intracranial neonatal neurosonography: an update

Intracranial Neonatal Neurosonography: An Update

Jane E. Benson, M.D.,* Marcus R. Bishop, B.Sc.,† and Harris L. Cohen, M.D.‡

*Assistant Professor of Radiology and Pediatrics and ‡Visiting Professor of Radiology, Russell H. Morgan Department of Radiology,Division of Pediatric Imaging, Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A.; †Senior Medical Student,

Guy’s, King’s and St. Thomas’ School of Medicine, Dentistry, and Biomedical Sciences, London, England

Summary: This article reviews salient features of a normal neonatal cranial ultrasoundexamination with suggestions concerning techniques that take advantage of new de-velopments in ultrasound technology. It also illustrates pathologic findings in suchareas as congenital abnormalities, intracranial hemorrhage, and infection. Recent pub-lications on the subject of neurodevelopmental outcome are explored, pointing out howvarying descriptions of intraventricular hemorrhages affect their results. Key Words:Infant—Neonate—Cranial ultrasound—Brain.

Learning Objectives: After reading this article and com-pleting the posttest, the reader should be able to:

● Describe the images that comprise the basic neurosono-graphic examination of the infant head.

● Describe the use of alternate sonographic windows andcolor Doppler ultrasound in finding intracranial pathol-ogy.

● List the characteristics that distinguish grades of intracra-nial hemorrhage.

● Identify abnormalities such as periventricular leukoma-lacia, Dandy–Walker complex, and agenesis of the cor-pus callosum.

Over the past two decades, neurosonography has maturedas a clinical tool and is now the standard of care in allneonatal intensive care units. Its diagnostic value in screen-ing and follow-up examinations as well as its safety areuncontested. Advances in sonographic equipment, however,have prompted refinements in technique and a reevaluationof what is recognized as pathology. Technological improve-ments, accessibility of Doppler-capable and color–Doppler-capable transducers, improvements in technique, availabil-ity of high-resolution linear probes, and extension of thehead ultrasound examination to include analysis of the fetusand the child beyond the age of fontanelle closure have all

aided the advancement of neurosonographic diagnosis. Thegreater availability of computed tomography and magneticresonance imaging for the evaluation of the smallest infantshas led to some interesting correlations. Grey-scale real-time neurosonography is commonplace in the care of thepremature infant, and color-flow and power Doppler arereadily available for their roles in certain clinical circum-stances. Obstetricians, neonatologists, and developmentalpediatricians also have an interest in cranial ultrasound as aprognostic indicator for neurodevelopmental outcome in theintermediate and long-term and as an immediate diagnostictool for acute cranial pathology.

NORMAL EXAMINATION

The basic neurosonographic examination in the neonateis performed through the anterior fontanelle in real-timeusing a sector or linear-array transducer with a frequency of7 MHz or higher. At times, a 5-MHz transducer may beused for the larger/older infant or for patients with a largeamount of scalp hair. In addition, very high-frequency trans-ducers (10 MHz or more) may aid the examination of su-perficial structures such as the extraaxial spaces or the su-perior sagittal sinus. The examiner positions the transduceron the anterior fontanelle in the coronal and sagittal orien-tations, angling as indicated in Figure 1 to obtain the imageplanes described in this article.

Imaging in the Coronal Plane: What Do We See?Figures 2 and 3 show some of the images obtained when

examining the brain through the anterior fontanelle in a

The authors have disclosed that they have no significant relationshipswith or financial interests in any commercial company pertaining to thiseducational activity.

Address correspondence and reprint requests to Jane E. Benson, M.D.,Central Radiology, Johns Hopkins Hospital, 600 N. Wolfe Street, Balti-more, MD 21287. E-mail: [email protected]

Ultrasound QuarterlyVol. 18, No. 2, pp. 89–114© 2002 Lippincott Williams & Wilkins, Inc., Philadelphia

89 DOI: 10.1097/01.RUQ.0000013843.41981.40

FIG. 2. Normal brain, anterior fontanelle approach. A. Coronal imagethrough the frontal lobes showing interhemispheric fissure (arrows) (cor-responds with I in Figure 1B). B. Coronal image through the frontal hornsof the lateral ventricles (solid arrow), sonographic dropout from the floorof the frontal vault (dashed arrow), and superior sagittal sinus (dottedarrow) (corresponds with II in Figure 1B. Normal temporal horns are notdistended sufficiently to be visible. The cavum septum pellucidum is verysmall in this near-term infant (asterisk). C. Coronal image through the atriaof the lateral ventricles (corresponds with V in Figure 1B). The beam isangled posteriorly. Choroid plexus is visible within the lateral ventricles,with slight separation from the ventricular wall indicating a ventricular sizethat is at the upper limit of normal. The lateral ventricle is imaged with itsanterior (solid) and posterior (dashed) borders marked by arrows. Thisimage is too posterior to include thalamus. The area between the ventriclesrepresents the paired pericallosal gyri (G). Incidentally noted is a somewhatprominent anterior extraaxial space marked by asterisks.

FIG. 1. A. Sagittal image planesthrough anterior fontanelle approach: 3 ismidline, whereas 2 and 1 are progres-sively more laterally angulated. B. Coro-nal image planes through the anterior fon-tanelle approach: I and II are more ante-r ior ly angula ted , I I I -VI is moreposteriorly angulated. From: Cohen HL,Blitman NM, Sanchez J. Neurosonogra-phy of the infant: The normal examina-tion. In: Timor-Tritsch IE, MonteagudoA, Cohen HL, eds. Ultrasonography ofthe prenatal and neonatal brain NewYork: McGraw-Hill, 1996: 403–22. Re-produced with permission of the Mc-Graw-Hill Companies.

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Ultrasound Quarterly, Vol. 18, No. 2, 2002

coronal plane. The transducer is angled slowly from front toback, imaging parenchyma and ventricular system fromfrontal brain at the level of the orbits to the subtentorialcerebellar hemispheres, the midline cerebellar vermis, andthe even more posterior echoless cisterna magna. We typi-cally document several hardcopy images in sequence. At thefrontal horns, one can note whether the ventricular size isnormal or if there is ventricular dilatation. The presence ofa corpus callosum can also be noted. Inferior to the corpuscallosum, the medial walls of the frontal horns and bodies ofthe lateral ventricles abut, forming the septum pellucidum.When these walls are separated by fluid, as they are in mostinfants, this is called the cavum septum pellucidum. Onecan note the interhemispheric fissure, which is the potentialspace between the two frontal lobes. Some people refer tothis normal appearance as the anchor sign.1 The anchor ismade of an apparent echogenic line representing the medialsurfaces of the two frontal lobes as they abut anterior to thecorpus callosum.

Angling the transducer slightly more posteriorly allowsimaging of the bodies of the lateral ventricles. Their size isthe key indicator of ventriculomegaly in the coronal plane.Further posterior angulation will show the occipital lobesand the paraventricular white matter. At any point whileexamining the patient in a coronal plane, one may angle thetransducer to the extreme right or left. This allows one toimage the periphery of the brain and enables assessment ofany possible extraaxial collection. An extraaxial collectionmust be suspected any time the brain border is sharply de-fined. It normally fades into the calvarial echogenicity.

Coronal imaging is limited in the more cranial portions ofthe brain, i.e., toward the vertex, but allows the comparisonof parenchymal echogenicity of the right and left halves ofthe brain. This will hopefully readily allow assessment ofthe increased echogenicity of hemorrhage, edema, or infarc-tion. At the brain periphery is the Y-shape Sylvian fissure,in which the branches of the middle cerebral artery tribu-taries can be seen to pulsate on real-time imaging. They maybe insonated by duplex or color Doppler.

The intraventricular choroid plexus has the same appear-ance on coronal views as on sagittal views: a tubular echo-genic mass seen within each lateral ventricle. Another ben-efit of examination in a coronal plane is that each choroidcan be compared with its contralateral mate. The fact thatthe echogenicity of the normal choroid plexus is the same asthat of relatively acute intraventricular hemorrhage (IVH) isnoteworthy. Contralateral comparisons of echogenicity andshape aid in making the diagnosis. The normal lateral wallof the ventricular body hugs the choroid plexus. Significantdistance between the choroid and the lateral ventricular wallsuggest ventriculomegaly.

Imaging in the Sagittal Plane: What Do We See?The midline sagittal view provides the most information

concerning structural brain malformations (Fig. 4). The im-age plane is determined by three points: the genu and sple-nium of the corpus callosum and the fourth ventricle. Themedian view allows one to image the crescentic corpuscallosum, the largest of the medial interhemispheric com-missures, just above the cavum septum pellucidum. Thecorpus callosum is classically described as hyperechoiccompared with normal brain parenchyma; however, it maybe isoechoic, particularly in the very young premature in-fant. The corpus callosum is definitively more echogenicthan the echoless fluid of the cavum septum pellucidum.Pathologists note a cavum septum pellucidum in 100% ofnewborn premature infants, with a decreasing incidence upto age 6 months. This structure is not imaged as often inroutine head ultrasound, but it certainly is more often seenin the premature infant and may disappear during the first 2months of life. Babcock and Farrugia2 reported imaging ofcavum septum pellucidum in 42% of newborns and 62% ofpremature newborns. Knowledge of the presence of thisnormal structure prevents confusion with a high-riding thirdventricle.2–4 Often, one may see a more posterior extensionof the septum pellucidum, termed the cavum vergae. Occa-sionally, there may be an even more posterior inferior fluid-filled area, said to be the cavum velum interpositum, whichis distinct from the cavum vergae5 (Fig. 5).

Superiorly, the corpus callosum is surrounded by themore echogenic pericallosal sulcus, in which lie the peri-callosal arteries. The pericallosal sulcus, in turn, is sur-rounded by the more rostral and superior cingulate gyrus.The cingulate gyrus and the more superficial or rostral gyricourse in a direction relatively parallel to that of the corpus

FIG. 3. Cerebellum and cisterna magna. Coronal image using the ante-rior fontanelle approach. Coronal view corresponding with IV in Figure 1Bshows the subtentorial components of the brain. Cerebellar hemispheres(H) are seen lateral to the echogenic midline vermis (V) of the cerebellum.Inferior to the vermis is an echoless triangle that is the cisterna magna(CM). T � right temporal brain. Arrows point to the echogenic interhemi-spheric fissure line, demonstrating the anchor sign. cc � corpus callosum.

INTRACRANIAL NEONATAL NEUROSONOGRAPHY 91


callosum and do not extend to the third ventricle. Thesegyri, as is true of all gyri, are echopenic when comparedwith the echogenic sulci separating them. As can be notedwith somewhat more difficulty in the fetus, the gyral/sulcalpattern of the brain becomes more prominent and more

complex, particularly on the midline views of the medialportion of the brain, as gestational age increases (Fig. 6).This maturational complexity will increase independently ofbrain volume in a growth-restricted infant.6 Classic pathol-ogy images of Dorovini-Zis3 show these differences forvarious gestational ages, with a relatively featureless patternat 22 weeks maturing into the typical adult pattern at 40weeks. Gyral/sulcal pattern identification may aid in deter-mination of the gestational age of a newborn.7,8 Knowledgeof postmenstrual age may aid in the identification of casesof agyria, in which there is little evidence of gyri. Branchesof the anterior cerebral artery run within the midline sulciand may be seen to pulsate within them. These vessels canbe imaged with color Doppler imaging.

Inferior to the corpus callosum and the cavum septumpellucidum is the third ventricle, which can be seen, occa-sionally with difficulty, on the median section. It is certainlyseen readily, when it is pathologically enlarged, with itscharacteristic anterior recesses. The circular, solid structurethat may be seen within it represents the massa intermedia,a secondary interhemispheric commissure.5

The choroid plexus may be seen as an echogenic structurein the roof of the third ventricle. This echogenicity mayextend caudally through the aqueduct. Infratentorially, a tri-angular, echoless area representing the fourth ventricle isseen anterior to the characteristically echogenic vermis ofthe cerebellum. Good technique requires the examiner to

FIG. 5. Posterior angled coronal view using the anterior fontanelle ap-proach, showing a large cavum vergae (CV).

FIG. 4. A. Midline sagittal view (corresponds with 3 in Figure 1A). A. C-shape corpus callosum with its rostrum (r), genu (g), and body (b) is noted.Triangular echopenic area below the letters is the small cavum septum pellucidum in this patient. Inferiorly, the echogenic vermis can be seen (V). Atriangular echopenic area seen anterior to the vermis is the fourth ventricle (4). (T) represents where the paired thalami join in the midline. This is a youngfetus and minimal gyri are seen. B. Right parasagittal view (corresponds with 2 in Figure 1A). The entire lateral ventricle (straight arrows) is imaged. Thehead of the caudate lobe (Ca) is seen anterior and somewhat superior to the right thalamus (T). Echogenic choroid plexus (c) is seen within the body ofthe lateral ventricle, particularly in the area of the atrium. Exaggerated echoes (curved arrows) are seen in the periatrial white matter, created by ananisotropic effect on white matter fibers, probably at 90° to the ultrasound beam. This normal finding is important to note, because it may simulate theechogenic phase of periventricular leukomalacia. S � echogenic skull/base of brain.



have the entire brain imaged on the screen, from the point oftransducer placement to the echogenic calvarium at the baseof the brain.

The paramedian images are obtained by angling the im-aging beam laterally using the axis of the anterior fonta-nelle, then angling the posterior aspect of the beam evenmore laterally to include the curve of the temporal horn. Thekey paramedian views are those of the lateral ventricles andthe nearby structures. Often, one must move the transducerslightly to the periphery of one side of the anterior fonta-nelle and image across to the contralateral lateral ventricleto obtain a satisfactory image.8 Each lateral ventricle can be

evaluated for its frontal portion, body, atrial or trigonal por-tion, and temporal and occipital portion. Some areas of thelateral ventricle, particularly the occipital horns, may not bereadily imaged when there is no hydrocephalus. In mostinstances, the entire lateral ventricle may be seen in oneparasagittal plane; however, especially if the ventricularsystem is dilated, portions of it must be imaged with moreangulation to the right or left of the body of the lateralventricle. The oval head of the caudate nucleus can be seenmeeting the circular thalamus at the thin, echogenic caudo-thalamic groove.

Lateral ventricular size is assessed on both parasagittal

FIG. 6. Comparison of gyral pattern in a premature (A,C) and full-term (B,D) infant. The Sylvian fissure visible in the coronal sections (A,B) is dividedand more extensive in the full-term infant (arrows). Sagittal views show an absence of gyri (C) compared with quite an extensive gyral pattern (D). Alsovisible (B,C) are corpus callosum (cc), interhemispheric fissure (i), frontal (f), temporal (t), and occipital (o) horns of the lateral ventricle, choroid plexus(C), atrium of the lateral ventricle (a), head of caudate (Ca), and thalamus (T).



and coronal views. Ventriculomegaly is assessed by mostsonologists by gestalt rather than by specific measurements.Normal ventricles are largest at the atrium. Lateral ven-tricles may normally be somewhat asymmetric, with the leftventricle slightly larger than the right, and the occipitalhorns more prominent than the frontal horns. Asymmetry ismore common in premature infants, probably because of arelatively less well-developed cerebral cortex than in full-term infants. Narrowed, slit-like ventricles, once believed tobe definitive evidence of cerebral edema, can be seen inmany normal full-term infants, particularly in the frontalhorns. Clinical findings or other abnormal features must benoted before considering narrow ventricles as abnormal.9,10

Along the floor and within each body of the two lateralventricles is the choroid plexus. Each lateral ventricle’s cho-roid plexus is homogeneously echogenic and tubular, with asmooth border. The choroid plexus extends from the fora-men of Monro to the atrium of the lateral ventricle, where itis largest in dimension, and then curves anteriorly and in-feriorly, extending into the tip of the temporal horn of thelateral ventricle. The choroid plexus does not extend into theoccipital horn of the lateral ventricle or anterior to the fo-ramen Monro, its egress to the third ventricle. As noted inthe discussion of midline images, the choroid runs along theroof of the third ventricle. It is also present within the roofof the fourth ventricle but cannot be imaged sonographi-cally.

In the search for possible periventricular leukomalacia orposthypoxic encephalopathy on parasagittal views, a key

area to analyze is the periventricular area, particularlyaround the ventricular trigone. The physician must be cau-tious about making a diagnosis of abnormality when notingthe normally prominent echogenicity of the peritrigonalwhite matter.11 Use of the orthogonal coronal views and asearch for asymmetry of the two sides of the brain as evi-dence of true pathology are useful. Follow-up examinationscan be confirmatory.12 In the far periphery of the braincortex, one may also note the middle cerebral artery tribu-taries pulsating in the Sylvian fissure.

Alternate Sonographic WindowsAs long ago as 1983, Mercker et al.13 described a lateral

approach to the calvarium to note extraaxial collections.Transcranial ultrasound relies on low-frequency transducers(often 2 or 3 MHz) to penetrate the thinner, squamous por-tion of the temporal bone after fontanelle closure.14 It maybe used to assess for hydrocephaly or IVH even earlier ifuse of the fontanelle is precluded by, for example, a localintravenous site.15 We have used the transcranial approachmost often in children who we have followed-up over a longperiod of time for hydrocephalus and treated hydrocephalyor in children in whom the families espouse a particular fearof radiation exposure. Sound penetration and the imagefield of view become more limited with time. Transcranialultrasound allows good visualization of the brain stem andthe basilar artery in the interpeduncular cistern by imagingin a plane parallel to the canthomeatal line (Fig. 7).16

Sutures are wide in the small infants, bridged by fibroustissue that allows sonographic entry not only through thecoronal, lambdoidal, and sagittal sutures but also throughthe metopic, mendosal, and squamosal sutures found almostexclusively in the infant skull (Fig. 8). A recent improve-ment in transcranial ultrasound imaging of neonates hasbeen the use of the mastoid fontanelle as an imaging portal

FIG. 7. Normal brain. Transtemporal approach through the left side, withthe patient facing the reader’s right, using a low-frequency probe. Choroid(C) is seen in the atrium of the lateral ventricle. Midbrain (M) and aqueductof Sylvius (arrow) are seen in cross-section. This frontal third of the brainis not included in the image.

FIG. 8. Infant skull showing normal open sutures. These serve as sono-graphic windows to the brain. Reproduced with permission of the Mc-Graw-Hill Companies.



(posterolateral approach). The mastoid fontanelle is locatedat the junction of the posterior parietal, temporal, and oc-cipital bones. The transducer is positioned approximately 1cm posterior to the ear and 1 cm above the tragus. Imagingthrough the mastoid fontanelle allows better visualization ofthe midbrain and the contents of the posterior fossa thandoes traditional anterior transfontanelle imaging. This ap-proach allows the use of higher-frequency transducers thandoes traditional transcranial ultrasound. The method hasproven particularly useful in assessing posterior fossa andcerebellar hemorrhage as well as deep venous sinus throm-bosis and basal cistern subarachnoid hemorrhage because ofthe closer proximity of the transducer to these regions.17

The foramen magnum can be accessed with the patientprone and the head flexed, which is particularly useful forexamining the medulla and low-lying cerebellar tonsils.This technique combined with the mastoid fontanelle ap-proach16 better-evaluates anatomy particularly relevant in

infants with meningomyelocele. The transtemporal and pos-terolateral fontanelle approaches have been useful in Dopp-ler imaging (described later), whereas the posterior fonta-nelle provides access to the posterior fossa structures18 (Fig.9). Midbrain structures, such as the thalamus, can also beseen from the posterior fontanelle, but the angle of approachof the ultrasound beam can cause artifactual echogenicity,particularly in the thalamus.19

ABNORMAL EXAMINATIONPreterm neonates (those born at <32 weeks gestation and

weighing <1,500 g) have the greatest demand for head so-nography, because cerebral events such as germinal matrixhemorrhage predominate in the population. Screening ismandatory in this group and the high incidence of positiveresults prompts regular sonographic follow-up. These in-fants frequently have comorbidity that complicates theirmanagement. Many stressors are suggested in the pathogen-

FIG. 9. A. Coronal imaging planes through the posterior fontanelle. Sagittal viewsare obtained by rotating the transducer 90° (reproduced with permission of theMcGraw-Hill Companies). B. Coronal view using the posterior fontanelle approach.Brackets demarcate the debris-filled extraaxial space, which is wider than normal.Contained debris in this setting could represent hemorrhage or infection. Choroidplexus is visualized in the lateral ventricles (C). C. Right parasagittal view using theposterior fontanelle approach visualizing frontal lobe (F) and choroid plexus (C).There is mild ventriculomegaly and blood in the ventricular atrium (arrow).



esis of cerebral pathology. Some of these relate to the careof other systems. Thus, diagnosis of potentially progressiveor reversible cerebral pathology is essential to optimize thecare provided.

The timing and frequency of screening examinationshave been the subject of several recent reviews, becausethese have implications for cost-effectiveness of care. Aninitial scan between days 3 and 7 of life supplemented by asecond scan between days 10 and 14 identify most clinicallyand developmentally important lesions.20,21 Another groupadvocates a scan in the second week only.22 At our institu-tion, a scan is performed at 4 to 6 weeks postnatal age toexclude unsuspected periventricular leukomalacia (de-scribed later).

The diagnosis of intracranial pathology has relied on the

departure from the accepted standards of imaged anatomy,often aided by the appearance of asymmetry. However, therefinement of equipment and the experience of practicehave uncovered some imaging pitfalls that should be re-membered as one evaluates images (Fig. 10).

Intraventricular HemorrhageIntraventricular hemorrhage is the most commonly diag-

nosed cerebral event in the preterm neonate. Over the past20 years, there has been much debate concerning the patho-genesis of the condition. Most bleeds originate in the ger-minal matrix, which is a single-cell-thick, subependymal,microvascular network. The germinal matrix is an area ofneuronal and glial cell proliferation, which appears duringthe 10th week of gestation in the wall of the third ventricle

FIG. 10. Coronal (A), coronal with more posterior angulation(B), and left parasagittal (C) views using the anterior fontanelleapproach. Term infants have small ventricles and the echo-genicity of the brain parenchyma is greater than that of theirlower-gestational-age counterparts. This set of images showspathologically small ventricles and echogenic parenchyma.Smaller ventricles can be an indication of cerebral edema causedby infection or ischemic insult. Often in such cases, the entirebrain is homogeneously increased in echogenicity and normalcerebral landmarks are difficult to find. Diagnosis: herpes en-cephalitis.



and migrates throughout the ventricular system. It beginsinvolution early in the second trimester, shrinking to a sub-ependymal focus adjacent to the foramen of Monro in thegroove between the caudate head and the thalamus duringthe 32nd week. The large caliber of the vessels coupled withminimal connective tissue support predispose the networkto rupture; hence, most hemorrhages occur in those neonatesborn between the limit of viability and the 32nd week ofgestation. These bleeds are synonymously termed germinalmatrix hemorrhage or subependymal hemorrhage. A smallproportion of intracranial hemorrhage has been shown tooccur as a result of venous occlusion, capillary ischemia,choroid plexus hemorrhage, and reperfusion injury in theolder neonate.

Subependymal bleeding is diagnosed when there is focalechogenicity in the caudothalamic groove, near the foramenof Monro (Fig. 11). There may be bulging into the ventricu-lar space on the sagittal view. Bilateral symmetric subepen-dymal hemorrhage is not rare, but the sonographer must becareful to distinguish this entity from the normal passage ofechogenic choroid plexus through the foramina to the roofof the third ventricle. Another possible mimic to be distin-guished are the hyperechoic caudate nuclei sometimesfound in postischemic infants; however, they can be seen inothers without such antecedent history.23 Similarly, in-creased echogenicity and the “lumpy, bumpy” appearanceof the normally bright and smoothly bordered choroidplexus in the lateral ventricles suggest the presence of ad-herent blood clots from intraventricular hemorrhage. How-ever, the choroid plexus of very premature infants (e.g.,born at 24 or 25 weeks gestation and weighing <500 g) are

proportionately more bulky and can present a confoundingappearance. On occasion, Doppler evaluation may be per-formed to show the presence of normal flow within thechoroid plexus—no flow signal can be located in a clot. Thechoroid plexus is not normally found in the occipital hornsor within the frontal horns anterior to the foramina ofMonro. The highly echogenic choroid may simulate theimage of IVH in its earliest stages, after fibrin depositionand before clot retraction and lysis. The examiner musttherefore be wary of what appears to be choroid either in theoccipital horn or, more importantly, anterior to the positionof the foramen Monro (i.e., in the frontal horns). A particu-larly thickened area of choroid should be considered withsuspicion. It is useful to examine the occipital horns of thelateral ventricles for layering blood products on follow-upscans. Patient position affects where layering is seen: a su-pine patient will have layering in the occipital horns,whereas if the head is turned to the side, the layers will bein both lateral ventricles (Fig. 12).

The grading system for IVH has been a topic of muchdebate during the past 20 years, and there has been nouniversally accepted rule. In 1978, Papile first described ahierarchy consisting of four grades based on the presence ofventricular blood and the degree of ventricular dilatation.24

This system was revised by Volpe 11 years later,25 when hededuced through autopsy studies that parenchymal bleedswere not a direct extension from the ventricular cavity,hence excluding them from his criteria. Volpe describedonly three grades, which related to the degree of intraven-tricular blood on parasagittal view. Grading systems in usetoday vary widely, with many institutions defining their

FIG. 11. A. Coronal view through the third ventricle (dashed arrow) using anterior fontanelle approach. Subependymal hemorrhage is seen in the wallof the right lateral ventricle. B. Right parasagittal view of the same patient showing subependymal hemorrhage with central cystic area in the caudothalamicnotch, caudate head (Ca), and thalamus (T). Diagnosis: grade I IVH, subacute.



own criteria, which poses a problem in standardization ofdata. Even when numerical grades are used, they may notreflect the original definitions. It is well known that over thecourse of time, ventricular size may increase without anyadditional new hemorrhage. The grading systems as origi-nally formulated by Papile and Volpe do not take this intoaccount. Consequently, a child’s condition may appear tochange from a grade II to III as posthemorrhagic hydro-cephalus develops. Our institution uses a modified Papilegrading system, in which grade II includes IVH with no orminimal ventricular dilatation (Fig. 13), grade III includesmoderate to prominent ventricular dilatation with IVH(Figs. 12,14,15), and grade IV describes an associated in-traparenchymal hemorrhage, which need not be a directextension of intraventricular blood (Fig. 16). Table 1 sum-marizes and compares these three systems.

Many comparison studies concerning outcome (describedin a later section) have used “mild,” “moderate,” and “se-vere” descriptors. Mild IVH refers to Volpe grade I andPapile grade I, moderate IVH refers to Volpe grade II andPapile grade II-III, whereas severe IVH relates to Volpegrade III and Papile grade III-IV. As mentioned before,low-grade IVH appears as an area of echogenicity withinthe subependyma, hence the subependymal hemorrhage orgerminal matrix hemorrhage designations. Moderate IVHresults when there is extension of blood into the ventricularcavity with associated ventricular dilatation. Severe IVHoccurs when there is a large volume of intraventricularblood, often with gross ventriculomegaly and, according to

Papile’s system, intraparenchymal hemorrhage. Manysonologists and sonographers, however, would classify thepicture in Figure 15 as severe IVH, despite there being noapparent periventricular echodensity.

Sonography is often used to track the evolution of IVH.As echogenic intraventricular blood clot organizes, it be-comes more echolucent, maintaining for a while an echo-genic periphery. Similarly, blood clot adhering to the cho-roid plexus or ventricular wall is initially echogenic, thenshrinks and becomes more echolucent centrally. When itdissolves, echogenic debris may be seen in dependent por-tions of the ventricles. Bleeding in the subependymal areawill also evolve from echogenic to more echopenic. A cystwill develop in this area in many individuals with resolutionof their clot (Fig. 17).

Bleeding into grey or white matter can sometimes bedetected by the asymmetric echogenicity it causes. In sub-arachnoid hemorrhage, the brain surface becomes muchmore echogenic as the arachnoid becomes thick and in-flamed. Where it is doubled-back, for example in the Syl-vian fissure, changes may be more obvious, and there maybe asymmetry with the other side when viewed in coronalplane. Similarly, the posterolateral ultrasound approachbrings the transducer closer to the basal cisterns whereblood clot may be visible.26 Subdural hemorrhage, particu-larly if the collection is over the cerebral convexity, may bevisible only with a high-frequency linear transducer and astand-off pad. It is suggested by evidence of a too-readily-seen brain border.

FIG. 12. Coronal view through the lateral and third ventricles using theanterior fontanelle approach. There is blood bilaterally within the lateralventricles and blood within the third ventricle (solid arrow). A blood–cerebrospinal fluid level is visible because of patient positioning with theleft side down. Diagnosis: grade II-III IVH.

FIG. 13. Coronal view through the body of the lateral ventricles usinganterior fontanelle approach. Blood is seen within the left lateral ventricle(dotted arrow) and a right-side subependymal hemorrhage is seen (dashedarrow). The left-side IVH extends down into the temporal horn (solidarrow). Diagnosis: left grade I and right grade II IVH.



Posterior Fossa HemorrhageThe exact cause of posterior fossa hemorrhage remains

unknown; however, correlation with difficulty in labor hasled to the theory that stretching of the tentorium and falxmay cause a laceration resulting in it—a similar mechanismof injury to subdural hemorrhage in the infant.27 Gudino28

reported that half of sonographically diagnosed cerebellarhemorrhage was secondary to dystocic delivery. Direct

trauma to the cerebellum itself may also be responsible.Diagnosis is of clinical significance because it relates todevelopment of psychomotor retardation, cerebellar signs,cognitive defects with learning difficulties, and epilepsy.

Cerebellar hemorrhage is an underdiagnosed entity, beingnoted less commonly than subependymal hemorrhage eventhough it is found in 10% to 25% of very low birth weightinfants at autopsy.29 Cerebellar hemorrhage has the same

FIG. 14. Coronal (A) and right parasagittal (B) views using the anterior fontanelle approach. There is blood clot in the dilated left lateral ventricle (solidarrow) and clot within the right lateral ventricle with a central cystic area, suggesting a subacute phase (dotted arrow). Thalamus � T. Diagnosis: subacutegrade III IVH.

FIG. 15. Coronal (A) and left parasagittal (B) views using the anterior fontanelle approach. A. Moderate hydrocephalus of both lateral ventricles, withleft ventricular clot containing an echopenic center, which is consistent with clot aging. There is further clot within the atrium, left occipital horn, and lefttemporal horn (B). Diagnosis: grade III IVH



sonographic features as other intraparenchymal bleeds (Fig.18). Acutely, it appears homogeneously echogenic. Withtime, it becomes more heterogeneous and eventuallyevolves into a hypoechoic lesion. There may be loss indefinition of the cerebellum and fourth ventricle on the mid-line sagittal view. Tentorial deviation and hydrocephalushave also been reported.30 The echogenic folia of the cer-ebellum effectively camouflage hemorrhage when viewedthrough the standard vertex windows. However, lateralizingthe approach, through the temporal bone or the posterolat-eral fontanelle, can make hemorrhage and cysts more vis-ible.29 Similarly, the pons and medulla become more acces-sible from these angles.

Extracorporeal membrane oxygenation (a lung bypass de-vice using semipermeable membranes for exchange of oxy-gen and carbon dioxide; used in neonates and infants withpotentially reversible lung disease) has been linked to thedevelopment of intraparenchymal hemorrhage, including

cerebellar hemorrhage after birth, though the pathogenesisremains to be determined. Putative mechanisms include im-mature vascular autoregulation and hypoxic-ischemic epi-sodes that result in endothelial damage and bleeding. Theseare exacerbated by the heparinization necessary for the ex-tracorporeal membrane oxygenation procedure. Dailyscreening neurosonography is the standard for monitoringbrain status. Development of any intraparenchymal hemor-rhage or IVH can be grounds for termination of extracor-poreal membrane oxygenation. However, these scans maynot be cost-effective after 5 days.31

Periventricular Leukomalacia and PorencephalyPeriventricular leukomalacia (PVL) represents ischemic

damage within the white matter tracts with subsequent re-sorption and scarring. It is most often visualized in the opticradiations in the trigone and peritrigonal area of the lateralventricle and just anterolateral to the frontal horns. Acutely,

TABLE 1. Intracranial hemorrhage: comparison of nomenclature systems

Papile Modified Papile Volpe

Grade I Subependymal hemorrhage Subependymal hemorrhage Germinal matrix hemorrhage with no orminimal IVH (<10% area on parasagittalview)

Grade II Intraventricular blood Intraventricular blood with no or minimalventricular dilatation

Intraventricular blood (10%–50% of ventriculararea on parasagittal view)

Grade III Intraventricular blood with ventriculardilatation

Intraventricular blood with prominentventricular dilatation

Intraventricular blood (>50% of ventricular areaon parasagittal view)

Grade IV Intraventricular blood and ventriculardilatation with extension intoparenchyma

Parenchymal abnormality (venous infarct vs.extra-ventricular extension) with or withoutintraventricular blood

Not applicable

FIG. 16. Coronal (A) and right parasagittal (B) views using the anterior fontanelle approach. There is clot distending the right lateral ventricle throughthe temporal horn (solid arrow), with associated paraventricular hemorrhage in superolateral parenchyma (dashed arrows). This could represent either anextension of right ventricular clot or an associated parenchymal infarct. The wall of the moderately dilated left lateral ventricle is echogenic, consistent withventriculitis, and possibly secondary to hemorrhage. B. Clot (Cl) extending through the dilated right lateral ventricle. A small volume of cerebrospinal fluidanterior to the clot is seen within the frontal horn (solid arrow). Diagnosis: grade IV IVH.



PVL is seen as a hyperechoic area. However, the criss-crossing fibers in the normal white matter give it a degree ofechogenicity that makes distinguishing acute PVL from nor-mal difficult, particularly in the paraatrial region where fi-bers perpendicular to the ultrasound beam reflect morebrightly than surrounding areas (the anisotropic effect). Di-rect comparison between the two hemispheres on coronalview from the anterior and the posterior fontanelles can be

helpful, because comparing images from these approachescan “subtract” the artifact caused by fiber reflection alone.Asymmetry allows easier identification of PVL.

The regions affected by PVL reflect the distribution ofthe anterior and middle cerebral arteries and the “watershedarea” between the two circulations.32 Although the patho-genesis of PVL is still unclear, an underdeveloped vaso-compensation response in the face of hypotension, charac-

FIG. 17. A. Right parasagittal view using the anterior fontanelle approach. There is a cyst-like collection that is consistent with either a largesubependymal hemorrhage or an intraventricular clot. Caudate � Ca, thalamus � T. B. Coronal view using the left transtemporal approach definitivelyshows the lesion to be subependymal hemorrhage.

FIG. 18. A. Coronal view using the anterior fontanelle approach with moderate posterior angulation. Cystic structure (arrow head) is seen within leftsubtentorial brain parenchyma. This view suggests arachnoid cyst or abnormal vascular structure. Lateral ventricles (arrow) are normal in size. However,transcranial view using the posterolateral fontanelle approach (B) reveals that the cyst is actually part of a larger complex area, with a prominent echogeniccomponent (arrow). This proved to be subacute cerebellar hemorrhage. Images courtesy of Dorothy Bulas, M.D., Children’s Hospital Medical Center,Washington D.C.30. Reproduced with permission of the McGraw-Hill Companies.



teristic of the premature neonate, has been implicated.33

With time (days to weeks), cellular degeneration results incyst formation and eventual evolution of fluid-filled cavities(Fig. 19).

The timing of an ischemic insult is often of interest toclinicians. When there is obvious white matter hemorrhage,this is fairly easy. Unfortunately, however, the echogenicityof the preceding edema without hemorrhage may have beentoo subtle to appreciate, and the appearance of cysts in thewhite matter several weeks after the onset of PVL is oftenthe first indication that there has been an ischemic episode.With the passage of additional weeks, the tiny cysts fill withfibrous and glial cells and disappear from sonographicview.27 Magnetic resonance imaging, however, can still de-tect areas of previous damage.

Encephalomalacia after larger, more focal infarctions

most often evolves into cystic spaces in the parenchyma. Ifone of these porencephalic spaces lies close to one of thelateral ventricles, then the tissue between them thins, thespace merges with the ventricular system, and normal-pressure ventriculomegaly results (Fig. 20).

These larger areas of infarction and hemorrhage oftencross regions of arterial supply and can be attributed todisturbances of venous drainage (Fig. 21). The infant brainhas two pathways for venous drainage: centrally (to theperiventricular system and the straight sinus) and peripher-ally (through surface veins to the sagittal and transversesinuses). When draining veins are obstructed, the tissuesthat they drain become congested and ischemic. This hasbeen advanced as another cause of brain parenchymal in-farction. It was initially advanced by Volpe25 as the mecha-nism by which IVH leads to periventricular hemorrhage:

FIG. 19. A. Right parasagittal image using the anterior fontanelle ap-proach. There is clot in the dilated body of the right lateral ventricle (Cl) andan echogenic area superior to the lateral ventricle (solid arrows). Image isconsistent with grade IV IVH or grade III IVH with acute PVL. The samepatient, only days later, showed acute cystic PVL superior and lateral to thefrontal horns (B), adjacent to the lateral ventricular body, and in periatrialarea (arrows) (C), corresponding with the echogenic area in A.



intraventricular blood increases the intraventricular pres-sure, interfering with central venous drainage. Hemorrhagenear the frontal horns is thought to be caused by congestionof terminal veins around the lateral ventricles.26 Similarly,meningeal irritation from bleeding or infection can throm-bose veins draining cerebral convexities and cause infarc-tion in areas that lie outside the normal arterial watershedregions.

Fluid-Filled Spaces

MidlineSeveral benign, fluid-filled midline structures can be en-

countered in the neonatal head. They have been mentioned

previously in connection with normal findings on the coro-nal and sagittal planes. The lateral ventricles normally meetin the midline beneath the corpus callosum. As was men-tioned previously, by term gestational age, the shared wallsfuse and become the septum pellucidum. At earlier gesta-tional ages, this potential space is still filled anteriorly withcerebrospinal fluid (CSF) and called the cavum septum pel-lucidum. This space can extend posteriorly to beneath thesplenium of the corpus callosum, where it is called thecavum vergae (Fig. 5). Both of these spaces can be seen onboth coronal and midline sagittal view. An additional smallspace just inferior and posterior to the splenium may alsoremain open and is called the cavum vellum interpositum.

FIG. 20. Coronal (A) and left parasagittal (B) using anterior fontanelle approach. A. Dilated circular structure (brackets) not consistent with the lateralventricle, representing either an infarct or a porencephalic cyst with central clot (Cl). B. The space is a porencephalic cyst merged with the lateral ventricle(solid arrows), with central clot (Cl). C,D. Retrospective look at the previous scan 14 days earlier, which was reported as normal. There is potentialabnormality on the coronal image (C), with an echopenic area extending further caudally on the left than on the right (solid arrow) and on the midlinesagittal image (D) where the corresponding echopenic region is seen (dotted arrow).



This space is seen best on the midline sagittal view (Fig.22). It should not extend past the curve of the splenium.

A fluid-filled space in that same location larger than thecavum velum interpositum might be better termed as anarachnoid cyst (Fig. 23). This term refers to a cyst thatforms within the arachnoid layer and is thus bound on allsides by arachnoid matter. They are most frequently foundin the cisterns and fissures, where the arachnoid is naturallymore plentiful. When in the midline, Doppler ultrasound isuseful in interrogating this space and ensuring that there areno flow signals within it that would indicate a vein of Galen

aneurysm (see later). An adjacent midline area, over thequadrigeminal plate, may also be the site of an arachnoidcyst.

Structures in the posterior fossa can be seen on midlinesagittal view from the vertex or from alternative windowssuch as the posterior fontanelle or the posterolateral fonta-nelle. The cisterna magna is the CSF space around the cer-ebellum. It is usually only a few millimeters in thickness,but it can have prominence, earning it the name mega cis-terna magna. Although this is considered part of the Dandy–Walker spectrum (see later), it can also be idiopathic. How-

FIG. 22. Midline sagittal views from two patients (A,B). Anterior fontanelle approach is used, showing cavum septum pellucidum, cavum vergae (CV),cavum velum interpositum (CVI), the vermis of the cerebellum (V), fourth ventricle (solid arrow), and the cisterna magna (dotted arrow).

FIG. 21. Coronal (A) and right parasagittal (B) views using the anterior fontanelle approach. A. Approach is performed with steep posterior angulation.B. Approach is performed with steep lateral angulation. Bright echoes are seen in both images within cortical parenchyma that do not correspond with adefinite arterial zone. This was later proven to be a venous infarct.



ever, its presence should prompt careful evaluation of thefourth ventricle and corpus callosum. A prominent cisternamagna may be simulated by a subtentorial arachnoid cyst.

Off MidlineOff the midline, cystic spaces are more suspicious.

Arachnoid cysts are usually round and can be found over thesurface of the brain, under the temporal lobes, and in theSylvian or interhemispheric fissures. Migrational anomaliesor early fetal ischemic events can leave areas of the calvarialvault unoccupied. These fill with CSF and are often irregu-lar in outline.

Cysts in the choroid plexus are common, occurring in 1%to 3% of normal patients.12,15 They have uncertain etiology.Most are small (2–3 mm) and not multiple. Large (>10 mm)and multiple cysts can be associated with chromosomal ab-normalities such as trisomy 18.27 This is an important issuein fetal ultrasound because of genetic counseling issues. Aproportion of choroid plexus cysts are thought by some tobe remnants of previous hemorrhage. It must also be re-membered that infants can have rare pathologies such aschoroid plexus papilloma and choroid plexus carcinoma.Choroid plexus in the lateral ventricles passes through eachforamina of Monro to reach the third ventricle. A cyst in thisportion of the choroid could simulate resolving subependy-mal hemorrhage.

The finding of cysts (or, as some pathologic studies haveshown, pseudocysts without an epithelial lining) in the re-gion of the frontal horns or the head of the caudate nucleussuggests the possibility of previous hemorrhage, infection,or other insult.34 This is based on the fact that as subepen-

dymal germinal matrix hemorrhages resolve, they becomeincreasingly echolucent and cyst-like. However, when theyare an isolated finding, most of these cysts are withoutproven antecedent injury and fail to correlate with anythingbut normal neurologic outcome (Fig. 24).35,36

Extraaxial spaces are more prominent in babies withyoung gestational age. This is because of cerebral immatu-rity. Full-term babies normally have small spaces. Thesespaces can increase in thickness during hospitalization for

FIG. 24. Coronal image using the anterior fontanelle approach. Anteriorwatershed cystic PVL (arrow) superolateral to the right lateral ventricle.

FIG. 23. Coronal and midline sagittal views (A,B) using the anterior fontanelle approach. An echolucent area is seen in the midline, which is possiblycavum vergae. However, sagittal view shows position to be outside the normal location for this and for cavum velum interpositum. Doppler ultrasoundconfirmed no internal flow. Diagnosis: arachnoid cyst.



reasons that are unclear (Fig. 14A). Similarly, the ventricu-lar system can enlarge slightly and subsequently revert tonormal. In cases of brain atrophy in which there is volumeloss, subarachnoid fluid can be seen as echoless materialwithin the interhemispheric fissure separating these frontallobes. Prominent extraaxial spaces anterior to the frontallobes with normal interhemispheric fissure thickness cansometimes be seen in normal patients during the first year oflife, however. This has sometimes been referred to as sub-dural effusions of infancy.1 Pathologic enlargement of ex-traaxial spaces can occur in communicating hydrocephalus,subarachnoid hemorrhage, subdural hemorrhage, bacterialmeningitis, and postischemic atrophy (Fig. 25). High-frequency linear array transducers may aid in the analysis ofthese spaces.

HydrocephalusThere are no absolute dimensions of normal ventricles;

however, the overall size of ventricles remains relativelyunchanged over the course of time37 while brain paren-chyma develops around them. Cerebrospinal fluid is pro-duced by the choroid plexus within the lateral and thirdventricles. Fluid from the lateral ventricles flows throughthe foramina of Monro into the third ventricle, and fromthere, it flows into the fourth ventricle via the aqueduct ofSylvius (a relatively long and narrow canal). From thefourth ventricle, fluid can enter either the cisterna magna viathe foramen of Magendie or the basilar cisterns by eitherlateral foramen of Luschka. The spinal subarachnoid spacereceives 20% of the CSF load, which later joins the other80% to wash over the cerebral convexities. Hydrocephalus

is classified as being either obstructive or nonobstructive,but imaging cannot always distinguish between the two. Ingeneral usage, “hydrocephalus” tends to imply obstructivecausation. In this article, “ventriculomegaly” will be usedmore generically to describe any enlargement of the ven-tricles.

Hydrocephalus is the most common congenital malfor-mation in neonates who survive to infancy; however, it isassociated with a poor outcome, with normal cognitivefunction developing in only 38%.38,39 Indications for asonographic examination are an enlarged head, prominentseparation of the cranial sutures, a full fontanelle, or signs ofneurologic abnormality. Hydrocephalus represents an in-creased volume of fluid within the ventricular systemcaused by abnormal production, passage, or drainage ofCSF. Obstruction is the most common cause of hydroceph-alus and can be divided into two categories: noncommuni-cating hydrocephalus, in which the obstruction is at a pointwithin the ventricular system, and communicating hydro-cephalus, in which there is decreased absorption or an ob-struction beyond the ventricular system. When CSF be-comes contaminated with blood, inflammation of the mem-branes with which it comes in contact occurs. Inflamedmembranes swell, and normally tight channels throughwhich CSF flows (e.g., foramina of Monro, aqueduct ofSylvius) become obstructed. The most frequent cause ofobstruction is posthemorrhagic ventriculitis, but infectiousmeningitis has similar results. Dilation of the frontal andoccipital horns are measurable indicators of developing hy-drocephalus; however, the atria of the lateral ventricles isoften the first area that dilates.15 Another sign of mild ven-

FIG. 25. A. Coronal view using the anterior fontanelle approach showing a normal, prominent, extraaxial space along the interhemispheric fissure(asterisk). B. Similar projection on a different patient showing dilated lateral ventricles (V) and prominent extraaxial space secondary to atrophy (ex vacuophenomenon).



tricular enlargement is interposition of CSF lateral to thechoroid plexus, because there is often good apposition of thechoroid plexus with the lateral ventricular walls in a normalscan.5 When the inflammation involves the arachnoidgranulations, decreased absorption overloads the systemwith excess CSF.

Nonobstructive ventriculomegaly is seen when there isincreased volume of CSF, such as from increased produc-tion (as from a choroid plexus papilloma) or decreased brainvolume caused by postischemic atrophy (Fig. 14B). Merg-ing of periventricular cysts with the ventricular space willincrease the overall size of the ventricle while retaining thepotential for normal CSF pressure.

The most common causes of congenital hydrocephalusare aqueductal stenosis, myelomeningocele (with associatedArnold–Chiari malformation), communicating hydrocepha-lus, and Dandy–Walker malformation. These diagnosessuggest themselves by different combinations of ventricularenlargement relating to the anatomic level of obstruction(Fig. 26). The midline sagittal view is optimal for evaluationof third and fourth ventricle dilation. Coronal views areuseful in comparing lateral ventricle size for disparity inasymmetric hydrocephalus and for assessing the temporalhorns. Potential causes of acquired hydrocephalus arepostinflammatory (commonly intrauterine infection withcytomegalovirus or toxoplasmosis), posthemorrhagic(IVH), or masses, which may be vascular (vein of Galenaneurysm) or, rarely, neoplastic in origin.40,41

Chiari MalformationsHans von Chiari described four unrelated congenital

hindbrain anomalies in the early 1900s. However, the mod-

ern definition of the Chiari malformations excludes thetypes III and IV that he proposed. Type I is best evaluatedwith magnetic resonance imaging, which shows caudal dis-placement of the cerebellar tonsils and inferior cerebellumbelow the foramen magnum. Diagnosis of the type II mal-formation is an important finding by virtue of its associationwith meningomyelocele. Patients with these malformationsare often noted to have a small posterior fossa and efface-ment of the cisterna magna.42 An anteroposterior measure-ment of 2 mm or smaller for the cisterna magna is sugges-tive of effacement. The Chiari type II malformation is as-sociated with hydrocephalus. There may be colpocephaly, anonspecific form of ventricular dilatation in which the pos-terior horns are more dilated than the anterior horns, whichis probably a result of aqueductal narrowing (Fig. 27).

Dandy–Walker ComplexThe Dandy–Walker complex is a trio of posterior cystic

malformations all related to defective development in theroof of the fourth ventricle. They are the classic Dandy–Walker malformation, the Dandy-Walker variant, and themega cisterna magna. They share a relationship with mid-line abnormalities (agenesis of the corpus callosum, holo-prosencephaly) and migrational disorders (schizencephaly,posterior cephaloceles).42

The classic Dandy–Walker malformation consists of se-vere fourth ventricle dilatation manifesting as a posteriorfossa cyst when it extends posteriorly. It is caused by asso-ciated aplasia or dysplasia of the cerebellar vermis. Thecerebellar hemispheres are compressed and the tentorium iselevated. Hydrocephalus rapidly develops in most cases if itis not present at birth (Fig. 28).

The Dandy–Walker variant has less severe fourth ven-tricle dilation, probably because of milder cerebellar vermishypoplasia. It has twice the incidence of the classic Dandy–Walker malformation and is more easily missed.

The mega cisterna magna represents 54% of the Dandy–Walker malformations. An isolated enlargement of the cis-terna magna of more than 10 mm is the usual sonographicfinding, with the cerebellar vermis remaining intact. Ven-triculomegaly is an unusual finding (Fig. 29).43

Agenesis of the Corpus CallosumThe corpus callosum is the largest cerebral commissure

connecting the cerebral hemispheres. The rostral (later an-terior) part forms between the 12th and 20th week of ges-tation; the caudal (later posterior) part forms thereafter.44

Agenesis of the corpus callosum can be caused by primary(developmental) dysgenesis, when there is an insult to thegrowing brain early in fetal life, such as a vascular or in-flammatory event soon after the 12th week of gestation. Theanterior portion of the infant’s corpus callosum is present,but as development fails to progress after the insult occurs,the posterior portion is missing. When partial or completedestruction of the callosum is observed, particularly when

FIG. 26. Coronal view using the anterior fontanelle approach, showingsymmetric lateral ventriculomegaly, with dilatation of frontal and temporalhorns. The third ventricle is normal. Image is consistent with either con-genital or posthemorrhagic hydrocephalus.



the anterior portion is missing and the posterior portion ispreserved, this is thought to have occurred much later infetal life after normal development. It is termed secondarydysgenesis. Agenesis of the corpus callosum is commonlydiagnosed in utero; however, partial absence of the corpuscallosum is a difficult diagnosis to make in fetal life.45

Agenesis of the corpus callosum is suspected if there ispresence of ventriculomegaly (in particular, colpocephaly),teardrop configuration of the lateral ventricles, and in-creased separation of the frontal horns and bodies of thelateral ventricles into a parallel arrangement. Enlargement

and upward displacement of the third ventricle betweenseparated frontal horns creates the “bull’s head” configura-tion in the coronal ultrasound view. In primary agenesis, thepericallosal gyrus does not form, and the remaining gyri andsulci run perpendicular to the third ventricle, creating thepathognomonic “sunburst” sign (Fig. 30).46–48

Agenesis of the corpus callosum may be an isolated find-ing, but there are other malformations46 and genetic syn-dromes44 in as many as 80% of cases. These include anoma-lies such as polymicrogyria and cortical heterotopia (whichform the basis for fetal diagnosis with magnetic resonance

FIG. 28. A. Coronal image using the anterior fontanelle approach. The fourth ventricle (4) is open posteriorly, communicating with a prominent cysticarea (C) in the region of the cisterna magna through a defect in the cerebellar vermis, flanked by the cerebellar hemispheres (H). B. Midline sagittal viewusing the anterior fontanelle approach, with patient facing the reader’s right. The tentorium is lifted superiorly by the large subtentorial cyst (C). Dysgeneticvermis (V) projects into the cyst fluid. Diagnosis: classic Dandy–Walker malformation.27 Reproduced with permission of the McGraw-Hill Companies.

FIG. 27. A. Right parasagittal view through the anterior fontanelle. This newborn with repaired myelomeningocele and hydrocephaly has colpocephaly,with small frontal horn (F). B. Midline sagittal view through the anterior fontanelle showing prominent massa intermedia (M) in a dilated third ventricle(arrowheads). Infratentorial structures are displaced downward and are responsible for the inability to image the cisterna magna. Diagnosis: Chiari type IImalformation.27 Reproduced with permission of the McGraw-Hill Companies.



imaging;45), septotopic dysplasia, encephalocele, aqueduc-tal stenosis, intracerebral lipoma,49 interhemispheric arach-noid cyst, hydrocephalus, Dandy–Walker malformation,and Chiari type II malformation.50,51

Prognosis for children with agenesis of the corpus callo-sum is dependent on their associated anomalies. Isolatedagenesis of the corpus callosum is said to correlate with a

higher incidence of febrile convulsion but an otherwise nor-mal developmental outcome.52

HoloprosencephalyHoloprosencephaly represents the disordered separation

of midline structures within the prosencephalon during thefourth through eighth weeks of embryogenesis. There arethree recognized variants based on the severity of the con-dition: alobar, semilobar, and lobar.

Alobar holoprosencephaly, the most severe form, occurswhen there is complete failure of separation of the cerebralhemispheres, resulting in a single ventricular cavity, fusionof the thalami, and absence of the corpus callosum, falxcerebri, optic tracts, and olfactory bulbs. Sonography re-veals a thin, primitive cerebrum completely covering asingle ventricle. The monoventricle is often horseshoe inshape, partially because of third ventricle impingement inthe form of a dorsal cyst (Fig. 31).

Semilobar holoprosencephaly occurs when there is partialseparation posteriorly of the cerebral hemispheres, withvariable degree of fusion of the thalami, and absent olfac-tory bulbs and corpus callosum. There is generally morecerebral tissue and a smaller monoventricle on sonography.

In lobar holoprosencephaly, complete separation of thecerebral hemispheres has occurred, making the sonographicdiagnosis somewhat more difficult. The frontal horns maybe closer together than usual and the septum pellucidum isabsent, creating what is, in fact, a monoventricle.

Holoprosencephaly is associated with midline facial ab-normalities. A child presenting with such features should

FIG. 30. A. Midline sagittal view using the anterior fontanelle approach. Arrows show the direction of gyri toward the third ventricle. This is the sunburstsign in complete agenesis of the corpus callosum. (M) marks the enlarged massa intermedia. B. Coronal view with moderate posterior angulation using theanterior fontanelle approach, showing gross dilatation of the occipital horns. This is colpocephaly in a child with partial agenesis of the corpus callosum.Also note that the ventricles have a parallel configuration.

FIG. 29. Midline sagittal view using the anterior fontanelle approach. Acystic space is seen inferoposterior to the echogenic cerebellum. Diagnosis:mega cisterna magna.



undergo intracranial analysis. Abnormalities may rangefrom hypotelorism to cyclopia to even cebocephaly.Whereas the more severe forms of facial abnormality andcerebral fusion often correlate, alobar holoprosencephalymay occur without any facial signs.53

Vascular MalformationsA midline mass in the tentorial region that shows turbu-

lent flow is most likely a vein of Galen aneurysm (Fig. 32).This is technically a misnomer. It is better described as anarteriovenous malformation that can draw flow from thala-mostriate, choroidal, and anterior cerebral arteries.54 Itstributaries can be assessed sonographically. Studies duringand after embolization can determine the degree of throm-bosis achieved. If shunting is extreme, the infant may pre-

sent with intractable cardiac failure. If the malformationgrows more slowly, the presenting symptoms may be sei-zures or hydrocephalus.

Other vascular malformations can be found within thebrain parenchyma itself. These can be cavernous malforma-tions where the caliber of feeding arteries and draining veinsis normal and there is no arteriovenous shunting. Similarly,a venous malformation consists of a collection of dilatedmedullary or cortical veins that drain into a single, dilated,venous structure, also with no arteriovenous shunting. Cap-illary telangiectases are collections of dilated capillaries.The diagnosis of these three classes of lesions depends ontheir size and location. Many are found incidentally at au-topsy and never cause symptoms, but some may be associ-ated with seizures or hemorrhage.38

Lenticulostriate VasculopathyThe sonographic finding of linear branching echogenicity

within the thalamus and basal ganglia is indicative of len-ticulostriate vasculopathy (LSV). This represents calcifica-tion of the arterial wall and perivascular infiltration ofmononuclear cells in medium-size branches of the middlecerebral artery, which supply the thalamus and basal gan-glia. Care must be taken when evaluating LSV with a pos-terior fontanelle approach. Schlessinger19 has shown thisapproach to result in an anisotropic effect, with normal fi-bers simulating LSV. Anterior fontanelle views are oftenmore reliable (Fig. 33).

The finding of echogenic walls in lenticulostriate vesselswas initially attributed to perinatal asphyxia and TORCH(toxoplasmosis, others, rubella, cytomegalovirus, and her-pes simplex) infections when it was first described.55 How-ever, it is now recognized as a more common finding thatmay also be seen with chromosomal abnormalities, fetalalcohol syndrome, bacterial meningitis, and twin-to-twintransfusion syndrome. It can also be found in normal pa-

FIG. 32. Left parasagittal image(A) using the anterior fontanelle ap-proach. A large space with moderateechogenicity lies inferomedial to thelateral ventricle (V). It could repre-sent a cyst with proteinaceous fluid inthis image. However, a coronal im-age (B) using the anterior fontanelleapproach shows turbulent flowwithin the mass on color Doppler im-aging. Diagnosis: vein of Galen an-eurysm.

FIG. 31. Coronal view using the anterior fontanelle approach. A singleventricle (V) surrounds the fused thalami (T) of a 38-postmenstrual-weekfetus. Note the absence of the interhemispheric fissure. Diagnosis: alobarholoprosencephaly.27 Reproduced with permission of the McGraw-HillCompanies.



tients. Hence, LSV probably represents a nonspecific re-sponse to vascular injury. Some groups have implicatedrespiratory distress syndrome and cyanotic congenital heartdisease in the postnatal development of LSV;55,56 however,definitive evidence is still sought. It is thought by some thatthe sonographic finding alone is not evidence enough toconduct a TORCH screen.57 The condition can be associ-ated with later developmental delay, gross motor delay, anddeafness; its finding should prompt close neurologic andimaging follow-up.58

Color Doppler UltrasoundColor Doppler ultrasound has allowed rapid analysis of

fluid-filled structures to determine whether they represent

blood vessels or cystic areas of the brain. It has allowedvisualization of the low-flow vessels in the infant brain. Asa clinical tool, it has great potential, much of which is as yetunrealized. Basic research is still being performed.

One area in which color Doppler ultrasound has alreadymade a difference is in the recognition of venous structuresin the brain. Drainage of capillary blood to the surface ve-nous sinuses is through connecting veins that are easily tornor thrombosed. Superior sagittal sinus thrombosis occurs inthe clinical context of sepsis, meningitis, or dehydration.Detection of superior sagittal or other sinus thrombosis (Fig.34) can prompt early diagnosis and treatment. Chances ofobtaining a more diagnostic examination are maximizedwith the use of sensitive color-flow imaging equipmentcoupled with high-frequency linear transducers positionedparallel to the sinus. Vertex position works best for thesuperior sagittal sinus,59 whereas the posterolateral ap-proach can visualize the transverse sinuses. Power Dopplerhas been used when flow is too sluggish to be denoted byroutine color Doppler ultrasound.60 Asymmetry in regionalblood flow can indicate an area of ischemia with changestoo subtle for grey-scale images. A bland infarct (ischemiawithout subsequent hemorrhage) may be signaled by pe-ripheral luxury perfusion visible by power Doppler ultra-sound.61,62

Resistive index (RI) values in cerebral arteries have beenpublished for normal term infants63 but have not yet yieldeddefinitive standards for comparison among patients. How-ever, one intriguing use for the RI appears to be in predict-ing whether a baby with hydrocephalus might benefit fromshunting; graded compression on the fontanelle causes anincrease in RI in an infant with obstructive hydrocephalus,which is not as obvious in a case of nonobstructive ven-triculomegaly.64 In evaluating asphyxia, most groups havenoted increased RI with low diastolic flow as evidence of

FIG. 33. Right parasagittal view using the anterior fontanelle approach,showing mineralizing vasculopathy of the lenticulostriate arteries (arrows).

FIG. 34. Midline sagittal (A) and coronal (B) images through the sagittal suture using a high-frequency transducer. Color Doppler shows flow in arteriesand perforating veins but no color in the expected region of the superior sagittal sinus (arrows). Diagnosis: superior sagittal sinus thrombosis.



organ at risk for ischemia/necrosis. Siebert et al.14 note lowRI with increased diastolic flow as equally of concern as itis evidence of poor autoregulation of cerebral blood flow.

Role of Head Ultrasound in NeurodevelopmentalOutcome Studies

A large body of work has appeared in the clinical pedi-atric literature in recent years, charting the developmentalprogress of cohorts of neonatal intensive care graduates dur-ing the past two decades. Cranial ultrasound reports have amajor part in these retrospective studies, giving the appear-ance of comparability among the study populations. Intra-ventricular hemorrhage is often reported as mild, moderate,or severe, with associated degrees of ventricular dilatation.Severe IVH (Volpe grade III; Papile grade III-IV) has apoor prognosis, with posthemorrhagic hydrocephalus in theshort-term and cerebral palsy, developmental delay, andlearning difficulties in the long-term. Moderate IVH (Volpegrade II; Papile grade II-III) may result in cerebral palsy andpoor cognition, whereas mild IVH (Volpe grade I; Papilegrade I) may resolve with no clinical sequelae.

However, it is notable that studies from the past 5 yearshave found it more and more difficult to maintain the clearcause and effect relationships between imaged abnormali-ties and neurologic defects that previous studies had fos-tered. The increasing sophistication in ultrasound capabili-ties and the increasing availability of computed tomographyand magnetic resonance imaging for even the tiniest infantshave been a two-edged sword: more subtle abnormalitiesare found, but these have less definite links to neurodevel-opmental outcome.

Several studies have addressed the practice of using earlyhead ultrasound findings to predict neurologic outcome.This has shown good correlation with only the most obviousand overwhelming of US defects,65–69 whereas more minorabnormalities (choroid cysts, subependymal cysts, evanes-cent flares) had no apparent consequences. Correlating se-verity of neurologic deficit with lesion severity was alsounprofitable.70 White matter injury correlates best witheventual disability, but this is the most difficult to appreciatesonographically.71 Comparing studies is hampered by thelack of standardization in study design and also by the lackof standardized language to describe sonographic find-ings.72 Adoption of standard descriptions would aid thecompiling of more significant results in a shorter time.73

Correlation between ultrasound and magnetic resonanceimaging findings has been good;74–77 however, magneticresonance imaging often finds more lesions than suspected.A postmortem study found ultrasound to be less than satis-factory in the correspondence between images and actualpathologic anatomy.78 One possible explanation for this hasbeen alluded to previously: white matter edema withouthemorrhage can be difficult to image, but the breakdown ofneural tissue at the cellular level begins immediately after

ischemic damage. These changes are apparent on histologicexamination much earlier than can be detected by radiologicimaging, which requires damage at the tissue level. Mag-netic resonance imaging spectroscopy and positron-emission tomography scanning offer future possibilities forearlier detection of ultrastructural abnormality.

CONCLUSION

Ultrasound continues to be the best tool that we have forthe assessment of the brain of a sick neonate. New imagingtechniques and hardware hold great promise for seeing finerdegrees of detail. However, it behooves us to keep abreastof what our clinical colleagues are doing with the informa-tion that we provide for them. The conclusions they makecan, in turn, eventually drive what they request of us. It is upto us to continue to provide new perspectives in imagingand show how these can serve the well being of our tinypatients.

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intracranial neonatal neurosonography: an update

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