A 10 yo male under treatment for epilepsy. Birth history is significant - Full term hospital delivery, not cried immediately after birth, was in NICU for 1 month. Previous CT brain show mild focal widening of cortical sulci in parietal regions.
Hypoxic Ischemic Encephalopathy
HIE, formerly peri natal or birth asphyxia – a cerebral hypoperfusion injury.
Imaging wise best diagnostic clue is Gliosis involving peri rolandic cortex or para sagittal border zones, bilateral and often symmetric involvement. Basal ganglia damaged if ischemic event is profound and acute. Associated findings are microcephaly, secondary craniosynostosis, cerebral cortical and mid brain atrophy.
Patient with this finding often are term neonates with significant birth history like fetal distress prior to delivery, low Apgar score, required resuscitation at birth, metabolic acidosis (cord pH less than 7), Neurological abnormalities in first 24 hours. Maternal infection, pre-eclampsia and diabetes.
Seek inborn errors of metabolism if apparent HIE with normal Apgar OR if more than 1 HIE child in a family. Other causes can be Inherited prothrombotic disorders leading to arterial or venous occlusions are Protein CIS deficiencies, factor V Leiden mutation, antiphospholipid antibodies.
Epidemiology up to 2/1,000 (0.2%) live births.
Clinical presentation
Mild : Hyperalert/irritable, mydriasis, EEG normal
Moderate: Lethargy, hypotonia, ~ HR, Seizures.
Severe: Stupor, flaccid, reflexes absent; Seizures.
Periventricular leukomalacia (PVL) patient show Lower extremity spasticity.
Unilateral/focal lesions present with Hemiplegia / Hemiparesis.
Parasagittal cystic encephalomalacia show Spastic tetra paresis whereas Bilateral BG damage show Extrapyramidal cerebral palsy.
Reference : Diagnostic imaging Osborn
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