Perinatal ischemic brain injury may appear in premature and full-term babies and includes global hypoxic-ischemic encephalopathy (HIE) and perinatal stroke. The symptoms are similar and non-specific, and clinical neuroradiology plays an important role in defining the diagnosis, following up the patient, and determining the effect on maturation and prognosis. Radiological techniques include state-of-the-art brain ultrasound (US) coupled with color Doppler for the initial diagnostic approach and magnetic resonance imaging (MRI) with T1- and T2-weighted sequences, diffusion-weighted (DWI), or diffusion tensor imaging (DTI). Depending on the suspected pathology, susceptibility-weighted imaging (SWI) and perfusion imaging using arterial spin labeling (ASL) may also be applied. Mild to moderate HIE in full-term babies comprises parasagittal cortico-subcortical lesions in arterial watershed zones, while in premature babies, it manifests as periventricular leukomalacia (PVL), either focal or diffuse. In severe HIE in both full-term and premature babies, a “central” pattern of lesions develops in the areas most mature for age, and in the most severe cases of HIE, the whole brain is affected. Brain hemorrhagic disease (BHD) develops mainly in very premature babies and includes subependymal and intraventricular hemorrhage (IVH). Posthemorrhagic hydrocephalus and periventricular hemorrhagic infarction (PHI) may also occur. Perinatal stroke is classified into arterial ischemic stroke (AIS) and cerebral sinovenous thrombosis (CSVT). AIS develops in full-term and near-term babies and involves mainly the left middle cerebral artery (MCA) territory. CSVT affects mainly the superficial venous system and is associated with hemorrhagic infarcts.
KeywordsIschemia Stroke Periventricular Parasagittal PVL Brain hemorrhagic disease Germinal matrix hemorrhage Intraventricular hemorrhage Venous infarct Posthemorrhagic hydrocephalus
Apparent diffusion coefficient
Arterial ischemic stroke
Arterial spin labeling
Brain hemorrhagic disease
Cerebral blood flow
Cerebral sinovenous thrombosis
Deep medullary veins
Diffusion tensor imaging
Extremely low birth weight
Germinal matrix hemorrhage
Middle cerebral artery
Magnetic resonance angiography
Magnetic resonance imaging
Periventricular hemorrhagic infarction
Posterior limb of the internal capsule
Very low birth weight
Perinatal Ischemic Brain Injury
Perinatal ischemic brain injury is classified into global hypoxic-ischemic encephalopathy (HIE) and perinatal stroke, which is further classified into arterial ischemic stroke (AIS) and cerebral sinovenous thrombosis (CSVT). The clinical presentation of HIE and perinatal stroke is often similar, and imaging techniques, specifically brain ultrasound (US) and magnetic resonance imaging (MRI), play an important role in the differential diagnosis, guiding appropriate management that can improve the long-term outcome (Argyropoulou 2010; Badve et al. 2012; Hagberg et al. 2016; Ramenghi et al. 2009; Volpe 2009b).
Imaging Techniques and Recommended Protocol
Brain US is the first-line examination, comprising gray-scale imaging of the brain and color/pulsed Doppler of the vessels. State-of-the-art technique should be applied, using sectorial (5–8 MHz) and linear-array (5–12 MHz) transducers and multiple acoustic windows (the anterior, posterior, and mastoid fontanelles and rarely the foramen magnum). The whole brain is evaluated with the sectorial transducer through the anterior fontanelle, and five to seven coronal scans and five sagittal scans should be performed. For a more detailed evaluation of the midline structures, one coronal and one sagittal scan may be performed in addition with the linear-array transducer. The occipital lobes and the occipital horns of the lateral ventricles are evaluated better through the posterior fontanelle. The posterior fossa structures are evaluated better through the mastoid fontanelle, and at least one coronal and one axial scan should be performed using the linear-array transducer. Color/pulsed Doppler should be applied for evaluation of the spectra and the resistive index (RI) of the anterior and middle cerebral arteries and of the venous sinuses and, in very low birth weight (VLBW) premature babies, of the internal veins. In neonatal posthemorrhagic hydrocephalus, the need for shunt placement can be assessed by using the delta RI which is derived from RI with fontanelle compression baseline RI/baseline RI. Patients with a delta RI >45% need ventricular shunt placement. Color Doppler is also useful for early detection of subarachnoid hemorrhage by depiction of alternating blue and red echoes within the aqueduct of Sylvius. In full-term babies, the first US should be performed on appearance of symptoms, with a follow-up US 1 week later. In premature babies, and especially those that are VLBW, a first brain US coupled with color Doppler should be performed during the first 24–78 h to look for brain hemorrhagic disease (BHD) and to assess flow in the terminal veins. A second US should be performed by the end of the 1st week, to look for heterogeneous periventricular hyperechogenicity and/or cyst formation (Argyropoulou and Veyrac 2015).
MRI protocol for the evaluation of the neonatal brain
Slice thickness/gap (mm)
3D T1W SPGR
High TR (e.g., 3500)
SE EPI DWI
b values: 0, 700 mm2/s
3D FFE SWI
Evaluation of hemorrhage, HIE, AIS
Suspicion of arterial occlusion
Suspicion of sinovenous occlusion
Global Hypoxic-Ischemic Encephalopathy (HIE)
Depending on the severity of HIE, a clinical grading system has been established using three subgroups: mild (stage 1), moderate (stage 2), and severe (stage 3). Imaging findings depend on the severity of HIE, the maturation of the brain (full-term, premature), and the interval between the insult and the time of imaging.
HIE in the Premature Baby
Mild to Moderate HIE
Mild to moderate HIE in premature infants includes two main entities: periventricular leukomalacia (PVL) and BHD, which includes germinal matrix hemorrhage (GMH), intraventricular hemorrhage (IVH), hydrocephalus, and periventricular hemorrhagic infarction (PHI). HIE is more common in VLBW (<1500 g) premature infants, with PVL being the predominant form of injury, occurring in 50% of cases, and BHD appearing in only 5% of cases. The less severe diffuse form of PVL represents 90% of cases and the more severe focal form 5% of cases (Volpe 2009b). An increased incidence (20–30%) of PHI has been reported in premature infants with extremely low birth weight (ELBW, <750 g).
The Clinical Scenario
In the acute stage, most infants are asymptomatic, but some may present slight abnormalities of consciousness, movement, tone, and respiration. Less frequently, and especially in those with BHD, the presenting symptoms may be seizures, quadriparesis, stupor, and coma. Over 5–10% of premature babies will develop a severe motor deficit (cerebral palsy), sensory disabilities (visual and hearing problems), and mental retardation. Over 25–50% may develop less severe deficits such as cognitive, behavioral, and attention problems (Argyropoulou 2010; Volpe 2009b).
Periventricular Leukomalacia (PVL)
The development of PVL is associated with a number of interacting risk factors, mainly related with prematurity. The most important risk factors are immaturity of the arterial vascular bed, with the presence of short and long penetrating arteries that are end arteries, low CBF <5.0 mL·100−1 g−1 (the normal CBF in adults is 50 mL·100−1.g−1) in the white matter (WM), impaired cerebrovascular autoregulation (with either a pressure-passive flow or a narrow range of blood pressure over which the CBF is maintained), and the vulnerability of the oligodendroglia precursors to hypoxia-ischemia and maternofetal infections. Short and long penetrators are end arteries, and the corresponding parenchyma represents watershed areas. Hypoxia and ischemia occur in a context of impaired cerebrovascular autoregulation that results in compromised blood flow at the end of long and short penetrators and between them. Ischemia at the end of long penetrators results in the more severe focal form of PVL, while ischemia at end of short penetrators and between the long penetrators results in the diffuse, less severe form. Both forms of PVL may coexist; the focal form is characterized by death of all cell elements around the lateral ventricles, while the diffuse form is characterized by apoptotic cell death of the oligodendroglia precursors (OLp). Mature oligodendrocytes provide myelin, so that death of OLp results in hypomyelination and decreased WM volume. OLp are highly vulnerable to free radicals due to the oxidative stress induced by ischemia and reperfusion. Free radicals, in association with a high content in iron, lead to apoptotic cell death of the OLp. An increased incidence of diffuse PVL has been reported in association with BHD, and the iron released from the degradation of hemoglobin has been considered responsible. Finally, maternofetal infection may promote the development of PVL by affecting the vascular bed and the CBF but also through toxic effects on OLp. Apart from WM involvement in the context of PVL, transient neuronal populations located within the WM are also affected from hypoxia-ischemia. A decrease of subplate neurons located in the subcortical WM and of the late-migrating GABA-ergic neurons located in the central WM has been reported in patients with PVL. Volumetric deficits in the thalamus, the basal ganglia, and the parieto-occipital cortex of patients with PVL have been related to involvement of these neuronal populations. Late-onset focal PVL occurring after the immediate neonatal period has also been reported after viral infections (rotavirus, human parechoviruses) (Volpe 2009b).
Brain Hemorrhagic Disease (BHD)
BHD starts with bleeding in the germinal matrix, which is a highly vascular collection of neuroglial cells located near the head of the caudate nucleus under the ependyma of the lateral ventricles. The vessels of the germinal matrix are characterized by a paucity of pericytes and an immature basal lamina. Increased fragility of the germinal matrix vessels, along with disturbances in CBF and platelet and coagulation abnormalities, is considered responsible for germinal matrix hemorrhage (GMH). Rupture of the ependyma leads to intraventricular hemorrhage (IVH). Posthemorrhagic hydrocephalus leads to compression of the terminal veins lying under the germinal matrix. Venous drainage of the WM takes place through a fan-shaped leash of short and long medullary veins which in turn drain into the terminal veins. Obliteration of these veins leads to the development of a periventricular hemorrhagic infarction (PHI) . The presence of blood in the cerebrospinal fluid (CSF) spaces initiates the development of arachnoiditis and hydrocephalus (Argyropoulou 2010; Couture et al. 2001).
Grade I corresponds to pure GMH
Grade II corresponds to GMH with IVH, without ventricular dilatation
Grade III corresponds to GMH with IVH and ventricular dilatation
Grade IV corresponds to a PHI
Profound asphyxia in preterm neonates follows the pattern of asphyxia in full-term babies, with the main difference being lack of involvement of the unmyelinated structures, such as the superior cerebellar vermis, the perirolandic cortex, and the PLIC.
Cerebellar lesions occur in VLBW premature infants and are divided into destructive lesions (hemorrhage, infarction) and cerebellar underdevelopment. Destructive lesions are more common and typically affect predominately one hemisphere.
Cerebellar development occurs rapidly between gestational weeks 24 and 30, with the superficial granular layer playing a key role. The latter acts as a germinal matrix and accounts for not only the development of the internal granular layer but also the establishment of connections necessary for the development of the cerebellar circuitry. Hypoxia-ischemia and impaired cerebrovascular autoregulation leading to hemorrhages in the supratentorial fossa are also responsible for GMH in the cerebellum. Hypoxia-ischemia, infection-inflammation, glucocorticoid exposure, and the deposition of hemosiderin on the surface of the cerebellum may interfere with proliferation and viability of the superficial granular layer and lead to cerebellar underdevelopment. Supratentorial PVL and PHI may further contribute to cerebellar hypoplasia through remote transsynaptic effects (Volpe 2009a).
Cerebellar hemorrhage is often unilateral, involving the superficial granular layer of one cerebellar hemisphere. Vermian hemorrhage may also occur when bleeding starts in the germinal matrix of the roof of the fourth ventricle. The incidence increases with decreasing birth weight, ranging from 17% in infants <750 g to 2% in infants >750 g. Cerebellar hemorrhage is often (77%) associated with supratentorial lesions, mainly hemorrhage. Predisposing factors coincide with those of supratentorial hemorrhage (i.e., impaired cerebrovascular autoregulation, a large patent ductus arteriosus) (Argyropoulou et al. 2003; Volpe 2009a).
Cranial US through the mastoid fontanelle shows a cerebellar hemorrhage as an echogenic area leading progressively to atrophy. MRI shows subacute cerebellar hemorrhage as high signal intensity on T1-W and T2-W images and, at later stages, reveals shrinkage of the affected lobe, along with signal loss on T2* and SWI, due to the presence of hemosiderin.
Interpretation Checklist HIE in Preterm Babies
Check birth weight: VLBW babies are more prone to development of HIE, and ELBW are more prone to PHI.
Check gestational age at birth: preterm babies show a less advanced gyration pattern than full-term babies, and the basal ganglia are hyperechoic compared to the WM.
Check the periventricular WM for heterogeneous hyper echogenicity.
Check the ventricular system for subependymal hemorrhage, IVH, and posthemorrhagic hydrocephalus, and measure the Delta RI.
Check with color Doppler the flow into the terminal vein. Check with color Doppler the presence of alternating blue and red color in the aqueduct of Sylvius.
Check for the presence of PHI.
Check the cerebellum for progressive decrease in size and for hemorrhage.
Check the gestational age at birth: preterm babies show a less advanced gyration pattern than full-term babies.
Check on T1-W and DWI the signal intensity of the PLIC.
Check on T1-W, T2-W, and DWI for signal abnormalities in the periventricular WM.
Check the lateral ventricles for enlargement.
Check the outlines of the lateral ventricles (irregular in focal PVL, regular in diffuse PVL).
Check the corpus callosum and the periventricular WM for thinning and for signal abnormalities.
Check the presence of blood by-products on T2* and SWI.
Check brain perfusion with ASL.
Follow-up Findings and Pitfalls
A normal brain US at the end of the first postnatal week does not preclude later development of the diffuse form of PVL.
Be aware of the timing of the examination to avoid misinterpreting a “pseudonormalization pattern” on DWI.
After 6 months of age, check the signal intensity of the PLIC on T2-W images. A high signal intensity is suggestive of a poor motor prognosis.
Progressive shrinkage of a cerebellum which was normal at birth may be seen in the context of BHD.
Check with T2* and SWI for the presence of blood by-products on the surface of the cerebellum, the brain parenchyma, and the ventricular wall.
HIE in Full-Term Babies
The incidence of HIE has decreased significantly because of improved perinatal care and nowadays is 1–6 per 1000 live births. HIE represents the third most common cause of neonatal death (23%), and the risk factors are preconceptional (maternal age >35 years, maternal thyroid disease, history of seizures, infertility treatment) and antepartum and postpartum (preeclampsia, genetic abnormalities, intrauterine growth restriction, breech presentation, gestational age >41 weeks, prolonged membrane rupture, abnormal cardiotocography, thick meconium, shoulder dystocia, tight nuchal cord, vacuum extraction, hypoglycemia, and increased plasma homocysteine) (Hagberg et al. 2016).
The main mechanism leading to HIE is impairment of cerebral blood flow and oxygen delivery, either prenatally or postnatally. Hypoperfusion of the brain induces a shift from aerobic (energy efficient) to anaerobic (energy inefficient) metabolism at a cellular level, leading to a rapid decrease of high-energy phosphorylated compounds, including adenosine triphosphate (ATP), phosphocreatine, and accumulation of lactic acid. Cellular membrane depolarization and transcellular ion pump failure inducing intracellular accumulation of Na+, Ca+, and water, lipid peroxidation, and production of toxic-free radicals such as nitric oxide (NO) represent the most important deleterious biochemical events responsible for cytotoxic edema and cell death. Upon recovery after resuscitation, secondary energy failure may occur, characterized by mitochondrial dysfunction leading to nuclear fragmentation. Early diagnosis and therapeutic intervention at the primary and secondary energy failure stages are crucial to improving the long-term neurodevelopmental outcome (Hagberg et al. 2016).
The Clinical Scenario
The clinical presentation is non-specific, with seizures and alteration of the level of consciousness, ranging from hyper-alertness through lethargy to stupor and coma.
Mild to Moderate Asphyxia
On MRI, diffusion imaging performed between 24 and 48 h after birth reveals restricted diffusion in the subcortical WM and the cortex of “watershed” areas (Fig. 12). A “pseudonormalization” pattern is observed at between 6 and 10 days, followed by increased diffusion afterwards. T2-W images show increased signal intensity with blurring of the cortical mantle, while T1-W images show hypointensity of the cortex and the subcortical WM with loss of gray/white matter differentiation. At around day 7, multiple cysts are observed, followed by shrinkage of the affected area comprising both the cortex and the subcortical WM, appearing with high signal on T2-W and low signal on T1-W images. A characteristic ulegyria pattern of the affected cortex is seen, with predominant atrophy of the cortex at the depths of the sulci, probably due to a lower perfusion compared with the apices (de Vries and Groenendaal 2010). ASL shows hypoperfusion, and SWI shows increased susceptibility of the medullary and sulcal veins.
Perinatal stroke is defined as “a group of heterogeneous conditions in which there is focal disruption of CBF secondary to arterial or cerebral venous thrombosis or embolic occlusion, between 20 weeks of fetal life through the 28th postnatal day, confirmed by neuroimaging or neuropathologic studies” (Lee et al. 2017).
Arterial Ischemic Stroke (AIS)
AIS is the most common cause of stroke in childhood and the second most common after adult stroke. It occurs in full-term and late-preterm infants but also in utero. The incidence of arterial infarction is 1 in 2300–5000 births, and the left middle cerebral artery (MCA) is the most commonly affected vessel. Boys are more commonly affected than girls and blacks more than whites. Risk factors for AIS include placental embolism, trauma, infection, asphyxia, acute blood loss, extracorporeal membrane oxygenation, and prothrombotic conditions. Long-term complications include hemiplegic cerebral palsy, epilepsy, and delayed language development (Lee et al. 2017).
The causal relationship of risk factors with AIS remains unclear. The normal hypercoagulability and the proinflammatory status of pregnancy associated with acquired risk factors might be responsible for the development of AIS.
The Clinical Scenario
AIS presents with non-specific signs, including seizures (the most common presentation), asymmetrical weakness, and early hand preference.
Coronal and sagittal US scans need to be performed. Parasagittal images demonstrate infarcts of the caudate nucleus, the putamen, and the pallidum anterior to the PLIC and infarcts of the ventrolateral thalamus posterior to the PLIC. US is often unable to detect superficial cortical infarcts. Color Doppler of the ipsilateral MCA may reveal either dilatation and increased flow and decreased RI, associated with late development of encephalomalacia and hemiplegia, or may be normal, associated with a normal outcome (Fig. 17a).
Subsequent development of motor sequelae is due to Wallerian degeneration and deafferentation resulting in atrophy of the ipsilateral cerebral peduncle, the PLIC, the mediodorsal thalamus, the body of the corpus callosum, and the corticospinal tract at the corona radiata (Husson et al. 2016)
In neonates with seizures, ASL and SWI performed early may show hyperperfusion and decreased susceptibility of the intramedullary and sulcal veins, respectively, in areas of restricted diffusion. The observed hyperperfusion is considered to be related to seizure activity and/or recanalization. Later, ASL shows hypoperfusion, and SWI shows increased susceptibility and more prominent intramedullary and sulcal veins.
Cerebral Sinovenous Occlusion
The incidence of venous infarction is about 1 per 100,000 children per year, 43% of which are neonates. Thrombosis within the superficial venous system is the more common, with involvement of the superior sagittal sinus starting in the parietal area, probably due to the oblique course of the draining veins (Badve et al. 2012; Ramenghi et al. 2009).
Prothrombotic states related to genetic (mainly G20210A prothrombin gene mutation and the presence of factor V Leiden) or acquired disorders (antiphospholipid syndrome) are risk factors. Venous thrombosis leads to increased venous pressure and the development of edema, due to transudation through the venous and capillary walls; this is often reversible. When venous pressure exceeds the local arterial perfusion pressure, arterial constriction occurs, further contributing to local ischemia. The arterial component of ischemia probably explains why most of the infarcts are located in the parasagittal subcortical areas which are missing meningeal, transmedullary, and deep collateral vessels (Ramenghi et al. 2009).
The Clinical Scenario
The clinical presentation is often non-specific, with early occurrence of thrombosis appearing with other comorbidities, such as respiratory distress, poor tone, fetal distress, asphyxia, and late occurrence (after 48 h) appearing with seizures, lethargy, apnea, and poor feeding (Ramenghi et al. 2009).
During the 1st week, MRI shows low signal intensity on T2-W and high signal intensity on T1-W images within the thrombosed vessel (Fig. 20). Interstitial edema of the parenchyma drained by the obstructed venous structure accounts for low signal intensity on T1- and high signal intensity on T2-W images. Most venous infarcts are hemorrhagic, and foci of increased or low signal intensity due to hemoglobin by-products may be seen in the affected parasagittal subcortical areas. Intraventricular hemorrhage and hemorrhagic thalamic lesions have been reported in almost 50% of perinatal CSVT. The appearance of a venous infarct is heterogeneous on DWI; increased diffusion occurs when interstitial edema is predominant and restricted diffusion when arterial vasoconstriction coexists. DWI shows a mixture of signal intensities in the hemorrhagic areas. MR venography (2D-TOF or 3D PC) is useful for evaluation of the patency of venous sinuses. Linear, radially distributed lesions that are hyperintense on T1-W and hypointense on T2-W images, associated with more peripheral cystic areas, have been described in the territory of the deep medullary veins. These lesions are thought to represent venous engorgement or thrombosis. At a chronic stage, the cystic areas disappear, and high signal intensity is observed, along with thinning of the WM around the frontal and occipital horns (Ramenghi et al. 2009). ASL shows in most cases of hypoperfusion in the infarcted area. SWI, due to increased susceptibility, shows prominent medullary veins in the affected area. Blood by-products of the hemorrhagic infarct are better visualized with SWI.
Interpretation Checklist: Cerebral Sinovenous Occlusion
Check the gestational age at birth: normal full-term babies show a more advanced gyration pattern than preterm babies, and the basal ganglia are almost isoechoic to the WM.
Check watershed areas for increased echogenicity of the subcortical WM.
Check the deep GM for increased echogenicity.
Check the cortex for increased echogenicity.
Check for increased echogenicity in the GM and WM in the territory of the MCA.
Check for flow in the circle of Willis.
Check for flow in the main venous sinuses.
Check for highly echogenic lesions (echogenicity higher than that of the choroid plexuses) in the territory of venous sinuses.
Check the gestational age at birth: normal full-term babies show a more advanced gyration and myelination pattern than preterm babies.
Check on T1-W images the presence of the normal high signal intensity in the PLIC.
Check for restricted diffusion in watershed areas, in the deep GM, the PLIC, and the territory of the MCA.
Check for low signal intensity on T1-W and high signal intensity on T2-W images and for increased diffusion in watershed areas, the deep GM, and the territory of the MCA artery.
Check on T1- and T2-W images for the “missing cortex sign.”
Check for hemorrhagic lesions in the territory of the venous sinuses.
Check the patency of arteries and veins with MRA.
Check perfusion on ASL (hyper or hypoperfusion).
Check the presence of blood by-products on T2* and SWI.
Check the medullary veins with SWI.
Follow-up Findings and Pitfalls
Check the watershed areas, WM and deep GM, and the territory of the MCA for the presence of multicystic encephalomalacia.
Check on T1-W and T2-W images the signal intensity of the PLIC.
Be aware of the history and previous examinations to avoid misinterpreting a “pseudonormalization” pattern.
On DWI, avoid misinterpretation of signal intensities related to hemorrhagic by-products.
Restricted diffusion in a venous infarct is related to arterial vasoconstriction.
A 26-week gestational age female neonate of low birth weight
Purpose of Imaging Studies
Systematic evaluation with brain US at 72 h of life and at the end of the 1st week of life
Brain US at 72 h of life and then weekly until term-equivalent age (40 weeks)
Brain MRI scan at term-equivalent age, including 3D turbo spin echo T1-W, axial T2-W, SWIP, and DTI
Brain US at 72 h of life is normal for age. Brain US at 36 gestational weeks equivalent shows ventriculomegaly with no other abnormality.
Brain MRI shows ventriculomegaly with regular ventricular outlines and thinning of the periventricular WM, compatible with the diffuse form of PVL.
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