Sonography of the Infant Brain - SD

Introduction

Good afternoon.

I'm Henrietta TLAs Rosenberg, director of pediatric Radiology at the Mount Sinai Medical Center in New York City.

I'm also professor of radiology at the Mount Sinai School of Medicine.

I'm very pleased to speak with you this afternoon about sonography of the infant brain.

We'll talk about anatomy, hemorrhage, and hypoxic ischemic disease.

Learning Objectives

The learning objectives for this talk include learning the performance of brain ultrasound in infants to learn the normal ultra sonographic brain anatomy and to learn the ultrasound appearance of brain hemorrhage and ischemia and their sequelae in premature and full term infants.

Transducer Frequencies and Fontanels

We use a variety of transducer frequencies in the infants in those babies who are quite large, those who are more than approximately five to six months of age and who are full term.

We will generally use a three megahertz probe.

We will at times have to use a Kline broad bandwidth so that we can penetrate to the depths of the brain.

Normally the fontanel, the anterior fontanel is opened until about nine to 18 months of age.

This could be open longer in babies who are premature or babies who have increased intracranial pressure.

In babies who are somewhat smaller, we may use a five megahertz and then in the babies who are premature or full term, we will in the neonatal period use an eight five megahertz.

For scalp lesions, we will generally use a linear array probe that is at least 10 megahertz, often going as high as 17 five.

The posterior fontanel is generally opened until zero to four months of age and may be open longer in premature infants and infants who have increased intracranial pressure.

Imaging Planes

Now we generally obtain our images using coronal and sagittal planes in the coronal plane, we're going to sweep the brain from anterior to posterior and we will be looking for certain landmarks.

Coronal Plane Anatomy

This is a drawing showing a coronal section of the brain In an infant, we can see the interhemispheric fissure.

We see the singular gyrus.

This hammock shaped area below the interhemispheric fissure represents the corpus callosum, and then below the corpus callosum, we have the right and left lateral ventricles which connect via the foramina of Monroe bilaterally to the third ventricle.

We also notice the Sylvan Fi in the region of the Sylvan Fisher.

We will visualize the pulsations of the middle cerebral artery just above the corpus callosum, we will see the peric collosal artery and within the cingulate gyrus we'll see the pulsations of the coloso marginal artery.

The goal of the sonogram is to image as much of the brain as we need to to have a complete evaluation, which implies that we will at times be leaking the transducer to the right and to the left to see over the convexes of the brain.

Sagittal Plane Anatomy

The object of the sagittal plane is to examine the midline structures for anomalies and to evaluate in a para sagittal plane, the ventricular system, as well as the parenchyma of the brain as we scan in a straight, anterior, posterior, or AP plane.

In the midline, we will see the corpus callosum, the genu, the body, the splenium, and just below the corpus callosum we'll have the septum lucidum.

Below that area we have the third ventricle.

We will see the mass intermedia when that ventricle is enlarged.

And then this continues through the aqueduct of Sylvia to the fourth ventricle.

We'll visualize the cerebellum and the ci sternum magna as well as the brainstem.

And depending upon the gestational age of the infant, we may or may not see the convolutional markings of the brain.

As we look at the para sagittal views, we'll image the ventricular system, and as we extend our view more peripherally, we'll see the substance of the brain parenchyma.

Bear in mind that when you're trying to visualize the ventricles, that the frontal horn is more medially positioned than the occipital horns, and so the anterior portion of the transducer needs to be more medially positioned than the posterior portion of the transducer.

Ultrasound Anatomy

Let's look at some of the ultrasound anatomy.

This is a very far anterior view.

This view is very far anterior because you can see the left and the right orbits.

The interhemispheric fissure is seen here and note that there are little areas of brighter echogenicity in the frontal lobes.

This is what is referred to as the periventricular blush.

It represents vascular markings as well as neurons as they extend from the deep white matter to the cortex of the brain.

As we extend our view a little bit more posteriorly, but still in the anterior plane, we see that there is interhemispheric fissure.

Here's the cingulate gyrus.

We can see the corpus callosum here as a hammock shaped structure that is very poorly a coic that is just below the brain parenchyma.

Here in the frontal lobes, we have a portion of the right lateral ventricle, a portion of the left lateral ventricle, and we're beginning to get into the areas of the cau nuclei bilaterally represented by these slightly brighter areas of increased echogenicity.

We're also beginning to see these y shaped structures that represent the syl fissures.

As we come back just a little bit more posteriorly to an anterior mid coronal view, we again see the interhemispheric fissure.

With the cingulate gyri, we can see the corpus callosum and image, the lateral ventricles.

Note that the inferior lateral aspect of the frontal horns are concave and that we can see the choroid plexus as it goes through the foramina of Monroe as brighter areas of echogenicity and choroid plexus in the region of the roof of the third ventricle.

The third ventricle may or may not be seen on the anterior mid coronal views.

Note the syl fissures bilaterally and also the bright genicity that is in the region of the hippocampal gyrus bilaterally.

As we look at the region of the temporal lobes, the little dots that we see centrally in the temporal lobe represent the temporal horns a little bit more posteriorly.

We get to the mid posterior coronal view.

Note in this view that we see this pie shaped area of bright echogenicity that represents the cerebellum.

A little bit farther back, we've reached the posterior coronal view and we see these bright areas of increased echogenicity that are the gloma of the choroid plexus, which we'll look at in more detail.

When we look at the para sagittal views, these are generally quite symmetric.

As we look a little bit more posteriorly, we see the per ventricular blush around the posterior portions of the brain, and we're looking here at the occipital lobes.

The periventricular blush represents vascular markings as well as neurons that are coursing from the deep white matter to the cortex of the brain.

One may encounter a variant where there is asymmetry in the size of the choroid plexus that is basically physiologic and not indicative of an abnormality.

Note that the right side of the baby's head is up on this particular view.

Remember that the choroid plexus is buoyed up by only one part of the roof plate, so that if there is a change in the position of the baby's head, the side that's up tends to appear larger than the side that is down.

Notice when we turn the baby's head the other way with the left side up, we now see that this gloss of the choroid plexus looks as though it is larger.

It really isn't.

This is an artifact of positioning.

If there's ever a question, you can always turn the baby's head, of course, with the support of the nurses because most of these babies are attached to life support systems and it is extremely important not to dislodge an endotracheal tube or other intravascular catheters or enteric tubes.

Extra-Axial Fluid Spaces

Also consider the extra axial fluid spaces.

We measure routinely the sano cortical width by identifying the superior sagittal sinus measuring from the sinus to the outer margin of the cortex of the brain.

In a normal baby, we'll see that the Sano cortical width measures 0.4 to 3.3 millimeters.

We also routinely measure the cranial cortical width.

This is the depth from the cranium to the cortex, and this should not measure more than 0.3 to 6.3 millimeters.

We measure the interhemispheric fissure and this should not measure more than 8.2 millimeters.

Here's the ultrasound rendition.

We're measuring from the superior sagittal sinus to the cortex of the brain bilaterally, and we're measuring from the cranium to the cortex of the brain as well as the interhemispheric fissure, and all of these numbers fit into a normal range.

Gyri and Corpus Callosum

Also, consider the presence, the number, and the configuration of the gyri which are proportional to the gestational age of the infant.

Notice that it is not until 26 weeks gestation that we begin to see the development of the cingulate, sulcus and gyrus as the babies mature from 26 weeks gestation up to full term, there is an increase in the number of convolutional markings until at term there are multiples.

This is an important detail to be aware of as there are certain congenital anomalies of the brain that are associated with lack of formation of the convolutions.

The corpus callosum should be looked for on every brain ultrasound study.

This is the largest medial interhemispheric commissure that contains fibers that interconnect the cerebral hemispheres, thus allowing for sharing of memory and learning between the two sides of the brain.

The corpus callosum forms during the third to fourth fetal month.

It grows as a bud from the lamina.

Terminis grows upward and backward while the brain grows laterally and posteriorly notice too that there is a fluid space below the corpus callosum.

This is the cavem septum lucidum and the more immature the baby is, the younger the gestational age, there will be a posterior extension to this fluid-filled space called the cave virga.

This should not be mistaken for a cyst within the brain.

So here we have the genu, the body, the splenium of the corpus callosum, and here we see the ultrasound image of this anatomy.

This is the genu of the corpus callosum, the body, the splenium with the baby's head facing to our left and the posterior aspect of the baby's head.

To our right, this is a cingulate gyrus, and here we can see that there is bright echogenicity right below the cavem septum lucidum and the posterior extension, the cavem virga.

This represents the choroid plexus in the roof of the third ventricle.

This is third ventricle, and you might question why does this third ventricle not look quite as koic as the fluid that's in the cave septum lucidum and the cavem virga.

The third and fourth ventricles are extremely slender.

They measure no more than approximately one to two millimeters in width, and therefore it is somewhat difficult to get an image that does not pick up specular reflectors from the brain tissue on both sides of these midline ventricles.

So here we have the third ventricle with the region of the aqueduct.

Sylvia going down into the area of the fourth ventricle, we have the cerebellum.

This very brightly a coic structure due to the fact that it's quite vascular and there are multiple convolutional markings.

Below the cerebellum is the ci sternum magna, and this should be looked for on every midline ultrasound view.

And here we have some increased echogenicity in the region of the brainstem.

Notice that the brain itself in terms of the parenchyma is a relatively hypoechoic structure.

So here's the genu, the body and the splenium of the corpus callosum third and fourth ventricles.

This is a baby who's somewhat more mature.

You can see that there are more convolutional markings.

There are a little bit serpiginous, which happens as they develop.

And here we have the genu, the body in the splenium of the corpus callosum with a remnant of the Cajun septum lucidum.

This line that you see centrally represents a septal vein.

Again, choroid plexus in the roof of the third ventricle, the aqueduct, the fourth ventricle, the brainstem cerebellum and cisterna Magna notice that once the babies become full term, there is less visualization of the Calum septum lucidum.

Sometimes it is totally obliterated by that age.

And here we see the genu, the body, the splenium of the corpus callosum, the choroid plexus in the roof of the third ventricle.

Here's the fourth, the brainstem, the cerebellum, and the cisterna.

Magna sagittal views allow us to visualize the lateral ventricles and we see here the bony structures of the cranial vault.

This is the anterior, the middle, and the posterior cranial fosse.

We have more convolutional markings seen on this particular image and we can see the various parts of the lateral ventricle.

This is the frontal horn, the body, the atrium of the lateral ventricle where the body, the occipital horn, and the temporal horns meet housed within the atrium of the lateral ventricle is the gloss of the choroid plexus.

This should be very smooth and it should taper toward the coth thalamic groove as well as toward the temporal horn.

We should not see choroid extending into the occipital horn of the lateral ventricle.

Note that there is an area anterior to the coth thalamic groove that is called the germinal matrix, and we'll talk about this in more detail in a minute.

We also have the region of the caudate nucleus and the area of the thalamus.

You'll notice there are little fine lines that radiate back from the posterior aspect of the body of the lateral ventricle as well as the exhibital horn.

This is the periventricular blush that I alluded to when we talked about the coronal plane imaging, and these represent the vascular markings as well as the nerve fibers that extend from the deep white matter to the periphery of the brain.

The initial description was that these lines were reminiscent of the strokes of an artist's brush.

Extremely important to see this detail and to be sure that it is less e coic than the gloma of the choroid plexus.

If this area becomes brighter than the choroid plexus.

We need to be concerned about hemorrhagic and necrotic changes, and we'll talk about that when we discuss ischemic disease of the premature brain.

Going back a little bit more towards the lateral aspect, we can see the Sylvie and Fi and if we would turn on Doppler, we would see the pulsations of the middle cerebral artery.

And coming out a little bit farther laterally, we see the area of the insula.

We also get another view that's known as the occipital mastoid view where we use the probe right behind the ear along the region of a little opening in the skull known as the mastoid fontanel.

It's really only possible to see through this area in very young babies, and this allows us to see the lobes of the cerebellum.

Notice here, the right lobe, the left lobe, and we can see the area of the ci sternum magna a little bit easier to see when we put it into a view which is in a more vertical presentation.

Evaluation of Hemorrhage

Let's consider the use of ultrasound for the evaluation of hemorrhage.

This has really evolved as the imaging modality of choice as a very sensitive and accurate way to diagnose subependymal hemorrhage as well as intraventricular hemorrhage and paraventricular hemorrhage.

It is a useful predictor of outcome.

We can do this examination right at the baby's bedside without radiation, without contrast material and without sedation.

I wanna take one minute to just talk about ventricular size.

People always ask what is the normal size of a lateral ventricle?

And a general rule of thumb is that if you measure the frontal horn from one border to the other in a cross-sectional image, this really should not measure more than approximately two to three millimeters tops.

Intracranial Hemorrhage in the Premature Infant

We're gonna start our discussion of hemorrhage in the infant brain by talking about intracranial hemorrhage in the premature infant.

Those infants who are prone to intracranial hemorrhage generally are less than 32 weeks gestation.

They weigh less than 1500 grams at birth, and there is a significant incidence of hemorrhage in very tiny preemies up to 70% in babies who have assisted ventilation.

Most of the hemorrhages occur within the first three days of life.

Most major hemorrhages are noted on day one, and about 91% of the babies with hemorrhage have the diagnosis made by the end of the first week of life.

The risk factors are multiple.

First of all, prematurity and low birth weight hemorrhage in the premature infant is more common in male babies than female babies.

It's more common in babies who are part of a multiple gestation, which of course is a high risk factor for being born premature if there's prolonged labor, any type of trauma at delivery.

If there's a problem with hyperosmolarity, hypercoagulation, hypoxia pneumothorax, and patent ductus arteriosis, one of the most important factors that affects the risk for intracranial hemorrhage in the premature infant is the fact that premature babies have very little, if any, autoregulation as regards the cerebral circulation.

Therefore, anything that causes an increase or decrease in cerebral blood flow can be directly transmitted to the brain if the systemic blood pressure suddenly goes up or down.

The area of the germinal matrix is extremely fragile and prone to hemorrhage.

And then there is a problem regarding intra cerebral vasodilatation, which can happen in the presence of hypertension, hypercapnia acidosis, and vasoactive substances such as prostaglandin.

Classification of Hemorrhage

We use a classification that is based on serial ultrasound findings where we consider basically for grades for grade zero.

This is a normal brain with grade one hemorrhage.

This refers to hemorrhage involving the germinal matrix and also hemorrhage that is in the region of the choroid plexus.

The gloma portion in the atrium of the lateral ventricle grade two hemorrhage includes intraventricular hemorrhage, no ventricular dilatation with or without germinal matrix hemorrhage.

It used to be thought that intraventricular hemorrhage was a breakthrough of germinal matrix hemorrhage, but we've seen many babies who have intraventricular hemorrhage but no evidence of germinal matrix hemorrhage.

Grade threes according to the literature, refers to intraventricular hemorrhage, ventricular dilatation, and germinal matrix hemorrhage.

Based on a study that we've done in babies with grade three hemorrhage, we derived a sub classification in these babies that distinguishes between mild, moderate and severe degrees of intraventricular hemorrhage and ventricular dilatation.

Babies with mild are referred to as grade three A.

Those with moderate hemorrhage and dilatation are referred to as grade three B, and grade three C refers to babies with severe IVH and severe ventricular dilatation.

These babies may or may not have germinal matrix hemorrhage, whether they're an A or a B or a C within the grade three category.

We decided to do this study because we noticed a long time ago that when parents were confronted with news that their baby had hemorrhage in the brain, they often became extremely anxious and had difficulty bonding with their baby.

What we learned from our study is that there's quite a significant difference between mild hemorrhage, moderate and severe in terms of the outcome.

We'll talk a little bit more about this later, but suffice it to say that babies with mild hemorrhage and dilatation often have no structural damage to the brain on follow-up, whereas the babies with more severe intraventricular hemorrhage and ventricular dilatation have structural changes and often need therapy with grade four hemorrhage.

In addition to intraventricular hemorrhage, ventricular dilatation with or without germinal matrix hemorrhage, there is additional hemorrhage into the parenchyma of the brain.

So basically our classification allows for identification of infants in whom structural changes may be expected to resolve or progress and allows for identification of infants who may require intervention.

Most grade one and two hemorrhages show normal follow up on ultrasound most grade three a's show normal follow up on ultrasound or no changes.

Most grade three B's and C's have persistent structural changes, and with grade four hemorrhage, there is development of a communicating poor and cephalic cyst in the region of the parenchymal hemorrhage.

Germinal Matrix

Just a few words about the germinal matrix.

The germinal matrix is located just adjacent to the coth thalamic groove.

It is the zone of neuronal and glial cell proliferation.

It is highly cellular, richly vascular and metabolically active in the developing brain.

This area of the germinal matrix involutes by 34 weeks gestation, at which point it is no longer as vulnerable to developing hemorrhage.

The germinal matrix is quite susceptible to hypoxic changes.

Now when there's hemorrhage in the germinal matrix, we suspect this based on the fact that we will notice a small area of bright echogenicity that is inferior lateral to the frontal horn and posterior to the foramen of Monroe.

It may be unilateral, it may be bilateral.

Larger hemorrhages may cause focal compression of the inferior lateral margin of the ventricle germinal matrix hemorrhages may result in subependymal cysts within a few weeks after the insult.

And here we can see the right and left lateral ventricles with small cysts in the region of the germinal matrix.

This is the choroid plexus at the region of the forer of Monroe bilaterally as well as choroid plexus in the roof of the third ventricle.

So again, here is the thalamic groove.

There's a bright area of increased echogenicity adjacent to it.

One might ask, how do we know that this is hemorrhage?

For we know that non shadowing calcification could look the same, tumors could look the same.

Areas of infections such as an abscess that contains densely packed purulent material could look like this.

Just as in any other imaging study, we have to consider the gestational age of the baby and the risk factors.

So in a premature baby, an area of bright echogenicity in this very vulnerable portion of the brain is consistent with germinal matrix hemorrhage.

Now, choroid plexus hemorrhage may be manifest only by the presence of a somewhat lumpy, bumpy appearance to the gloma of the choroid plexus or even to other parts of the choroid plexus.

So here's the germinal matrix hemorrhage, and this is the area of the choroid plexus hemorrhage.

Intraventricular Hemorrhage

Now, intraventricular hemorrhage can result from intraventricular extension of a germinal matrix hemorrhage.

It may actually arise from the region of the choroid plexus, it may be unilateral or bilateral.

Initially, blood appears brightly.

A coic on ultrasound and it may be difficult to identify in a non dilated ventricle, and at times may be difficult to differentiate from a germinal matrix hemorrhage.

A large hemorrhage will form a cast of the ventricle.

This is an example of a very immature baby.

Notice.

There are no convolutional markings.

This is the interhemispheric fissure, the region of the corpus callosum.

Here's the cavem septum lucidum, and this is the left lateral ventricle, normal size choroid plexus, choroid plexus in the roof of the third.

These are the hippocampal gyri.

Notice choroid plexus here, but also notice that within the right lateral ventricle there is a small area of brightly, a coic material consistent with hemorrhage.

As we look somewhat more posteriorly, notice there are no convolutional markings implying this baby is less than 26 weeks gestation.

And notice that there is an area of bright echogenicity lying dependently within the occipital horn of this ventricle consistent with intraventricular hemorrhage.

Here's the para sagittal view, the frontal horn, the body, the atrium housing the gloma, which tapers toward the coth thalamic groove and the temporal horn.

And here we see the area of hemorrhage that is located dependently in the occipital horn.

So grade two is hemorrhage within the ventricle with no dilatation of the ventricular system.

I mentioned before that sometimes it can be difficult to decide is the hemorrhage in the ventricle or is it adjacent to the ventricle?

As a subependymal hemorrhage and very meticulous scanning is necessary to make that differentiation In a baby who has dilatation of the lateral ventricle, we begin to consider grade three hemorrhage.

If there's no parenchymal hemorrhage to put it into a grade four classification, it's important to know where the walls of the ventricle are.

Always look for the append lining, which is slightly koic even in babies who don't have hemorrhage.

And here we can see that there is essentially a normalized frontal horn, but as we get towards the occipital horn and towards the temporal horn, we see that there's dilatation.

There's also bright echogenicity that's in excess of the echogenicity that we would normally see in the region of the gloma of the choroid plexus.

There's some in the temporal horn, some in the occipital horn, and there is a bright area of echogenicity in the germinal matrix.

So this is mild hemorrhage, mild dilatation with germinal matrix hemorrhage consistent with a grade three A.

Now notice the difference in the appearance of a grade three B hemorrhage, which is moderate IVH moderate ventricular dilatation, and in this particular baby also includes germinal matrix hemorrhage.

So if we outline the ventricle here, we see that there is moderate dilatation of the ventricle.

This bright area of echogenicity represents the germinal matrix hemorrhage, and then there is a moderate size area of bright echogenicity that's occupying parts of the frontal horn and the body even extending into the atrium of the lateral ventricle, and there's increased echogenicity in the occipital horn as well as some in the temporal horn.

So this is a moderate degree of hemorrhage and dilatation as well as a germinal matrix hemorrhage.

So this is a grade three B.

Notice the extreme difference between the mild and the moderate degrees of intraventricular hemorrhage and dilatation compared with severe IVH severe ventricular dilatation and germinal matrix hemorrhage.

Here we have a very far anterior coronal view of the brain demonstrating large areas of bright echogenicity within the frontal horns right side greater than left.

Notice that instead of the ventricle maintaining a concave lateral wall, it's now convex, which raises the question of increased intraventricular pressure, and this is consistent with intraventricular hemorrhage that is severe.

Coming a little bit more to a mid coronal view, we see the right lateral ventricle, the left, and here we have the third ventricle.

We could see hemorrhage extending through the forer of Monroe from these dilated ventricles which are severely dilated into the third ventricle.

A posterior coronal view shows bright echogenicity more so than what we would expect with just the choroid plexus.

It's quite broad on the left side as well, but not quite as extensively.

So we have bilateral grade three hemorrhage.

Notice the para sagittal view.

There is an entire cast of the lateral ventricle formed by this huge amount of hemorrhage.

The frontal horn, the body, the atrium of the lateral ventricle in continuity with the body, the occipital horn, which is filled with blood as well as the temporal horn.

In fact, the echogenicity is so bright compared to the gloma of the chloride plexus that it totally silhouettes out the borders of the choroid plexus.

Resolution of Hemorrhage

Now what happens when there is a hemorrhage within the ventricular system?

Basically the clot will undergo a process of internal liqui faction.

The clot will retract from the ventricular walls, it will undergo fragmentation and absorption.

At times, septations will persist and characteristically.

There will be thickening and brighter echogenicity in the append lining that is obvious within one to six weeks after the hemorrhagic insult.

Sometimes there are some disruptions noted in the region of the append.

Well, here's the same baby.

As we look at the ensuing process of attempt at resolution, there is bright echogenicity in the region of the germinal matrix.

Here's the Kath thalamic groove, which is also showing some central decreased echogenicity indicating that it is beginning to undergo early liquefaction.

And then we notice that the bright echogenicity that was previously seen as a cast of the lateral ventricle is no longer totally brightly a coic, but we see a bright line that is the outline of where that major hemorrhage occurred.

Often people have difficulty seeing the difference between the clot as its undergoing resolution and the walls of the ventricle.

So I'm gonna show you the outline of the walls of the ventricle.

There's thickening and bright echogenicity in the frontal horn in the body of the lateral ventricle extending all the way out to the occipital horn.

Here's the temporal horn, and this is usually due to a glio reaction or adherence of blood cells to the append lining of the brain.

Here is the gloss of the choroid plexus tapering toward the coth thalamic groove and the temporal horn.

Notice that there is preservation of the per ventricular blush, so this is a clot undergoing liquefaction and undergoing retraction from the ventricular walls.

Well, so far as the ventricular enlargement is concerned, initially the enlargement is due to distention by the hemorrhage.

This enlargement may resolve, it may persist, it may progress.

One of the problems that is always of concern when there is a hemorrhage that is more severe than a grade three A is that the babies can develop post hemorrhagic hydrocephalus.

It may be obstructive, which is usually at the aqueduct of sylvius or it may be communicating.

And in this situation, the cerebral spinal fluid is not resorbed by the arachnoid granulations usually because of some hemorrhage around the brain as well.

There may also be an inflammatory type of appendicitis that can cause persistent ventricular magaly.

When the ventricles are large, it's not uncommon for the neonatologists if they see a enlarging head circumference to use lumbar punctures to try to relieve the pressure by removing some of the fluid at times ventricular punctures will be made to relieve the pressure by aspirating fluid.

At times when shunts are done too early and there is residual clot within the ventricle, the side holes of the shunt tube can become clogged and the shunt will be totally ineffective.

Well, here's the same baby that we looked at with a grade three C hemorrhage.

That's severe hemorrhage dilatation and in this particular baby also germinal matrix hemorrhage and we see that approximately a month and a half later there is marked dilatation of both the right and the left lateral ventricles as well as the third and the fourth ventricles.

Here's the midline sagittal view where picking up one of the ventricles, very wide foramen of Monroe, we see that there is an koic appearing third ventricle with the cerebral spinal fluid outlining the mass intermedia.

There's also a very prominent fourth ventricle.

Here's a good example of how the third and fourth ventricles may appear to be filled with koic fluid.

When the ventricle is widened, there are no specular reflectors that will be picked up by the ultrasound transducer, and so this is a very useful way of knowing that there is in fact dilatation of the third and fourth ventricles.

Here we can see some pressure on the cerebellum and we're looking at this very enlarged posterior horn of the lateral ventricle.

This is just an artifact and notice how compressed the occipital cortex is as well as the decreased depth of the parietal and the frontal parenchyma.

Grade Four Hemorrhage

Now with grade four hemorrhage, in addition to ventricular dilatation and intraventricular hemorrhage, there may or may not be germinal matrix hemorrhage, but there is hemorrhage in the brain parenchyma over time.

Usually within several weeks to a couple of months, there will be liquifaction of the infant brain In the area of insult with hemorrhage, the infant brain is relatively quite liquid and extremely vulnerable to degradation of the tissue.

In the presence of hemorrhage, intraparenchymal hemorrhage is most often a form of hemorrhagic paraventricular infarction.

It is associated with intraventricular hemorrhage in approximately 80% of cases and occurs on the side with more severe IVH.

The distribution is often frontal parietal, but it can extend into the occipital areas as well.

Over time, the po cephalic cyst will be demonstrated as a communicating cyst with the associated lateral ventricle.

Example.

This is a coronal view of the brain In an infant who has moderate dilatation of the left lateral ventricle, the right lateral ventricle is not seen distinctly because there is an bright area of increased echogenicity, not only in the region of the ventricle but in the subependymal region and in the brain parenchyma.

As we look more posteriorly, the findings show in distinctness of the ventricle with this huge area of hemorrhage in the parietal occipital region.

This is the choroid plexus in the atrium of the left lateral ventricle.

It appears that there's some hemorrhage in this ventricle as well and hemorrhage extending into the posterior portions of the right lateral ventricle.

The para sagittal view shows in distinctness of the lateral ventricle.

It appears that there is a germinal matrix hemorrhage, but in addition to hemorrhage in the region of the ventricle, there's also a frontal parietal occipital hemorrhage in the parenchyma.

While about one month later on this coronal view, we see that the lateral ventricles have enlarged that there is now convexity to the lateral walls of the lateral ventricles, presuming increased intracranial pressure.

The third ventricle is large, the temporal horns are large and notice that there is bright thickened append themal lining bilaterally thought to be due to a glio reaction or adherent blood cells.

There is also a large amount of contained material within the ventricle in the region of the previous hemorrhage.

It's beginning to undergo clot retraction and liquefaction, and at first look, one might think that the hemorrhage in the parenchyma is actually resolving satisfactorily because it looks like there are parts that show the same echogenicity as the unaffected brain parenchyma.

What in fact is happening is that this clot is undergoing dissolution and we can see that there's actually continuity and communication of this clot in the parenchyma with the intraventricular clot and there's still quite a bit of bright genicity within the brain parenchyma.

This is the beginning of the formation of a communicating poor cephalic cyst, para sagittal view baby's head is facing.

To our left, we see the frontal horn, the body, the atrium of the lateral ventricle, occipital horn, temporal horn.

Notice the thickened, the penal lining, and the fact that there is now beginning destruction of the deep white matter in the region of the previously noted grade four hemorrhage.

Also note that the intraventricular clot that had formed a cast of that ventricle is undergoing retraction from the walls of the ventricle and is undergoing internal liquefaction intraventricular hemorrhage depending on the severity may resolve within days to months.

And this is the left lateral ventricle we see the thickened dependable lining, the enlargement of the ventricle.

This is the gloss of the choroid plexus.

There's hemorrhage in the temporal horn as well as some residual clot in this very prominent occipital horn.

Well, one month later, this is what this unfortunate little baby's brain looked like.

We see that there is further dilatation of the left lateral ventricle and that there is complete destruction of the brain tissue in the region of the previous intraparenchymal bleed.

Para sagittal view confirms the tissue breakdown in the frontal parietal region extending into the more anterior portions of the occipital region and notice how little parenchyma there is left in this brain from the pressure of the poor cephalic cyst and the dilated ventricle.

Paraventricular Hemorrhagic Infarction

A few words about paraventricular hemorrhagic infarction.

It's thought that the parenchymal hemorrhage is basically due to increased pressure in the terminal vein in the subependymal region, which drains the medullary veins in the per ventricular white matter.

When there is a germinal matrix hemorrhage, intraventricular hemorrhage complex, the pressure from the hemorrhage can obstruct the terminal vein in the periventricular white matter.

This results in increased intraparenchymal and periventricular pressure, which can impair the blood flow to the brain from the arterial side and ultimately infarction can occur.

This is an example from Dr. George Taylor's work of a 26 week gestation infant who had a germinal matrix hemorrhage.

As we see just to the right of the Cajun septum lucidum and below this right lateral ventricle, there's some dilatation of the left lateral ventricle.

There's also a little hemorrhage in the germinal matrix on the left, but notice that there is satisfactory flow in the terminal veins as well as the internal cerebral vein.

Here's another example.

We can see that the terminal veins are displaced and draped over these bilateral germinal matrix hemorrhages, but there is satisfactory flow.

Contrast that with this.

This is a baby who has a grade four hemorrhage marked dilatation of both lateral ventricles.

We can see the more anterior parts of the ventricle here, the temporal horn, the temporal horn, lots of clot within the left lateral ventricle extending into the region of the deep white matter.

There's also clot within the temporal horn of the right lateral ventricle.

Notice what happens to the flow in the terminal veins.

On the right side, we see satisfactory flow into the internal cerebral vein, but on the left side, because of the pressure from this severe hemorrhage that has afflicted this baby's left lateral ventricle and the parenchyma, there is pressure on the vein so that there is inappropriate venous return.

There's quite a bit of morbidity and mortality associated with intracranial hemorrhage in the premature infant.

Once the grade of the hemorrhage is more than a grade one and two, grade one and two hemorrhage, the risk of morbidity and mortality is about the same as in a baby who has no hemorrhage, which is about 12 to 18% in terms of morbidity.

Grade three and four though is associated with a significant risk of major neurological handicaps such as developmental delay, mental retardation, motor disabilities, and contralateral hemiparesis of a grade four hemorrhage.

Intracranial Hemorrhage in the Term Infant

Now, intracranial hemorrhage in the term baby is far less common than in premature infants.

It generally is associated with asphyxia birth trauma, apneic episodes, seizures and coagulation defects, and the distribution of blood is quite different than the pattern that we've described with premature infants.

Here's an example of an infant who had been treated with heparin for a complication of an umbilical artery catheter that resulted in occlusion of the aorta and a renal artery.

We see a very bright area of increased echogenicity overlaying the region of the right lateral ventricle as well as the thalamus.

One might question how do we know this is hemorrhage?

Well, we know that this particular baby was treated with heparin and was at risk for bleeding, but tumor could look like this.

Non shadowing calcification, early abscess formation with tightly compacted purulent material could have the same appearance.

The most important thing is to understand the baby's gestational age and the clinical history as one comes to a conclusion as to what the underlying etiology is.

Now intracranial hemorrhage in the term infant may be clinically asymptomatic.

It is more likely to be involving the cerebral hemispheres, the cerebellum, the subarachnoid space, the subdural space, as well as the epidural space.

It's more common in infants who are small for gestational age.

There's a higher incidence in vaginal deliveries and a higher incidence in infants of color.

Cerebellar hemorrhage is an uncommon event.

It is associated with germinal matrix hemorrhage and intraventricular hemorrhage in preemies.

It's associated with traumatic delivery and coagulation defects.

In full term neonates, there is generally a very poor prognosis for cerebella hemorrhage as it is frequently fatal.

And here's an example.

This is a an occipital mastoid view where we see the cerebellum and we see this bright area of echogenicity that is involving the right cerebellar hemisphere.

A little bit easier to see on the view when we turn the baby's head on the film in the direction that we would like to see the cerebellum.

So this has a very poor prognosis.

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Penal hemorrhage in term infants can be difficult to diagnose with Ultrasound.

Ultrasound is less accurate for the diagnosis of subependymal hemorrhage.

Not so much anymore for cerebella hemorrhage because of the fact that we use the occipital mastoid views.

But the reason it's difficult to see the subependymal hemorrhage is that often it's not possible with ultrasound to see entirely over the convexity of the brain.

Subependymal hemorrhage is associated with asphyxia trauma and disseminated intravascular coagulation.

Typically we'll see increased echoes and widening of the horizontal portions of the sylvan fissure.

Subdural and epidural hemorrhage is usually secondary to trauma.

In term infants, it is difficult to detect with ultrasound.

We can use a standoff pad, a high frequency transducer, and we may use axial transtemporal views to aid in the diagnosis.

CT and MRI are the preferred imaging modalities for evaluation of extra axial hemorrhage and fluid collections.

Extra-Axial Fluid Spaces in Hemorrhage

We talked earlier on about how to measure the extra axial fluid spaces, and this is the ultrasound correlation in a baby who has an increase in the extra axial fluid spaces suspicious for hemorrhage.

So this is OC cortical, cranial cortical and interhemispheric fissure.

This baby came in to the ultrasound lab because of an enlarged head circumference was the child of two lawyers who had adopted the baby and had no clinical findings that they reported to the pediatrician, but the pediatrician was concerned that the baby's head circumference had grown outta proportion to the size of the baby's body.

While the coronal view shows that there is a separation of the outer margin of the brain from the inner margin of the cranial vault.

So there's increase in the extra axial fluid space, more so on the left than on the right, and there's some brighter echogenicity in the fluid around the right cerebral hemisphere suspicious for hemorrhage.

Note too that there is dilatation of the right and the left lateral ventricles and we don't see the septum lucidum here.

This is choroid plexus at the forer of Monroe bilaterally and here we see dilatation of the third ventricle.

As we scan more posteriorly in this coronal view, again, we see the bilateral enlargement of the extra axial fluid spaces left larger than right, but right more echogenic than left.

And this is choroid plexus coming around the areas of the atria of the lateral ventricles.

This area here looks somewhat unusual in that there is less echogenicity.

Well para sagittal view shows the frontal horn, the body, the atrium of the lateral ventricle, temporal horn, choroid plexus, and this large area that's devoid of echogenicity suspicious for apor cephalic cyst.

Here's the opposite side, notice the increased extra axial fluid space.

Same thing here and more echogenic.

And we have a ventricle that is mildly dilated compared to this which is mild to moderately dilated.

And here's the CT scan.

We see that there is apor cephalic cyst communicating with the occipital horn of this lateral ventricle that there is dilatation of the occipital horn.

The ventricle is relatively larger on the right side than the left, that there is a loss of brain parenchyma in the occipital region and that there are bilateral subdural collections.

Plain film of the skull documented the presence of multiple fractures.

So this baby actually was a victim of unsuspected child abuse until the physician noted the enlarged head circumference and sent the baby for imaging.

Here's another infant who came in because of seizures with a large head circumference greater than the 97th percentile.

We see on the left side that there is a normal extra axial fluid space, but here we see that there is a subdural collection that is quite hyper coic.

Here's another view looking at the same area.

So remember with sono, look at the extra axial fluid spaces we can be visualized.

And here we can see on the sagittal view that on the right side there is a large echogenic collection, which is thought to be hemorrhage.

Cephalohematoma is a bleed under the periosteum that is confined by the sutures.

As we look at this axial view of the skull, we can see the midline and the lateral ventricles, and there is this collection that is confined by the sutures outside the cranial vault.

Very commonly we see a mirror image artifact, which again we see with this cone down view.

This was scanned through a gel pad.

Subgaleal hematoma is a collection that is basically seen around the entire scalp of the baby's head.

As we look at the coronal as well as the sagittal views, we see that there is a hyper coic collection in the soft tissues around the cranial vault with no underlying abnormality.

At times we will actually identify bony abnormalities in the region of a subgaleal hematoma or a cephalohematoma.

In this axial view, we see the cranial vault and we see this large collection around the cranial vault in this baby with a subgaleal hematoma.

And in addition, we could see that there is a fracture of the underlying bone.

Hypoxic Ischemic Disease

Let's go on now and talk about the next type of insult to the infant brain.

Periventricular leukomalacia known as PVL.

This is hypoxic ischemic disease.

In the premature infant, We see an incidence of approximately four to 15% of PVL in low birth weight infants.

These are infants who weigh less than 1000 grams.

There is an association of PVL with maternal chorioamnioitis.

This is a condition that results in infarction and necrosis of the periventricular white matter.

Typically the frontal cerebral white matter near the forter of Monroe, as well as at the level of the optic radiations adjacent to the trigones of the lateral ventricles.

It's thought to be related to the fact that the vasculature in the per ventricular regions is immature and is actually a watershed area.

The junctional zone of the end arteries lacks collateral circulation in combination with a lack of cerebral vascular autoregulation.

In premature babies, they are at very high risk for having hemorrhage as well as necrosis.

Typical typical findings of PVL Include during the first 10 days, generally bilaterally, symmetric coarse gular broadbands of bright echogenicity in the periventricular white matter.

We may see these changes in up to about 28% of patients who actually have PVL so that the sensitivity of ultrasound in the first 10 days is not high.

Babies with PVL are generally attached to life support systems and therefore are not able to be safely taken to MRI for evaluation of the brain, even though this is a more sensitive examination.

To identify the findings of periventricular leukomalacia within the first 10 days of life with PVL, there's white matter gliosis, there's hemorrhage and there is edema in the brain, particularly in the deep white matter.

Typical ultrasound findings when we can see them consist of very bright coarse increased genicity in the deep white matter paralleling the lateral walls of the lateral ventricles.

Here we see the choroid plexus in the right ventricular atrium, and here we see the choroid plexus in the left lateral ventricular atrium.

Bright coarse echogenicity suspicious for hemorrhagic necrosis.

Right para sagittal view shows that there is a bright area of increased echogenicity in the deep white matter in the region where we normally would see the fine lines of the expected periventricular blush.

Remember that the choroid plexus is the brightest echogenicity within the brain.

And when the deep white matter echogenicity is similar to the choroid plexus or brighter than that, one has to be concerned about hemorrhage.

If we scan the brain within two to three weeks after the initial insult, what we'll see in the deep white matter are multiple small cysts due to necrosis and cavitation.

This is a mid posterior coronal view.

We're picking up the choroid plexus within the atrium of the left lateral ventricle.

There's a little bit of rotation of the baby's head, and so we're only picking up a small part of the gloss of the right lateral ventricle.

But notice that there's still bright echogenicity in the deep white matter with little tiny cysts scattered throughout.

And this is the parietal occipital region in a very far posterior coronal view, showing the bright echogenicity with the superimposed tiny areas of cystic necrosis and cavitation.

Right para sagittal view shows the extent frontal parietal occipital and we see a similar phenomenon in the left side of the brain.

So this is very typical of what happens within the two to three week period after the insult.

If we wait a little bit longer, somewhere between one and three months, we'll see that the cysts become larger.

We may see multiple cysts or the tissue between the cysts may disintegrate, and so it will look like there are single cysts.

These cysts range in size from millimeters to about two centimeters.

Over time, these small cysts may collapse and disappear and white malio scars can develop.

Thus, it's important to image these babies at the two to three week interval after birth because if we have a baby in which we can't see the changes within the first two weeks of life, if we miss our opportunity to see the cystic degeneration and we wait so long that the cysts may collapse and disappear, we may never know that there were structural changes to the brain.

There may also be decrease in the cerebral myelin.

The ventricles can get larger, particularly in the region of the trigone and the occipital horns.

As the brain undergoes atrophy, some of the largest cysts may resolve or they can develop into non communicating porn cephalic cysts.

And here's the same baby a couple of months later in which we see that there are multiple coalesced large cystic spaces in the deep white matter that are totally separate from these prominent right and left lateral ventricles.

This is the cavem septum lucidum note that there is still maintenance of the concavity of the lateral walls of the lateral ventricles, implying that this is atrophy and not increased intraventricular pressure.

Here's the para sagittal view of one of the cerebral hemispheres.

The opposite side looked identical.

We see that there are multiple cystic spaces in the deep white matter consistent with periventricular leukomalacia.

PVL is associated with major neurodevelopmental handicaps.

The babies can have developmental delay.

They may develop symmetric spastic diplegia, the lower extremities more so than the upper extremities.

The necrosis basically involves the descending fibers from the motor cortex, which run in the periventricular frontal white matter.

And so these babies can become quite spastic.

If they have very severe lesions, they may have spastic quadriparesis.

And the sooner these babies get enrolled in physical therapy programs, the better chance they will have to reduce the spasticity.

They may also have severe visual impairment and cortical blindness intellectual deficits are less common.

So this is basically the insult that leads to cerebral palsy.

Hypoxic Ischemic Encephalopathy in Full Term Infants

Now, full term babies have a different pattern of insult when they are exposed to hypoxia or ischemia.

That results in encephalopathy during the 36th to 40th week of gestation.

The watershed area of the brain moves towards the cortex by 44 weeks.

The watershed is between the end fields of the anterior, the middle, and posterior cerebral arteries and is completely peripheral.

And so hypoxic ischemic encephalopathy in full term infants is more likely to involve the cortex and the subcortical regions of the white matter.

There are some findings that we can look for on ultrasound.

Initially, the findings are indicative of changes that could suggest cerebral edema.

Remember too that patients who have encephalitis can have similar findings.

But again, the gestational age, the clinical presentation and lab analysis of cerebrospinal fluid can help differentiate edema can result from encephalitis as well.

So typically what we're going to see initially, a slit like ventricles where the lumen of the lateral ventricle is extremely difficult to discern.

There will be obliteration of the extra axial fluid spaces, ssci and interhemispheric fissure.

There will be increased cerebral echogenicity diffusely or perhaps more superimposed focal areas of increased echogenicity.

And it can be seen in the subcortical areas, the periventricular white matter, the phite, and the basal ganglia.

Here's an example of cerebral edema.

And I can remember the first time I saw this on ultrasound where the technologist called and said, I just can't seem to demonstrate the architecture of the brain and the normal anatomy.

And they started playing with the dials of the machine to see whether or not they could clarify the image.

Well, in fact, with cerebral edema, we lose the usual architectural markings.

Notice that there is increased echogenicity.

There's a little bit of patchy superimposed, increased echogenicity.

We don't see the interhemispheric fissure.

Well, we can't really see the lateral ventricles well because of the fact that there is edema and compression of the ventricles.

This is a mid posterior coronal view, and I think you can recognize the compressed gloma of the choroid plexus as they wrap around the atria of the lateral ventricles.

But overall hazy increased echogenicity with some areas appearing somewhat more patchy.

Here's the midline view.

Difficult to see the detail completely of the corpus callosum, but we can surmise that this is the corpus callosum, partial obliteration of multiple sci.

We can't really see the third and fourth ventricles.

Well, here's the region of the cerebellum, and this is a very far sagittal lateral view of the insula with marked decrease in the visualization of the cerebral sulci.

And here's the sagittal view, showing the region of the lateral ventricle demonstrating that we can't see the lumen of the lateral ventricle because of the pressure of the cerebral edema causing the walls of the ventricles to be immediately contiguous with each other throughout the ventricle.

This is the gloss of the choroid plexus and there's also some obliteration of the fine lines in the periventricular blush.

What happens later on is that the brain can undergo atrophy, which will be manifested by increase in the size of the ventricles and increase in the size of the extra axial fluid spaces, including the fluid around the sulci and between the brain.

In the region of the interhemispheric fisure, multi multicystic encephalomalacia can develop secondary to necrosis.

And this is a baby who had had cerebral edema.

In follow-up, we see the enlargement of the lateral ventricles.

Notice the maintenance of the concavity of the lateral walls, which is consistent with atrophy rather than increased intraventricular pressure.

Notice the widening of the extra axial fluid spaces.

Here's the para sagittal view showing the dilatation of the lateral ventricle as well as the increase in the extra axial fluid space consistent with atrophy that developed secondary to hypoxic ischemic disease.

Another baby, in addition to having increase in the extra axial fluid space over time and dilatation of both right and left lateral ventricles had small areas of cystic degeneration scattered throughout the cerebral hemispheres.

So this is a rather extensive dense, hypoxic ischemic insult that involved the cerebral hemispheres bilaterally.

Cerebral Cortical Infarction

Cerebral cortical infarction is uncommon in neonates and young infants.

Predisposing factors include prematurity, asphyxia, congenital heart disease, polycythemia, which can result in hyper viscosity and decreased arterial perfusion, trauma, meningitis and thromboembolism.

Most often it is in a distribution of the middle cerebral artery.

And initially we'll see during the acute phase an absence of gyral definition, an absence of vascular pulsations, altered parenchymal echogenicity, a territorial type of distribution, possible midline shift and ventricular compression.

After there is some resolution, one may see return of the pulsations of the brain gradually and the development of cystic spaces.

It's quite common for infants who have had a cerebral cortical infarction to develop seizures and hemiplegia following a stroke.

Here's an example of a baby who was born with thrombocytopenia and petee.

It was noted during intrauterine life.

And then on this postnatal sonogram that there is severe dilatation of the right lateral ventricle.

There are areas of bright echogenicity within the frontal horn in the body, in the occipital horn within this ventricle consistent with hemorrhage and the very far para sagittal view shows that there is a large area of bright echogenicity with hypoechoic appearance somewhat more centrally implying ischemic tissue breakdown and developing cephalic.

Here's a coronal view that is set side by side with the CT scan showing the dilatation of the right lateral ventricle, mild dilatation of the left la I'm gonna fix that.

Showing the moderate to severe dilatation of the right lateral ventricle, mild to moderate dilatation of the left lateral ventricle and the tissue down in the cerebral hemisphere adjacent to the ventricle.

Summary

So in summary, we've discussed insults to the infant brain that consists of hemorrhage and hypoxic ischemic disease.

Thank you very much.