A 9 yo male with recurrent seizures, delayed mile stones. Birth history significant 8 month preterm hospital delivery, not cried immediately after birth.
Axial flair images of brain
Bilateral medial occipital cortical Gliosis, ex vacuo dilatation of adjacent lateral ventricles with undulating wall owing to paucity of periventricular white matter. An associated mild diffuse cerebral cortical atrophy.
Imaging wise : Perinatal Hypoxic / Hypoglyemic Brain Injury needs consideration.
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 may be 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
Imaging wise : Perinatal Hypoxic / Hypoglyemic Brain Injury needs consideration.
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 may be 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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