Maternal-fetal medicineInfection and fetal neurologic injuryUgwumadu, AustinAuthor Information Department of Obstetrics & Gynecology, St George’s Hospital, London, UK Correspondence to: Austin Ugwumadu MRCOG, Consultant/Senior Lecturer in Obstetrics & Gynaecology, Department of Obstetrics & Gynecology, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK. Tel: +44 20 8725 0506/0501; fax: +44 20 8725 1975; E-mail: firstname.lastname@example.org Current Opinion in Obstetrics and Gynecology: April 2006 - Volume 18 - Issue 2 - p 106-111 doi: 10.1097/01.gco.0000192999.12416.95 Buy SDC Metrics Abstract Purpose of review Antepartum fetal exposure to infection/inflammation is a more important risk factor for brain injury than intrapartum hypoxia in both the term and preterm neonate. Such preexisting infection/inflammation might also provide the platform for subsequent intrapartum hypoxic–ischaemic damage. This review will discuss the complex interaction between fetal inflammatory response and neurotoxicity, and focus on the clinical implications of the synergistic interaction between infection/inflammation and hypoxia–ischaemia. Recent findings Current evidence indicates that inflammatory mediators are directly neurotoxic, and also sensitize the fetal brain tissue to a greater magnitude of damage by subsequent hypoxia–ischaemia by lowering the threshold at which hypoxia initiates neuronal cell apoptosis/cell death. Summary Further studies are urgently needed to characterize the fetuses at risk of damage, the duration of exposure required to cause injury, the influence of gestational age and whether Caesarean section may be protective. Until then clinicians should maintain a high level of surveillance in labours complicated by infection and avoid additional exposure to hypoxic–ischaemic insults. © 2006 Lippincott Williams & Wilkins, Inc.