Perinatal infections, prematurity and brain injury.

PURPOSE OF REVIEW

The association between perinatal infection and brain injury is widely accepted but a cause-and-effect relationship has not yet been proven. This article summarizes available evidence and current primary publications for debate.

RECENT FINDINGS

Work completed during the review period has reinforced current understanding of perinatal infection, prematurity and brain injury. In animal experiments: lipopolysaccharides have been further implicated in brain injury, not only as a cause of brain injury but also as mediators of preconditioning and protection. Recent studies suggest that cerebral injury following low-dose lipopolysaccharide administration may become compensated in adulthood. Other studies have emphasized the complexity of the response by showing that plasma cytokine levels may not reflect those in the central nervous system or inflammatory events in the brain.

SUMMARY

Perinatal infection and maternofetal inflammation is strongly associated with preterm birth. Inflammation probably represents an important mechanism for cerebral damage, and both overt lesions and maldevelopment can result. Epidemiological data and multiple animal models to link infection, inflammation and brain damage exist, but proof of causation is elusive.