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CEREBRAL ISCHEMIA IN NEONATES:
FROM SONOGRAPHY TO CT TO MRI
FERRACIOLLI SF, MD; TUFIK SB, MD; OLIVEIRA NETO A, MD; COMMANDER CW, MD; FEITOSA
EAF, MD; MATSUOKA MW, MD, PhD; LUCATO LT , MD, PhD; LEITE CC, MD, PhD; CASTILLO M,
MD.
UNIVERSITY OF SÃO PAULO - BRAZIL
UNIVERSITY OF NORTH CAROLINA - USA
INTRODUCTION
Perinatal ischemic stroke occurs around the time of birth with
pathological or imaging evidence of focal or diffuse infarctions. It is
caused by a heterogeneous group of conditions that lead to
disruption of cerebral blood flow secondary to arterial or venous
thrombosis or emboli between 20 weeks of fetal life through the
28th postnatal day.
Incidence of neonatal acute ischemic stroke is about 1:4,000-5,000
full-term newborns.
Perinatal ischemic stroke is an under diagnosed condition as not all
such infarctions are symptomatic during the neonatal period and
may go on unrecognized without brain imaging.
INTRODUCTION
Diffuse hypoxic-ischemic brain injury results in neonatal hypoxicischemic encephalopathy (HIE). Because of differences in brain maturity
at time of insult, severity of hypotension, and duration of insult, there
are 4 distinct patterns of injury. Cranial US and CT reveal periventricular
leukomalacia, germinal matrix hemorrhage, and hydrocephalus. MRI is
the most sensitive modality for evaluating these injuries.
In preterm neonates, mild hypotension causes periventricular
injury while severe hypotension causes infarction of the deep
gray matter, brainstem, and cerebellum. In term neonates,
mild hypotension causes parasagittal cortical and subcortical
injury while severe hypotension causes injuries of the lateral
thalami, posterior putamina, hippocampi, corticospinal tracts,
and sensorimotor cortex.
GOALS
To review the spectrum of acute cerebral neonatal ischemia
from regional infarcts to diffuse anoxia emphasizing the
benefits of MRI vs. CT and sonography.
Pertinent literature is reviewed and cases showing the
importance of MRI in each of these settings compared to
CT and sonography were selected from the teaching files of
2 academic institutions.
CLINICAL FINDINGS
Clinical presentation of perinatal stroke varies from nonspecific
symptoms to obvious neurological symptoms. Seizures are most
common in children with ischemia, especially newborns. Many patients
are symptomatic in the first 48 hours of life while in n a few patients,
the event may be clinically silent.
Newborns are particularly susceptible to stroke due to the perinatal
activation of coagulation mechanisms and the most involved vascular
territory is the middle cerebral artery, especially the left side. The
predominance of left side lesions is probably due to differences in
vulnerability/maturation or presence of vascular asymmetries. The left
hemisphere may be more vulnerable to embolic lesions due to
hemodynamic differences from a patent ductus arteriosus or through a
direct route involving the left common carotid artery.
CLINICAL FINDINGS
Perinatal stroke is a common cause of long-term neurologic disability and the
leading cause of hemiplegic cerebral palsy; 41% of children after neonatal
stroke have cognitive impairments.
Perinatal asphyxia is the most important cause of HIE resulting in hypoxemia
and hypercapnia. The exact pathophysiology of HIE is not understood but lack
of sufficient blood flow and decreased blood oxygen lead to loss of cerebral
autoregulation and diffuse injury. The nature of the injury depends on the
severity of hypotension and degree of brain maturation.
An encephalopathic neonate has low Apgar scores at delivery and metabolic
acidosis in cord blood. Within 24 hours of life an infant may develop apnea,
seizures and abnormal EEG which is helpful in predicting outcome including
likelihood of death and significant long-term neurologic sequelae such as spastic
quadriplegia or diplegia.
CLINICAL FINDINGS
Perinatal asphyxia is the most important cause of Hypoxic Ischemic
Encephalopathy (HIE), resulting in hypoxemia and hypercapnia.
Although the exact pathophysiology of HIE is not completely
understood, lack of sufficient blood flow in conjunction with decreased
oxygen content in blood leads to loss of cerebral autoregulation and
diffuse injury. The exact nature of the injury depends on the severity of
hypotension and the degree of brain maturation.
An encephalopathic neonate may have low Apgar scores at delivery and
metabolic acidosis documented in cord blood. Within the first 24 hours
of life, an infant may develop symptoms of apnea and seizures with
abnormal EEG. Abnormal EEG may be helpful in predicting outcome
including likelihood of death and significant long-term neurologic
sequelae such as spastic quadriplegia or diplegia.
IMAGING FINDINGS
SONOGRAPHY
CT
MRI
Selected Cases
SONOGRAPHY (US)
US provides an easy, accessible, convenient, noninvasive,
relatively low-cost screening examination at bed-side. It imparts
no ionizing radiation exposure and is sensitive for detection of
hemorrhage, periventricular leukomalacia (PVL), and
hydrocephalus. Doppler interrogation and assessment of
resistive index (RI) provide information on cerebral perfusion.
It is operator dependent and less sensitive to structural
abnormalities in the cerebral convexities and brainstem.
Parenchymal abnormalities identified at US can be non-specific
and the cystic lesions that characterize HIE appear aproximately
4 weeks after the ischemic event, not allowing an early
diagnosis of this pathology.
CT
CT is the least sensitive modality for evaluation of HIE and
focal infarcts because of the high water content in the
neonatal brain and high protein content of CSF which
result in poor parenchymal contrast resolution. In addition,
CT has the inherent disadvantage of radiation exposure.
However, CT provides a rapid mode of cranial screening
for hemorrhage in sick neonates without the need for
sedation.
MRI
It is the most sensitive and specific technique for
examining infants with suspected HIE and has no ionizing
radiation.
MR imaging is often not possible because the need for
sedation of sick neonates, lack of optimal safe transport,
and limited access to a unit at smaller facilities.
Studies have focused on the utility of early MRI (firsts days
of life) compared to later MRI (after 1 week) and
concluded that early MRI does not underestimate lesions.
MRI
DWI obtained between 24 hours and 8 days of life is very
sensitive for detection of cytotoxic edema but does not
correlate well with extent of ischemic injuries and does not
predict outcome.
MR spectroscopy reveals an elevation of lactate in ischemic
areas.
Conventional MRI sequences can rule out other causes of
encephalopathy (cerebral infarction, cancer, hemorrhage).
MRI PATTERNS OF INFARCTIONS
I. Watershed
• Between cortical arterial territories.
• Subcortical brain infarcts in white matter along and slightly above the
lateral ventricles.
II. Focal.
• Involves only a part of the brain usually an arterial territory.
III. Diffuse
• Involves the entire brain, white and gray matter
• Involves predominantly the posterior temporal, occipital and parietal
regions as in hypoglycemia.
• Involves the basal ganglia and thalami.
IMAGING FINDINGS COMPARISON
Imaging findings of focal/regional cerebral ischemia are
straightforward and easily diagnosed with MRI. CT is less
helpful but superior to US.
In cases of diffuse acute anoxia, US may show subtle
findings such as cortical sulci effacement and increased
echogenicity in the central brain. MRI especially with DWI
clearly shows the abnormalities while CT does not
contribute to the diagnosis.
MRI is the best tool to show the diffuse acute anoxia.
IMAGING FINDINGS COMPARISON
SELECTED CASES
WATHERSHED INFARCTIONS
Severe HIE. Axial CT and DWI//T2 MR images. There are multiple acute
infarcts in watershed distributions including the corpus callosum. The
findings are subtle on CT and DWI/T2 are clearly superior.
WATHERSHED INFARCTIONS
Severe HIE. US reveals increased echogenicity in periventricular white
matter and CT low density in same regions. T2 image show high signal in
white matter and prominence of deep medullary veins while DWI show
periventricular and callosal infarctions.
FOCAL INFARCTION
Focal infarct in a neonate. US, CT and DWI/T2 MR images show a focal
right parietal infarction. In this example, MRI is clearly superior to CT and US
where the lesion is not seen.
FOCAL INFARCTION
Focal infarction. CT shows subtle left frontal hypodensity (arrowhead). The
lesion is seen more clearly as high signal on DWI and T2 image shows loss of
cortical ribbon in same location (arrow).
FOCAL INFARCTIONS
Focal infarctions. US is normal while T2 image obtained 1 hour later
shows loss of posterior cortical ribbon and DWI show high signal in the cortex
posteriorly.
DIFFUSE INJURY
Diffuse HIE. US shows an area of increased echogenicity in the right posterior brain
(arrowhead) and a CT shows subtle edema and loss of gray/white matter
differentiation in same location. MR T2 image shows diffuse injuries with loss of
cortical ribbon and high signal in white matter and deep gray nuclei.
DIFFUSE INJURY
Severe hypoxic-ischemic injury. US shows questionable high echogenicity in basal
ganglia (arrowheads). T2 and DWI MR images show near complete absence of cortical
ribbon, high signal from deep gray matter, and diffusely hyperintense white matter
and restricted diffusion especially anteriorly and posteriorly.
CENTRAL INFARCTIONS
Severe HIE. US shows subtle increased echogenicity in basal ganglia especially on
the left. Axial T1 pre- and post contrast images show high pre contrast T1 signal and
contrast enhancement in basal ganglia and thalami. Cortical ribbon is absent. In this
example, MRI is clearly superior to US although findings are seen on US.
TAKE-HOME MESSAGES
Acute anoxic brain injury in neonates results in severe
neurologic disability and mortality. Recognition of the
typical imaging findings can lead to an earlier diagnosis
which may aid in determining therapy, outcome and family
counseling. Although US is the screening method of choice,
findings tend to be subtle and need MRI confirmation in
most patients.
MRI is the gold standard because its higher sensitivity and
findings are more specific than US and CT.
REFERENCES
18.
Rutherford, MA et al: Magnetic resonance imaging of white matter diseases of prematurity. Neuroradiology (2010) 52:505–521.
Huang, BY; Castillo, M: Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. RadioGraphics March-April 2008, Volume 28
Number 2.
Ghei, SK et al: MR Imaging of Hypoxic-Ischemic Injury in Term Neonates: Pearls and Pitfalls. RadioGraphics 1048 July-August 2014, Volume 34
Chao, CP et al: Neonatal Hypoxic - Ischemic Encephalopathy: Multimodality Imaging Findings. RadioGraphics October 2006, Volume 26.
Liauw, L et al: Hypoxic-Ischemic Encephalopathy: Diagnostic Value of Conventional MR Imaging Pulse Sequences in Term-born Neonates.
Radiology April 2008, Volume 247: Number 1.
Charon, V et al: Comparison of early and late MRI in neonatal hypoxic–ischemic encephalopathy using three assessment methods. Pediatric
Radiology. 2015 Dec; 45(13):1988-2000.
Agut, T et al: Early identification of brain injury in infants with hypoxic ischemic encephalopathy at high risk for severe impairments: accuracy of MRI
performed in the first days of life. BMC Pediatr. 2014 Jul 8;14:177.
Shankaran, S et al: Neonatal Magnetic Resonance Imaging Pattern of Brain Injury as a Biomarker of Childhood Outcomes following a Trial of
Hypothermia for Neonatal Hypoxic-Ischemic Encephalopathy. J Pediatr. 2015 Nov; 167(5):987-93.e3.
Machado, V et al: Perinatal ischemic stroke: a five-year retrospective study in a level-III maternity. Einstein (Sao Paulo). 2015 Jan-Mar.
Martinez-Biarge, M et al: Predicting motor outcome and death in term hypoxic-ischemic encephalopathy. Neurology. 2011 Jun 14;76(24):2055-61.
Spring in ’t Veld, LG et al: Serial 1- and 2-Dimensional Cerebral MRI Measurements in Full-Term Infants after Perinatal Asphyxia.
Neonatology. 2016 Mar 12; 110(1):27-32.
Dinan, D et al: Easily Overlooked Sonographic Findings in the Evaluation of Neonatal Encephalopathy: Lessons Learned From Magnetic Resonance
Imaging. Semin Ultrasound CT MR. 2014 Dec; 35(6):627-51.
Cauley, KA et al: Apparent diffusion coefficient histogram analysis of neonatal hypoxic–ischemic encephalopathy. Pediatr Radiol. 2014 Jun;
44(6):738-46.
Okabe, T: Early magnetic resonance detection of cortical necrosis and acute network injury associated with neonatal and infantile cerebral infarction.
Pediatr Radiol. 2014 May; 44(5):597-604.
Badve, CA et al: Neonatal ischemic brain injury: what every radiologist needs to know. Pediatr Radiol. 2012 May.
Gunny , RS et al: Imaging of Perinatal Stroke. Magn Reson Imaging Clin N Am. 2012 Feb;20(1):1-33.
Izbudak, I et al: MR Imaging of theTerm and Pre term Neonate with Diffuse Brain Injury. Magn Reson Imaging Clin N Am. 2011 Nov; 19(4):709-31.
Kitamura, G et al: Hypoxic-Ischemic Injury: Utility of Susceptibility-Weighted Imaging. Pediatr Neurol. 2011 Oct; 45(4):220-4.
19.
Vermeulen, RJ et al: Diffusion-weighted and Conventional MR Imaging in Neonatal Hypoxic Ischemia. Radiology. 2008 Nov; 249(2):631-9.
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