Investigators from the Department of Neurology, Children’s Hospital and Harvard Medical School, Boston and the Neuroepidemiology Branch, Bethesda take issue with the terms hypoxic-ischemic and post-asphyxial encephalopathy when the etiology is frequently in doubt. These authors prefer the simple descriptive terms, neonatal or newborn encephalopathy for infants with a clinically defined syndrome of impaired neurologic function, which includes lethargy, coma, hypotonia, impaired primitive reflexes, depressed or absent respirations and seizures. Difficulties in initiating respiration and maintaining tone and consciousness may be caused by factors that predate birth or onset of labor. Neonatal encephalopathy grading schemes previously described in the literature (Sarnat and Sarnat, Low et al, Levene et al, Amiel-Tilson and Ellison, Fenichel) are considered qualitative rather than quantitative and their potentially correctable limitations are discussed. [1]

COMMENT. In a previous issue of Pediatric Neurology [2], Dr. Alan Hill of the University of British Columbia Children’s Hospital, Vancouver, reviewed the diagnosis, classification, pathology and management of hypoxic-ischemic cerebral injury in the term newborn. Grade III severe HIE, manifested by coma, hypotonia, seizures, abnormal brain stem and autonomic function, and increased intracranial pressure, is associated invariably with death or severe neurologic sequelae. Grade II moderate HIE, with lethargy/stupor, hypotonia, suppressed reflexes and seizures, has a poor outcome in 20-40% of infants. Grade I mild HIE, characterized by hyperalertness, jitteriness, exaggerated Moro and stretch reflexes, is transient with duration less than 24 hours and recovery is complete. The author emphasizes that the clinical features of hypoxic-ischemic encephalopathy are not specific and that similar symptoms may be caused by metabolic disorders, infection or cerebral dysgenesis.