Neonatal encephalopathy occurs in 1–6 of every 1000 live full‐term births and is a major cause of neurodevelopmental disability1
: 15–20% of affected infants will die during the postnatal period, and an additional 25% will sustain permanent clinical deficits.2
The deficits of greatest concern include functional motor and cognitive deficits. Functional motor deficits are often described as cerebral palsy, a non‐progressive motor or postural disorder originating in early life. Cognitive deficits include mental retardation or subnormal intellectual function resulting in impaired language skills, learning, executive functions or social ability.
Hypoxic‐ischaemic encephalopathy certainly accounts for a substantial fraction of neonatal encephalopathy, yet many newborns with this condition have no documented hypoxic‐ischaemic insult.4
There is continuing controversy as to whether neonatal encephalopathy is primarily related to insults sustained in the antepartum or intrapartum period.5
Although many risk factors, such as maternal hypothyroidism, pre‐eclampsia, preterm premature rupture of the membranes and chorioamnionitis, are clearly prenatal,6
recent evidence from prospective cohorts of neonatal encephalopathy using magnetic resonance imaging (MRI) shows that most brain injury actually happens at or near the time of birth.7
For the purpose of this review, the term “neonatal encephalopathy” is used instead of “perinatal asphyxia” in recognition of the variable timing of injury resulting in this syndrome.
The American College of Obstetricians and Gynecologists task force on neonatal encephalopathy and cerebral palsy concluded that an acute intrapartum event could only result in cerebral palsy of the spastic tetraplegic type and could not result in isolated cognitive deficits, such as mental retardation.9
Earlier studies on neurodevelopmental outcomes after fetal hypoxia and other presumed causes of asphyxia did not identify infants with isolated cognitive deficits,10
yet few population‐based studies exist.5
Nevertheless, in examining the long‐term outcomes of children with neonatal encephalopathy or risk factors for hypoxia‐ischaemia, some studies have shown that isolated cognitive deficits may occur in the absence of functional motor deficits.11
In this era of potential treatments for neonatal brain injury, including hypothermia, we need a better understanding of the motor and cognitive outcomes of survivors of neonatal encephalopathy. Furthermore, understanding the spectrum of neurodevelopmental outcomes after neonatal encephalopathy will allow clinicians and researchers to identify children requiring early intervention and continued follow‐up to maximise their potential for independent function throughout development.
This review will consider whether long‐term cognitive deficits can occur in the absence of functional motor deficits after neonatal encephalopathy. We will examine evidence from animal models and human studies and consider the role of newer imaging techniques, such as MRI.