Abstract
Excerpt: In the first edition of this report, the Task Force on Neonatal Encephalopathy and Cerebral Palsy outlined criteria deemed essential to establish a causal link between intrapartum hypoxic events and cerebral palsy. It is now known that there are multiple potential causal pathways that lead to cerebral palsy in term infants (see Fig 1), and the signs and symptoms of neonatal encephalopathy may range from mild to severe, depending on the nature and timing of the brain injury. Thus, for the current edition, the Task Force on Neonatal Encephalopathy determined that a broader perspective may be more fruitful. This conclusion reflects the sober recognition that knowledge gaps still preclude a definitive test or set of markers that accurately identifies, with high sensitivity and specificity, an infant in whom neonatal encephalopathy is attributable to an acute intrapartum event. The information necessary for assessment of likelihood can be derived from a comprehensive evaluation of all potential contributing factors in cases of neonatal encephalopathy. This is the broader perspective championed in the current report. If a comprehensive etiologic evaluation is not possible, the term hypoxic–ischemic encephalopathy should best be replaced by neonatal encephalopathy because neither hypoxia nor ischemia can be assumed to have been the unique initiating causal mechanism. The title of this report has been changed from Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology to Neonatal Encephalopathy and Neurologic Outcome to indicate that an array of developmental outcomes may arise after neonatal encephalopathy in addition to cerebral palsy.