Abstract

Neurology| September 01 1999 Elevated Cytokines and Cerebral Palsy AAP Grand Rounds (1999) 2 (3): 30–31. https://doi.org/10.1542/gr.2-3-30 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Elevated Cytokines and Cerebral Palsy. AAP Grand Rounds September 1999; 2 (3): 30–31. https://doi.org/10.1542/gr.2-3-30 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search toolbar search search input Search input auto suggest filter your search All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: cerebral palsy, cytokine, interferons Source: Grether JK, Nelson KB, Dambrosia JM, Phillips TM. Interferons and cerebral palsy. J Pediatr. 1999;134:324–332. In a retrospective study, Grether et al investigated the association between spastic cerebral palsy (CP) and serum levels of neonatal interferons (IFNs), other inflammatory cytokines, thyroid hormones, complement and coagulation factors. The subjects were selected from a population based case-control study of CP risk factors conducted in the San Francisco area between 1983 and 1985. One hundred and ninety-two children were identified with CP at 3 years of age. From this group, a subset of children with moderate to severe spastic CP was selected based upon the availability of archived blood from newborn metabolic screening and neonatal exposure to intrauterine infection, asphyxia or maternal problems in the second half of pregnancy. Also included was a small group of children with no apparent cause for their CP. The final study cohort included 31 mostly term children with spastic CP for whom neonatal blood spots were available, and 65 children of unknown gestational age and weight randomly selected from the control group. Blood was eluted from blood spots that had been stored over time at −15°F and analyzed for various constituents. Fourteen of the 31 children with spastic CP were found to have levels of all 3 IFNs higher than any child in the control group and were at or above the maximum adult normal values. IL-1, 6, 8, TNF alpha and other inflammatory mediators were also high in this group. In contrast, thyroid hormones, total T4, T3 and complement proteins C3, 4 and 9 were lower than in the controls. Seven of the 9 children with increased IFNs had spastic diplegia, a subtype of CP. In the remaining 17 of the cases, IFNs were low and in the range observed in the control group. The concentration of other cytokines, thyroid hormones and complement were also within the normal range. Although these children with CP had no evidence of inflammation, 70% of them had one or more coagulation factors that were abnormal. The most frequent form of CP in this group was spastic hemiplegia. The etiology of CP remains elusive in the majority of children. Recently, strong epidemiological evidence has been presented linking maternal intrauterine infection with neonatal white matter disease or periventricular leukomalacia (PVL) in the preterm infant. Yoon reported a correlation between elevated cytokines in amniotic fluid, histologic chorioamnionitis, PVL on neurosonography and CP.1 In children who died with PVL, immunohistochemical studies have shown an overproduction of cytokines in hypertrophic astrocytes and microglial cells of the CNS.2,3 Sixty to 100% of neonates with PVL develop CP, most commonly spastic diplegia. Cytokine mediated inflammatory reactions appear to be involved in the evolution of brain damage. In this small (N=31) retrospective exploratory study, Grether et al found that nearly half of the 31 children with CP had evidence of inflammation during the neonatal period with markedly elevated serum IFNs and other inflammatory mediators. This is the first report... You do not currently have access to this content.

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