Systematic review of chorioamnionitis and cerebral palsy

Wu, Yvonne W.

doi:10.1002/mrdd.10003

Cited by 212 publications

(138 citation statements)

References 51 publications

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“…In fact, in Wu's meta-analysis, no two studies used the same definition of clinical chorioamnionitis. 41 We have no reason to think there would be differential misclassification between cases and controls, therefore, our risk estimates remain valid but of reduced magnitude. In addition, we underestimated the true prevalence of maternal infection because we could not assess infection that occurred outside the period of delivery.…”

Section: Discussionmentioning

confidence: 82%

Maternal Infection and Risk of Cerebral Palsy in Term and Preterm Infants

et al. 2004

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We tested the hypothesis that term and preterm infants exposed to maternal infection at the time of delivery are at increased risk of developing cerebral palsy (CP). STUDY DESIGN:A population-based case-control study was conducted using Washington State birth certificate data linked to hospital discharge data. Cases (688) were children r6 years old, singleton births, hospitalized during 1987 to 1999 with an ICD-9 diagnosis code for CP. Controls were 3068 singleton birth infants randomly selected from birth records for the same years without CP-related hospitalizations. Infection information was available only for the birth hospitalization. RESULTS:Infants of women who had any infection during their hospitalization for delivery were at increased risk of CP (odds ratio (OR) 3.1, 95% confidence interval (CI) 2.3 to 4.2). This was observed for term deliveries (OR 1.8, 95% CI 1.1 to 2.8) and preterm deliveries (OR 2.3, 95% CI 1.3 to 4.2). CONCLUSIONS:Our results suggest that maternal infection is a risk factor for CP in both term and preterm infants.

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Section: Discussionmentioning

confidence: 82%

Maternal Infection and Risk of Cerebral Palsy in Term and Preterm Infants

et al. 2004

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“…Intrauterine infection greatly increases the risk of periventricular leukomalacia (PVL) and cerebral palsy in premature infants and term infants (Grether and Nelson, 1997;Wu and Colford, 2000;Wu, 2002), and cytokines have been implicated in this association (Dammann and Leviton, 1997). Elevated levels of IL-6 in fetal cord blood and of IL-6 and IL-1b in amniotic fluid are associated with white matter lesions and cerebral palsy in premature infants (Yoon et al, 1996;Yoon et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Prenatal Infection and Risk for Schizophrenia: IL-1β, IL-6, and TNFα Inhibit Cortical Neuron Dendrite Development

Gilmore¹,

Jarskog²,

Vadlamudi³

et al. 2004

Neuropsychopharmacol

236

158

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Prenatal exposure to infection increases risk for schizophrenia, and we have hypothesized that inflammatory cytokines, generated in response to maternal infection, alter neuron development and increase risk for schizophrenia. We sought to study the effect of cytokines generated in response to infectionFinterleukin-1b (IL-1b), tumor necrosis factor-a (TNFa), and interleukin-6 (IL-6)Fon the dendritic development of cortical neurons. Primary mixed neuronal cultures were obtained from E18 rats and exposed to 0, 100, or 1000 units (U)/ml of IL-1b, TNFa, IL-6, or IL-1b þ TNFa for 44 h. MAP-2-positive neurons were randomly identified for each condition and the number of primary dendrites, nodes, and total dendrite length was determined. We found that 100 U of TNFa significantly reduced the number of nodes (27%, p ¼ 0.02) and total dendritic length (14%, p ¼ 0.04), but did not affect overall neuron survival. A measure of 100 U IL-1b þ TNFa significantly reduced the number of primary dendrites (17%, p ¼ 0.006), nodes (32%, p ¼ 0.001), and total dendritic length (30%, po0.0001), although it did not affect overall neuron survival. At 1000 U, each cytokine significantly reduced the number of primary dendrites (14-24%), nodes (28-37%), as well as total dendritic length (25-30%); neuron survival was reduced by 14-21%. These results indicate that inflammatory cytokines can significantly reduce dendrite development and complexity of developing cortical neurons, consistent with the neuropathology of schizophrenia. These findings also support the hypothesis that cytokines play a key mechanistic role in the link between prenatal exposure to infection and risk for schizophrenia.

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“…Others, however, have reported that chorioamnionitis is an antecedent of echolucency (50). Virtually all placentas and umbilical cords that have fetal vasculitis also have inflammation of the membranes, but only approximately half of placentas with membrane inflammation have fetal vasculitis (21,51).…”

Section: Discussionmentioning

confidence: 99%

Bronchopulmonary Dysplasia Is Not Associated with Ultrasound-Defined Cerebral White Matter Damage in Preterm Newborns

et al. 2004

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Bronchopulmonary dysplasia (BPD) and cerebral white matter damage (WMD) are neonatal disorders that occur most commonly in those who are born much before term. In a large multicenter database, we sought to determine whether the two disorders occur together more frequently than expected and whether BPD and other neonatal respiratory characteristics are more common among infants who develop ultrasound-defined WMD than among those who do not. In a sample of 904 infants who were born before the 30th week of gestation and survived until 36 wk postmenstrual age, we did not find a co-occurrence of BPD and WMD above what would be expected by chance. Confounding does not seem to account for this lack of association between WMD and BPD. In conclusion, our findings do not support the hypothesis that BPD contributes to the occurrence of sonographically defined WMD. Preterm infants are exposed to a number of antenatal and postnatal challenges that, in concert with their immaturity, render them susceptible to a wide range of neonatal disorders. Among these, bronchopulmonary dysplasia (BPD) and cerebral white matter damage (WMD) are prominent entities.BPD was initially identified as a chronic neonatal lung disease that occurred in preterm infants who were exposed to prolonged ventilation with high airway pressure and high inspired oxygen concentrations (1). More recently, a "new" BPD was defined as a form of neonatal chronic lung disease, characterized by aberrational lung alveolarization and vascular development (2). Changes in neonatal practice, including the introduction of exogenous surfactant, increased use of antenatal glucocorticoids, and sophisticated ventilatory support strategies, might play a role in this changing clinical phenomenology of BPD. Antenatal effects apparently gain pathogenetic importance (3), and major research emphasis is being placed on inflammatory pathomechanisms (4). The current terminology has now returned from "chronic lung disease" to BPD (5). The new definition of BPD-"receiving O 2 at 36 wk postconceptional age"-has been shown to be a better predictor of abnormal pulmonary signs and symptoms at age 2 (83%) (6) than the 38% achieved by previously suggested definition of BPD-"receiving O 2 at 28 d of life" (7).

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Systematic review of chorioamnionitis and cerebral palsy

Cited by 212 publications

References 51 publications

Maternal Infection and Risk of Cerebral Palsy in Term and Preterm Infants

Maternal Infection and Risk of Cerebral Palsy in Term and Preterm Infants

Prenatal Infection and Risk for Schizophrenia: IL-1β, IL-6, and TNFα Inhibit Cortical Neuron Dendrite Development

Bronchopulmonary Dysplasia Is Not Associated with Ultrasound-Defined Cerebral White Matter Damage in Preterm Newborns

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