Magnetic Resonance Imaging in (Near-)Term Infants with Hypoxic-Ischemic Encephalopathy

Abstract

Hypoxic-ischemic encephalopathy (HIE) is a major cause of neurological sequelae in (near-)term newborns. Despite the use of therapeutic hypothermia, a significant number of newborns still experience impaired neurodevelopment. Neuroimaging is the standard of care in infants with HIE to determine the timing and nature of the injury, guide further treatment decisions, and predict neurodevelopmental outcomes. Cranial ultrasonography is a helpful noninvasive tool to assess the brain before initiation of hypothermia to look for abnormalities suggestive of HIE mimics or antenatal onset of injury. Magnetic resonance imaging (MRI) which includes diffusion-weighted imaging has, however, become the gold standard to assess brain injury in infants with HIE, and has an excellent prognostic utility. Magnetic resonance spectroscopy provides complementary metabolic information and has also been shown to be a reliable prognostic biomarker. Advanced imaging modalities, including diffusion tensor imaging and arterial spin labeling, are increasingly being used to gain further information about the etiology and prognosis of brain injury. Over the past decades, tremendous progress has been made in the field of neonatal neuroimaging. In this review, the main brain injury patterns of infants with HIE, the application of conventional and advanced MRI techniques in these newborns, and HIE mimics, will be described.

Keywords: diffusion-weighted imaging; hypoxic-ischemic encephalopathy; magnetic resonance imaging; magnetic resonance spectroscopy; neonatal encephalopathy; neonatal neuroimaging; outcome prediction; perinatal asphyxia.

Figure 1

MRI performed on day 5 in a newborn born with Apgar scores 0/2/5 who received therapeutic hypothermia for HIE. Although the signal intensity of the posterior limb of the internal capsule appears normal on T1-weighted imaging (A), DWI shows extensive diffusion restriction in the basal ganglia and thalami (B), and the perirolandic cortex (C). The infant died after redirection of care.

Figure 2

MRI was performed on day 4 in a term infant who was born with Apgar scores of 1/5. Amplitude integrated EEG initially showed a continuous normal voltage background pattern and cooling was not started. The infant developed seizures at 10 h after birth. MRI shows a watershed predominant pattern of injury, with T2-weighted imaging showing loss of distinction between the gray and white matter at the cortex of the occipital lobes and the left frontal lobe (A) and DWI (B) showing diffusion restriction in these areas. The infant had a normal outcome at 18 months of age.

Figure 3

MRI performed on day 3 after birth, showing near total injury with extensive injury in the white matter, BGT, brainstem and cerebellum. Abnormalities are often more subtle on T2 weighted imaging in the first days after the hypoxic-ischemic insult (A) and are best seen using DWI on early MRI (B,C). Except for the dentate nuclei, the signal in the cerebellum is not increased and therefore the term ‘the white brain’ was coined. The infant died after redirection of care.

Figure 4

MRI performed on day 3 in an infant born with Apgar scores of 3/4/6 who received therapeutic hypothermia for severe HIE. MRI showed posterior cerebral artery stroke, presenting as increased signal intensity and loss of cortical gray and white matter differentiation on T2 weighted imaging (A) and a low signal intensity on ADC mapping (B). Injury was also noted in the BGT. ¹H-MRS performed in the BGT shows a lactate peak, presenting as a doublet peak at 1.33 ppm.

Figure 5

MRI performed on 10 days after birth showing injury of the mammillary bodies, presenting as decreased signal intensity on T1 weighted imaging (indicated by the white arrows on (A), swelling and increased signal intensity on T2-weighted imaging (B), and diffusion restriction on diffusion-weighted imaging (C). Diffusion restriction is also noted in the hippocampi, which is often seen in combination with mammillary body injury.

Figure 6

MRI performed on day 7 showing punctate white matter lesions. While these lesions are subtle on T1 weighted imaging (A), the abnormalities are much clearer and more numerous on the ADC map (B). Susceptibility weighted imaging can be used to rule out hemorrhagic abnormalities (C).

Figure 7

MRI was performed on day 3 in an infant born with Apgar scores of 9/10 who developed intractable seizures within the first hours after birth. T2 weighted imaging shows the decreased distinction of the gray and white matter at the cortex (A). DWI shows extensive diffusion restriction with sparing of the anterior periventricular white matter and an asymmetrical distribution of white matter injury in the parieto-occipital lobes (B). The infant died on day 5 after redirection of care and was subsequently diagnosed with Molybdenum cofactor deficiency.