Echogenic Lesions in Cranial Sonography by Dr. George Taylor.
In this talk, we will discuss focal echogenic lesions seen in cranial sonography in an effort
to expand the differential diagnosis of these lesions beyond the simple hemorrhage.
These seven infants, each of whom have a focal echogenic lesion, they look quite similar.
However, each of them has a different diagnosis that we will summarize at the end of the talk.
The differential diagnosis of these lesions includes, in addition to hemorrhage, focal
neuronal ischemia or stroke, both primary and secondary calcifications, gliosis, hypermyelinization,
melanosis, and fat.
Although they can have a very similar appearance, one can usually narrow the differential diagnosis
somewhat by knowing the gestational age, how old the child is post-gestationally, knowing
both the history and type of hypoxemia or asphyxia, and the presence of associated anomalies.
These three infants show the typical pattern of premature hemorrhage, extending on the
left side from germinal matrix through intraventricular in the center and intraparenchymal peripherally
on the right side.
These hemorrhages are typically brightly echogenic initially and gradually become liquefied and
less echogenic over time.
However, hemorrhages in term and near-term infants are often different in location, and
cause, and appearance.
Here are two near-term infants with a clotting abnormality.
The infant on the left side has a brightly echogenic thalamic hemorrhage.
The infant on the right has post-hemorrhagic hydrocephalus and a moderately echogenic clot
in the parietal bone.
Both infants were infants of mothers who had lupus and had platelet antibodies.
In patients who have poorly clotted blood, the blood can range in echogenicity from the
typical brightly echogenic blood to loosened blood.
And often the blood will have an echogenicity similar to surrounding brain.
So the extent of the hemorrhage may be difficult to assess initially, because there is very
poor distinction between blood and underlying brain.
This is particularly the case in infants who are treated with ECMO where there is a cuagulopathy
that is quite common during this time.
In another child who is near-term with critical coarctation of the aorta, we see a flame shaped
hypertensive hemorrhage in the deep white matter.
Now this patient has had diffuse hypoxic ischemic injury-- is full term.
And we can see these focal bright bands of increased echogenicity surrounding the gyri
in the central portions of the brain.
These represent secondary hemorrhages in the subcortical U-fibers.
And so secondary hemorrhage can be seen as brightly echogenic lesions that occur not
as result of a clotting abnormality, but as a result of underlying abnormal brain.
And then here we have a child who is approximately 30 weeks, who has symmetric bilateral basal
ganglia, echogenic lesions that are moderately bright.
But rather then, unlike hemorrhages they do not exhibit a mass effect.
They do not displace normal structures.
And so in this situation we need to include focal neuronal ischemia.
At pathology this child had focal neuronal injury in the basal ganglia.
This child has very similar echogenic lesions in both the putamina and globus pallidus as
seen on ultrasound and post-mortem CT and MRI.
This child was treated with ECMO for pulmonary hypertension.
And in pathology we expected to see focal hemorrhages.
However, on the growth specimen there was no abnormality.
Only during microscopic analysis did we see that these were related to microcalcifications.
So microcalcifications can occur secondary to ischemia after one to several weeks post-insult
and can result in diffuse and rather even focal echogenic lesions throughout the deep
white matter.
The other pattern of calcifications that we see is seen in this child who is 37 weeks,
and presents with seizures.
You'll note, in addition to the multiple coarse calcifications that are in the periventricular
white matter, this infant has a very limited sulcation despite being near term.
This child had been infected with cytomegalovirus during pregnancy.
And these focal calcifications represent secondary granuloma formation from the CMV infection.
Here's another infant who has brightly echogenic symmetric lesions in the basal ganglia.
This child is now four weeks post the hypoxic ischemic injury.
And these lesions gradually appeared over the last week.
At autopsy, when this child died two days later, these areas represented focal gliosis.
We do not generally see gliosis in premature infants.
And this is a phenomenon that's only seen in term or near-term infants.
Now here is another child who is term, who had low Apgar scores following repeated compression
of the cord during labor.
Now three to four weeks post-birth we now see these brightly echogenic symmetric basal
ganglia lesions without mass effect at all.
At pathology these were status marmoratus.
This is an unusual condition.
We've only seen two cases at our institution that were seen on ultrasound.
They're seen more commonly in term than pre-term infants and are seen in this situation of
repeated episodes of brief ischemia, such as repeated cord compression.
These lesions affect the glutamate-bearing neurons in areas that are very rich in these
neurons such as the basal ganglia.
There is neuronal loss and secondary gliosis.
But the most striking part of this is the hypermyelinization of the basal ganglia and
capillary proliferation.
This results in bright light bulb like appearance to the basal ganglia, typically there and
in the thalamus.
This infant was term, being treated with ECMO for pulmonary hypertension, and developed
a geographic pattern of increased echogenicity involving the distribution of the right middle
cerebral artery, here seen in the image to the left, compared to the normal side on the
right side of the screen.
This is at day one.
By day eleven we can see that this lesion has become very dense.
There is loss of sulcal demarcation with a mass effect.
And on CT we can see that this was a middle cerebral artery stroke with secondary hemorrhage.
Now the size of the hemorrhage on CT is much smaller than the echogenic lesion on ultrasound.
So it is very difficult for ultrasound to distinguish between hemorrhage and stroke
or ischemia, because they have a very common and very similar appearance.
Focal stroke early on shows a pattern of diffused geographic increased echogenicity with preservation
of the gyral and sulcal pattern, and diminished vascular pulsations on color Doppler.
After two to three days in the next week or so, there is progressive increase in echogenicity
with loss of the anatomic definition, and the appearance of this peripheral luxury perfusion
very well shown on color Doppler.
And late, after several weeks, now we see atrophy, generalized or regional atrophy,
and reduced cerebral blood flow.
Focal stroke seems to be, has a distribution in the middle cerebral artery.
Almost exclusively it is unilateral in the majority of cases.
And it has an interesting predilection to the left side compared to the right.
We see this in patients with polycythemia, or hypercoagulable states, in patients who
have embolized from other sources, patients who have been exposed to cocaine prenatally,
patients who have had a vascular anomaly or generalized circulatory failure.
Now the other area, or the other type of focal echogenic lesion is commonly seen in patients
who have other anomalies of the brain.
And here we see this 39 week infant who is dysmorphic and has seizures.
And what we see on the sagittal mid-line image is only a partially formed corpus callosum,
and these brightly echogenic lesions in the midline, posterior to the genu of the corpus
callosum.
In this situation these brightly echogenic lesions represent callosal lipomas.
In patients who have severe vasculitis or vasculitis secondary to meningitis, one can
see focal areas of ischemia and stroke as shown in this patient who had Citrobacter
cerebritis and extensive coagulative necrosis of the right frontal lobe.
Over time the brightly echogenic lesions seen in the upper right image gradually devolved
into a liquefactive area of anomaly.
It is very difficult to tell the difference between an abscess and liquefied ischemic
brain in these infants.
Finally, we have another child who presented at six months of age with the clinical diagnosis
of meningitis.
And we see a very heterogeneous echogenic mass in the left hemisphere of the child.
And initially this was thought to be a hemorrhage.
However, on color Doppler sonography we can see that this echogenic lesion has hyperemia
and flow within the lesion.
So it cannot be a clot.
This child had a choriod plexus carcinoma.
These are unusual, but at times difficult to separate between a clot and a tumor without
color Doppler sonography.
And finally have a child with a giant melanocytic nevus in a bathing suit distribution.
These infants may have congenital neurocutaneous melanosis in between 2 and 45% of patients.
If this is a neurocutaneous melanosis they may develop melanocytic tumors in the leptomeninges.
A small percentage of these infants will have the nevus degenerate into melanoma.
And in this child, we have multiple focal echogenic lesions throughout the posterior
fossa and mid-brain that were thought to be neurocutaneous melanosis.
So we go back to the original seven infants that we saw where the lesions include germinal
matrix hemorrhage, basal ganglia ischemia, neurocutaneous melanosis, a callosal lipoma.
In the second row we have gliosis.
We have diffuse basal ganglia calcification, secondary to ischemia.
And finally, we have a choroid plexus carcinoma.
I hope that this talk helped expand the differential diagnosis of echogenic lesions in cranial
sonography.
Please help us improve the content by providing us with some feedback.