3. Introduction
An extremely important neuroimaging technique in neonates & infants.
Well-established technique in providing clinically important information in a
convenient and safe bedside environment
First line investigation in assessment of the unwell or hemodynamically
unstable neonate.
Best line of investigation : MRI
4. Evolution of Cranial USG
EVOLUTION OF
CRANIAL USG
<1980 1980-2000 1990-2000
B – MODE USG
TRANSCRANIAL
DOPPLER
A – MODE USG
5. Advantages of cranial ultrasound
o Safe
o Bedside- compatible
o Reliable
o Early imaging
o Serial imaging :
Brain maturation
Evolution of lesions
o Inexpensive
o Suitable for screening
6. Indications
Screening for hemorrhage or parenchymal injury
Premature infants – all < 1500 g or < 32 weeks gestation
Follow-up of hemorrhage, post-hemorrhagic ventricular dilatation and peri-
ventricular leucomalacia
Congenital malformations of brain
Follow-up of antenatally detected brain abnormalities
Cranial dysmorphism
Sudden deterioration in clinical conditions
Signs and symptoms of CNS disorders
7. Methods of cranial ultrasonography:
All aseptic precautions should be
followed
Must be done in a warm environment
When baby is quiet or after feeding
Baby is placed in the supine position
Care should not be taken to not move
the infant
Transducer should be cleaned
thoroughly before and after the
examination
Coupling gel is applied to the
transducer
8. Methods of cranial ultrasonography:
Select the appropriate probe
Select the appropriate preset
Adjust the depth, gain and time gain
compensation settings
Probe is then firmly placed over the
fontanelle
Pressure over the anterior fontanalle
should be avoided, especially in the
premature critically ill neonate
9. Types of probes
High-frequency
sector/phased array
transducer with a small
footprint probe
• Transducers: 5 – 7.5 – 10
Mhz
• Preterm : 7.5 Hz
• Standard examination : use
7.5 – 8 MHz
Higher frequency linear
transducer (10 Mhz) in tiny
premature infant and/or
superficial structures
Lower frequency sector /
linear transducer ( 5 Mhz)
in Large infant, thick hair,
and/or deep structures
12. SONOGRAPHY PRINCIPLES
The normal brain is always nearly symmetric. But symmetric is NOT ALWAYS normal.
White matter looks like white matter, Grey matter looks like grey matter.
(Grey matter – Hypoechoic, White matter – Hyperechoic)
CSF – Anechoic
Choroid plexus / small hemorrhages / areas of infarct – Hyperechoic
Echogenicity of white matter < Echogenicity of choroid plexus
Subarachnoid space – Anechoic with vessels
Subdural space – Anechoic without vessels
17. Corpus Callosum
• Horizontal bundle of nerve fibers connecting
both hemispheres
• Largest white matter structure consisting of
more than 200 axons
• Components:
Rostrum
Genu
Body
Splenium
18.
19. Basal Ganglia
• Collection of grey matter
structures at the base of the
brain
• Components:
Caudate Nucleus
Globus pallidus
Putamen
• Caudothalamic groove
20.
21. Ventricular System
• Series of chambers in the brain filled with
cerebrospinal fluid.
• Contains Choroid Plexus
• Components:
Paired lateral ventricles
Third ventricle
Fourth ventricle
22. LATERAL VENTRICLE
FORAMEN OF MUNROE
THIRD VENTRICLE
CEREBRAL ACQUEDUCT
FOURTH VENTRICLE
FORAMEN OF LUSCHKA AND MAGENDIE
SUBARCHANOID SPACE
SAGITTAL SINUS
24. Choroid Plexus
• Network of epithelial cell, capillaries and connective tissue
• Creates CSF and filters waste
• Located in lateral, 3rd and 4th ventricles
• Hyperechoic.
3 DOT SIGN
25. Acoustic windows
Anterior fontanelle - Most
cranial ultrasounds are
performed used till 12 – 14
months)
Supplemental windows :
1. Posterior fontanel
2. Mastoid fontanel
3. Temporal window
Imaging through a
supplementary window
should be performed if any
abnormality is detected in
sagittal or coronal plane.
27. CORONAL VIEWS
Transducer should be placed in the middle of
the Anterior fonatnel
Plane - passing from ear to ear. Marker on
transducer should point to baby’s right
Transducer is angled as far forward and
backward as possible to scan coronal images
in sequential manner
28. CORONAL PLANES
C1 – Frontal lobes
C2 – Frontal horns of lateral ventricle
C3 – Third ventricle
C4 – Posterior to foramen of Monro( level of cerebellum)
C5 – Level of trigone of lateral ventricles
C6 – Level of occipital lobes
35. SAGITTAL PLANE
Transducer rotated at 90 degrees for
scanning in sagittal plane
Probe should be parallel to the AP
diameter of the cranial vault, marker
should point towards baby’s noise.
46. Normal variants mimicking pathologic
abnormalities
1. Persistent fluid filled spaces
2. Mega cisterna magna
3. Assymetric ventricular size
4. Choroid plexus variants
5. Periventricular cystic lesions
6. Hyperechoic white matter pseudolesions or periventricular halo
7. Immature sulcation in premature infants
8. Lenticulostriate vasculopathy
9. Calcar avis
47. Persistent fluid filled spaces
Common finding in
healthy neonates
Occasionally persist
into adulthood and
are a normal variant
of no significance
Include:
1. cavum septi
pellucidid ( CSP)
2. cavum vergae
3. cvaum veli
interpositi
48. Cavum Septum Pellucidum
• Midline fluid filled structure between anterior horns of lateral ventricle
• Fetal neurodevelopment marker
• Usually fuses by 6 months, persists in 15% of adults
52. Mega Cisterna magna
The typical cisterna magna is less than 8 mm in
both the sagittal and axial planes.
A mega cisterna magna measures greater than
8 mm and is seen in 1% of post-natally imaged
brains.
A mega cistern magna is a normal variant
distinguished from an arachnoid cyst by its lack
of mass effect .
53. Assymetric ventricular size
• Normal ventricles measure less than
10 mm in transverse diameter
• 60% of full term and 30 % of
premature infants having ventricles
smaller than 2- 3 mm.
• Asymmtery between the sizes of the
ventricles has been observed in 20 –
40 % of infants.
54. Choroid plexus variants
• Choroid cysts smaller than 1 cm are incidentally
noted in 1 % of infants at autopsy.
• At prenatal US, it is predictive of autosomy 18
especially if large,and bilateral
• Variation sin shape of choroid plexus can be seen –
lobular or bulbous variants
55. Connatal cysts
String of pearls
Also called subfrontal / frontal horn
cysts
Seen most often during early
postnatal period and may regress
spontaneously
Appear as bilateral symmetric cysts
adjacent to the frontal horns, just
anterior to the foramina of Monroe.
Usually appear in multiples and
appear as a string of pearls.
56. Hyperechoic white matter pseudolesion
/periventricular halo
Apparent echogenic areas that are
visualized only in one plane
Occur as artifacts due to anisotropic
effect
Additional images obtained at a 90
degree angle resolve the finding and
prevent misinterpretation.
Periventricular white matter
pseudolesions and halos are
normally less echogenic than the
adjacent choroid plexus
57. Immature sulcation
Infants born before the 24th week possess a smooth cerebral convexity
exhibiting only the occipito-parietal and sylvian fissures
A diagnosis of lissencephaly should not be made in newborn < 24 weeks
of gestation
58. Lenticulostriate Vasculopathy
Nonspecific thickening of
the lenticulostriate artery
walls secondary to a variety
of pathologic conditions
and infections
Seen on sonography as
unilateral or bilateral
branching, linear or
punctate increased
echogenicity within the
thalami
Resolves in 32 – 50 % of
premature infants.
59. Calcar Avis
It is a paramedian protusion
of the calcarine gyrus into the
medial aspect of the lateral
vent at the junction of trigone
with the occipital horn.
It may simulate a
intraventricular hemorrhage.
61. GerminalMatrix
• Fetal structure that involutes by 36 weeks
• Highly vascularized structure
• Located in the subependymal region of the
caudo-thalamic groove
• Origin of hemorrhage in premature infants.
62. Intra-cranial hemorrhage – Germinal matrix hemorrhage
More common in premature infants (50%)
Most common neurological complication in preterm infants
20 – 25 % are asymptomatic
90% of hemorrhages occur in first week of life, 1/3rd on first day
Follow with weekly Ultrasound to evaluate for hydrocephalus
68. Grade IV – Intra-ventricular hemorrhage
evolution
69. Periventricular leucomalacia(PVL) or White
matter necrosis ( WMN)
Hallmark of hypoxic ischemic insult in preterm neonates
Leuco : white, malacia : softening
It is a white matter disease that affects the periventricular zones.
Causes : Ischemia , infection, vasculitis
PVL presents as areas of increased periventricular echogenicity.
occurs most commonly in premature infants (<33 WOG (38% PVL) and
<1500 g birth weight (45% PVL).
70. DeVries classification of PVL grading
• Grade I : Prolonged periventricular flare
present for 7 days or more.
• Grade II : Presence of small – localized
fronto-parietal cysts.
• Grade III : Extensive periventricular cystic
lesion involving occipital and fronto-parietal
white matter
• Grade IV : Areas of extensive sub-cortical
cystic lesions.
76. Pattern of hypoxic ischemic injury
Neonate Moderate Severe
Premtaure Periventricular leucomalacia
Thalamic, basal ganglia and
brainstem
Term
Parasagittal white matter in
cortex
Thalamic, basal ganglia,
brainstem and perirolandic
white matter
77. Hydrocephalus
Excessive accumulation of CSF
in the ventricular system or
subarachnoid spaces or both.
Results from imbalance in
absorption and production of
CSF or due to an obstruction to
the free flow of CSF.
Types :
1. Communicating ( Extra-
ventricular obstruction)
2. Non- communicating ( Intra-
ventricular obstruction)
79. LEVENE INDEX : Up to 40 weeks
* Absolute distance between the falx and the lateral
wall of the anterior horn in the coronal plane at the
level of third ventricle.
VENTRICULAR INDEX : > 40 weeks
*Ratio between the lateral sides of the
ventricles and the biparietal diameter.
80. CRANIAL DOPPLER SONOGRAPHY
Vessels identified in Cranial Doppler :
ACA ( A1 and distal segment), internal carotid artery and basilar
artery, internal cerebral veins and vein of Galen
Superior sagittal sinus and straight sinus
AF and trans-temporal (squamous portion of temporal bone)
approach
Circle of willis is best seen through transtemporal approach
81. Brain – low resistance vascular bed.
Continuous forward flow should be
seen in arteries in both systole and
diastole
Doppler Imaging :
o Circle of Willis
o Region of vein of Galen
Normal RI : 0.6 – 0.9
<0.5 and > 0.9 : Abnormal
82. Resistive index
• Highest in premature and decreases upto 2
years of age.
• General approximation :
Premature – 0.8
Term – 0.7
1 year – 0.6
2 year – 0.5
83. TYPES OF
CYSTS
LOCATION
CONNATAL CYST
At or just below the supero-lateral
angles of frontal horn or body of
lateral ventricles and anterior to
foramen of Monroe
SUBEPENDYMAL
CYST
Below the external angles of frontal
horn or body of lateral ventricles
and posterior to foramen of Monroe
PERI-
VENTRICULAR
LEUCOMALACIA
Above the angles
Periventricular cystic lesions
84. Congenital brain anomalies
Disorders of
organogenesis
Disorders of
diverticulation
Disorders of
sulcation and
migration
Disorders of
histiogenesis
Chiari II malformation
Dandy walker malformation
Corpus callosal agenesis
Schizencephaly
Lissencephaly
Holoprosencephaly
Vein of Galen malformation
Pellucidal agenesis
92. Vein of Galen Malformation
• Fistulous connection
between cerebral arteries
and median prosencephalic
vein.
• m/c AV malformation in
neonatal period
• 2 types :
Choroidal - 90%, presents
in neonate as chf and
intracranial bruit
Mural – presents in infancy
with developmentak delay,
seizures and hydrocephalus
93. Limitations
Image quality is dependent on the size of the acoustic window available
Evaluation of superficial structures id difficult
Myelination is not visualized
Diffuse white matter injury are not very well detected
Presence of scalp hair
94.
95. References
1 . Rumack CM, Levine D. Diagnostic ultrasound. Elsevier Health Sciences;
2017 Aug 8.
2. Allan, P.L., Baxter, G.M. and Weston, M.J., 2011. Clinical Ultrasound, 2-
Volume Set E-Book: Expert Consult: Online and Print. Elsevier Health
Sciences.
3. AIIMS – MAMC – PGI’s Comprehensive textbook of Diagnostic Radiology
Describe a screening head ultrasound
Know the screening protocol for cranial usg
Perform a head ultrasound
Role of MRI : can detect brain maturation, can detect lesions that are difficult to be detected on sonography
Allows detection of diffuse and noncystic white matter lesions in preterm infants and diffusion weighted imaging allows very early detection of hypoxic ischemic brain injury.
A - mode : for demonstration of midline shift
B – mode : for pathologies
Safe – no ionizing radiation
Incubator safe , no hassle of shifting the baby
Premature infants : m / c cause of intra-cranial hemorrhage
Seizures, hypotonia, microcephaly and unexplained poor feeding at term
Aims : Exclude/demonstrate cerebral pathology
Assess timing of injury
Assess neurological prognosis
Help make decisions on continuation of neonatal intensive care
Optimize treatment and support
– hand washing, sterile gowns caps, masks and gloves
AF is small : phased array transducers of small footprint and wide insonation angle ( 140 degrees)
7.5 – optimal visualization of per-and intra- ventricular areas of brain
Superficial structures : cortex, subcortical white matter, sas and sss
Deeper structures : posterior fossa and basal ganglia in full term infants
Sector probe with small footprint : provides a sector filed of view, generates a cone shaped image originating from a small apex
The brain is divides into 3 main parts- the cerebrum/ forebrain : most cephaliod portion , cerebellum(hindbrain) and the brainstem which starts from below the crebellum all the way down to the spinal cord/canal and consists of pons, midbrain and medulla. The bra
in has many convolutions called the sulci nd gyri,these increase the surface area of the brain accumulating more brain tissue.
The cerebrum is divided into 4 sections: frontal and parietal : by central sulcus…frontal, parietal and temp by lateral sulcus/ sylvian fissure.
The cerebrum is also divided into 2 hemispheres : the right and the left.. These hemispheres are connected by corpus callosum
(posterior view of a sheep brain showing CC, rt nd left hemispheres, cerebellum and spinal cord)
Translation of brain anatomy to sonography needs understanding of sonographic physical principles.
NORMAL BRAIN IS ALWAYS NEARyT SYMMETRIC. This fact allows for detection of early changes of infarction or focal ischemia.
The superficial pia mater should be seen as a thin, well-defined hyperechoic layer immediately overlying the hypoechoic cortical gray matter, which in turn overlies the hyperechoic white matter.
.
SUBARCHANOID SPACE : contains many vessels unlike subdural. it is symmeteric
This image displays normal gray- white matter differentiation in a term neonate. (rule of 3 : all these 3 layers are usually seen an are distinguishable)
SUBARCHANOID SPACE : contains many vessels unlike subdural. it is symmeteric
(PRESSURE OVER THE ANTERIOR FONTANELLE SHOULD BE AVOIDED IN PREMATURE INFANTS – AS IT CAN SUBARCHANOID SPACE OBLITERATION)
The superficial pia mater should be seen as a thin, well-defined hyperechoic layer immediately overlying the hypoechoic cortical gray matter, which in turn overlies the hyperechoic white matter
This image displays normal gray- white matter differentiation in a term neonate. (rule of 3 : all these 3 layers are usually seen an are distinguishable)
(PRESSURE OVER THE ANTERIOR FONTANELLE SHOULD BE AVOIDED IN PREMATURE INFANTS – AS IT CAN SUBARCHANOID SPACE OBLITERATION)
These are the structures which we see almost always and are important to rule out anomalies and for orientation to landmarks
Sonographic image showing IF : red line and rt + left cerebral lobes/hemispheres
Anatomical drawing of the same.
Within the interhemispheric fissure, we have falx cerebri – which is the invagination of the dura matter, it goes down into the groove (dura matter is covering of the brain/ part of meninges) -- this is an anatomical section showing the falx and surrounding dura.
Green colour – tentorium that separates cerebrum and cerebellum
This is a deep horizontal fissure, where as interhemi fissure was a deep longitudinal and midline fissure.. this is horizontal and lateral
IT IS ECHOGENIC - COZ OF THE PRESENCE OF MCA IN IT
(Insula : involved in consciousness/related to emotions: empathy,compassion / reg of body homeostasis:taste,perception/motor control to name a few)
It is a very important and large structure that connects both hemispheres…(picture :we can see the fibers cross over, this is one hemi and other hemisphere, they are all the nerve fibers—they allow communication between 2 hemispheres)
IMPORTANT FOR EYE MOVEMENTS, COGNITION, AND TACTILE LOCALIZATION
REPORTEDLY LARGER IN FEMALES
Sonographic coronal image showing CC and white matter tracts going out ( inter fissure, lat vent, CSP , 3rd vent)
Sonographic sagittal image showing the components .
Important in motor learning/ eye movements/motivation. Between the caudate and thalamus- we have caudothalamic groove which is important for sonography- site for germinal bleeds.
caudate : hypoechoic
Echogenic choroid plexus.. CTG is the area where germinal cortex is present.(which well discuss it a little later)
Any echogenicities same or more ehogenic to CP when seen in CTG indicated haemorrhage.
In very young fetuses, vent system has germinal matrix all around
Points
Typically in USG we can only see CP in lat vent and in the roof of the 3rd vent , 3 echogenic foci : 3 DOT SIGN
Choroid plexus in a premature infant has a lumpy bumpy appearance with prominent echogenicity. Shouldn’t be confused with a intra-ventricular clot.
Echogenic choroid plexus is not seen in the frontal horn anterior to the foramin of monro or occipital horns.
Doppler evaluation – chroid plexus flow is seen and absent in hemorrhagic clot.
AF : opens till 2 years but we scanning is : 1till 2-14months
PF : opens upto 3months
Excellent window to image the supratentorial part of the brain
Located at the junction of coronal and sagittal sutures
Remains open for the first 12 – 14 months of age.
(Parasagittal view – probe to be angled right and left fro mid-sagittal view
In very premature babies we can also see the outline of the lens when angulated anterior enough
@ level of frontal horn
Lateral ventricles are larger in preterm infants
CSP – fkuid filled space bw frontal horns
Cc – lies superior to CSP giving rise to tram-line appearance
Caudate nucleus present below lateral ventricle
s
Third ventricle seen b/w lateral ventricles and csp
Foramen on monro is seen in this view
Sylvian fissure is seen in this plane . Y-shaped structure In term infants and wide-open in preterm infants
Important view to assess basal ganglia for edema, ischemia and hemorrhage.
Lenticulostriate vasculopathy
CP : LARGEST PART WE SEE IN LAT VENT CALLED AS GLOMUS, anatomical depection of it is seen in this – very lumpy looking tissue .. It is key to notice the perivent white matter. / aka peritrigonal blush (post and superior to trigone of vent)
PVWM : IS HOMOGENOUS IN ECHOGENICITY AND should be EQUAL OR LESS ECHOGENIC THAN CP. IF HYPERECHOIC THAN CHOROID PLEXUS, we need to think of ischemias : PVL
Ventricular cavities should diverge at this plane, if they are seen parallel, cc dysplasia should be suspected
(There are many parallel fibers in this region and coz of the placement of the probe in coronal section, it producses wave which hit these fibers at 90 degrees/ perpendicular : creating a blush like appearance )
First view : midline
Second : thru caudothalamis groove / para sagittal view
Thiird : at the level of PVWM and slyvian fissure / tangential para sagittal
Midline parasagittal :
Csp
cavum vergae ( if present)
Corpus callosum
3rd ventricle with massa intermedia
Cerebral aqueduct
Fourth ventricle
Cerebellum
brainstem
At the level of CTG .. Any echogenicity in that area around 1 cm : germinal matrix haemorrage..
Choroid plexus usually starts 1/3 rd after the begenining of the thalamus
The choroid tucks up in the caudothalmic groove of the lateral ventricle. It does not extend beyond the caudothalamic grooves into the frontal horns.
Important view to assess basal ganglia and lenticulostriate vasculopathy
Further angulation of the transducer laterally results in a section lateral to the lateral ventricles.
The sylvian fissure is the landmark in this view
At the level of insular cortex/ sylvial fissure.
Structures seen : parietal lobe, temporal lobe
Assess periventricular white matter, periventricular flare and cystic periventricular leucomalacia
Used to visualized occipital horns, glomus of cp and periventricular white matter
Located at jn of sagittal and lamboid suture.
Fuses by 3 months
CA indicates calcar avis; Ch, choroid plexus; CH, cerebellar hemispheres; LV, lateral ventricle trigone; OH, occipital horn; OL, occipital lobe; SA, subarachnoid space; and T, tentorium.
Occipital horns are anechoic as they have no choroid plexus.
Baby with their heads laying down, he most dependent portion of the vent susytem is the occipital horn..so if we are unsure of blood in the vent system , we can use this view and any echogenicity in occ horns indicates hemorrhage
These planes are extremely useful for detecting dependently layering clot and clot attached to the choroid plexus. So CP on doppler exhibits vascularity but clot: lack of vascular flow
(peritrigonal blush : fibers are almost parallel so no blush is seen usually, in suspected cases of PVL this view can be used to rule out )
Right above the ear where the ear meets temporal part of the skull.
Circle of willis can be visualized.
Axial view , similar to view calculating bpd in anc
Posterior to the ear behind the helix. At the jn of temporal, parietal and occipital bones.
best view for cerebellum, brainstem ( pons and midbrain)
May not fuse till 2 years of age
Place the probe parallel to the ear to obtain a coronal view. Sweep the probe back and forth to identify the cerebellar hemispheres, vermis, third and fourth ventricle, pons and cisterna magna.VERMIS IS ECHOGENIC.. Cerebellar hemispheres are hypoechoic compared to vermis.
Fuses by 3-6 months. ( fusion starts from the posterior to anterior – so the first to get obliterated is cavum vergae)
ABSENCE IS ASSOCIATED WITH CNS ABNORMALITIES : SEPTO OPTIC DYSPLASIA , CALLOSAL AGENESIS
This is a diagram showing vent system – deep to it we have CSP and CV which is a continuation of CSP (posterior cystic portion )…CV is present in some babies and is continuation of CSP and it goes all the way down to the end of CC.)
Anterior to foramen of monro – csp
Posterior to monro – cavum vergae
N THIS BABY CSP AND CV ARE NOT EVEN PRESENT- THEY ARE OBLITERATED.
CVI : structure is good to place doppler to rule out vein of galen aneurysm or any other venous aneurysms
NOT ASSOCIATED WITH ANY CONGENITAL ANOMALIES
Not seen after 2 years of age normally
Dd : arachnoid cyst
CISTERNA MAGNA : normal 3– 8mm , unlike archanoid cyst it doesn’t cause any mass effect when enlarged . And it can be diff from dandy walker by visualization of vermis.
ASYM VENT SIZE: ventricular size smaller as infants mature .. Normal <10mm in transverse..
Asym vent size can be diff from entriculomegaly(colpocephaly) as colpo co-occurs with agenisis of corpus callosum / chiari 2 malformations.
Colpocephaly - disproportionate prominence of the occipital horns of the lateral ventricles.
Radiologically, diagnosis of colpocephaly becomes more likely when the ratio of the posterior horn to anterior horn of lateral ventricle width (P/A ratio) is ≥3.
Dd for colpocephaly – normal pressure hydrocephalus
The choroid plexus does not extend into the frontal or occipital horns, so hyperechoic material in these areas should suggest pathology. Isolated cysts and measuring less than 1cm, they are considered a benign finding
When choroid cysts are found to be multiple, bilateral, or greater than 1 cm in size, this may suggest a chromosomal abnormality .
Connatal cysts are always found in immediate proximity with the frontal horns where they are found in multiples and exhibit a string of pearls appearance ..they undergo Spontaneous regression..
Located at the superolateral margin of junction of frontal horn and body of lateral ventricles
(Believed to be caused by deficient coarctation of the ventricles)
Anisotropy effect is an ultrasound artifact where an echogenicity is seen / echogenic structure is seen due to an oblique insonating angle and this disapperas when the plane is changed.
@24wks : occipital fissure is seen.. @28wks : cingulate gyrus and at around 30 wks sulcal branching occurs and sulci and gyri are seen.
Lack of sulcation in term – abnormal.
Lack of cingulate gyrus – corpus callosal agenesis
Lissencephaly is a heterogeneous group of disorders of cortical formation characterized by a smooth brain, with absent or hypoplastic sulci and is strongly associated with subcortical band heterotopia ( this condition is characterized by a band of grey matter located deep to and roughly paralleling the cortex, with either normal or pachygyric overlying cortex)
Pachygyria – broad gyri
Insignificant
Depicts insult to the neonatal brain
Seen with torch, neonatal hypoglycemia, fetal alcohol syndrome, uncomplicated prematurity
CALCAR AVIS : it is a paramedian protusion of the calcarine gyrus into the medial aspect of the lateral vent at the junction of trigone with the occipital horn. it may simulate a intraventricular hemorrhage. A, AF
parasagittal view shows a rounded masslike image mimicking an intraventricular clot within the occipital horn (arrow). B, PF parasagittal view we can see that the mass is the calcar avis (arrow) DUE TO ITS continuity with the occipital white matter and the calcarine fissure (CF).
It is a present in premature babies and it is also a fetal structure that involutes by 36 weeks. it is very important coz it is where the bleeds in premature infants begin.
It consists of highy vascularized network of premature neural cells which later becomes the glial cells.. These capillaries are very tiny and delicate and can rupture with any change In the fetocerebral vascular perfusion. Rapid change in the blood pressure, these tiny capillaries rupture and blood starts to accumulate in CTG and when it breaks the vent lining or ependymal lining, it enters the vent and becomes IVH.
PREMATURE INFANTS LACK BARORECEPTORS. 1st appears at 7th week, maximum at 23 weeks , involute by 36 weeks
Grade 1 and 2 bleeds generally have a good prognosis.Grade 3 and 4 bleeds have variable long-term deficits, but outcome in grade 3 hemorrhages is usually good when no parenchymal injury has occurred.
80 % of grade 1 progress to garde 2
intracranial hemorrhage confined to the caudothalamic groove/ sub-ependymal regionIt is staged as grade 1 hemorrhage., < 1cm
In the acute phase these bleedings are hyperechoic, changing to iso- and hypo-echoic with time.
Non hemorrhagic hyperechogenicity – infections, term babies
80 % of grade 1 progress to grade 2 On the left a grade 2 intracranial hemorrhage.On the coronal image only the cavum septi pellucidi is seen.Both lateral ventricles are filled with blood, but there is no ventricular dilatation.
On the left the same patient after 3 days.The ventricles are dilated and clot formation is seen.Secondary hydrocephalus occuring several days after a grade 2 bleed should not be mislabeled as grade 3 hemorrhage.
Ependyma is very fragile and ruptures and blood spills inti the ventricles.
Blood forms a cast of the ventricle.
Large Intra-ventricular hemorrhage with ventriculomegaly
Ventricular lining becomes echogenic reflecting ventriculitis
20% increase in mortality
35% increase in neurologic deficits
Large highly reflective areas fill the ventricles producing a cast like appearence
Grade 4 intracranial hemorrhageOriginally these grade 4 hemorrhages were thought to result from subependymal bleeding into the adjacent brain.Today however most regard these grade 4 hemorrhages to be venous hemorrhagic infartions, which are the result of compression of the outflow of the veins by the subependymal hemorrhage.
On the left a grade 4 hemorrhage.There is a large subependymal bleeding but also a large area with increased echogenicity in the brain parenchyma lateral to the ventricle.This is probably the result of a venous infarct.
These venous infarctions resolve with cyst formation.These cysts can merge with the lateral ventricle, finally resulting into a porencephalic cyst.On the left a different patient with a grade 4 hemorrhage at a later stage with extensive cyst formation.
50 % increase in mortality, 90 % increase in neurological deficits like cerebral palsy and spastic doiplegia
Day 1 , Day 2 – No bleed
Day 3 – Intra-parenchymal hemorrhage extending into ventricles
Day 4 – Intra-ventricular clot ( increasing in size) with periventricular echogenicity suggestive of ischemia and necrosis
Day 7 – Clot retraction
Day 28 – Cystic encephalomalecic changes.
In prematures this white matter zone is a watershed zone between deep and superficial vessels, very vulnerable to hypoxic ischemic insult
Normally the echogenicity of the periventricular white matter should be less than the echogenicity of the choroid plexus.
Detection of PVL is important because a significant percentage of surviving premature infants with PVL develop cerebral palsy, intellectual impairment or visual disturbances.More than 50% of infants with PVL or grade III hemmorrhage develop cerebral palsy.
Periventricular cysts ar eusually < 2-3 mm and carry poor prognosis
The term flaring is used to describe the slightly echogenic periventricular zones, that are seen in many premature infants in the first week of life.During this first week it is not sure if this is a normal variant or a sign of PVL grade 1.Flaring persisting beyond the first week of life is by definition PVL grade 1.
Follow up is needed to differentiate flaring from PVL grade I.The case on the left shows a premature infant with flaring.At follow up no cyst formation was found and after the first week a normal periventricular white matter was seen.
PVL is diagnosed as grade 1 if there are areas of increased periventricular echogenicity without any cyst formation persisting for more than 7 days.Increased periventricular echogenicity is however a nonspecific finding that must be differentiated from the normal periventricular halo or normal hyperechoic 'blush' posterosuperior to the ventricular trigones.Suspect PVL if the echogenicity is asymmetric, coarse, globular or more hyperechoic than the choroid plexus.The abnormal periventricular echotexture of PVL usually disappears at 2-3 weeks.PVL can be differentiated from hemorrhages because PVL lacks mass effect.
The images on the left demonstrate a PVL grade 2 with small periventricular cysts.The echogenicity has resolved at the time of cyst formation.2% of the preterm neonates born before 32 weeks develop cystic PVL.The severity of PVL is related to the size and distribution of these cysts.Cystic PVL has been identified on cranial ultrasounds on the first day of life, indicating that the adverse event was at least 2 weeks prenatal rather than perinatal or postnatal.
US is highly reliable in the detection of cystic WM injury (PVL grade II or more), but has significant limitations in the demonstration of noncystic WM injury (PVL grade I).This deficiency of neonatal cranial US is important, because noncystic WM injury is considerably more common than cystic WM injury.
PVL is diagnosed as grade 3 if there are areas of increased periventricular echogenicity, that develop into extensive periventricular cysts in the occipital and fronto-parietal region.
PVL is diagnosed as grade 4 if there are areas of increased periventricular echogenicity in the deep white matter developing into extensive subcortical cysts.PVL grade 4 is seen mostly in fullterm neonates as opposed to PVL grade 1-3, which is a disease of the preterm neonate. Flaring persisting beyond the first week of life is by definition is PVVL garde 1.
Cystic spaces that replace brain tissue with wihite matter necrosis
AHW defined as the diagonal width of the anterior horn measured at its widest point in the coronal plane), and thalamo-occipital distance (TOD) (defined as the distance between the outermost point of the thalamus at its junction with the choroid plexus and the outermost part of the occipital horn in the parasagittal plane.
Ventricular index - Ratio between the lateral sides of the ventricles and the biparietal diameter.
FRONTAL HORN RATIO
RIGHT : THERE IS BALOONING OF THE VENTRICLES and the INDEX MEASUREMNETS UNDERESTIMATES THE SEVERITY OF THE VENT WIDENING
THESE MEASUREMENTS CAN BE COMPARE TO THE REFERENCE CURVE AND ARE QUITE USEFUL FOR FURTHER FOLLOW UP.
Color Doppler imaging is used to screen the vasculature for patency and resistance to flow in cerebral veseels
In the coronal : we look for circle of willis with internal carotids / MCA/ ACA ..In the sagittal : sagittal sinus and vein of galen
Circle of willis can be seen from transtemporal also if fontanelle are closed. Adv of transtemporal view is PCA can also be clearly seen
RI : decreases with the age ( from 0.9 to 0.5) Lower values may indicate acute hypoxia or ischemia, which may trigger increased diastolic flow through cerebral vasodilation. Higher values may suggest cerebral swelling where intracranial pressures rise higher than systemic pressures leading to decreased diastolic flow
Subependymal cysts and germinolytic cysts both occur at caudothalamic groove and Subependymal cysts are the sequlae of germinal matrix hemorrhages and congenital geminolytic cysts are commonly seen in metabolic disorders maternal cocaine consumption.(zellwegers), neurotropic infection, (cmv, rubella),
Histogenesis: Development of cells into tissues.
Organogenesis: Development of tissues into
organs.
Neural tube closure (dorsal induction: 3-4 weeks’
gestation)
Diverticulation (ventral induction: 5-6 weeks’
gestation)
Diverticulation :
Posterior fossa cyst commun icating with 4th ventricle ( arachnoid cyst and enlarged foramen magnum do not)
Large posterior fossa
Hypoplastic cerebellar vermis and laterally displaced cerebellar hemispheres
Frequently associated with other anomaies
Image :There is an enlarged posterior fossa with a large CSF cystic space communicating with the 4th ventricle. The vermis is not identified and suspected to be absent or hypoplastic. There is high attachment of the tentorium. The anterior and mid-body of corpus callosum are present. Findings are most consistent with a Dandy-Walker malformation.
Batwing configuration of frontal horns (
Small posterior fossa with low-lying tentorium
Interdigitating gyri
Large massa intermedia
Chiari Imalformation is simply the downward displacement of the cerebellar tonsils, without displacement of the fourth ventricle or medulla. Chiari II malformation is the most common and of greatest clinical importance because of its almost universal association with myelomeningocele.
Chiari III malformation is a high cervical encephalomeningocele in which the medulla, fourth ventricle, and virtually the entire cerebellum reside.
Classic sonographic findings of the Chiari II malformation involve the entire brain.
Anterior and inferior pointed frontal horns- Batwing configuration
Enlarged lateral ventricles with occipital horns larger than frontal horns- Colpocephaly
Third ventricle appearing only slightly enlarged
Enlarged massa intermedia fills third ventricle.
Elongation and caudal displacement of fourth ventricle, pons, medulla, and vermis
Nonvisualized fourth ventricle because of
compression
Partial absence of septum pellucidum
Interhemispheric fissure
Wide, especially after shunting
Interdigitation of gyri causes serrated appearance
Ansence of corpus callosum
Hydrocephalus
100 % have myelomeningocele
80 % have associated anomalies
Parallel lateral venticlees
Elevated 3rd ventricle
Absent cingulate gyrus and sulcus
Sunburst sign – radially arranged sulci
Probst bundles impress upon lateral ventricles ( failure to fuse)
Rare congenital brain malformation resulting from incomplete separation of two hemispheres due to failure of midline cleavage of prosencephalon
Types : lobar, alobar and semilobar ( lobar – least severe type – midline abnormalities – fusion of cingulate gyrus and anterior frontal lobes)
Alobar – single large posteriorly located ventricle and fused thalami
Single ventricle and fused thalami.
No falx or interhemispheric fissure
Right – mr image
Semilobar – intermediate between alobar and lobar
Most commonly fused at the thalami and anteriorly
Can have associated facial anomaly
Partially separated thalamus
Hypoplastic falx and interhemispheric fissure
Rare cortical malformation manifesting as a grey matter lined cleft( single or bilateral) extending from ependymal to pia mater i.e from cortex to ventricular system
Type 1 : closed lip
Type 2 : open lip – easily diagnosed on usg an echo –free cavity extends from surface of brain to fuse with lateral wall of lateral ventricle
Image : open-lip schizencephaly show bilateral clefts
(c) with wide openings to the ventricular (v) system.
Lack of gyration and sulcation
Thickened cortex
Colpocephaly
Homogenous or pseudoliver appearance to the brain parenchyma
Figure of 8 appearance due to shallow sylvian fissure
Can result from intra-uterine infection
Small acoustic win dows can affect image quality and some structures and abnormalities remain difficult to visualize.