Sage Journals: Discover world-class research

Abstract

French

Neurosonography (NSG) is pivotal for rapid, point-of-care neonatal brain assessment. This review elucidates the comprehensive applications of NSG in pediatric care, emphasizing its role in early diagnosis and management of pathologies affecting the pediatric head—such as scalp lesions, misshapen calvarium, ventricular distortions, and cerebrovascular abnormalities, and its specific role in conditions like hypoxic-ischaemic encephalopathy (HIE) across different neonatal gestational ages. We explore its diagnostic advantage in critical care settings, particularly for infants with stroke risk in sickle cell disease, ECMO-related complications, screening for therapeutic hypothermia, and routine neonatal intensive care unit monitoring. This review discusses the recommendations based on the timing of brain injury (preterm and term) and describes technical considerations that enhance diagnostic accuracy. Ultimately, this article advocates for its incorporation into routine neonatal screening to improve neurodevelopmental outcomes, underscoring its importance in clinical decision-making and long-term management of pediatric brain disorders.

Keywords

neurosonography HIE BESS subpial haemorrhage neonatal stroke neonatal infection ECMO-related complications

Introduction

Neurosonography (NSG) is an initial imaging modality for assessing the neonatal brain. NSG can be performed bedside in the intensive care unit with no radiation exposure. It has several advantages as it is readily available, cost-effective, real-time, and portable compared to MRI. The NSG aims to detect brain injury, structural abnormalities, and understand the timing and evolution of parenchymal injury. It also aids in making accurate diagnoses to facilitate clinical decision-making and monitor the growth and brain maturation in the neonatal period.

With technological innovation, improved image resolution, and faster processing, NSG is reliable in the early diagnosis of brain injury in infants at risk of neurodevelopmental impairment, allowing timely initiation of optimal therapy and eventually improving neurological outcomes. In this review, we highlight the indications of NSG and emphasize the technique and sonographic anatomy with a systematic approach to the diverse spectrum of pathologies affecting the head, including neonatal haemorrhages, sutural abnormalities, hypoxic-ischaemic encephalopathy, congenital masses and malformations, and cerebrovascular abnormalities.

Indications

NSG plays a critical, multifaceted role in evaluating pediatric brain abnormalities, primarily indicated for screening all newborns with suspicion and risk of brain injury. The American Institute of Ultrasound in Medicine practice parameters outline the specific indications for NSG in neonates and infants.^1,2 This article presents an anatomically based framework, beginning with the outermost scalp, followed by skull and sutures, extra-axial spaces, brain parenchyma, ventricles, and intracranial vessels, as described in Table 1.

Table 1.

Indications of Neurosonography.

Scalp	Collections, benign and malignant masses, inclusion cysts, vascular masses
Skull and calvaria	Abnormal shape, plagiocephaly, craniosynostosis, delayed or premature closure of fontanelle
Extra axial space	Benign enlargement of subarachnoid space, extra-axial collections and haemorrhages, secondary effacement
Parenchyma	Hypoxic ischaemic injury, haemorrhage, stroke, infections, congenital tumours, and congenital malformations
Ventricles	Hydrocephalus, post-haemorrhagic ventricular dilatation, ventricular-periventricular cysts
Vessels	Hypoxic ischaemic injury, stroke, vascular malformations, and thrombosis

Timing of Neurosonography in Neonates

Preterm Infants (<31 + 6 Weeks Gestational Age)

For preterm infants born at ≤31 + 6 weeks, the position statement by the Canadian Pediatric Society recommends NSG for routine surveillance at 4 to 7 days to detect germinal matrix haemorrhage (GMH), intraventricular haemorrhage (IVH), and early ventricular dilatation.³

In infants with Grade 2 or higher IVH or white matter injury, a follow-up NSG should be performed every 7 to 10 days. If ventricular dilatation or worsening post-haemorrhagic ventricular dilatation (PHVD) occurs, the imaging frequency should be intensified, at least weekly initially and as clinically indicated later.³

Term-corrected NSG is recommended for preterm infants born before 26 weeks’ gestation and for infants born between 26 + 0 and 31 + 6 weeks gestational age in case of additional risk factors or previous moderate-to-severe abnormality, including grade 3 or higher IVH, PHVD, or cystic periventricular leukomalacia (PVL).³

Preterm infants (32 + 0 to 36 + 6 Weeks Gestational Age)

For the late and moderately preterm infant (32 + 0 to 36 + 6 GA) with additional risk factors, an NSG is recommended 4 to 7 days after birth, followed by repeat imaging at 4 to 6 weeks in case of imaging abnormality on initial NSG. Term-corrected NSG is not routinely recommended for late and moderately preterm infants.³

Technique and Settings

NSG is preferably done through the cranial incubator in the NICU and at the bedside or in the ultrasound room during infancy and childhood. During the examination, adequate care should be taken to avoid moving the infant and causing any disturbance to the incubator temperature and pressure over the anterior fontanelle for optimal Doppler assessment.

NSG starts with grey-scale imaging performed through the anterior fontanelle in coronal and sagittal planes using the multifrequency phased array, curved array, and linear array transducers (5-18 MHz). The choice of transducer frequency is a compromise between resolution and penetration with the optimal near-field resolution of higher frequencies and better penetration depth of lower frequencies. The focus point is centred on ventricular areas and can be altered based on the region of interest. Appropriate gain adjustment helps interpret the imaging findings reliably, and adequate depth of view is necessary for better assessment of the posterior part of the brain. Coronal planes are acquired through the anterior fontanelle with anterior-to-posterior angulation with the transducer marker pointing to the right side (7 standard planes).^2,4 Sagittal imaging uses a mid-sagittal view with the transducer pointing anteriorly, and left and right parasagittal views extend from the midline through the caudothalamic grooves, deep white matter, insula, Sylvian fissures, and peripheral cortex on both sides (7 standard planes)^2,4 (Figure 1A and B). Cine loops may also be obtained to supplement the coronal and sagittal images. Additional images are acquired through the posterior and mastoid fontanelles. The primary and supplemental imaging windows, their advantages, and relevant sonographic anatomy are described in Table 2, Supplemental Videos 1 to 3.

Figure 1.

(A) Sagittal graphic representation showing standard coronal planes performed through the anterior fontanelle, at the level of frontal lobes (C1); frontal horns of the lateral ventricle (C2); lateral ventricles at the level of foramina of Monro (C3); lateral ventricles posterior to the foramina of Monro (C4); quadrigeminal plate cistern and cerebellum (C5); echogenic glomi of the choroid plexus (C6); and posterior to the occipital horns including parietal and occipital lobes (C7). (B)

Table 2.

Imaging Windows, Advantages, and Relevant Sonographic Anatomy.

Imaging windows	Imaging plane	Applied sonographic anatomy
Anterior fontanelle	• Coronal images—Levels • Frontal lobe • Frontal horns of the lateral ventricle • Third ventricle • Posterior to foramen of Monro • Trigone of lateral ventricle • Occipital lobes	• Grey-white matter differentiation, gyral pattern, and sulcal spaces are assessed for symmetry and echogenicity. • Failure to appreciate normal layers, that is, thin echogenic superficial pia mater, hypoechoic grey matter and relative hyperechoic white matter, is abnormal (focal haemorrhage or infarction). • Hyperechogenecity of the periventricular white matter more than the choroid plexus is abnormal (haemorrhage vs periventricular leukomalacia). • Intraventricular echogenicity within the frontal horn of the lateral ventricle anterior to the foramen of Monro and in the occipital horn posterior to the calcarine sulcus should raise concern for intraventricular haemorrhage as these areas are devoid of choroid plexus. • The anterior horn width and the ventricular index are measured at the level of the foramen of Monro in the mid-coronal plane. • Doppler assessment of the anterior cerebral artery in the sagittal plane at the level of the genu of the corpus callosum and bridging veins in the coronal plane to differentiate BESS from extradural and subdural collections.
Anterior fontanelle	Sagittal images—Levels ➢ Mid-sagittal plane ➢ Parasagittal planes (right and left) ➢ Through lateral ventricles ➢ Through the insula
Posterior fontanelle	Coronal and sagittal images	• Better evaluation of atria and the occipital horns of the lateral ventricle. • Subtle intraventricular haemorrhage in the occipital horn and suspected holoprosencephaly.
Mastoid fontanelle	Axial +- coronal	• Excellent depiction of posterior fossa structures, including transverse sinus, sigmoid sinus, torcula, and cisterna magna. • Assess aqueduct obstruction, brainstem, and cerebellar bleeds. • Evaluate infratentorial anomalies such as Dandy-Walker syndrome and cerebellar hypoplasia.
Temporal window	Ideally, axial images of both sides	• Look for the brainstem and cerebellum. • Doppler assessment of the Circle of Willis and the middle cerebral artery.

Colour Doppler images are mandatory when screening arterial and venous structures. Doppler imaging assessment of the anterior cerebral artery (ACA) at the genu and the region of the superior sagittal sinus (SSS) and vein of Galen are an integral part of the assessment. Spectral tracing with peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistive index (RI) is essential to evaluate hypoperfusion, ischaemia, and cerebral oedema in post-haemorrhagic ventricular dilatation and underlying cardiac abnormalities. Power Doppler and B-flow imaging help assess hyper- and hypoperfused areas.

Finally, high-resolution linear array transducer images are obtained to assess the convexity subarachnoid spaces, peripheral cortex, and deeper brain structures. Linear images are also used to assess the scalp, sutures, extra-axial spaces, and vascular structures.

Teaching Points

In preterm neonates, to ascertain periventricular leukomalacia, the findings must be confirmed on 2 orthogonal planes as prominent periventricular echogenicity could be due to the anisotropic effect caused by the perpendicular ultrasound beam striking the peri-atrial white matter tracts.

In preterm neonates, the RI tends to be elevated (up to 0.90) due to low intracerebral diastolic flow velocities. In term infants, it can be as low as 0.65, reflecting improved diastolic flow due to physiologic transition.⁴

The ACA RI has to be carefully evaluated in cardiac disease, primarily due to variability in the end-diastolic flow. The intracranial arteriovenous malformations demonstrate irregular and biphasic spectral patterns.

Normal Variants of the Brain on Neurosonography

Adequate awareness of the imaging appearances on neurosonography is necessary to avoid potential misdiagnosis, and the normal variants are described in Table 3.

Table 3.

Normal Variants of the Brain on Neurosonography.

Normal variants	Imaging appearance on Neurosonography
Premature brain sulcation	The lack of sulcation in extreme prematurity should not be confused with malformations of cortical development. Conversely, the smooth brain in a term neonate should raise concern for cortical malformation.
Peritrigonal echogenicity	The symmetric near homogenous echogenic appearance of posterior periventricular white matter in preterm infants disappears in the early neonatal period. The findings should be confirmed on orthogonal planes to exclude periventricular haemorrhage and leukomalacia.
Lenticulostriate vasculopathy (LSV)	One or 2 unilateral or bilateral curvilinear hyperechogenicity with branching patterns in the basal ganglia is considered a normal variant. High-grade (3 or more striations) LSV could be seen in patients with hypoxia, congenital infections and genetic abnormalities.
Benign enlargement of the subarachnoid space in infancy (BESS)	Symmetric frontal and parietal extra-axial space widening with interhemispheric width beyond 6 mm in infants with macrocephaly that spontaneously resolves by 2 y of age. The CSF space follows the gyral contour with the presence of subarachnoid cortical veins and lacks adjacent gyral flattening.
Asymmetric lateral ventricles	Mild asymmetric lateral ventricles are common in preterm newborns and tend to normalize during the first month of life. They could persist into postnatal life without periventricular white matter volume loss or abnormal echogenicity.
Connatal cysts	Single or multiple, unilateral or bilateral small cystic lesions adjacent to the superolateral margins of the frontal horns of the lateral ventricles. They are located along the external angle of the lateral ventricles and usually disappear within the first year of life.
Cavum septum pellucidum (CSP), cavum vergae (CV), and velum interpositum (CVI)	A fluid-filled single midline cavity, located between the lateral ventricles. The component anterior to the foramen of Monro is labelled CSP, and the posterior is CV. CVI is a simple, unilocular, thin-walled cystic lesion in the pineal region between the forniceal columns above the level of internal cerebral veins. Non-visualization of the CSP in the antenatal period could be associated with anomalies such as callosal agenesis, septo-optic dysplasia, schizencephaly, and holoprosencephaly.
Mega cisterna Magna	Retrocerebellar cerebrospinal fluid accumulation of more than 10 mm. The cerebellar vermis, tentorium, and posterior fossa show preserved morphology with no mass effect.
Choroid plexus cysts	Incidental small choroid plexus cysts are unilateral without clinical significance and genetic abnormalities. On the other hand, large bilateral choroid plexus cysts in appropriate clinical settings should raise suspicion for Trisomies.

Pathologies

Scalp: NSG is the preferred initial imaging technique for evaluating pediatric scalp lesions as it allows detailed assessment of lesion morphology, echogenicity (solid or cystic), vascularity, and potential intracranial extension.^5,6 After the neonatal period, the occipital and post-auricular lymph nodes (benign or malignant) are the frequently encountered pediatric scalp lesions.⁷ Common infantile scalp conditions include:

Cephalohaematoma: Subperiosteal haemorrhage confined by the periosteum that does not cross sutures, except in craniosynostosis (Figure 2).⁷

Subgaleal Haematoma: Occurs between the galea aponeurotica and pericranium due to emissary vein rupture, allowing the haematoma to cross the sutures and midline (Supplemental Figure 1).⁸

Caput Succedaneum: A serosanguineous fluid accumulation in the subcutaneous tissue, typically crossing sutures and midline.⁹ It is commonly associated with prolonged labour and vacuum-assisted delivery (referred to as Chignon).¹⁰

Haemangiomas: A benign vascular tumour presents at or immediately after birth with internal vascularity on US and often undergoes gradual involution (Supplemental Figure 2).^7,11 Vascular malformations, on the other hand, are small at birth and continue to grow.¹²

Ectodermal inclusion cysts: Dermoid and Epidermoid cysts are midline or off-midline seen frequently in the frontotemporal region, as well-defined, avascular, and hypoechoic structures on US, occasionally containing calcifications, fat or mucinous material (Supplemental Figure 3).^7,13 Epidermoid cysts are often sub-periosteal compared to dermoid cysts, which are usually superficial to the periosteum.⁷

Langerhans Cell Histiocytosis: Often affects the calvarium, appearing as a solid lesion on US, originating from the diploe with asymmetric outer and inner table destruction.⁷

Figure 2.

Newborn following vacuum-assisted delivery. The panoramic ultrasound image reveals the right parietal heterogeneous echogenic collection, suggesting cephalohaematoma (star), which does not cross the midline or sutures.

Teaching point: Subgaleal haemorrhage may extend into the neck and can be associated with fractures; it should be looked for in neonates with unexplained blood loss.^7,14

Skull and sutures: NSG is occasionally used to assess fractures, and in the absence of scalp haematoma, it is difficult to differentiate from accessory sutures.¹⁵ Rarely organized cephalhaematoma can present as calvarial deformity. US demonstrates patency of fontanelles and identifies cranial sutures as hypoechoic lines between hyperechoic bony plates.^16,17

Abnormal head shape: Posterior calvarial deformity is usual in infants due to posture, resulting in positional or deformational plagiocephaly.¹⁸ Craniosynostosis is caused by the premature fusion of one or more cranial sutures, whether non-syndromic or syndromic, seen as the absence of the hypoechoic suture gap (Figure 3). It most commonly affects the sagittal suture and often requires surgical intervention.^17-19

Figure 3.

Three-month-old female with anterior plagiocephaly. Coronal ultrasound image with linear array transducer shows fusion of the right coronal suture, in keeping with coronal craniosynostosis (arrow) compared to the patent coronal suture on the normal left side (dashed arrow).

Teaching point: The metopic suture may close as early as the third month of life and can be constitutional in the absence of trigonocephaly and hypotelorism.¹⁶

Extra-axial Space: Enlarged extra-axial spaces can result from diverse conditions, including extra-axial collections, haemorrhages, parenchymal atrophy, or ECMO-related. BESS can be transiently observed in infants. Small extra-axial spaces can be physiological.^20,21

Epidural Haemorrhage (EDH): A rare bleed, often seen with post-forceps delivery, characterized by mass effect with or without skull fracture.²⁰

Subdural Haemorrhage (SDH): Typically associated with a traumatic birth, SDH appears as focal extra-axial collection displacing the hyperechoic arachnoid (Figure 4). It lacks traversing vessels and may have associated mass effect.^21,22

Subarachnoid Haemorrhage (SAH): Difficult to detect sonographically as they usually lack mass effect. SAH can be suspected in cases with thickened echogenic sulci and prominent extra-axial CSF space with internal echoes.²⁰

Subpial Haemorrhage (SPH): SPH accounts for ~15% of perinatal haemorrhages, presenting as gyriform echogenicity with characteristic sulcal splaying.²³ Larger SPH lesions may show a yin-yang appearance (Figure 5). The hypoechoic extra-axial component reflects a partially clotted haemorrhage, and the hyperechoic intra-axial component indicates cortical involvement.^24,25

BESS: Associated with macrocephaly, presents as enlargement of subarachnoid space extending along the falx cerebri on US (Figure 6). Doppler assessment shows traversing cortical vessels.^20,21,26

Figure 4.

Five-month-old patient with increasing head circumference. Coronal ultrasound image with a linear array transducer shows bilateral subdural collections (stars) with internal echoes in the medial parietal parafalcine region, causing mildly effaced underlying subarachnoid spaces (arrows).

Figure 5.

Two-day-old with premature baby for screening. Coronal ultrasound image with a linear array transducer reveals bilateral inferior temporal extra-axial gyriform mixed echogenicity causing sulcal widening (arrows). The larger subpial haemorrhage along the right inferior temporal region shows a Yin-Yang appearance (inset image in left upper corner).

Figure 6.

Six-month-old male with a head circumference above 97th percentile for age and sex-matched controls. Coronal ultrasound image with a linear array transducer demonstrates enlarged extra-axial CSF spaces with normal traversing vessels, suggesting benign enlargement of the subarachnoid sulcal spaces (BESS).

Teaching point: EDH and SDH can lead to effacement of the sulcal spaces. SPH typically causes sulcal widening, which can often be challenging to distinguish from an echogenic cortex when small.²⁷

Parenchyma

Hypoxic-Ischaemic Encephalopathy (HIE): HIE affects both term and preterm infants, with injury patterns determined by the severity and period of hypoxia in the perinatal period (Table 4). The gestational age is vital as the cerebral watershed areas differ between term and preterm infants due to ongoing myelination and cerebrovascular maturation.^20,21,26,28

Table 4.

Key Imaging Findings in Hypoxic-Ischaemic Encephalopathy.

HIE type	Regions affected	Imaging findings
GM-IVH	Germinal matrix and ventricles	GM-IVH ± ventricular enlargement, periventricular hemorrhagic infarction (PVHI)
PVL	Periventricular white matter	Periventricular hyperechogenicity and cyst formation (>2 wk)
Severe preterm HIE	Thalamus, globus pallidus, hippocampus, dorsal brainstem, cerebellum	Increased thalamic echogenicity, relative sparing of Basal ganglia
Mild to moderate term HIE	Cortical-subcortical white matter	Watershed cortical-subcortical echogenicity and sulcal effacement
Severe term HIE	Putamen, lateral geniculate, caudate, and perirolandic cortex	Sulcal effacement, loss of grey-white differentiation, slit-like ventricles.

Preterm HIE: The primary watershed areas in preterm infants are the periventricular white matter and germinal matrix.

Germinal Matrix-Intraventricular Haemorrhage (GM-IVH): The germinal matrix containing fragile blood vessels is susceptible to fluctuations in systemic blood pressure and oxygen levels.^26,29 Most haemorrhages happen within the first 3 to 4 days of life (critical window).^30,31 NSG is essential for monitoring high-risk infants, especially those born before 30 weeks and extremely low birth weight and for the grading of GM-IVH.^20,28,32

Grade 1: Confined to the germinal matrix (Figure 7A).

Grade 2: Extends into the lateral ventricle without dilatation (Figure 7B).

Grade 3: Grade 2 with ventricular dilatation in early/initial scan with AHW measuring >6 mm (Figure 7C).

Periventricular Haemorrhagic Infarction (PVHI): Rare ischaemic injury affects brain tissue adjacent to a GM-IVH (5% of cases), often resulting from damage to terminal subependymal veins (Figure 7D). PVHI has a high risk of long-term neurological impairment.^21,31,33 It is critical to assess whether PVHI is unilateral or bilateral, extent of involvement and the presence of midline shift.²¹

Cerebellar Haemorrhage: Haemorrhage in the external granule cell and subependymal layers (cerebellar germinal zones) haemorrhages are rare but more frequent in babies with very low birth weight (<750 g), traumatic delivery, and ECMO babies (Supplemental Figure 4).^21,28,30,34

Figure 7.

Parasagittal ultrasound image with a linear transducer array (A) shows echogenic focus in the caudothalamic groove (Grade I—GMH-IVH). Coronal images (B and C) with a linear transducer array show echogenic focus in the left caudothalamic groove and temporal horn of the right lateral ventricle in B (Grade II—GMH-IVH) and right caudothalamic groove bleed with right frontal and temporal horns extension and mild ventricular enlargement in C (Grade III—GMH-IVH). Coronal image with a curvilinear transducer array (D) shows bilateral germinal matrix haemorrhages with ventricular extension and left periventricular haemorrhagic infarction (Grade III + PVHI) (arrow).

Teaching point: Imaging through the mastoid fontanelle should be obtained to enhance the detection of cerebellar haemorrhages.²⁰

Periventricular Leukomalacia (PVL): A slowly evolving HIE affecting white matter, often appears around 7 to 10 days as increased echogenicity in the fronto-parietal periventricular regions (Figure 8), more than the echogenicity of choroid plexus, may evolve into cyst.^20,28,35 Cystic PVL is a more severe form (Supplemental Figure 5), typically noticeable after 2 to 3 weeks and is associated with long-term developmental impairment, including cerebral palsy.^28,30,36 PVL should be assessed using MRI at term-equivalent age to help predict neurodevelopmental outcomes.³

Figure 8.

A 5-day-old preterm boy with mild HIE. Coronal ultrasound image with a linear array transducer demonstrates the asymmetric increased echogenicity in the bilateral periventricular white matter confirmed in a follow-up MRI study (not shown).

Teaching point: Periventricular hyperechogenicity in a term baby with or without haemorrhage should raise concerns for other underlying causes, such as COL4A mutation and metabolic disorders.³⁷

Severe HIE: Targets areas with high metabolic activity and early myelination, such as the thalamus, globus pallidus, brainstem, and cerebellum.^26,28,38,39 NSG may show increased echogenicity in the thalamus within 48 to 72 hours of severe hypoxic-ischaemic episodes (Figure 9).²⁸ Doppler studies often show high end-diastolic flow and decreased RI (<0.6) due to cerebral vasodilation.^4,26,40

Figure 9.

Newborn with prolonged labour and severe preterm HIE. Coronal ultrasound image with a linear array transducer demonstrates diffusely increased echogenicity of the deep and periventricular white matter and bilateral gangliothalamic region (stars) with effacement of the sulci and ventricles.

Term HIE: HIE in term infants presents differently due to more advanced brain maturation.

Mild to Moderate HIE: Involves peripheral watershed regions, showing increased echogenicity in the subcortical white matter with accentuated grey-white matter differentiation of the parasagittal frontal and parietal regions.^20,21,26,39 Prolonged hypoxia may involve basal ganglia and often cause widespread echogenicity with cerebral oedema, slit-like ventricles, effaced extra-axial CSF spaces, and low RI in the Doppler study.^21,26,39

Severe HIE: Targets more advanced myelinated areas, including the caudate nucleus, putamen, perirolandic cortex, ventrolateral thalamus, hippocampus, and dorsal brainstem.^{20,21,26,28,39} In severe cases, cortical and subcortical injury may lead to sulcal effacement, loss of grey-white matter differentiation, and slit-like ventricles (Figure 10). ACA RI below 0.55 correlates with poor neurodevelopmental outcomes (Supplemental Figure 6).^32,41

Figure 10.

Term baby with severe HIE. Coronal ultrasound image with a curvilinear array transducer reveals diffuse increased echogenicity involving the visualized brain parenchyma with slit-like ventricles, effaced sulcal spaces, and low resistive index (not shown).

Teaching point: Watershed cortical-subcortical term HIE is challenging to assess on US and requires careful evaluation of the peripheral brain, often MRI correlation.²⁶

Choroid Plexus Haemorrhage: Choroid plexus haemorrhage is relatively rare, more common in term infants with hypoxia.²⁰ It appears as an irregular, heterogeneous, bulky choroid plexus on ultrasound.²¹

Neonatal Stroke

Arterial ischaemic stroke is the predominant type of stroke in the neonatal period, most commonly affecting the middle cerebral artery (MCA) territory. Risk factors include birth-related trauma, coagulation and congenital cardiac disorders, vasospasm from perinatal infections, dehydration, and maternal cocaine use.^20,42 NSG findings of acute arterial infarction typically reveal focal increased echogenicity with loss of grey-white matter differentiation, sulcal effacement (Figure 11), and peripheral hyperaemia (luxury perfusion).^26,42 However, early detection of acute stroke on ultrasound can be challenging due to limited sensitivity and the often-asymptomatic presentation in neonates. As the infarction evolves, it may lead to encephalomalacia and volume loss.^20,42

Venous sinus infarcts and thrombosis often occur in the context of perinatal injuries, infections, and hypercoagulable states.^20,28,42 Doppler ultrasound can identify venous thrombus and absent flow, often showing echogenic brain parenchyma and sometimes associated haemorrhage (Supplemental Figure 7). Thalamic involvement is usually associated with the straight sinus and vein of Galen thrombosis, and superior sagittal sinus thrombosis often involves the bilateral parasagittal cortex and subcortical white matter.^20,42-44

Figure 11.

Two-day-old term baby with left upper extremity arterial clot for screening US head before initiation of heparin. Coronal ultrasound image with a linear array transducer reveals a hyperechoic and bulky left basal ganglia (star), concerning for neonatal ischaemic infarction, confirmed on MRI (not shown).

Teaching point: In suspected neonatal stroke, careful assessment of the grey-white matter junction and any asymmetry of parenchymal echogenicity, cerebral sulci, and ventricles could aid in diagnosis.

Neonatal Infections

Congenital infections, particularly TORCH (TOxoplasmosis, Rubella, Cytomegalovirus [CMV], and Herpes simplex virus), frequently cause a range of intracranial abnormalities (Figure 12). These include intracranial calcifications, cortical malformations, cerebral and cerebellar dysgenesis, callosal agenesis, germinolytic cysts, white matter cystic changes, ventriculomegaly, microcephaly, and lenticulostriate vasculopathy (LSV).^26,45,46

Cytomegalovirus (CMV) is the most common congenital infection in neonates. Early exposure (before 20-24 weeks) leads to severe brain abnormalities and microcephaly, while later infections result in milder manifestations such as periventricular calcifications and white matter changes, cortical malformations, and cysts (Figure 12).^26,45,47

Toxoplasmosis, the second most common, often presents with ventriculomegaly and randomly distributed calcifications.^20,26,45

Zika virus is notably associated with severe microcephaly and profound cortical malformations.⁴⁸

Figure 12.

Seven-day-old girl, serology positive for congenital CMV infection. Coronal ultrasound image with a linear array transducer shows tiny periventricular echogenic foci (circle), from suspected calcifications, left germinolytic cysts (not shown), and abnormal sulcation (arrows), suggesting polymicrogyria.

Acquired infections in neonates can be bacterial, viral, or others. Though rare, bacterial meningitis and meningoencephalitis are severe and commonly caused by Group B Streptococcus, E. coli, H. influenza, and Listeria.^21,49 NSG findings include thickened echogenic meninges, floating echoes or collections in extra-axial space (Figure 13), cerebral oedema, and ventriculomegaly.^26,49 Viral meningitis and meningoencephalitis, most commonly neonatal herpes, can involve grey and white matter, leading to extensive brain necrosis, multifocal brain necrosis, and eventual multi-cystic encephalomalacia.^49,50

Figure 13.

Two-month-old female admitted for H Influenza meningitis. Coronal ultrasound image with a linear array transducer reveals diffuse echogenic thickening of the leptomeninges and prominent extra-axial spaces with internal echoes (arrows). Mildly increased echogenicity of the ventricular wall is concerning for ventriculitis. Findings were confirmed on contrast MRI (not shown).

Teaching point: Serial ultrasound helps monitor complications such as cerebritis, abscess formation, and hydrocephalus.

Congenital Malformations: Congenital malformations are rare and often require an MRI for complete evaluation.^20,26 Neonatal ultrasound demonstrates variable sensitivity in diagnosing and characterizing these conditions.

Supratentorial Malformations

Corpus Callosum (CC) Abnormalities: Agenesis or dysgenesis of the CC can occur in isolation or with other anomalies. NSG findings include widely separated frontal horns, colpocephaly, and an elevated third ventricle (Figure 14). Sagittal views demonstrate poor visualization of the pericallosal gyrus with an abnormal anterior cerebral artery (ACA) course.^51,52

Absent septum pellucidum: The absence of septum pellucidum (Figure 14) can occur in isolation or result from abnormal prosencephalic segmentation, resulting in holoprosencephaly. It is often associated with various congenital syndromes, including Aicardi, Apert, and Kallman.^53,54

Neuronal migration disorders: Could be genetic or from perinatal insult, including polymicrogyria (Figure 12), open lip schizencephaly, grey matter heterotopia, and focal cortical dysplasia. These are difficult to diagnose due to peripheral location and ongoing brain maturation but should be suspected with asymmetric gyration-sulcation patterns.^20,26

Figure 14.

Coronal ultrasound image with a linear array transducer demonstrates the absence of septum pellucidum and agenesis of the corpus callosum with parallel oriented lateral ventricles, “Viking horn” appearance (arrows) and a prominent and high-riding third ventricle (star).

Teaching point: Rarely, non-visualized septum pellucidum may be attributed to secondary destruction as observed with severe hydrocephalus and hydranencephaly.⁵³

Infratentorial Malformations

Enlarged Posterior Fossa: Dandy-Walker Malformation (DWM) is characterized by large posterior fossa cystic formation with hypoplastic vermis and raised torcular confluence (Supplemental Figure 8), frequently accompanied by hydrocephalus. On the other hand, Blake’s Pouch Cyst results from the failure of the foramen of Magendie to fenestrate and have a normal but rotated vermis.^26,55

Small Posterior Fossa: Chiari II Malformation involves a small posterior fossa with effaced retro cerebellar space and cerebellar tonsillar herniation. This condition often presents with a myelomeningocele, which is typically treated prenatally. Untreated cases may show a characteristic “banana sign” in the US due to the cerebellum wrapping the brainstem.^55,56

Teaching point: Neonates with supratentorial hydrocephalus should undergo Us with mastoid views to assess and exclude posterior fossa disorders.

Brain Tumours: Perinatal brain tumours are rare and generally have poor prognosis. Most are supratentorial, include teratomas, astrocytomas, choroid plexus papillomas, and ependymomas.^57,58 NSG typically show heterogeneous masses with disrupted brain anatomy. Teratomas are the most common neonatal brain tumour, usually presenting as large, midline, heterogeneous masses that may replace a significant portion of the brain (Supplemental Figure 9). Choroid plexus papilloma may appear homogeneous or heterogeneous in the US.^20,58

Teaching point: Rarely, benign hypothalamic hamartomas and vascular malformations can mimic sinister brain tumours in the US, necessitating the use of a multimodality approach for accurate differentiation.

Ventricles

Hydrocephalus: An abnormal ventricular dilatation, which may be obstructive, non-obstructive, or secondary to ex vacuo dilation from parenchymal volume loss.²⁶ Advanced stages may show fenestration of the septum pellucidum. Anterior horn width is the most sensitive measure for detecting ventriculomegaly.^30,40

Post-haemorrhagic Ventricular Dilation (PHVD): PHVD arises due to obstruction within the ventricular system or inflammatory response (eg, ventriculitis or arachnoiditis) secondary to haemorrhage.²⁸ It is commonly seen in premature neonates with high-grade GM-IVH. The grading of PHVD is based on the anterior horn width (AHW) and ventricular index (VI). Mild ventriculomegaly is indicated by 3 to 5 mm, moderate by 6 to 10 mm (Supplemental Figure 10), and severe by values over 10 mm. Ventricular index above 97th percentile is seen in moderate PHVD and >97th percentile plus 4 mm in severe forms. The size of the largest ventricle should be utilized for grading PHVD after the first week of life.^30,40

Ventricular-Periventricular cyst: Often recognized based on their location. Subependymal cysts from evolving germinal matrix haemorrhage and germinolytic cysts are seen in the caudothalamic groove. Additionally, cavum velum interpositum or pineal gland cysts and arachnoid cysts may project into the posterior third ventricle.^47,59,60

Teaching point: Caudothalamic groove cystic lesions in a term baby should raise suspicion for germinolytic cysts associated with congenital infections, metabolic disorders, and genetic conditions.

Vessels

Doppler ultrasound is essential in evaluating various neonatal brain conditions, including ischaemia, thrombosis, and cardiac- and ECMO-related complications. It also helps distinguish subdural fluid collections from BESS and assess intracranial vascular masses.

a. Doppler Examination of the ACA: This is routinely performed at the genu of the corpus callosum due to its ease and reproducibility. Elevated RI with or without diastolic flow reversal is observed in conditions involving significant left-to-right shunting (eg, large patent ductus arteriosus [PDA]), as well as in raised intracranial pressure such as hydrocephalus and cerebral oedema.^4,61 Conversely, a reduced RI with elevated diastolic velocities (Supplemental Figure 6) is typically seen in neonates with HIE.^4,61

b. Venous Doppler: The SSS can be evaluated through the open sagittal suture to detect venous thrombosis. Other fontanels can serve to assess the other cerebral venous sinuses. The reduced flow in the SSS may mimic thrombus, particularly in neonates undergoing cooling therapy or those on ECMO. Spectral waveform analysis can clarify the diagnosis. Neonates with cardiac pathology, ECMO support, or positive pressure ventilation may show pulsatile venous waveforms (Supplemental Figure 11), indicating elevated venous pressures or altered haemodynamics.^62-64

c. Vascular Malformation: A pulsatile vascular mass located posterosuperior to the third ventricle is characteristic of a Vein of Galen malformation (Figure 15), caused by arterialization of the prosencephalic vein from multiple arterial feeders.^20,26

Figure 15.

A 1-day-old female, born at 30 + 6 weeks of gestational age, with a vein of Galen malformation. Sagittal ultrasound image with a linear array transducer shows an enlarged vein of Galen, in keeping with aneurysmal malformation of the vein of Galen.

Teaching point: The anterior portion of SSS may be hypoplastic and should not be mistaken for a thrombus.

Specific Conditions

Transcranial Doppler (TCD) in Sickle cell anaemia: TCD remains a critical non-invasive tool for assessing stroke risk in children with sickle cell disease (SCD). Current guidelines recommend that screening begin at age 2 and be repeated annually (Supplemental Figure 12). For children with cognitive decline and normal TCD results, MRI screening is advised according to the guidelines.^65-68

Normal TCD: Time-averaged mean maximum velocity (TAMMV) of <170 cm/s in the MCA and internal carotid artery (ICA).

Conditional TCD: TAMMV between 170 and 199 cm/s, indicating a moderate stroke risk and requiring more frequent screening (every 3-6 months).

Abnormal TCD: TAMMV ≥200 cm/s, significantly increasing the risk of ischaemic stroke and warranting prophylactic chronic transfusions.

ECMO-Related Complications: Infants receiving ECMO therapy are at heightened risk of intracranial haemorrhage due to need for anticoagulation, with this risk further exacerbated by prematurity and cerebral venous congestion. Daily NSG monitoring, particularly within the first 7 days, is essential for early detection of bleeding (Supplemental Figure 13), embolic infarcts, and venous sinus thrombosis. Doppler findings often reveal variable resistive indices and pulsatile venous waveforms. Ventricular and extra-axial space enlargement, with or without haemorrhage, is also seen in these patients.^69-71

Therapeutic Hypothermia: NSG plays a vital role in cooling therapy for neonates with moderate to severe HIE. Before initiating cooling, NSG is used to rule out intracranial haemorrhage, which would contraindicate the therapy. Once cooling begins, serial NSG monitor cerebral haemodynamics, including resistive indices, to assess for evolving brain injury or recovery. Additionally, ultrasound helps detect complications such as cerebral oedema, haemorrhage, and ischaemia, ensuring real-time monitoring throughout the therapy and allowing for prompt therapeutic adjustments and improved outcome predictions.^72-74

Summary

This article provides an in-depth evaluation of the role of neonatal neurosonography in diagnosing and managing brain pathologies. NSG is indispensable in the early diagnosis, treatment planning, and prognosis of neurological conditions in neonates and infants, especially in the NICU setting. Doppler ultrasound further enhances diagnostic capabilities by providing crucial insights into cerebral blood flow dynamics and guiding interventions in HIE, hydrocephalus, and other cerebrovascular disorders. Additionally, the use of transcranial Doppler for stroke risk assessment in children with sickle cell disease underscores the broader application of neurosonography in pediatric neuroimaging.

Supplemental Material

sj-tiff-1-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-1-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-10-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-10-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-11-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-11-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-12-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-12-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-13-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-13-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-14-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-14-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-15-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-15-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-16-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-16-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-2-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-2-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-3-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-3-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-4-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-4-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-5-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-5-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-6-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-6-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-7-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-7-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-8-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-8-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Supplemental Material

sj-tiff-9-caj-10.1177_08465371241308849 – Supplemental material for Pediatric Neurosonography: Comprehensive Review and Systematic Approach

Supplemental material, sj-tiff-9-caj-10.1177_08465371241308849 for Pediatric Neurosonography: Comprehensive Review and Systematic Approach by Neetika Gupta, Shivaprakash B. Hiremath, Isabelle Gauthier, Nagwa Wilson and Elka Miller in Canadian Association of Radiologists Journal

Footnotes

Acknowledgements

To the CAR-ASM 2024 team for inviting our work for submission in the CARJ.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

Neetika Gupta

Shivaprakash B. Hiremath

Supplemental Material

Supplemental material for this article is available online.

References

Dudink

Jeanne Steggerda

Horsch

; eurUS.brain group. State-of-the-art neonatal cerebral ultrasound: technique and reporting. Pediatr Res. 2020;87(Suppl 1):3-12.

AIUM Practice Parameter for the Performance of Neurosonography in Neonates and Infants. J Ultrasound Med. 2020;39(5):E57-E61.

Guillot

Chau

Lemyre

. Routine imaging of the preterm neonatal brain. Paediatr Child Health. 2020;25(4):249-262.

Lowe

Bailey

. State-of-the-art cranial sonography: part 1, modern techniques and image interpretation. AJR Am J Roentgenol. 2011;196(5):1028-1033.

Meuwly

Lepori

Theumann

, et al. Multimodality imaging evaluation of the pediatric neck: techniques and spectrum of findings. Radiographics. 2005;25(4):931-948.

Kim

Yoo

Jeon

Kim

. Ultrasonography of pediatric superficial soft tissue tumors and tumor-like lesions. Korean J Radiol. 2020;21(3):341-355.

Bansal

Oudsema

Masseaux

Rosenberg

. US of pediatric superficial masses of the head and neck. Radiographics. 2018;38(4):1239-1263.

Davis

. Neonatal subgaleal hemorrhage: diagnosis and management. CMAJ. 2001;164(10):1452-1453.

Nicholson

. Caput succedaneum and cephalohematoma: the cs that leave bumps on the head. Neonatal Netw. 2007;26(5):277-281.

10.

McQuivey

. Vacuum-assisted delivery: a review. J Matern Fetal Neonatal Med. 2004;16(3):171-180.

11.

Fefferman

Sarvis Milla

. Ultrasound imaging of the neck in children. Ultrasound Clinics. 2009;4(4):553-569.

12.

Kollipara

Dinneen

Rentas

, et al. Current classification and terminology of pediatric vascular anomalies. AJR Am J Roentgenol. 2013;201(5):1124-1135.

13.

Morrow

Oliveira

. Imaging of lumps and bumps in pediatric patients: an algorithm for appropriate imaging and pictorial review. Semin Ultrasound CT MR. 2014;35(4):415-429.

14.

Chang

Peng

Kao

Hsu

Hung

Chang

. Neonatal subgaleal hemorrhage: clinical presentation, treatment, and predictors of poor prognosis. Pediatr Int. 2007;49(6):903-907.

15.

Chaturvedi

Stanescu

Blickman

Meyers

. Mechanical birth-related trauma to the neonate: an imaging perspective. Insights Imaging. 2018;9(1):103-118.

16.

Rozovsky

Udjus

Wilson

Barrowman

Simanovsky

Miller

. Cranial ultrasound as a first-line imaging examination for craniosynostosis. Pediatrics. 2016;137(2):e20152230.

17.

Cacciaguerra

Palermo

Marino

, et al. The evolution of the role of imaging in the diagnosis of craniosynostosis: a narrative review. Children (Basel). 2021;8(9):727.

18.

Marino

Ruggieri

Marino

Falsaperla

. Sutures ultrasound: useful diagnostic screening for posterior plagiocephaly. Childs Nerv Syst. 2021;37(12):3715-3720.

19.

Rozovsky

Barrowman

Miller

. Centile charts for cranial sutures in children younger than 1 year based on ultrasound measurements. Pediatr Radiol. 2018;48(5):701-707.

20.

Caro-Domínguez

Lecacheux

Hernandez-Herrera

Llorens-Salvador

. Cranial ultrasound for beginners. Transl Pediatr. 2021;10(4):1117-1137.

21.

Riedesel

. Neonatal cranial ultrasound: advanced techniques and image interpretation. J Pediatr Neurol. 2018;16(2):106-124.

22.

Di Salvo

. A new view of the neonatal brain: clinical utility of supplemental neurologic US imaging windows. Radiographics. 2001;21(4):943-955.

23.

Lim

Shin

Kim

Chung

Hahn

Cho

. Ultrasound findings of subpial hemorrhage in neonates. Ultrasonography. 2023;42(2):333-342.

24.

Barreto

ARF

Carrasco

Dabrowski

Sun

Tekes

. Subpial hemorrhage in neonates: what radiologists need to know. AJR Am J Roentgenol. 2021;216(4):1056-1065.

25.

Assis

Kirton

Pauranik

Sherriff

Wei

. Idiopathic neonatal subpial hemorrhage with underlying cerebral infarct: imaging features and clinical outcome. AJNR Am J Neuroradiol. 2021;42(1):185-193.

26.

Maller

Choudhri

Cohen

. Neonatal head ultrasound: a review and update-part 2: the term neonate and analysis of brain anomalies. Ultrasound Q. 2019;35(3):212-223.

27.

Cain

Dingman

Armstrong

Stence

Jensen

Mirsky

. Subpial hemorrhage of the neonate. Stroke. 2020;51(1):315-318.

28.

Maller

Cohen

. Neonatal head ultrasound: a review and update-part 1: techniques and evaluation of the premature neonate. Ultrasound Q. 2019;35(3):202-211.

29.

O’Leary

Gregas

Limperopoulos

, et al. Elevated cerebral pressure passivity is associated with prematurity-related intracranial hemorrhage. Pediatrics. 2009;124(1):302-309.

30.

Mohammad

Scott

Leijser

, et al. Consensus approach for standardizing the screening and classification of preterm brain injury diagnosed with cranial ultrasound: a Canadian perspective. Front Pediatr. 2021;9:618236.

31.

O’Shea

Counsell

Bartels

Dammann

. Magnetic resonance and ultrasound brain imaging in preterm infants. Early Hum Dev. 2005;81(3):263-271.

32.

Richer

Riedesel

Linam

. Review of neonatal and infant cranial US. Radiographics. 2021;41(7):E206-E207.

33.

Fritz

Polansky

O’Connor

. Neonatal neurosonography. Semin Ultrasound CT MR. 2014;35(4):349-364.

34.

Volpe

. Cerebellum of the premature infant: rapidly developing, vulnerable, clinically important. J Child Neurol. 2009;24(9):1085-1104.

35.

Rennie

Hagmann

Robertson

Rennie

. Neonatal Cerebral Investigation. 2nd ed. Cambridge University Press; 2008.

36.

Hand

Shellhaas

Milla

; COMMITTEE ON FETUS AND NEWBORN, SECTION ON NEUROLOGY, SECTION ON RADIOLOGY. Routine neuroimaging of the preterm brain. Pediatrics. 2020;146(5):e2020029082.

37.

Reddy

Doyle

Hanagandi

, et al. Neuroradiological mimics of periventricular leukomalacia. J Child Neurol. 2022;37(2):151-167.

38.

Grant

. Acute injury to the immature brain with hypoxia with or without hypoperfusion. Magn Reson Imaging Clin N Am. 2006;14(2):271-285.

39.

Varghese

Xavier

Manoj

, et al. Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury. Indian J Radiol Imaging. 2016;26(3):316-327.

40.

James

. Practical guide to neonatal cranial ultrasound (CrUS): basics. Paediatr Child Health. 2018;28(9):424-430.

41.

Dinan

Daneman

Guimaraes

Chauvin

Victoria

Epelman

. Easily overlooked sonographic findings in the evaluation of neonatal encephalopathy: lessons learned from magnetic resonance imaging. Semin Ultrasound CT MR. 2014;35(6):627-651.

42.

Fichera

Stramare

Bisogno

, et al. Neonatal cerebral ultrasound: anatomical variants and age-related diseases. J Ultrasound. 2024;27(4):993-1002.

43.

Merlini

Hanquinet

Fluss

. Thalamic hemorrhagic stroke in the term newborn: a specific neonatal syndrome with non-uniform outcome. J Child Neurol. 2017;32(8):746-753.

44.

Canedo-Antelo

Baleato-González

Mosqueira

, et al. Radiologic clues to cerebral venous thrombosis. Radiographics. 2019;39(6):1611-1628.

45.

Neuberger

Garcia

Meyers

Feygin

Bulas

Mirsky

. Imaging of congenital central nervous system infections. Pediatr Radiol. 2018;48(4):513-523.

46.

Fabre

Tosello

Pipon

Gire

Chaumoitre

. Hyperechogenicity of lenticulostriate vessels: a poor prognosis or a normal variant? A seven year retrospective study. Pediatr Neonatol. 2018;59(6):553-560.

47.

Fernandez Alvarez

Amess

Gandhi

Rabe

. Diagnostic value of subependymal pseudocysts and choroid plexus cysts on neonatal cerebral ultrasound: a meta-analysis. Arch Dis Child Fetal Neonatal Ed. 2009;94(6):F443-F446.

48.

Ribeiro

Werner

Lopes

FPPL

, et al. Central nervous system effects of intrauterine Zika virus infection: a pictorial review. Radiographics. 2017;37(6):1840-1850.

49.

Schneider

. Neonatal brain infections. Pediatr Radiol. 2011;41 Suppl 1:S143-S148.

50.

Epelman

Daneman

Kellenberger

, et al. Neonatal encephalopathy: a prospective comparison of head US and MRI. Pediatr Radiol. 2010;40(10):1640-1650.

51.

Bhat

. Neonatal neurosonography: a pictorial essay. Indian J Radiol Imaging. 2014;24(4):389-400.

52.

Hernanz-Schulman

Dohan

Jones

Cayea

Wallman

Teele

. Sonographic appearance of callosal agenesis: correlation with radiologic and pathologic findings. AJNR Am J Neuroradiol. 1985;6(3):361-368.

53.

Hosseinzadeh

Luo

Borhani

Hill

. Non-visualisation of cavum septi pellucidi: implication in prenatal diagnosis? Insights Imaging. 2013;4(3):357-367.

54.

Nagaraj

Calvo-Garcia

Kline-Fath

. Abnormalities associated with the cavum septi pellucidi on fetal MRI: what radiologists need to know. AJR Am J Roentgenol. 2018;210(5):989-997.

55.

Barkovich

Raybaud

. Congenital malformations of the brain and skull. In: Barkovich

Raybaud

, eds. Pediatric Neuroimaging. 6th ed. Wolters Kluwer; 2018:405-632.

56.

de la Cruz

Millán

Miralles

Muñoz

. Cranial sonographic evaluation in children with meningomyelocele. Childs Nerv Syst. 1989;5(2):94-98.

57.

Alamo

Beck-Popovic

Gudinchet

Meuli

. Congenital tumors: imaging when life just begins. Insights Imaging. 2011;2(3):297-308.

58.

Sugimoto

Kurishima

Masutani

Tamura

Senzaki

. Congenital brain tumor within the first 2 months of life. Pediatr Neonatol. 2015;56(6):369-375.

59.

Epelman

Daneman

Blaser

, et al. Differential diagnosis of intracranial cystic lesions at head US: correlation with CT and MR imaging. Radiographics. 2006;26(1):173-196.

60.

Lowe

Bailey

. State-of-the-art cranial sonography: part 2, pitfalls and variants. AJR Am J Roentgenol. 2011;196(5):1034-1039.

61.

North

Lowe

. Modern head ultrasound: normal anatomy, variants, and pitfalls that may simulate disease. Ultrasound Clin. 2009;4(4):497-512.

62.

Taylor

. Intracranial venous system in the newborn: evaluation of normal anatomy and flow characteristics with color Doppler US. Radiology. 1992;183(2):449-452.

63.

Dean

Taylor

. The intracranial venous system in infants: normal and abnormal findings on duplex and color Doppler sonography. AJR Am J Roentgenol. 1995;164(1):151-156.

64.

Miller

Daneman

Doria

Blaser

Traubici

Jarrin

, et al. Color Doppler US of normal cerebral venous sinuses in neonates: a comparison with MR venography. Pediatr Radiol. 2012;42(9):1070-1079.

65.

DeBaun

Jordan

King

, et al. American Society of Hematology 2020 guidelines for sickle cell disease: prevention, diagnosis, and treatment of cerebrovascular disease in children and adults. Blood Adv. 2020;4(8):1554-1588.

66.

Bernaudin

Verlhac

Arnaud

, et al. Long-term treatment follow-up of children with sickle cell disease monitored with abnormal transcranial Doppler velocities. Blood. 2016;127(14):1814-1822.

67.

Reeves

Madden

Freed

Dombkowski

. Transcranial Doppler screening among children and adolescents with sickle cell anemia. JAMA Pediatr. 2016;170(6):550-556.

68.

Modolo

Luvizutto

Hamamoto Filho

, et al. Transcranial Doppler as screening method for sickling crises in children with sickle cell anemia: a Latin America cohort study. BMC Pediatr. 2022;22(1):368.

69.

Rubin

Gross

Ehrlich

Alexander

. Interhemispheric fissure width in neonates on ECMO. Pediatr Radiol. 1990;21(1):12-15.

70.

von Allmen

Babcock

Matsumoto

, et al. The predictive value of head ultrasound in the ECMO candidate. J Pediatr Surg. 1992;27(1):36-39.

71.

Barnacle

Smith

Hiorns

. The role of imaging during extracorporeal membrane oxygenation in pediatric respiratory failure. AJR Am J Roentgenol. 2006;186(1):58-66.

72.

Robertson

Hagmann

Acolet

, et al. Pilot randomized trial of therapeutic hypothermia with serial cranial ultrasound and 18-22 month follow-up for neonatal encephalopathy in a low resource hospital setting in Uganda: study protocol. Trials. 2011;12(1):138.

73.

Alfaifi

. Use of cranial ultrasound prior to the start of therapeutic hypothermia for newborn encephalopathy. Cureus. 2023;15(4):e37681.

74.

Sanislow

Singh

Yang

Inder

El-Dib

. Value of cranial ultrasound at initiation of therapeutic hypothermia for neonatal encephalopathy. J Perinatol. 2022;42(3):335-340.

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.01 MB

2.49 MB

2.07 MB

2.96 MB

1.14 MB

0.69 MB

1.09 MB

1.68 MB

1.50 MB

1.69 MB

1.98 MB

1.84 MB

2.40 MB

2.53 MB

3.88 MB

3.44 MB

2.13 MB