Defining cerebral palsy: pathogenesis, pathophysiology and new intervention

Abstract

Cerebral palsy (CP) affects 2/1 000 live-born children. There are several antenatal factors, including preterm delivery, low birth weight, infection/inflammation, multiple gestations, and other pregnancy complications, that have been associated with CP in both the preterm and term infant, with birth asphyxia playing a minor role. Due to the increasing survival of the very preterm and very low birth weight infant secondary to improvements in neonatal and obstetric care, the incidence of CP may be increasing. The topics of neonatal encephalopathy and CP, as well as hypoxic-ischemic encephalopathy, are of vital importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause CP have been advanced previously by both the American College of Obstetricians and Gynecologists and the International Cerebral Palsy Task Force. This review will cover the progression toward defining the pathogenesis and pathophysiology of cerebral palsy. Four essential criteria were advanced as prerequisites if one is to propose that an intrapartum hypoxic-ischemic insult has caused a moderate to severe neonatal encephalopathy that subsequently results in CP. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis (pH <7.0 and base deficit of 12 mmol/L or more); 2) early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks' gestation; 3) CP of the spastic quadriplegic or dyskinetic type, and 4) exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders. Other criteria that together suggest intrapartum timing are also discussed. The focus of this paper is to explore antenatal antecedents as etiologies of CP and the impact of obstetric care on the prevention of CP.