Chorioamnionitis and Cerebral Palsy in Term and Near-Term Infants

Wu, Yvonne W.; Escobar, Gabriel J.; Grether, Judith K.; Croen, Lisa; Greene, J; Newman, Thomas B.

doi:10.1097/00006254-200405000-00011

Cited by 63 publications

(79 citation statements)

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“…In our series a history of premature rupture of membranes was found in 6% of the study subjects. Studies have shown that chorioamnionitis is an independent risk factor for CP among term and near-term infants [17]. Multiple pregnancy has been considered an important prenatal risk factor for CP [2].…”

Section: Discussionmentioning

confidence: 99%

Magnetic resonance imaging, risk factors and co-morbidities in children with cerebral palsy

et al. 2010

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Cerebral palsy (CP) continues to be a major problem in India. The present study provides an insight into the various clinical and neuroradiological correlates of CP. The study included 102 children with CP and was subjected to magnetic resonance imaging (MRI) of the brain. Forty-seven (46%) patients belonged to the 1-3 years age group and 84 (82%) were born at term. Of 102 children, 39 (38%) were delivered at home. Based on their tone and topographic pattern of weakness, it was found that 47 (46%) had spastic diplegia and 35 (34%) spastic quadriplegia. Hemiplegic, dystonic, and atonic CP accounted for the remaining 20%. The occurrence of severe birth asphyxia, which is rarely seen in developed countries, continues to be a major problem in developing countries, and accounted 64 (62%) of the patients. Cognitive delay (82%) was the most common co-morbidity, followed by seizure disorder (52%), feeding difficulties (22%) and visual abnormalities (29%). Ninety-one (89%) children had an abnormal MRI. Periventricular white matter injury (PWMI) was observed in 48 (47.1%), followed by diffuse encephalopathy (29%). Focal lesions (6%) and malformations (3%) were less common. In children with spastic diplegia, PWMI was the most common MRI abnormality, whereas in spastic quadriplegia, diffuse encephalopathy was most common. MRI scans help in revealing the pathologic basis of CP and had strong correlations with clinical findings.

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Section: Discussionmentioning

confidence: 99%

Magnetic resonance imaging, risk factors and co-morbidities in children with cerebral palsy

et al. 2010

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“…Evidence of intrauterine infection, evidenced by histological chorioamnionitis in the placenta and membranes or intrapartum pyrexia is associated with a 4-5 fold increase in cerebral palsy (RR 4.7, 95% CI 1.3-16.2) in term infants 28 .…”

Section: Introductionmentioning

confidence: 99%

Cerebral palsy: causes, pathways, and the role of genetic variants

MacLennan

Thompson

Gécz

2015

American Journal of Obstetrics and Gynecology

360

288

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Cerebral palsy (CP) is heterogeneous with different clinical types, comorbidities, brain imaging patterns, causes, and now also heterogeneous underlying genetic variants. Few are solely due to severe hypoxia or ischemia at birth. This common myth has held back research in causation. The cost of litigation has devastating effects on maternity services with unnecessarily high cesarean delivery rates and subsequent maternal morbidity and mortality. CP rates have remained the same for 50 years despite a 6-fold increase in cesarean birth. Epidemiological studies have shown that the origins of most CP are prior to labor. Increased risk is associated with preterm delivery, congenital malformations, intrauterine infection, fetal growth restriction, multiple pregnancy, and placental abnormalities. Hypoxia at birth may be primary or secondary to preexisting pathology and international criteria help to separate the few cases of CP due to acute intrapartum hypoxia. Until recently, 1-2% of CP (mostly familial) had been linked to causative mutations. Recent genetic studies of sporadic CP cases using new-generation exome sequencing show that 14% of cases have likely causative single-gene mutations and up to 31% have clinically relevant copy number variations. The genetic variants are heterogeneous and require function investigations to prove causation. Whole genome sequencing, fine scale copy number variant investigations, and gene expression studies may extend the percentage of cases with a genetic pathway. Clinical risk factors could act as triggers for CP where there is genetic susceptibility. These new findings should refocus research about the causes of these complex and varied neurodevelopmental disorders.

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“…CA is now universally recognised as a major second trimester disease and a leading cause of preterm birth, fetal/neonatal morbidity and mortality [5,13]; however, scanty information on the effects of CA in the term fetus/newborn is available to date. In fact, CA-complicated term pregnancies have been related to depressed Apgar scores, neonatal encephalopathy with a strongly increased risk of developing cerebral palsy [13,24,28,29], infection [1], high risk of intubation in the delivery room [1], fetal death [19], and fetal growth restriction [21,27]. However, a large fraction of CA remains subclinical (subclinical histological CA (s-HCA) [9,12,25] and no recognisable clinical signs of CA at birth are known to date.…”

Section: Introductionmentioning

confidence: 99%