tertiary, um, injuries on top

5:16

of the primary insult.

5:19

So, you know, as a radiologist, like,

5:22

it's actually very important and even more so in this, uh,

5:24

perinatal neonatal period to, to know the clinical history

5:27

because there are many, uh, different factors that can lead

5:30

to kind of a final common pathway for injury.

5:33

So you want to look in the note, um,

5:35

and if you really need to actually contact the clinician

5:38

and ask, uh,

5:39

get whatever information you can about prenatal history,

5:42

you know, uh, what was the fetal course that they have?

5:44

Regular checkups, right? Was anything detected?

5:47

Uh, maternal things, you know, gestational diabetes,

5:50

preeclampsia, you know, all of these things

5:51

that might affect the health of the fetus.

5:54

Uh, what was the gestational age at birth?

5:55

Were they premature? Were they term?

5:58

Um, and then postnatally, what was the delivery course?

6:01

Was there an assisted delivery?

6:03

Uh, was it a, you know, normal delivery?

6:05

Was the, uh, baby requiring res resuscitation

6:09

or support, you know, what were their AP GORE scores?

6:12

Uh, were they looking a little blue?

6:13

And then, um, afterwards, what, uh, what testing was done?

6:17

If they're in the nicu, you know, what are their labs?

6:20

Uh, what, what might that entail in terms of, you know,

6:22

metabolic disruptions and whatnot.

6:26

So let's talk a little bit about gestational age.

6:28

Um, preterm by definition,

6:30

preterm birth is anything less than, uh, 37 weeks, uh, uh,

6:35

since the last menstrual period, uh, at the time of birth.

6:38

And we round down to the last completed week.

6:40

So even 36 weeks,

6:41

six days would be considered a late preterm,

6:43

obviously very mild, right?

6:46

But now that is technically a preterm.

6:47

And so the more preterm you are,

6:49

the more immature these these structures are,

6:51

and the more likely you are to have, uh, brain injury, uh,

6:54

multi-organ injury and long-term complications.

6:57

Um, term is anything, you know, between like 37 to 41,

7:01

but full term technically is the, you know,

7:03

around the 40 week period, you could be, you know,

7:06

early term or late term.

7:08

Uh, there's also post-term, so 42 weeks or higher.

7:12

And, uh, this is also associated with complications,

7:14

you know, oligohydramnios

7:15

and placental, um, you know, degradation and so forth and,

7:19

and, uh, macro somia.

7:21

So typically they will induce, um, a pregnant lady if,

7:24

if she goes beyond, uh, 42 weeks to, to avoid that, okay?

7:29

So the term neonate, uh, officially means, uh, up to 28 days

7:33

after birth, uh, no matter gestational age.

7:36

Uh, in colloquially,

7:38

they also call this the newborn period, although that's a looser term.

7:42

Um, infant is up to 12 months, right?

7:45

The term baby is, uh, is also used generically,

7:48

but some people will use that, uh,

7:49

for a wider sprint up till they're walking.

7:51

And now, let's talk about corrected age.

7:53

So if you're preterm, right,

7:55

then you're actually gonna be behind on your milestones.

7:57

So you can't use the normal pediatric milestones like

7:59

walking, rolling, right?

8:01

Because you're actually behind.

8:02

So let's say you were born at 34 weeks, right?

8:04

So you're actually six weeks behind from a full term baby.

8:07

So you need to actually correct for

8:09

that prematurity when you look at the milestones.

8:11

So until at, you know, at birth,

8:13

they are actually negative six weeks, right?

8:16

And so not until they reach, uh, six weeks chronological age

8:19

after birth, will they actually catch up

8:21

with the full term baby in terms of milestones.

8:23

So that's the idea of corrected age for maturity. Okay?

8:27

So imaging modality. So in the neonate, um, we often start

8:31

with head ultrasound because it's, um, you know,

8:33

there's no ionizing radiation.

8:35

It's fast bedside exam.

8:36

And so, uh, they can go through various fontanelles,

8:39

which are essentially these, you know, like open, uh,

8:41

you know, non ossified, uh, fibrous things, um,

8:44

in the skull, uh, that actually the sutures

8:47

and fontanels are there

8:48

because they can mold

8:49

as the baby goes through the birth canal, right?

8:51

So you have some level of plasticity,

8:53

and then as the brain grows, it keeps the sutures open

8:55

and they start to, uh, narrow

8:57

and fuse over time, depending on age.

8:59

So the anterior fontanel actually stays open, you know,

9:02

till about 14, 18 months of age.

9:04

So obviously throughout the infancy,

9:05

you can still insensate through it.

9:07

And so you can see in the chronol

9:09

and the satchel plane, um,

9:10

the ventricles nice gray white distinction here,

9:13

the corpus callosum, uh, the cerebellum, if you're lucky

9:16

as well, we don't typically do ct, you know,

9:20

because of the ionizing radiation,

9:21

but let's say if there's a trauma, right?

9:23

Accidental or, um, non-accidental, um, any concern for, um,

9:27

you know, uh, hemorrhage for fracture, um,

9:30

rapid screening, if, uh, Mr.

9:32

Mrs not immediately available,

9:34

that might be within the risk benefit ratio.

9:36

And so here, uh, you can see that the neonates have, uh,

9:39

water your brains in adults, right?

9:40

Because they're not myelinated yet.

9:42

And so it is, uh,

9:43

a little bit more hypodense here, and that's normal.

9:46

And the overall volumes are fuller too, right?

9:48

So unlike the, the atrophy you see the adult brain, right?

9:51

You, you actually have a relatively smaller, uh,

9:54

ventricle subretinal spaces for, for much

9:56

of the infancy childhood.

9:58

Now you can have the, uh, so-called benign enlargement

10:01

of subarachnoid spaces, transiently, you know,

10:03

run nine months or so in self resolving run two

10:05

or three years, but, uh, not in the neonate.

10:07

And then you have these sutures, right?

10:09

The sutures and fontanels that I mentioned.

10:11

So these are gonna, um, gonna be pretty open and,

10:14

and maybe a little overlapping if, uh,

10:16

they had a vaginal burst, right?

10:17

Going through the canal there.

10:19

Uh, and then they, they actually narrow pretty rapidly in

10:22

the first like month or so.

10:23

So then you have like a couple millimeters,

10:24

and then they steadily, uh, narrow over time

10:26

and have different, uh, age related times of closure.

10:30

So, for example, the atopic suture in the frontier, uh,

10:33

closes earliest, uh, can be, you know, four months

10:35

or sometimes even a little bit earlier.

10:38

And then we have mr, which is really the workhorse

10:40

for all of our problem solving.

10:42

So I wanna show you this, uh,

10:43

because this is what a normal, uh,

10:46

term neonatal Mr should look like, right?

10:48

So I have these arrows here on

10:50

what are called the posterior limbs of internal capsules.

10:52

If you've got the, you know, anterior limb,

10:53

the genu posterior limb.

10:55

And so you see that that's pretty much the only part

10:58

of the neonatal brain that's myelinated, right?

10:59

Because what do you have to do when you're born?

11:01

You have to cry and reach out for mom,

11:02

and that's pretty much it.

11:04

So, uh, this T one shortening myelin is fat

11:07

and protein, right?

11:08

So you're gonna get T one bright T two dark,

11:11

uh, kind of signal here.

11:12

And so it's pretty much that, uh, posterior third

11:15

to posterior half of the ic

11:17

or the click, uh, should be myelinated.

11:19

If you're, uh, full term infant, obviously you're preterm,

11:22

it might be a little less,

11:24

but if you're not seeing it at all

11:25

or barely, then you have to be suspicious

11:26

that maybe there's something obscuring it, right?

11:28

Like, um, maybe an edema from an, uh,

11:31

hypoxic ischemic injury.

11:33

And so here, this is the,

11:34

the apparent diffusion coefficient map from the diffusion.

11:37

Um, and so there's nothing restricted

11:38

that's as it should be, right?

11:40

This is a perfusion, uh,

11:41

what we call arterial spin labeling.

11:43

And so you see that again, right?

11:45

The basal ganglia are the most robust, um,

11:48

and the cortico spinal tract.

11:49

So they have good flow

11:51

because they're actively developing as a result

11:53

because they have more flow.

11:55

Normally, if you have a hypoxic ischemic insult,

11:57

they will be selectively vulnerable to a severe, um, HII

12:02

because they are taking more blood flow baseline,

12:05

but still, the rest of the brain does have,

12:07

you know, a reasonable flow.

12:08

It's just not as much as the actively

12:10

developing myelinating areas.

12:13

So that's important too. And then Mr.

12:15

Cytoscopy another advanced tool, right?

12:17

So we can do voxels,

12:18

usually they'll do one over the basal ganglia,

12:20

like a single voxel one over the, uh, white matter.

12:23

Um, and then you can basically

12:25

get the different metabolites.

12:26

This here is a long echo MRS,

12:29

and so we're just cleaning up the baseline here,

12:31

essentially just looking at the major metabolites.

12:33

And so again, in contradistinction to adults where they have

12:37

that hunter angle that's supposed to go up, right?

12:39

So your NAA from your neurons is higher than your

12:42

choline from your cell membranes.

12:43

Well, the infants are still, you know,

12:46

they have some anaerobic metabolism, even more

12:48

of their preterm, but basically at term age, right?

12:51

They still are undergoing a combination

12:53

of aerobic and anaerobic.

12:55

So the NAAP, uh, area under the curve of the NAA peak,

12:58

right, is around like two thirds of the choline.

13:01

And that's actually normal to have that slight down slope.

13:03

They can have a little bit of lactate

13:04

and lipid again, because of that.

13:06

Um, some of that physiologic immature in heric metabolism.

13:09

So that's actually what a normal MRS looks like,

13:12

and that'll be important for us later on.

13:15

Okay? So MRI considerations, um, in babies, right?

13:18

You, they have to be stable

13:19

before they can go down for MR mri.

13:21

So if they're, you know, difficult delivery,

13:22

they have all this like support devices

13:24

that are MRI incompatible, uh, maybe they're preterm

13:27

and they have this, you know, huge surface area

13:29

to volume ratio, so they're losing heat, right?

13:31

So you need to incubate them.

13:33

Uh, they also sometimes like

13:35

to move like any patient, right?

13:36

So you might have to do the so-called

13:38

feed and swaddle, right?

13:39

So that they get postprandial,

13:40

and then you can like wrap 'em up real tight.

13:42

Um, sometimes if they're still moving,

13:44

and it's important that you get that detail, you might need

13:46

to do sedation or even, um, general anesthesia depending on

13:49

how suspicious you are.

13:50

Obviously, we don't love to give general anesthesia, uh,

13:54

to kids below two or three years of age, uh,

13:56

because there's some literature showing

13:58

that there's long-term, uh,

13:59

neurodevelopmental effects, right?

14:01

But again, it's all about the risk benefit ratio, okay?

14:04

So then imaging wise, right?

14:06

You have to decide what kind

14:07

of scanner you you wanna use, right?

14:09

The standard ones are three T and 1.5 T, of course.

14:12

Uh, and three T gives you much nicer brain detail.

14:15

You can do more, uh, with the advanced imaging.

14:17

Uh, but there are a number of emerging platforms, low field,

14:21

more accessible, mrs.

14:22

Uh, which, uh, slightly, slightly, uh, lower image quality,

14:26

uh, less capability for advanced imaging.

14:28

Uh, but some of these are self shielded, right?

14:30

So they can actually be on the floor, uh,

14:32

in the nicu, right?

14:33

And, um, even if they have some lines

14:35

and tubes, they may still be, um, safe enough to not,

14:38

you know, deviate within the scanner.

14:40

But obviously you, you need to, uh, work

14:42

with your MRI safety people and do testing and all of this

14:45

because, uh, these are more non-standard devices.

14:47

But the idea is that if you're not sta,

14:48

the baby's not stable enough

14:50

to be taken all the way down to radiology.

14:51

And MRI, some of these units are kind of more point of care

14:55

and may allow for, for more, uh, real time scanning.

14:59

Um, and then obviously devices, if they have support lines

15:02

and things like ECMO is a big no-no, right?

15:04

You have a lot of deviation in the, in the vessel and stuff.

15:07

Uh, but some of the other lines

15:09

and tubes, depending on, uh, screening

15:11

and compatibility, you know,

15:12

gold EG leads can be scanned, uh, in MR mri.

15:15

So, uh, it just depends on what they have

15:17

and whether those things can be taken out

15:19

or switched out for MRI compatible or conditional ones.

15:22

And then what sequences are you just doing like a basic

15:24

screening and rule out, uh,

15:26

or are you're looking for high level migrational anomalies

15:29

and that you need like, that really good, uh,

15:31

good advanced imaging.

15:33

You wanna run some advanced sequences.

15:35

So again, that all kind of relates back to sedation,

15:37

anesthesia, and then contrast again,

15:40

like a gadolinium deposition in children,

15:42

even the macrocyclic agents have a little bit of that,

15:44

and the babies have a very

15:46

immature blood brain barrier, right?

15:47

So we don't know what the long-term effects are.

15:49

So typically we are not gonna give contrast

15:51

unless there's a tumor or infection, uh, concern, right?

15:54

And then of course, in those cases,

15:56

you can, um, and then timing.

15:58

So that's the kind of the biggest pitfall, right?

16:00

Is that the, the findings

16:02

of the neonatal brain imaging depend very much on the timing

16:06

after birth or after the insult.

16:08

So, um, some places, uh,

16:10

not too many a minority do immediate imaging within the

16:13

first one or two days after birth.

16:15

The reason that a lot of places don't do this is

16:17

because I'll get to it later,

16:18

but, uh, they often will do cooling

16:20

or other, you know, uh, supportive therapies.

16:22

And so that kind of gets the baby outta circulation

16:24

for MRI compatibility.

16:26

So, uh, there are places that do early scans, uh,

16:29

within the first, let's say three to five days.

16:31

There are places that do later scans within the first,

16:34

like one or two plus weeks, right?

16:36

Or at the time of discharge, some do both.

16:39

Uh, and then of course, follow up

16:41

after discharge when the, when the, uh, baby's older.

16:45

And, uh, each of these has pros and cons, right?

16:47

So it's actually incredibly heterogeneous practice

16:50

variations across the country and across the world.

16:53

And so I'm gonna just talk about all

16:54

of the different possibilities, kind of at a high level.

16:57

Um, but if you look at, uh, the major, um, you know,

17:01

clinical trials and, uh, landmark publications, most

17:03

of them are talking about either early and or late imaging

17:05

and comparing the two, okay?

17:08

So normal myelination, we have to know about normal

17:10

before we can diagnose a abnormal.

17:12

So I talked about this a little bit in that other slide,

17:14

but essentially myelination happens starting in the fifth,

17:17

about the fifth fetal month.

17:18

Um, and it starts in the peripheral nervous system,

17:20

and then it goes, um, in kind of, um, stereotype direction.

17:24

So it'll actually, uh, go up from inferior disappear.

17:26

So it will go from the peripheral

17:28

to the spinal cord brainstem, right?

17:30

Brainstem, cerebellum, and then starts to get into, uh,

17:33

the sial chest at the time of birth.

17:35

It tends to go from central to peripheral, right?

17:38

And then also generally speaking, posterior to anterior, uh,

17:41

so that the frontal lobes, the executive areas,

17:43

myelinate last, but also the eloquent

17:45

tracts will myelinate earlier.

17:47

So, like I said, those corticospinal tracts and,

17:49

and the, the clicks, um,

17:50

visual cortex sensor motor cortex areas

17:53

that you really need to use, right?

17:54

The babies are gonna mature those faster.

17:57

Um, and so myelin is fat and protein, right?

18:00

So again, at birth, right, you just have the clicks

18:02

that are involved, T one bright, T two dark,

18:04

and then over time.

18:07

So by, uh, there's a saying T one at one,

18:10

T two at two, right?

18:11

So the idea is that by one year

18:13

of H you have essentially inverted the contrast.

18:16

So you have enough male island on board

18:17

to have white matter being white, uh, on the T one,

18:21

just like you'd seen an adult,

18:22

even though it's not complete yet.

18:24

And then it takes another year.

18:25

So about two years of age where you actually get the,

18:28

the full, uh, T two hypo, uh, intensity out

18:31

to the periphery, uh, to have the kind of adult pattern.

18:34

So you can date, you know, myelination on T one up

18:37

to one year of age, and then T two up to two,

18:39

assuming they don't have some kind of genetic or epilepsy

18:41

or something that would slow myelination, um, flare.

18:46

So that's kind of like macroscopic suppression of fluid.

18:48

And so when you have intra myelin edema

18:51

that you're looking at, so the why is it T two dark?

18:53

Basically you're forcing out as you, my,

18:55

you force out the free water between the layers

18:57

of the myelin sheet, so it looks dark on T two.

19:00

Um, but flares looking more like

19:02

macroscopic collections, right?

19:04

So the picture is actually very confusing in

19:07

neonates in young children.

19:08

And so, um,

19:10

I can always tell if a place is like a serious children's

19:12

hospital by whether they ran flare on kids less than two

19:15

or three years of age, it's just not helpful.

19:17

Um, in most cases, maybe like tumor infection, if you wanted

19:20

to do a post contrast flare to look at, you know,

19:22

superimposed edema, leptin, menal disease.

19:24

But in general, like doing a pre contrast flare in young

19:28

children really, uh, is, is kind of a waste

19:30

and can actually cause more confusion.

19:34

Okay? So let's go into classic cases.

19:36

So, uh, preterm, so preterm brain injury.

19:39

So there's a couple classifications

19:42

of preterm birth clinically, so indicated as an iatrogenic.

19:45

So the mom had preeclampsia, right?

19:47

There was, um, you know, rupture of memories or something.

19:50

And basically the, the, the child has to be delivered.

19:52

There's no choice otherwise to keep them, you know,

19:55

in utero would cause more harm.

19:56

And then there are spontaneous ones, right?

19:59

So, um, for whatever reason, genetic

20:00

or some environmental thing, you know, maybe lifestyle

20:03

with smoking, whatever, uh, for whatever reason,

20:06

the preterm birth just starts spontaneously.

20:08

And it's really a cascade of vascular and

20:10

or inflammatory factors that leads to this

20:12

that we're still really trying to understand better.

20:15

Um, and the problem of course, with preterm birth is

20:17

that you have many immature organ systems.

20:19

The neuroglial precursors are all immature.

20:21

Birth is a traumatic event going from in utero to ex utero.

20:24

And so you have these, you know, fryable vessels

20:27

and other things that are being damaged

20:29

with the primary insult,

20:30

and then also secondary and tertiary, right?

20:32

So you're getting ongoing destruction cycle

20:35

and then long-term dis maturation, um, therapy.

20:40

So they have tocolytic to try to slow down delivery.

20:42

And then just things to help decrease inflammation,

20:45

reduce infection, keep the, you know, uh, small,

20:49

small child warm, um, keep them ventilated, right?

20:52

And then the big one for preterm is this kangaroo care,

20:55

which is, you know, what's kangaroo care?

20:57

So it's basically like skin to skin contact

20:59

between the mother and the baby.

21:00

So it helps both of them, right?

21:01

It helps with the bonding, it helps with like microbiome

21:05

and, you know, breast milk and stuff.

21:06

So that the, the, this neonate is getting like the,

21:10

you know, a lot of the kind

21:11

of protective factors from the mother

21:12

that they have lost from,

21:14

from being the preterm birth and so forth.

21:16

So the idea is like, like this tree kangaroo, right?

21:18

Is that basically, you know, if you,

21:20

if you look at a newborn,

21:21

kangaroo is this tiny pink hairless thing,

21:23

and it has to crawl its way up to the pouch

21:25

and like find the, find the tet.

21:27

So, you know, honestly, like humans have it a lot easier

21:30

'cause we have all this exogenous support,

21:32

but yeah, that's the idea, right?

21:33

So basically it has to sit in there and mature

21:34

and have skin to skin contact, okay?

21:37

So, uh, preterm brain injuring, um, imaging.

21:40

Uh, so the, they're gonna have an immature brain, right?

21:44

So less ated, less myelinated than a term, uh, infant.

21:47

Um, there's certain characteristic patterns we see

21:50

with preterm brain, the white matter injury, right?

21:53

Because the white matter is still, uh, developing.

21:55

You can have punctate lesions, punctate white mi lesions.

21:58

You can have diffuse, um, excessive, uh,

22:00

T two hyperintense signal, just like all the white matters,

22:03

kinda a little bit of dus.

22:04

Uh, you can have the so-called paraventricular leia

22:07

where you actually get cystic degeneration, um,

22:09

in these watershed areas around the medullary veins

22:12

that are draining, um, intraventricular hemorrhage.

22:15

So this is the pepe, you know,

22:16

classic ultrasound classification.

22:18

And what I wanted to point out about the IVH grading one

22:21

to four is that it's actually a progression, right?

22:23

So you have the, the, uh, germinal matrix, the, um,

22:27

gives rise, it matures and migrates, right?

22:29

And forms your, uh, neuroglial structures.

22:31

But, uh, it involutes uh, it migrates

22:34

and involutes by like 35 weeks, right?

22:37

So basically the last place at it invol is

22:40

the co thalamic groove.

22:41

And so in a mild preterm birth, right, that's

22:44

what you might just see the grade one

22:45

hemorrhage in the co thalamic groove.

22:47

Um, grade two is when you actually have

22:49

intraventricular hemorrhage.

22:50

It could be some layering blood products,

22:51

or it could just be some, a penal, uh, hemosiderin staining.

22:55

The, uh, the lining if it's already resorbed.

22:58

Uh, grade three is when you have ventricular magaly, right?

23:00

So now you're actually clogging some of the outflow tracks,

23:03

so you're actually getting some hydrocephalus.

23:05

And then grade four, um,

23:06

they talk about parenchymal involvement,

23:08

but it's not just any parenchymal involvement.

23:10

'cause some of that could be white matter

23:11

injury, but it's distal.

23:12

It's the idea that the, the clot is actually occluding,

23:16

the medullary venous drainage enough

23:18

that you're getting a medullary venous arm infarct

23:20

around the periventricular white matter.

23:22

So it's a direct result of having clot,

23:24

like clogging the drainage pathway.

23:26

So it's actually a progression.

23:28

I'll show you examples of that.

23:30

And then cerebellar hemorrhage often under recognized.

23:32

But, uh, really important

23:33

because preterm birth really has a lot

23:35

of long-term cognitive effects.

23:36

And we've come to understand in, in last, uh, decade

23:40

or so, that the cerebellum is not just

23:42

responsible for balance, right?

23:43

There's a lot of like higher level

23:45

of cognitive executive function.

23:47

And so that, that relates again, to

23:49

that kinda long-term

23:50

neurocognitive effects of preterm birth.

23:52

And so there are, uh, infra editorial, uh,

23:55

external granule cells, which are kind of the analogs

23:57

of the germinal matrix that are migrating out

23:58

and those that are also susceptible to injury.

24:01

Okay? So timing people do not recommend MR for early,

24:05

you know, preterm birth

24:06

because like, you know, it's gonna be abnormal,

24:08

it's gonna have some of these findings.

24:10

So ultrasound for screening is fine.

24:12

And then if you see something, uh, you know,

24:14

fluidly abnormal, you can get an MR to confirm.

24:17

But again, that just kind of tells you what etiology,

24:18

you know, it's gonna be abnormal if they're premature, uh,

24:22

the term equivalent, you know?

24:23

So basically once their corrected age is like 40 weeks, like

24:26

before they're about to be discharged

24:28

and they're stable, that's been much more successful in the

24:30

literature for predicting long-term outcome

24:32

because you're looking at the complications

24:34

of the original insult and it's better for prognostication.

24:37

So, and they're gonna be more stable for mentioning as well.

24:39

So if you had to choose on generally speaking, it's better

24:42

to do term equivalent.

24:44

Uh, you can do early,

24:45

but again, that's more for just, uh, understanding, okay?

24:48

So preterm ultrasound, uh, has, you know,

24:51

different manifestations, right?

24:52

So you can have some of this kinda

24:54

what periventricular white matter injury.

24:57

You could have this grade three IV H with the coto thalamic,

25:00

you know, an intraventricular hemorrhage and hydrocephalus.

25:02

And you see that echogenic kind of debris

25:04

along the ventricles.

25:06

So normal germinal matrix can also be echogenic,

25:08

but it's very well defined and curve.

25:09

And you're, you're not gonna get that extra

25:11

debris and distension.

25:12

And here's a grade four intraventricular hemorrhage.

25:15

So now you have so much, uh, clot, right?

25:17

Asymmetric here that it's actually plugged up the met vein.

25:20

So you have this radiating per

25:22

ventricular hemorrhagic infarct.

25:23

So, um, the ultrasound echogenicity is tricky

25:27

'cause it can be like a little bit of white matter injury.

25:29

It can be some mineralization, it can be hemorrhage, right?

25:31

So be a little careful because many things can look

25:33

echogenic, right?

25:34

But it's really looking at the secondary signs as well.

25:37

And you see that all of these have like this kind

25:39

of an immature ation pattern, right?

25:41

Of the preterm infant as well. Okay?

25:44

So at um, at Mr right, uh,

25:46

preterm interventricular hemorrhage, so this is

25:48

that grade one Cato thalamic groove grade

25:51

two in the ventral clinic.

25:52

You see, it's not just that layering,

25:53

but you see that on T two

25:55

or susceptibility, you see that kind

25:56

of like dark line, right?

25:58

That shows that you had hemorrhage,

25:59

even if it's completely resorbed,

26:01

you can still see that cirrhosis.

26:03

Here's grade three with some distension and shunting,

26:06

and then here's that grade four

26:07

where you're clogging up the ventricles,

26:08

and now you have that peri ventricular hemorrhagic, uh,

26:10

venous infarct, and then the late complications, right?

26:14

So this doesn't just stay like this, right?

26:16

Basically involutes

26:17

and, uh, the term porn cephalic, it's a white matter,

26:20

you know, relatively clean line cyst

26:22

because again, in neonates they have very immature, uh,

26:25

glymphatic system.

26:26

So the astrocytes are these glial cells that cause

26:29

astro gliosis, right?

26:30

So the scarring after injury.

26:33

And so those things are not mature

26:34

until the first couple years of life.

26:36

So when you get an injury like this as opposed to an adult,

26:38

it can be a very clean cavity.

26:39

And so that's porn cephalic.

26:41

So basically these things can, um, can involute,

26:44

you can have cirrhosis,

26:45

you can have trans mantle porn cephalic, essentially, so

26:48

that you have almost no residual cortical mantle.

26:50

And then you can have the dreaded complication,

26:52

which you see in many preterm infants

26:54

of the post hemorrhagic hydrocephalus.

26:56

You get all these adhesions, he post hemorrhagic adhesions

26:59

and isolation of the ventricles,

27:01

and it becomes very difficult to manage their hydrocephalus

27:04

because you have so many different loculation in here,

27:08

the white matter injury, um, so early.

27:11

So again, like, uh, there's,

27:13

there's obviously intraventricular hemorrhage board here,

27:15

but you see these separate areas of like little hemorrhagic,

27:18

and these are not next to the ventricle.

27:19

They're not caused by clot, right?

27:21

So these are actually separate areas of white matter injury

27:24

with blood fluid levels with this T one shortening

27:27

of dys myelination, um, cystic, you know, and,

27:31

and so these little areas, right?

27:32

So in the watery brain, it's gonna be baseline white matter,

27:36

uh, is is unmyelinated.

27:38

So it's gonna be T one dark T two bright, right? Emus brain.

27:42

And so on that background, you can see little areas

27:45

of white matter injury or dys myelination with this kind

27:47

of exci toxic insult, right?

27:49

Mineralization with this T one bright T two dark signal.

27:54

And the T two stuff is kind of more variable.

27:57

'cause um, you already, it's kind of already watery,

27:59

so it can be a little hard tell,

28:00

but the T one can actually be very, very helpful.

28:04

Um, and then late findings.

28:05

So if you just see this kind of like patchy, you know, uh,

28:08

periventricular white matter stuff,

28:10

and there's volume loss, right?

28:12

You suspect, right? Even if this is an adult, right?

28:14

And you're reading it that you suspect that they had some,

28:16

uh, preterm, uh, white matter injury.

28:19

Uh, when it's more profound,

28:20

they actually have this angular morphology.

28:22

It's the draining medullary vein.

28:24

So they kinda have this, uh, triangular shape to them

28:27

of the watershed, and then angular

28:29

exo dilation of the ventricles.

28:31

And here's the cystic periventricular lmia.

28:33

So actually cavitating now,

28:34

but again, that kind of para ventricular watershed.

28:37

And then here's one with like porn celi and adhesions,

28:39

and very, very thin cortical mantle.

28:41

A lot of, uh, white matter predominant volume loss.

28:46

All right? And then we have cerebellar hemorrhage.

28:48

So, uh, again, this can be on T two or susceptibility,

28:51

but you see these areas of, you know, dark signal

28:54

and you can have like a few foci, uh, or several

28:57

or even like diffuse threat, the cerebellum leading to,

29:00

you know, hemorrhagic infarct and hypoplasia and so forth.

29:04

Uh, so in the long term, so this is a ultrasound here,

29:06

you can actually see this, uh,

29:07

dinky little dinky little cerebellum.

29:09

And same thing on Mr. Here, right?

29:10

So it can be very, um, hypoplastic, uh,

29:14

because it's basically an acquired

29:16

insult as they're developing.

29:17

You can even have, uh, hypoplasia dysplasia

29:20

and cerebellar cluster, right?

29:21

So these were basically areas of injury, um, of hemorrhage.

29:24

And then the, the cerebellum,

29:26

which actually develops quite a bit postnatally in the

29:29

first, like two or three years of life will,

29:31

will foliate abnormally

29:32

around these areas of acquired injury.

29:36

Okay? So moving on to term brain injury.

29:38

Uh, so the physiology here, so again, there's

29:41

that primary secondary, tertiary insult,

29:43

but now it's kind of like directly related

29:45

to the delivery, right?

29:46

So before, right, the preterm, like some of

29:48

that stuff we couldn't control

29:49

because it might have been endogenous or, or the,

29:52

and the birth had to happen anyway.

29:54

Uh, but with the term, it's basically like you have some

29:56

kind of insult at the time of birth, around the time

29:58

of birth, the difficult delivery usually.

30:00

So we're, we're assuming that

30:01

that insult happened pretty much, you know, at that time.

30:04

So that initial insult could have been

30:06

hypoxic and or ischemic, right?

30:07

It could have been, um, the baby didn't get enough,

30:10

you know, good breasts, um, placental abruption, you know,

30:13

the cord, uh, ucoc cord,

30:17

um, anemia, right?

30:19

Maternal or fetal, right? So lots of different etiologies,

30:22

placental, you know, thromboemboli.

30:26

Uh, but it's not just that primary insult, right?

30:28

The secondary energy failure.

30:29

So this initial insult actually induces a whole metabolic,

30:33

pro-inflammatory cascade,

30:35

and that causes additional injury on top

30:37

of the primary insult.

30:39

And the brain essentially fails to autoregulate, you know,

30:41

they're, they're newborns, right?

30:43

So they don't have the most mature cerebral autoregulation.

30:45

Um, and so in many times you can actually get

30:48

a rebound hyperperfusion.

30:49

So initially you've got low flow, right from

30:52

that initial HIE and then HII,

30:56

and then, um, the brain will respond

30:58

and maybe overcorrect, right?

31:00

And so basically more blood flow comes in,

31:01

but that actually leads to all this like free radicals

31:04

and apoptosis

31:05

and all sorts of, uh, negative, uh, negative kind of, um,

31:09

feedback loops that that lead

31:11

to essentially a lot more injury than

31:13

just the initial insult.

31:15

And then, uh, long term, right?

31:17

Months to years, you can have chronic ongoing injury from,

31:20

from this process.

31:22

So we wanna kind of blunt that.

31:23

And so the, the, the really only scientifically proven, um,

31:28

there are a number of adjuvants you can do, but,

31:30

but they don't necessarily provide added.

31:32

They may minimize, they may decrease hospital stay,

31:35

but the overall outcomes don't really change on, on top

31:38

of this therapeutic hypothermia.

31:40

So the idea is that there's this window

31:42

for the secondary energy failure over the first six hours

31:44

after the birth that you can actually blunt this response.

31:47

And how do you do that? You, you cool the baby down, right?

31:50

From like 36, 37, you cool 'em down

31:52

to 33, 34 degrees Celsius for three, for three days.

31:56

And so you blunt that like hyperperfusion response, right?

31:59

So that you're not delivering the free radicals

32:01

and all this blood and inflammation to the RD damage brain.

32:05

So you minimize that, essentially

32:06

that secondary energy failure.

32:08

And then after that, you gradually rewarm them

32:10

back to normal temperature.

32:12

And so, because most MRI, uh, cooling, uh, sorry, uh,

32:15

most cooling systems are not MRI compatible,

32:18

this limits a lot of centers from doing the earlier imaging,

32:21

but as I said, right, you,

32:22

the immediate imaging is actually not as helpful as,

32:25

you know, like three to five days out.

32:26

So usually after rewarming and stabilization.

32:30

So, you know, around day four, if it's,

32:34

if you're really on the ball,

32:35

or maybe five to seven, if, if it takes some time,

32:38

is when you see the majority of post cooling HIE pa uh,

32:42

infants at most centers.

32:44

And, uh, that's, that's

32:46

what I think we're gonna show the most examples of.

32:49

So there's this little, um, uh, you know,

32:51

the vanilla ice I think was hot when I was growing up,

32:54

so I'm dating myself now, but he had a song, ice, ice baby.

32:57

But, uh, in, in the modern day, it probably is more useful

33:00

to, uh, to, to apply to this therapeutic hypothermia.

33:05

So basically they just wrap them in a, a blanket, right?

33:07

And they cool them and they pass the cooling fluid

33:10

constantly through their, their body and also their head.

33:13

Okay? So term brain imaging, uh,

33:16

there are multiple patterns described.

33:17

So it, it depends on the duration, severity of the imaging.

33:21

So you might have just like a few little, you know,

33:24

embolic things or whatever, writes a little punt injury.

33:27

But the two most common are the

33:28

watershed and the central patterns.

33:30

So watershed is just like adults, right?

33:32

It's between like A-C-A-M-C, A PCA

33:34

or the internal, like the recurrent artery of hubner

33:37

and the, you know, lenticular, trites and whatnot.

33:39

Um, posterior choroidal.

33:40

So, um, so those are like more border zone,

33:43

mostly white matter, uh, kind of pattern.

33:46

And that's what you see with your partial asphyxia, right?

33:50

So like, not total, but like partial, like usually shorter,

33:54

but could be prolonged, but still, like they,

33:56

they had some oxygen but it was reduced, right?

33:59

And the central pattern, that's when you

34:00

have like severe, right?

34:01

So, so if you have like a complete anoxia,

34:04

severe prolonged, right?

34:05

Then now the most metabolically active structures

34:08

that are selectively vulnerable, right?

34:09

The basal ganglia phite,

34:11

the cortico spinal tracts, the hippo camp I, right?

34:13

Those, the, the ones that require the most oxygen

34:16

and blood flow are gonna be selectively hit

34:18

because you have a complete anoxic situation.

34:21

Uh, there's also infant injury,

34:23

which is usually underestimated,

34:24

and that's typically seen with advanced cases.

34:25

And then you could have just diffuse.

34:26

So global injury, okay? So timing wise, right?

34:31

Uh, just like in adult stroke, right, the diffusion

34:34

will peak, you know, usually like two to three days after,

34:38

but it, you know, anywhere from one to four

34:39

as you get toward a week, right?

34:42

You start to have pseudo normalization

34:43

because the restricted diffusion in the swollen dying cell

34:47

membranes, the cell remains licensed.

34:48

So they release the edema into the, you know, uh,

34:50

interstitial space.

34:51

And so you get that, uh, pseudo normalization of the A DC.

34:54

So then after that you can't really use this.

34:57

So you can use the other things like I mentioned the T one

34:59

that dys myelination, um, on the watery brain background

35:02

that T one hyperintensity is helpful, often edema on top

35:07

of an already watery brain is hard to appreciate.

35:09

So it's pretty hard in many cases to see the T two

35:12

unless it's in a like myelinate area, like the clicks.

35:15

So that's usually more helpful late when you start

35:17

to see like the ence laia or the gliosis or whatever.

35:20

So it starts to present, uh, more in the late period.

35:23

Uh, but you can see it's very dependent on

35:25

kind of physiology and timing.

35:26

And then you can also do perfusion to look

35:29

that hyperperfusion response and metabolism.

35:33

Okay? So, um, HIE uh, ultrasounds can have a, a variety of,

35:37

uh, appearances, right?

35:38

So here's some kind of, you see that gray white interface

35:41

that's kind of blurred and you've got slit ventricles.

35:43

So this is a diffusely edematous brain,

35:45

but the location's pretty good 'cause we're now term, right?

35:48

Here's one of the central injuries.

35:49

So very echogenic basal ganglia compared

35:51

to like the white matter.

35:53

And then here's another one

35:54

where you actually have almost like a super scan.

35:57

So like you have diffuse kinda white matter injury here, uh,

36:01

and then it's actually kind of exaggerated contrast

36:04

with the, the more ous gray matter.

36:06

So you can have either decreased or increased contrast,

36:09

but both are abnormal, right?

36:11

And obviously you have to correct for ultrasound

36:12

artifacts and gain and things.

36:14

But again, like I think the clinical picture

36:15

and then being able to really look at

36:17

that gray white distinction and so forth is helpful.

36:20

Okay? So watershed

36:21

injury, you know, just like adults, right?

36:22

So these kinda like A-C-A-M-C-A PCA border zones, right?

36:25

So the cortex, the white matter kind

36:27

of paralleling the lateral ventricles

36:29

here, restricted diffusion.

36:31

You can see that the, the T two is, is sort of appreciable,

36:34

uh, edema on top of an already watery brain,

36:36

but it's not as easy to appreciate.

36:39

So having, it's all about timing, right?

36:42

Um, and then late, so this is called EULA gyre.

36:44

So, uh, the medullary arteries are penetrating in, uh,

36:48

to the, uh, you know, to these kind of like deep, deep sci.

36:52

And so it's kind of a watershed area if, if you're getting

36:55

that, um, uh, you know, low flow, uh, from cerebral artery.

36:59

So basically you get the selective kind of injury

37:01

to the deep ssci with relative span of surface gyre.

37:04

So it's like, uh, Latin for mushroom gyre.

37:07

And so we're not talking like your American mushrooms.

37:09

It's like not, not the straw mushrooms.

37:10

It's like those Asian oyster mushrooms

37:12

that have like really long stems and like tiny little tops.

37:15

So that's what this eulogy is.

37:17

And this is, this is a risk factor

37:18

for seizures, for example.

37:20

So you can see the border zone appearance, uh,

37:23

on follow-up can be, uh, bilateral,

37:25

but it can also often be asymmetric, right?

37:28

So these, all of these cases, uh, uh, have some level

37:31

of asymmetry, but there is actually bilateral

37:32

involvement watershed.

37:34

And this is, this just shows you that, you know,

37:36

although watershed injuries usually partial hypoxia

37:39

of its prolonged, you actually have pretty severe

37:41

sequelae, okay?

37:43

The central injury here, uh, so this is, uh, the a DC,

37:47

and you're seeing the restriction in

37:48

these critical areas, right?

37:49

High flow areas. So the corticospinal tracts,

37:52

the basal ganglia, um, classically the areas

37:55

that are selectively vulnerable

37:56

and the term infant are gonna be the, um, the, uh,

38:00

posterior pertamina right here.

38:01

And then the, uh, ventral lateral thalami.

38:03

So like these part of the thalami.

38:04

So when you see that pattern, that's pretty specific

38:07

for term HIE.

38:09

And so here, this is a little tricky,

38:11

but see, uh, the clicks, uh,

38:14

they're a little bit like, they're a little bit faded.

38:16

You're not seeing that T two darkness

38:17

for like a third to a half of it.

38:19

It's kind of blurred out.

38:20

There's maybe a little bit too much edema here.

38:22

And then the vent later thal line,

38:24

the posterior perin are actually a bit too T one, right?

38:27

So they're approaching the level of the clicks, right?

38:30

So something's not quite right in this whole central area.

38:33

And then the a SL perfusion just said that we, we have, uh,

38:36

re like essentially a reactive hyperperfusion in those same

38:39

injured areas because basically they have the ischemia,

38:41

now they're trying to rebound, but you see

38:43

that they're actually stealing

38:44

blood from the rest of the brain.

38:45

The rest of the brain has pretty slow flow,

38:47

and you have excessive profusion to these injured areas.

38:49

So that's that secondary energy failure,

38:51

and it steals from the rest of the brain.

38:52

And that's what we're trying to blunt with the cooling.

38:56

So late findings, so here you see the cystic degeneration.

38:59

So now, like very, very bright, uh, posterior pertamina

39:02

and ventral later th with some cystic degeneration,

39:05

very specific for, uh, neonatal HIE.

39:07

And then here, uh, this is older, uh, patient,

39:10

but you see again that posterior

39:11

pertamina ventral later thalami.

39:13

So if you see this in an adult or an older child

39:16

or whatever, and there's no history you can call it, right?

39:18

Because nothing else does this.

39:20

Um, and you can have as asymmetric, right?

39:22

So hemiplegia, uh,

39:24

you can have asymmetric central injury as well.

39:25

So this person, you know, uh, right hemisphere involvement,

39:28

they're gonna have more left sided symptoms, okay?

39:32

You can have large, uh, large artery infarcts,

39:34

uh, in term babies.

39:36

Um, it's not too common,

39:38

not like adults, right, who have strokes all the time.

39:40

But again, on the MCA stroke,

39:42

on the ultrasound restricted diffusion edema, again,

39:45

edema on top of a watery brain can be

39:46

hard to see if it's more subtle.

39:48

Um, interestingly, we usually don't find a, a clot, right?

39:52

Like there's nothing for neural IR to do.

39:54

It's usually the theory is

39:55

that maybe there's some placental emboli,

39:57

they kinda like flicked off and occluded

39:59

and then they kind of cleared out.

40:00

So we usually don't find the actual clot,

40:02

but you see there's restricted diffusion,

40:03

but on the a SL, there's actually a, a luxury perfusion.

40:07

And that MCs actually more hyperemic.

40:09

So again, that's that secondary energy failure.

40:11

So that's flooding the area with free radicals

40:13

and causing additional injury on top

40:15

of the original ischemia.

40:17

And so again, in the late phase, you can get, you know,

40:19

porn cephalic and eulogy in those mc distributions.

40:22

And so again, if you're seeing eulogy, that's pretty,

40:25

that's quite specific, that pattern.

40:27

Uh, those mushroom gyri

40:28

or cystic porn cephalic, it means

40:30

that they had a pretty early insult,

40:32

not necessarily perinatal,

40:33

but at least in the, you know,

40:35

first one max two years of life, right?

40:37

When they didn't have mature astrocytes.

40:39

So you can, you can, again, you can call it,

40:41

this is not an adult mc in far, this is definitely,

40:43

even if you had no priors,

40:45

you'd know this was earlier in life and then global injury.

40:49

Um, so, uh, these are tricky, right?

40:52

Because, uh, this, uh, here are some cases

40:54

where I think they were out outside the hypothermic window,

40:56

like they got transferred in, it was more than six hours.

40:59

So there was no point in starting the hypo in this

41:01

heart, starting the cooling.

41:03

But you do see there's some restricted diffusion centrally,

41:05

but there's some little spots peripherally too.

41:07

This is a little too emini.

41:08

And then you're losing the clicks, you're getting

41:10

that bright basal ganglia.

41:12

Too much edema here. So in follow up,

41:14

it's actually bloomed, right?

41:16

So this was like one or two days, this was five days.

41:19

And so you see that doing it too early, right?

41:21

Doing the imaging too early can actually really

41:23

underestimate the degree of, of, uh, end stage injury.

41:26

So here, yes, there's a central pattern,

41:28

but there's really diffuse diffusion restriction,

41:30

profound vasso ga and really diffuse edema.

41:32

You lose that gray white distinction.

41:34

Here's another example with a SL.

41:36

So again, you see some central restriction,

41:37

but it's a little too emus out here as well.

41:40

So it's really both central and peripheral patterns.

41:43

You see that rebound hyperperfusion

41:44

of the injured basal ganglia,

41:46

and then it's stealing from the surrounding brain,

41:48

you're losing the clicks.

41:50

And then here, uh, so you know, at day four or five, right?

41:53

You have profound blooms. So the entire brain is restricted.

41:57

The profusion actually is,

41:58

is more consistent between the two.

41:59

So it's been a better prognostic factor, right?

42:01

So you're still getting a, a ton

42:03

of rebound hyperperfusion, right?

42:05

Um, and, and then in the end stage, right,

42:07

you essentially have this like cystic HIE, right?

42:09

Very swollen and it all shrinks down.

42:13

So diffusion pitfalls, uh, just like in adults, right?

42:16

If you're not doing in the first like few days,

42:18

which often happens because you're cooling them and stuff,

42:21

or they're not stable, then

42:23

it could pseudo normalize, right?

42:24

So pseudo normalization, um, happens like around a week.

42:28

Uh, so timing is one thing. Also the gradient.

42:31

So what we call the B value, the gradient strength.

42:34

So babies are, are, uh, less an isotropic

42:37

'cause they're not myelinated, right?

42:39

So in adults, we typically do B of a thousand as a standard.

42:42

Uh, but in kids we often do B value seven or 800

42:46

because they're more watery, right?

42:47

There's nothing to measure. Um, you can go higher.

42:50

You could go to like, let's say B of 2000

42:52

and you could exaggerate the contrast,

42:54

but you could also over call, right?

42:56

Because you might be exaggerating the

42:57

normal physiologic contrast.

42:59

And if you're not familiar with that appearance,

43:00

you might over call, um, ischemia.

43:03

Uh, and you can also do synthetic gradients.

43:05

So I, I recommend that honestly,

43:06

because if you already have like two, two B value zero

43:09

and let's say 800, you can,

43:10

you can essentially generate other synthetic ones.

43:13

If you wanna just exaggerate contrast without trying

43:15

to overcall temperature's also an issue, right?

43:17

Because, uh, water molecules diffuse more slowly

43:21

at lower temperatures, right?

43:22

And more fast. So if you're cooling, you're gonna again, uh,

43:26

potentially overestimate the level of restriction.

43:28

And then as you rewarm

43:30

that pseudo normalization may actually be

43:31

stretched out in terms of time.

43:33

Um, so these were all kind

43:35

of like in the middle time period, like maybe like

43:38

around five to seven days where we did diffusion.

43:41

And as you can see, this one has only one spot,

43:43

but it was a moderate HII, it's just that, uh, a lot

43:46

of it had pseudo normalized by then.

43:48

This was a MCA large, uh, large vessel occlusion,

43:51

but only the lenticular trites are

43:53

like, you know, fully restricted.

43:54

The rest was partially pseudo normalized.

43:56

And then these areas again.

43:57

So, uh, if it's a severe insult, right, moderate

44:00

or severe, you have ongoing injury at day five to seven,

44:03

that's pretty, that's pretty bad, right?

44:04

Because normally the diffusion stuff comes down

44:07

and starts to pseudo normalize after four days.

44:09

So if you're still seeing diffusion restriction,

44:11

even if you're only seeing like a little spot,

44:13

but the fact that you're seeing it later on means

44:16

that you're probably dealing with a more serious insult,

44:18

if that makes sense.

44:21

Okay? And then, uh, spectroscopy.

44:23

So, uh, there's a saying

44:25

that spectroscopy is also something for the future, right?

44:27

It has a lot of potential, but it never seems

44:29

to quite hit it in clinical practice.

44:31

I mean, the babies, if they're moving, right?

44:34

Uh, you have this big voxel in a small head

44:36

and then there's a lot of variation

44:37

between scanners and things.

44:39

Uh, the tips I wanna give you, so a short echo is good

44:41

for metabolic disorders, right?

44:43

Because it's shorter. So you have a noisy baseline,

44:45

but you can, you can catch small metabolites, right?

44:48

So like, uh, things that you might not be able

44:50

to detect once you have a longer echo

44:52

and you clean up the baseline.

44:53

Um, so if you're looking for metabolic disorders,

44:55

do a short echo, long echo, uh, takes a little bit longer,

44:58

cleans up the baseline, so you just

45:00

get the major metabolites.

45:01

If you're just trying to grade HIE,

45:03

then do just the long echo

45:04

'cause you really are just concerned about the ratios.

45:07

And then the 1 44, the intermediate echo, like

45:09

that's really just academic, right?

45:11

The idea is that because of the j coupling

45:13

of the methyl group on the lactate doublet, right?

45:16

That you could invert

45:17

below the baseline if you had a lactate peak.

45:19

But honestly, this is really obvious.

45:21

If it's a big lactate doublet, you're,

45:23

it's not gonna be diagnostic dilemma.

45:24

So why would you waste time doing another one?

45:27

Uh, unless you want it for a talk or something.

45:29

And then, um, if it's a small one, right?

45:32

Uh, if it's a small one that like you're questioning like a

45:35

mild lactate peak of short echo, uh, by the time you get

45:38

to longer echo, it'll have decay, right?

45:39

So just because you have a small doublet

45:41

and you don't see it in invert, uh,

45:43

because it's all noisy in here at intermediate echo,

45:45

it doesn't mean it wasn't lactate.

45:46

Basically, if it's a narrow thing at 1.4 parts per million,

45:50

like I would call it lactate, right?

45:52

Um, it doesn't matter. Like I don't see the point

45:54

of doing this in general and then evolution wise, right?

45:58

Again, depending on the nature of the injury, right?

46:01

You can see like for example, this patient had progressive,

46:04

uh, HIE cons, you know, secondary energy failure.

46:07

So day four, day seven

46:08

and day 10, you see the lactate and lipids coming up.

46:11

You see the NAA coming down, right?

46:13

And so basically this, this, uh, this neonate was having

46:17

progressive, uh, injury metabolically, right?

46:20

But again, we never interpret these in isolation.

46:23

It's always in conjunction with all

46:25

of the basic anatomic imaging.

46:28

Okay? So last is the special cases.

46:30

So these are things like that, that they're kind

46:32

of slam dunk if you see them,

46:34

but you have to know that they exist.

46:36

All right? So hemorrhage, right?

46:37

So normal birth, they're going through the birth canal,

46:39

it's okay to have a little bit

46:41

of subdural slash intradural blood products, right?

46:43

I mean, who wouldn't after squeezing your head around,

46:45

but it should be like relatively little

46:47

and it should resorb, you know, um,

46:50

maybe in the first like few weeks or month after birth.

46:53

Okay? Delivery assist. So vacuum forceps, right?

46:56

These things can be pretty traumatic,

46:57

even sometimes a c-section if they're like yank in the head.

47:00

And so you can have subarachnoid, subdural,

47:03

you can also have something called sepe hemorrhage.

47:05

So there's this p uh, be beneath the p mater again

47:07

that the blood brainin bears immature

47:09

and neonate, so they don't have their gl lns.

47:12

And so there's this potential space.

47:13

And so you see this kind of triangular collections

47:15

and subarachnoid,

47:17

which is layer right along multiple socy gyre

47:20

and not push on the parenchyma,

47:21

but these actually create mass effect

47:23

because they're trapped, right?

47:24

Kind of like between one or two gyre and socy.

47:27

And so they create ischemia.

47:29

Classically, they're in the temporal

47:30

parietal regions, but they can be anywhere.

47:31

So that's sape hemorrhage.

47:34

Most newborns get vitamin K injection in their thigh within

47:37

six hours of birth to prevent this very thing.

47:40

So this family declined the injection.

47:42

And so, you know, the kid couldn't produce clotting factors.

47:45

So they presented with a lot of like subarachnoid,

47:47

subdural intraventricular hemorrhage, um,

47:50

and then a piece of head trauma.

47:51

So here we have a stella multidirectional fracture, we have,

47:54

you know, actual cortical vein thrombosis and kinking,

47:56

and then they can have these asymmetric ischemia.

47:59

Some people think it's like from the shaking

48:01

and maybe like the strangulation of one carotid

48:03

and so forth, okay?

48:06

Scalp collections. Uh, it's normal to have capitox itanium.

48:09

So that's basically, as you go through the birth canal, some

48:11

of that fluid gets forced into the connective

48:13

tissue and it resolves.

48:15

It's kind of along the co uh, the vertex here.

48:18

Uh, there's something called delayed sub bale,

48:20

neurotic collections of infancy.

48:21

So these don't, are not present at birth.

48:23

They, they come up like a couple weeks to like maybe,

48:26

you know, four, four plus weeks after,

48:29

and they're kind of boggy and fluctuate.

48:31

And so, uh, the idea is that maybe like, uh, there's some,

48:34

you know, impaired, you know, glymphatic

48:37

or lymphatic drainage, the,

48:38

and it's often associated with more difficult deliveries.

48:41

But these also will solve resolve,

48:42

and they're kind of like fluctuation.

48:44

And most importantly, they're delayed.

48:46

They don't actually, they're not present to birds,

48:47

and they're simple collections.

48:49

Uh, cephalohematoma.

48:50

So this one is actually limited by sutures

48:53

because it's actually periosteum.

48:54

We can see that there's some mineralization of this.

48:56

It's actually that outer layer

48:57

of the periosteum being uplifted

48:58

and the hemorrhage is going into that space, right?

49:01

And so these can actually ossify

49:03

and become part of the skull and just become an asymmetry.

49:06

But again, you see that thin mineralized layer

49:08

of periosteum, and they basically are delimited by suture.

49:11

So kernel, squamous suture,

49:13

sagal suture, they do not go beyond.

49:16

So gallic hematomas, just like in adults, right,

49:18

require an actual skull fracture, right?

49:20

So this, this, uh, kid had, uh, forceps, uh, delivery

49:24

and so has a lot of skull fractures, has some, a lot

49:26

of subdural blood products, venous sinus injury.

49:29

And then like a lot of subgaleal blood, um,

49:32

other scalp collections,

49:33

you can actually have meningo seals.

49:34

You can actually have herniated brain, right?

49:36

Not just, uh, it's like adual

49:37

bone defect in herniated brain.

49:39

So these can be anterior

49:40

or occipital, like fronto, ethmoidal nasal.

49:42

We see those more in the Asian population.

49:45

Uh, the posterior ones, uh, are more North America, Europe.

49:47

So you can have etre encephalocele in the parietal

49:49

region most commonly.

49:51

And so these are actually like, they were meningocele

49:53

and they kind of closed down.

49:54

And so you just have a little residual fibrovascular stock.

49:57

But a lot of times they're no longer communicating.

49:59

They're kind of functionally close.

50:00

It can just kind of resect this thing.

50:02

And so they have a little bit of, you know, a kind of,

50:04

everything's converging toward that area,

50:06

but essentially it functionally closed off.

50:09

Uh, and, and kind of occipital ones.

50:10

This is actually a qre three, right?

50:12

So you have a cervical occipital encephalocele, um,

50:14

you also have some interhemispheric, um, uh, holos,

50:18

cephalic, uh, superior vertex ones are pretty rare.

50:21

You can sometimes see that with amniotic, um, band syndrome.

50:25

And then basal encephalocele.

50:26

So the sphenoid ones, those are the, um, front

50:28

and nasal dysplasias are morning glory syndrome.

50:30

So they can have excavated optic discs, cleft palate,

50:34

duplicated odontoid

50:35

and pituitary, um, oral teratomas, uh,

50:38

hyper tism and so forth and so on.

50:40

So, um, a whole, like a, a kind of facial, um,

50:44

mid-face fusion syndrome, okay?

50:47

Vascular lesions. So just like in adults, right?

50:49

You can have cortical and medullary vein thrombosis,

50:51

but, uh, neonates are more, uh, predisposed

50:54

to prothrombotic conditions from the birth, from sepsis,

50:58

from hypoxia, ischemia, all of these things.

51:00

So you really wanna make sure

51:02

that this is a high level suspicion.

51:04

'cause uh, I think, I think this case was called trauma, um,

51:07

by an adult radiologist, right?

51:09

And it's like, yes, there is diffuse hypoxia

51:11

and there's a lot of, uh, peripheral,

51:14

but ag I mean, there aren't any subdurals, right?

51:15

And, and it's like, what is this?

51:17

So basically there was diffuse venous sinus thrombosis,

51:21

and then you had secondary arterial ization,

51:23

because if you get the impaired venous outflow over time,

51:26

the pressures build up.

51:27

And then you get little petee hemorrhages, right?

51:29

The capillary rupture, and then the pressures get so high

51:32

for venous outflow that you start to get secondary arterial.

51:35

So there's no, you know, arter large artery distribution

51:37

because the entire brain is in farting,

51:39

right from a longstanding venous thrombosis.

51:41

So very important, uh, to remember this diagnosis.

51:44

And the medullary veins can also be congested and immature.

51:47

And so you can see again, that T one shortening kinda linear

51:49

radiation engorgement thrombosis.

51:52

And so this can also give you kind

51:53

of like a white matter injury like pattern.

51:55

But the key is that you actually have a bunch of, uh,

51:58

congested metral veins through that whole area.

52:00

And very linear vein

52:02

and galin malformations, you know, this, uh,

52:04

essentially AV shunting, high flow shunting, right?

52:07

Uh, through the median cephalic vein,

52:10

they can have this turbulent yin yang flow, lots of,

52:12

you know, choroidal, uh, or mural feeders

52:15

and ischemia of the brain parenchyma,

52:18

and this is a good one to know,

52:19

the collagen four A mutations, uh, they can cause, uh,

52:23

neonatal or even antenatal, uh, hemorrhagic porn cephalic,

52:26

essentially it's, uh, the collagen four in the vessel walls

52:29

can give you hemorrhagic strokes throughout life, right?

52:32

So if you see like a fetal MRI

52:34

or a neonate with a bunch of like hemorrhagic, you know,

52:37

porn cephalic cysts, right?

52:38

You really have to invoke this diagnosis infection.

52:41

Uh, so congenital CMV, we've all seen it depends on

52:44

how early they were infected.

52:45

Uh, if it was early,

52:46

they can actually have severe migrational abnormalities.

52:48

They can have germal, uh, cysts, uh,

52:51

particularly in the interior temporal regions.

52:53

They can have, uh, migrational anomalies.

52:55

Uh, para ventricular calcifications, uh, Zika,

52:59

especially in the first trimester could give you very

53:01

severe, you know, volume loss,

53:03

migrational abnormalities, scalp rue.

53:05

So this is all like very, you know,

53:06

early developmental acquired, um, condition, uh,

53:11

vir, this is a good one to note.

53:12

It has the sunburst pattern.

53:14

There's oth a few other viruses can do this,

53:16

but that's to relate to the inflammatory microglia.

53:18

And so they can have this kinda radiating, uh,

53:20

restricted diffusion through their per ventricular regions

53:23

and some of the white matter tract, basal ganglia.

53:26

And then other, you know, bacterial conditions can give you

53:28

abscess formation, hemorrhagic meningitis and so forth.

53:32

Uh, congenital malformation,

53:33

so we all know chiri two, right?

53:35

The myelo cyl, mylo meninge,

53:37

it basically causes a prenatal CSF leak.

53:39

So the tonsils come down,

53:41

but also it affects the, the, uh, cortical folding, um,

53:45

and the migration because you have this essentially

53:47

developmental CSF leak, um, poly micro jia in a,

53:51

in an unmated child, it can be a little bit hard

53:53

to diagnose, but again, this is a very broad, you kind

53:56

of thickened, you know, irregular

53:58

fisure, uh, Sylvie and fisher.

54:00

And so even if you're not doing a sedated exam, right?

54:02

Just to see some of these 2D images to realize that,

54:05

you know, there's something not quite right about this.

54:08

Sylvie and Fisher, um, holo cephalic, different levels of,

54:12

uh, you know, frontal lobe mal rotation infusion,

54:14

not a subtle diagnosis, uh, tubulopathy,

54:16

if you see some crazy pan migrational type, you know,

54:19

supinator asymmetric, those are often mutations

54:23

of microtubules because those affect the,

54:25

the actual radial glial fibers along which the neuroglial

54:28

pro genders migrate.

54:29

So again, you know, medical genetics, um, and

54:31

or kind of neuro uh, neurology assessment can be helpful

54:35

for these neuro cutaneous disorders are marked

54:39

by their cutaneous manifestations as surge Weber.

54:41

With this, you know, blush over the eyebrow here.

54:44

And so actually this is the normal side, right?

54:46

This is the normally myelinated cortico spinal tract.

54:49

This side is accelerated, right?

54:51

So you have way more myelination T one shortening T two dark

54:54

than you should in a newborn.

54:56

And you see that there's these dysplastic veins, right?

54:58

So these enhances essentially a venous malformation.

55:01

And so, uh, the brain can't drain in the early stages,

55:05

so it actually has a lot of blood pooling

55:08

and it accelerates myelination.

55:09

It's only later on when those dysplastic, uh, you know,

55:12

cortical veins cannot drain the blood.

55:14

You start to get venous ischemia.

55:16

But in the very early phase, this is actually

55:18

what Sturge Weber looks like.

55:20

Tuber sclerosis, adenoma sedation, right?

55:22

So you can have a bunch of tubers,

55:23

which are essentially just migrational anomalies.

55:25

So again, unmyelinated watery brain.

55:28

So you actually have the inverse signal, right?

55:30

It's actually T one bright T two dark.

55:32

Once the patient myelinates, they look the opposite, right?

55:35

They look actually T one dark and T two bright, the tubers.

55:39

But this is what they look like, um, in a neonate.

55:41

And the calcification is really a late finding.

55:43

So usually you only get, uh,

55:44

very little a calcification early on.

55:47

Uh, this is a schematic overgrowth,

55:49

so they can have capillary malformation, poly, uh, dact,

55:52

poly micro gyre.

55:53

Um, and so this is all pi three ca, um, pathway,

55:57

and then neurotin melanosis.

55:59

So proliferation of melanocytes in the skin,

56:02

central nervous system.

56:03

Again, this is best done on the neonatal scan

56:06

because as a patient myelinates, these T one deposits start

56:09

to blur with the myelinating brain, uh,

56:13

inborn metabolic disorders.

56:14

So, um, the key here really is like working with, uh,

56:18

the newborn screening

56:19

or the pediatrician to see what the suspicion is

56:21

because they all have symmetric restricted diffusion, right?

56:24

Basal ganglia, maybe some white matter stuff.

56:27

And then they have char supposedly characteristic, you know,

56:30

spectroscopic signatures.

56:32

But unless you have the clinical suspicion

56:34

and the lab test, it's gonna be really hard to like look

56:36

for some very subtle peak.

56:38

But once you have the clinical suspicion

56:40

and you can say, okay, um, you know,

56:42

putting all this together, right?

56:43

This is an inborn error of metabolism.

56:45

And typically these patients, sometimes it can mimic HIE,

56:48

but they had a normal delivery

56:50

and then suddenly they just crump, you know, at some point

56:53

after birth maybe they had like a little illness

56:55

or a little minor trauma, and then they just like

56:57

decompensate rapidly.

56:58

That's the, uh, usually the history

57:00

for metabolic disorders acquired metabolics.

57:04

So hypoglycemia posterior, uh, circ, uh,

57:06

posterior circulation, it's probably like a press

57:09

like phenomenon, right?

57:10

So you have a poor auto autoregulation, you have, uh,

57:13

low glucose and it tries to like push, uh,

57:16

push the flow here,

57:17

but, uh, you end up getting a kind of posterior,

57:19

often visual cortical injury.

57:22

Um, unconjugated bilirubin, right?

57:24

Jaundiced infant right, will be particularly neurotoxic

57:28

to globus palus and turn.

57:29

And then in the chronic stage, you'll see atrophy,

57:32

um, hyperammonemia.

57:34

So some of these metabolic acidosis, right?

57:36

Can selectively injure the peric and insular regions

57:39

and the basal ganglia.

57:41

And then some cases of osmotic demyelination,

57:43

which actually this patient had HIE

57:45

and then on top of that had dis uh, osmotic dysregulation

57:48

because of the pituitary hypothalamic axis

57:51

and toxic conditions.

57:53

So again, just so you know,

57:54

kids put stuff in their mouths, right?

57:55

So, um, glipizide poisoning, um,

57:58

this was essentially like a diffuse cerebral edema,

58:01

but gabatone is, uh, used for infantile spasms.

58:03

And so that's a GABA analog.

58:05

So you can actually get, uh, some reversible, um, injury

58:08

to the, to the deep gray nuclei.

58:10

Um, withdrawal from

58:13

maternal opioids can give you a number of features.

58:16

And then even the synthetic opioids, like, uh,

58:19

because they don't clear well

58:20

and infants can give you quite a bit

58:21

of injury if you accidentally overdose.

58:24

And then finally, tumors. So, uh, neonatal tumors are rare.

58:27

Uh, a lot of them are these Desmoplastic Glo gliomas,

58:30

which are great, W2 grade one.

58:31

So they have some cystic components

58:33

and peripheral nodular components,

58:35

but they're pretty indolent even though they look bad.

58:38

Uh, the hemispheric GLIs are high grade,

58:40

and this is the infant types.

58:41

So these have been recently described,

58:42

so these are pretty aggressive.

58:44

And then, uh, teratoma, you know,

58:46

especially immature ones don't have a good prognosis.

58:48

But again, this is kinda, you know, uh,

58:50

germ cell restricted diffusion calcification.

58:54

All right, so that's everything.

58:55

Um, in conclusion,

58:57

neonatal brain physiology is very dependent

58:59

on clinical backgrounds.

59:01

So always look at the notes

59:02

and try to correlate when you're reporting a case,

59:04

there are characteristic imaging patterns with preterm

59:07

and term birth injury that we've described.

59:10

So recognizing

59:11

and being aware of those is, is very important.

59:13

And then any unusual features, all those, uh, kind

59:15

of more rare cases we just went over should prompt a

59:17

more detailed workup.

59:19

So thank you so much for your attention.

59:20

I'm happy to take a few questions if anyone has any.

59:23

Thank you so much Dr. Ho.

59:24

Yeah, and if you are okay to stick around

59:27

for a couple minutes, um, sure.

59:29

We got a couple questions in that q

59:30

and a feature, if you wanna pop that open, I can also.

59:34

Sure. Let's see. Okay,

59:36

first one says gray matter hemorrhage versus PVL occurs at

59:40

which age?

59:42

Gray matter gray matter hemorrhage.

59:44

So I think most of the hemorrhage,

59:47

the IVHI described is gonna be, oh, germinal matrix is,

59:49

I think is what they're saying, germal.

59:51

So it's all about the level of preterm.

59:53

So if you're just mildly preterm, you're likely

59:55

to have the germinal matrix just involuting

59:58

in the kaath thalamic groove.

59:59

So that's grade one. And the more preterm, if you get

60:01

to like vary your extreme preterm, you're more likely

60:04

to have a lot, you know, a lot more severe IVH,

60:07

the para ventricular leukomalacia,

60:09

so-called white matter injury.

60:10

Again, it's a gradation, right?

60:12

So, um, the, the more preterm your, uh, you are,

60:16

the more likely you are to have like a cystic PBL as opposed

60:18

to just some like mild focal areas.

60:22

What is correct time for ultrasound and MRI for HIE?

60:25

Again, this is like a loaded question

60:26

because every place does it a little bit differently.

60:28

I would say for the HIE, they found that, um,

60:32

the early scans, so like around that three to five day,

60:35

so like right after you, cool

60:37

and rewarm is kind of the best prognosticator.

60:40

Some people will do the late exam, so like a week

60:43

or two later, and it might help a little with complications,

60:46

but usually with the HIE, the term HIE,

60:49

you can actually predict that from the initial one, um,

60:52

unless it's really bad and it keeps going,

60:54

like a few of the cases I showed.

60:55

But those were, uh, comparing immediate to, to more

60:58

of a early, uh, exam more than early to late ultrasound.

61:03

You can do anytime so often they'll do daily ultrasounds in

61:06

the NICU to just monitor.

61:07

And again, like if you see some, uh, marked evolution,

61:11

right, then you can work it up with MRI and bring 'em down.

61:13

But ultrasound is very helpful 'cause you can do it bedside

61:15

and you can do it all the time.

61:16

I mean, you could do it multiple times

61:17

a day if you really wanted to.

61:20

Um, how to differentiate astrocytic gliosis,

61:23

which is T one hypertensive

61:24

with normal click T one hyperintensity, okay?

61:27

So, uh, the, the, the normal click that I showed you,

61:31

one half to one third, right?

61:33

So if it's missing, if it's less than that

61:35

or it's missing, that indicates

61:37

that there's some edema injury on board, right?

61:40

And then the astro gliosis in terms of T one shortening,

61:43

so usually that's in the white matter,

61:45

so it's farther from the click,

61:46

but it's, it's basically bright word's not supposed

61:49

to be like even the, the central injury

61:51

with the baso ganglia thalamus, right?

61:53

When I showed you, uh, that one of those cases,

61:55

like it was actually on the level of,

61:57

or brighter than the click, right?

61:59

So basically the click gets less T one bright, T two dark,

62:03

and these other areas get more.

62:04

So, right? So you basically have an inversion of the normal,

62:07

uh, of the normal pattern, um,

62:11

sape hemorrhage versus SAH, okay?

62:14

So SAH just like in an adult,

62:16

it just outlines multiple gyn soci and, and it just spreads

62:19

and it, it, uh, redistributes, right?

62:21

So it doesn't have any mass effect

62:23

where sapi has a triangular morphology, it's really limited

62:26

to one or maybe two soci that gets really big

62:29

and then it pushes, it causes a mass effect

62:31

on the adjacent cortex.

62:33

And that, um, sometimes ischemia as, as I showed, uh,

62:36

in those cases because it's delimited by that kind

62:39

of p mater, which is more closely opposed to the cortex,

62:43

unlike the SAH, which is subarachnoid space,

62:45

it can just kind of freely distribute.

62:47

Um, and then the spe space is pretty much seen in infants

62:50

and neonates as a potential space either

62:52

with difficult delivery or sometimes abusive head trauma.

62:55

It's occasionally been described in adults,

62:57

but I would say that is like really the exception, right?

62:59

So it's much more of a neonatal type thing.

63:02

Uh, it looks like, uh,

63:04

this person also asked about sh sape cortical hemorrhage.

63:09

I mean, if it's really intracortical, right?

63:10

You can co localize that on, on, uh, on an anatomic,

63:15

and typically those would be more punted

63:17

or let's say if it's an in from a hemorrhagic

63:19

infarct or something, right?

63:20

Then you'd see the secondary features, right?

63:22

But, uh, isolated cortical hemorrhage,

63:24

I would say would be pretty rare.

63:25

The, the case with the venous thrombosis

63:27

was a secondary feature, right?

63:28

That was basically capillary rupture from diffuse, uh,

63:32

and prolonged, uh, venous venous occlusion,

63:36

delayed sub apo neurotic hemorrhage, right?

63:39

So the delayed sub apo neurotic collections are usually

63:41

not hemorrhagic, right?

63:43

They're usually simple fluid,

63:44

maybe they'd be a little complex,

63:45

but they're not actually blood, right?

63:47

So subgaleal hemorrhage,

63:49

like actual blood products is typically

63:51

'cause you had a fracture, right?

63:52

And so you're getting just like an adult,

63:54

you're getting subdial hemorrhage from the skull fracture,

63:57

um, and then those would be present

63:59

immediately at birth too, right?

64:00

Because you had the trauma already.

64:01

So the delayed ones come up like two to four weeks after,

64:04

and they self-resolve and they're boggy

64:06

and fluctuate, right?

64:07

So they're just like simple fluid, right?

64:10

And it's more like impaired lymphatic

64:12

or g lymphatic drainage, right?

64:13

So there's no actual blood products

64:15

and you can move them around.

64:16

There's, and not necessarily an underlying skull fracture.

64:19

There might be some like difficult delivery,

64:21

but usually not an actual fracture, the cause

64:23

of early maturation and search Weber, well, like I said, um,

64:27

the, the search Weber has a venous malformation

64:29

of the face and of the brain, right?

64:31

And so your superficial cortical veins are not draining

64:35

effectively because they're malformed, right?

64:37

So basically the only drainage you have

64:39

is the deep venous drainage.

64:40

And so the blood is just sitting in your brain.

64:44

And so if a brain has more blood,

64:46

it's gonna mature fast, right?

64:47

The only problem is that as you grow,

64:50

just the deep venous drain is no longer sufficient, right?

64:52

To sustain a growing brain.

64:54

And that's why you start to undergo venous ischemia.

64:56

Then you get the T tram track calcification.

64:58

That's a late finding, right? Have you ever wondered why?

65:00

Well, that's the part nearest the superficial

65:03

cortical venous malformation, right?

65:04

So that dies off first because it's farthest

65:06

from the deep venous supply.

65:07

But you start preferentially shunting all the venous

65:10

drainage deep, and that's why you get your enhancing

65:13

medullary veins, your hyper enhancing cord plexus,

65:15

and then you get your progressive paral venous ischemia, uh,

65:20

T one hyperintensity and post lateral thalamus.

65:22

When should we call it normal versus abnormal?

65:24

Like in term HIE?

65:26

So you really shouldn't have, uh, so the,

65:29

the normal T one signal, so if you go back

65:32

and review this, uh, you know, uh, lecture, you'll see

65:35

that the T one signal in the petina

65:38

and ventral lato thalami is always less,

65:41

it's always less T one bright

65:42

and T two dark than the click, right?

65:44

And with the HIE, they invert, right? They equalizer invert.

65:48

So the click becomes less apparent and the putamen

65:51

and the ths become more apparent, right?

65:53

So it's basically inversion of the normal pattern.

65:57

When we have bilateral deep white matter abnormal

66:00

hyperintense signal in T two

66:01

and flare, how can we distinguish hypoxic ischemic

66:06

insult from leuko dystrophy for first MRI image?

66:10

So deep white matter.

66:13

So we should first of all don't do f flare neonate.

66:15

That's my first statement to you.

66:17

But abnormal T two, like high T two can be a lot

66:20

of things I could, it's usually like a watershed thing,

66:22

either in a preterm or a term, right?

66:25

Uh, it's basically edema on top

66:26

of like an already watery brain.

66:28

And so that this is called dci, right?

66:30

Diffuse excessive high signal intensity. That's the classic.

66:33

Like it's actually expected in a preterm

66:35

'cause you've got immature white matter.

66:36

Um, I would say like if you've,

66:39

if you're doing an early enough exam, right?

66:41

Within like four days

66:42

or so, you probably could see some, um, diffusion changes,

66:45

the a DC metrics.

66:47

So there are some a DC metrics gonna be useful.

66:49

So for example, with HIE, uh, in the click right,

66:52

if it's less than point 75 times 10

66:55

of the negative three millimeters squared per second,

66:57

as opposed to like more than 0.9 to one is normal, then

67:01

that's much more likely to have like, uh,

67:03

negative implications for HIE, um, outcomes for preterm,

67:08

uh, I think the, the cutoff was around like 1.4, right?

67:12

So if it's like higher than 1.4, in my experience, I try

67:14

to go to like maybe 1.7 or eight, right?

67:17

It, but I think it depends on your vendor.

67:19

But essentially you can use your kind of institutional a, d,

67:22

c norms to say like,

67:23

do do I think this is just heterogeneous T two,

67:25

like a mild thing,

67:27

or is this like actually more profound T two elevation

67:31

that I think could have like more,

67:32

more outcome significance and leukodystrophy.

67:35

So I have a whole nother talk on leukodystrophies,

67:37

but uh, genetic,

67:39

I assume we're talking about genetic leukodystrophies, uh,

67:41

neonatal onset ones, like honestly,

67:43

most leukodystrophies do not,

67:45

are not present at birth, right?

67:47

They, they occur, uh, depending on the level

67:49

of the mutation, anywhere from early

67:50

childhood to even adulthood.

67:52

Uh, but they have characteristic patterns, right?

67:54

They can have, uh, geographic appearances

67:57

leading in trailing edges.

67:59

Um, other things like maybe cranial nerve enhancement

68:02

or whatever, uh, they're gonna be symmetric,

68:05

like very symmetric, not asymmetric.

68:06

Like a lot of our cases, they're not gonna have the, uh,

68:11

isolated basal ganglia involvement, right?

68:12

So they, they might have like, you know, some white matter,

68:15

some basal ganglia stuff.

68:16

But the, I don't really think that any of the cases

68:20

that I've shown in this talk really are a differential

68:24

of leukodystrophy, honestly.

68:25

Like leukodystrophy has a very,

68:27

or even like polio dystrophies, right?

68:29

Just genetic metabolic conditions have a very different look

68:33

and presentation to them, right?

68:34

They could have abnormal faces, you could do, uh,

68:37

metabolic testing, right?

68:38

So some of the metabolic disorders that we showed right,

68:41

has some overlap, but again,

68:42

there's a clinical suspicion there's,

68:43

there's a very different kind of clinical presentation

68:46

and the imaging also looks different.

68:48

So any,

68:52

let's see, was there anything else?

68:53

Please suggest good articles for h Hi mimics, you know,

68:56

I think like radiographics or any

68:57

of those things, um, are pretty good.

68:58

Or some of the textbooks.

69:00

What is the normal ventricle size and neonates? Which plane?

69:03

Okay, so, uh, surprisingly like the, from from birth,

69:08

even actually prenatal through like, you know, maybe,

69:11

maybe the first year or so there, there's actually a pretty,

69:14

um, consistent, uh, ventricular size.

69:17

So I think, uh,

69:20

there's like a millimeter difference in the norm

69:22

between males and females.

69:23

I think the males were a little bit bigger, but it's usually

69:25

like, I would say 10, like 10 ish millimeters.

69:28

So like the, there's a, there's some criteria for this.

69:31

I, I forget the name of the person who, who established it,

69:33

but gag, I think, yeah, so 10 is a,

69:36

10 millimeters is a good number, right?

69:38

For like, for early, for early life neonate to infant

69:41

and even prenatal life.

69:43

Uh, if, if you're 12 or more, right?

69:47

And this is max, so I use the atrium,

69:49

I just use the diagonal measurement

69:51

of the atrium on like axial

69:52

or corona, wherever you get the biggest one.

69:55

And so if it's like more than 12, it's like mild.

69:57

If it's more than like 14, 15, that's moderate, right?

70:00

But also I think visually you can tell,

70:02

and then the question is ventricular

70:03

magaly, is that hydrocephalus?

70:05

Like are you seeing communicating, you know, uh,

70:08

like are you seeing adhesions or level obstruction?

70:10

Or are you dealing with an X vao, right?

70:12

Because if you're dealing with an X vacu, then yes,

70:14

it's ventricular magaly, but it's not really relevant

70:16

because it's because the, you've lost parenchyma.

70:19

So again, I think the, the, the visual

70:21

and kind of relating it to the physiology is important.

70:25

But there's some stuff in the chat here. Okay.

70:28

Uh, so how can we differentiate split

70:32

cord plexus from cord plexus hemorrhage?

70:36

I'm not entirely sure what it's meant by split, uh,

70:39

cord plexus, uh, cord plexus hemorrhage

70:42

or int ventricular hemorrhage.

70:43

I mean on ultrasound it's, it's, um, genic, right?

70:47

But so can normal, uh, cord plexus on mr,

70:51

it's pretty obvious because you have the susceptibility

70:53

and signal changes.

70:55

But on ultrasound, like I think having the kind

70:57

of asymmetric enlargement, heterogeneity,

70:59

some shaggy debris in the ventricle,

71:01

maybe enlarged ventricle could be helpful split.

71:04

Um, I mean there are cord plexus variant,

71:06

it's like there are cysts

71:08

and uh, xanthe, granial lumus,

71:09

which is not too common in a neonate.

71:11

But again, I think the morphology in the clinical history

71:15

and all of this are kind of helpful to you, right?

71:16

Because hemorrhage is kinda expansile, you know, like, it,

71:20

it might layer et cetera, et cetera.

71:23

Fat foci on CT brain and complex CHD.

71:26

So I mean, you can have fat emboli, right?

71:28

Um, I, uh, you and ecmo, right?

71:31

So the, the two things that can give you, like if you,

71:34

you're actually seeing bulk fat.

71:36

Like if you're seeing a fat density, um, on a ct,

71:40

then I assume you're talking about fat emboli, right?

71:42

The, the way to do, like if you look at mr, um,

71:45

you'd see like innumerable micro hemorrhages,

71:47

like starfield, yeah.

71:49

So long bone fractures can do that.

71:51

But uh, even like I saw a case the other day with a,

71:53

like an intraosseous, like a iv, right?

71:56

And so if you push the IV too hard

71:58

and then ECMO can do it, right?

71:59

Because you, especially the veo arterial ecmo,

72:01

but even the potentially the veo venous,

72:03

basically you're cutting down vessels

72:05

and you're creating like a, like an AV shunt, right?

72:07

And so the ECMO cases can look very much like, you know,

72:11

fat mbo, I, because they're basically just like micro MBO I

72:13

through, uh, you're, you're, you have like a instrumentation

72:16

that's giving you like a prothrombotic

72:18

and then you have like ab shunting.

72:19

So you might be dealing in a CHD case, you might be dealing

72:22

with a kid with ECMO potentially.

72:24

Um, that's, that's my thought on that.

72:28

We do SWI sequence our micro

72:29

hemorrhage is related to delivery.

72:32

Uh, not really like I would say subdurals, uh,

72:35

small subdurals are expected for delivery.

72:37

Uh, micro hemorrhages, if you're just seeing like one,

72:39

like one or two, I would not freak out about it.

72:42

I mean, like I said, the placenta,

72:44

we don't usually examine the placenta,

72:46

but people are realizing

72:47

that placental health is like a big part of,

72:49

of neonatal, you know, outcomes now.

72:51

And so if you look at some of these kids

72:53

with the large vessel occlusions

72:55

or even like, you know, venous thrombosis

72:57

or whatever, you see that the placenta actually looks very

72:59

ischemic and shaggy, you know, in those instances.

73:01

And so the placenta was not that healthy.

73:03

So if you had like a little placental clot

73:05

or something, it could just flick off

73:07

and cause a micro hemorrhage.

73:08

And I don't think that's a big deal. So if you see like one

73:10

or two, maybe that's okay

73:11

and you're seeing a lot of them, then you know,

73:13

you might worry about congenital heart disease

73:15

or some, you know, other prothrombotic state.

73:20

I think you got 'em all. Dr. Ho. Wow.

73:24

Thank you so much for answering all those questions

73:26

and for your phenomenal lecture today.

73:28

We really appreciate it.

73:30

Yeah, thanks so much. And again, people are welcome to,

73:32

uh, email me if they have any other questions.

73:34

Awesome. Yeah, thank you so much.

73:36

And thank you for everyone for asking those excellent

73:38

questions and for participating in today's NOOM conference.

73:41

You will be able to access a recording of today's conference

73:44

and all of our previous noom conferences

73:46

by creating a free account.

73:47

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

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Be sure to join us on Thursday,

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March 20th at 12:00 PM Eastern, where Dr.

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Samir Ranga will give a lecture entitled CT Evaluation

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of Pelvic Ring Injuries, patterns,

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classifications, and Approach.

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You can register for that@mrionline.com.

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Follow us on social media

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for updates on future noon conferences.

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