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MRI findings in infants with infantile spasms after neonatal hypoxic-ischemic encephalopathy
Dawn Gano1, Michael A Sargent, Steven P Miller
1Department of Pediatrics, University of California, San Francisco, California; Department of Neurology, University of California, San Francisco, California; Department of Pediatrics, University of British Columbia, Vancouver, Canada.
Insights
Infantile spasms in newborns with hypoxic-ischemic encephalopathy are linked to brain damage in the basal ganglia and thalami. This risk increases with extensive cortical injury or midbrain damage.
Area of Science:
- Neonatal neurology
- Pediatric neuroimaging
- Neurocritical care
Background:
- Neonatal hypoxic-ischemic encephalopathy (HIE) is a major cause of brain injury in newborns.
- Infantile spasms are a severe epilepsy syndrome that can develop after HIE.
- Understanding the patterns of brain injury associated with infantile spasms is crucial for prognosis and management.
Purpose of the Study:
- To determine the characteristic patterns of brain injury in infants who develop infantile spasms after HIE.
- To identify specific anatomical areas of brain injury associated with infantile spasms post-HIE.
Main Methods:
- A nested case-control study was conducted on term newborns with HIE.
- Magnetic resonance imaging (MRI) including diffusion-weighted imaging was performed on day 3 of life.
- MRI scans were analyzed for patterns of injury (basal ganglia/thalamus, cortical, brainstem, hypothalamus) and compared between infants with and without infantile spasms.
Main Results:
- Infantile spasms developed in 4.5% of newborns with HIE.
- Infantile spasms were significantly associated with basal ganglia/thalamus injury and total brain injury.
- Extensive cortical injury (>50%), midbrain injury, and hypothalamic abnormalities were also linked to infantile spasms.
Conclusions:
- Neonatal brain injury in the basal ganglia and thalami is a significant risk factor for developing infantile spasms after HIE.
- The presence of extensive cortical injury and/or midbrain injury further increases this association.
Background:
To evaluate the predominant pattern of brain injury and the anatomic areas of injury in children with infantile spasms following neonatal hypoxic-ischemic encephalopathy.
Methods:
A nested case-control study of infantile spasms in children with term neonatal hypoxic-ischemic encephalopathy was performed. All patients had T1/T2-weighted magnetic resonance imaging with diffusion-weighted imaging performed on the third day of life. Using a validated scoring system, the magnetic resonance imaging was classified as: normal, watershed, basal ganglia/thalamus, total, or focal-multifocal. Two study investigators scored additional anatomic areas of injury (cortical extent, levels of the brainstem, hypothalamus) on T1/T2-weighted magnetic resonance imaging and diffusion-weighted imaging blinded to the outcome. The predominant pattern of brain injury and anatomic areas of injury were compared between patients who developed infantile spasms and randomly selected controls.
Results:
Eight patients who developed infantile spasms were identified among a cohort of 176 term newborns with hypoxic-ischemic encephalopathy (4.5%). There were no significant differences in the perinatal and neonatal course between newborns who developed infantile spasms and controls who did not. The development of infantile spasms after neonatal hypoxic-ischemic encephalopathy was significantly associated with basal ganglia/thalamus and total brain injury (P = 0.001), extent of cortical injury greater than 50% (odds ratio = 11.7, 95% confidence interval = 1.1-158.5, P = 0.01), injury to the midbrain (odds ratio = 13, 95% confidence interval = 1.3-172, P = 0.007) and hypothalamic abnormalities (P = 0.01).
Conclusions:
The development of infantile spasms after hypoxic-ischemic encephalopathy is associated with injury to the basal ganglia and thalami on neonatal magnetic resonance imaging, particularly when extensive cortical injury and/or injury to the midbrain is present.
