Antenatal Antecedents and the Impact of Obstetric Care in the Etiology of Cerebral Palsy

Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, The University of Texas Medical Branch, Galveston, Texas 77555-0587, USA.
Clinical obstetrics and gynecology (Impact Factor: 1.77). 01/2009; 51(4):775-86. DOI: 10.1097/GRF.0b013e3181870994
Source: PubMed


Cerebral palsy (CP) affects 2/1000 live-born children. Multiple antenatal factors, including preterm delivery, low birth weight, infection/inflammation, multiple gestation, and other pregnancy complications, are mostly associated with CP in both the preterm and term infant, with birth asphyxia playing a minor role. Owing to the increasing survival of the very preterm and very low birth weight infant secondary to improvements in neonatal and obstetric care, the incidence of CP may be increasing. The focus of this paper is to explore antenatal antecedents as etiologies of CP and the impact of obstetric care on the prevention of CP.

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    • "Animal and human studies suggest that infection and inflammation lead to fetal inflammatory response, and that this inflammation is associated with brain injury and subsequent development of CP (Clark et al., 2008; Yoon et al., 2000). The host's defense to an inflammatory insult involves a group of intracellular proteins called damage-associated molecular pattern molecules or DAMPs, such as S100B (Lotze et al., 2007; Medzhitov 2008). "
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    ABSTRACT: To evaluate the association between cerebral palsy (CP) or infant death and putative cord blood biomarkers of neurologic injury, we performed a nested case-control secondary analysis of a multicenter randomized trial of magnesium sulfate (MgSO(4)) versus placebo to prevent CP or death among offspring of women with anticipated delivery from 24 to 31 weeks' gestation. Cases were infants who died by 1 year (n=25) or developed CP (n=16), and were matched 1:2 to a control group (n=82) that survived without developing CP. Umbilical cord sera concentrations of S100B, neuron-specific enolase (NSE) and the total soluble form of the receptor for advanced glycation end-products (sRAGE) were measured by ELISA in duplicates. Maternal characteristics were similar between the 2 groups. Cases were born at a lower gestational age (GA) and had lower birth weight compared with controls. There were no differences in concentrations of the three biomarkers and the composite outcome of CP or infant death. However, S100B was higher (median 847.3 vs. 495.7 pg/ml; P=0.03) in infants who had CP and total sRAGE was lower (median 1259.3 vs. 1813.1 pg/ml; P=0.02) in those who died compared with the control group. When corrected for delivery GA and treatment group, both differences lost statistical significance. In conclusion, cord blood S100B level may be associated with CP, but this association was not significant after controlling for GA and MgSO(4) treatment.
    International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience 06/2011; 29(8):917-22. DOI:10.1016/j.ijdevneu.2011.06.009 · 2.58 Impact Factor
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    • "Increased risk for cerebral palsy has most often been associated with chorioamnionitis (i.e. intra-uterine infection), although there is some evidence that extra-uterine maternal infections during pregnancy may also play a role (Murphy et al., 1995; Clark et al., 2008). Meta-analysis has indicated a significant association between chorioamnionitis and cerebral palsy for both preterm and term infants (Wu and Colford , 2000; Wu, 2002). "
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    ABSTRACT: Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy. Since 2000, a large number of studies have used rodent models of systemic prenatal infection or prenatal immune activation to characterize changes in brain function and behavior caused by the prenatal insult. This review provides a comprehensive summary of these findings, and examines consistencies and trends across studies in an effort to provide a perspective on our current state of understanding from this body of work. Results from these animal modeling studies clearly indicate that prenatal immune activation can cause both acute and lasting changes in behavior and CNS structure and function in offspring. Across laboratories, studies vary with respect to the type, dose and timing of immunogen administration during gestation, species used, postnatal age examined and specific outcome measure quantified. This makes comparison across studies and assessment of replicability difficult. With regard to mechanisms, evidence for roles for several acute mediators of effects of prenatal immune activation has emerged, including circulating interleukin-6, increased placental cytokines and oxidative stress in the fetal brain. However, information required to describe the complete mechanistic pathway responsible for acute effects of prenatal immune activation on fetal brain is lacking, and no studies have yet addressed the issue of how acute prenatal exposure to an immunogen is transduced into a long-term CNS change in the postnatal animal. Directions for further research are discussed.
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