Gross motor functions and immune parameters in children with spastic cerebral palsy: is there a link?

Cerebral palsy (CP) is a group of persistent motor and postural disorders that cause activity limitations, which are explained by non-progressive disorders in the developing brain [1]. Inflammation is detailed in the pathogenesis of most perinatal brain injuries, which contributes to the risk of cerebral palsy, including neonatal stroke, preterm birth, birth asphyxia, and infection [2, 3]. Systematic reviews of the clinical literature now support an association between higher levels of circulating pro-inflammatory mediators and the diagnosis of cerebral palsy, especially in prematurity [4]. However, the duration and extent of this inflammation, as well as the consequences for children with cerebral palsy, remain unclear. Inflammation in cerebral palsy may consist in a change in the cytokine status [4]; altered immune response [5]; adaptive immune changes, including the distribution and function of T- and B-cells [6], as well as other genetic and non-genetic changes in signaling pathways [7]. Inflammation following perinatal brain injury is commonly reported to change over time, between the acute and chronic phases of injury [8]. However, persistent inflammation (i.e., inflammation lasting months to years after the primary injury phase) has been postulated to have detrimental effects on the brain and may contribute to severe forms of the disease. This is supported by the persistent inflammation hypothesis, also known as programming effects, whereby prenatal, antenatal, or neonatal pro-inflammatory cytokines induce inflammation that contributes to long-term cytokine dysregulation [9]. The study in children with an early residual stage of cerebral palsy demonstrated the relationship between the functional level on the GMFCS scale (Gross Motor Function Classification System) and some indicators of immune status.