Distinctive neuroimaging pattern in term newborns with neonatal placental encephalopathy: A Case Series

Abstract: Background Identifying antepartum versus intrapartum timing and the cause of neonatal encephalopathy (NE) often remains elusive due to our limited understanding of the underlying pathophysiological processes and lack of appropriate biomarkers. Objectives This retrospective observational study describes a case series of term newborns with NE who displayed a recognizable magnetic resonance imaging (MRI) pattern of immediately post-natal brain abnormalities that rapidly evolved towards cavitation. Our aim is to: (i) report this neuroimaging pattern, (ii) look for placental determinants, and (iii) depict the outcome. Design/Methods Unicentric retrospective case series reporting the clinical, radiological, and laboratory findings of NE associated with a distinctive neuroimaging pattern, i.e., immediately post-natal extensive corticosubcortical T2 hyperintensities, followed by rapid corticosubcortical cavitation that does not match the neuroimaging picture of intrapartum hypoxic-ischemic encephalopathy (HIE). Results Seven term newborns presented bilateral corticosubcortical hyperintensities that were detected on T2 between day of life (DOL) 1-4, which rapidly evolved towards cystic encephalomalacia, i.e., between DOL9-12. All these newborns presented with moderate/severe NE. The outcome was either neonatal death or quadriplegic cerebral palsy (CP) and epilepsy. None of the reported patients fulfilled the criteria of a high likelihood of acute intrapartum HI or quadriplegic CP. All these newborns were exposed to chronic and/or acute placental inflammation and/or HI. Conclusions To further define the antepartum causes of NE, early neuroimaging and a placental exam are recommended. Brain T2 hyperintense injuries before DOL4 followed by rapid cavitation before DOL12 might be biomarkers of NE from an antepartum/placental origin.