Is late prevention of cerebral palsy in extremely preterm infants plausible?

Preterm birth continues to be associated with neurodevelopmental problems including cerebral palsy. Cystic white matter injury is still the major neuropathology underlying cerebral palsy, affecting 1-3% of preterm infants. Although rates have gradually fallen over time, the pathogenesis and evolution of cystic white matter injury are still poorly understood. Hypoxia-ischemia (HI) remains an important contributor yet there is no established treatment to prevent injury. Clinically, serial ultrasound and magnetic resonance imaging studies typically show delayed development of cystic lesions 2 to 4 weeks after birth. This raises the important and unresolved question as to whether this represents slow evolution of injury occurring around the time of birth, or repeated injury over many weeks after birth. There is increasing evidence that tertiary injury after HI can contribute to impairment of white and grey matter maturation. In the present review, we discuss preclinical evidence that severe, cystic white matter injury can evolve for many weeks after acute HI and is associated with microglia activity. This suggests the intriguing hypothesis that the tertiary phase of injury is not as subtle as often thought and that there may be a window of therapeutic opportunity for one to two weeks after hypoxic-ischemic injury to prevent delayed cystic lesions and so further reduce the risk of cerebral palsy after preterm birth.
Source: Developmental Neuroscience - Category: Neuroscience Source Type: research