Snp cytokine polymorphysms, perinatal infection and cerebral palsy

Abstract

Cerebral palsy (CP) is the most common neurological disorder in children attributed to non-progressive disturbances in the developing fetal or infant brain. The cause and pathogenesis of CP is multifactorial and continues to be poorly understood. Prematurity is considered to be the leading risk factor for the development of CP. In recent times, intrauterine infection/inflammation has been identified as the most common cause of preterm delivery and neonatal complications. Microorganisms or their products stimulate the production of cytokines and a systemic response termed FIRS (Fetal Inflammatory Response Syndrome) in the fetus. Activation of the cytokine network and elevated levels of proinflammatory cytokines can cause white matter brain damage and preterm delivery, as well as the future development of CP. The balance between pro- and anti-inflammatory cytokines in the neonatal brain is likely to be critical in determining the initiation, development and consequences of cerebral injury. Individual infants display a spectrum of severity of damage following apparently comparable insults. Such variation may depend on the complicated interaction of the multiple etiological factors and on the genetic susceptibility of the individual including polymorphisms in pro- and anti-inflammatory cytokine genotypes.