Antenatal magnesium sulfate decreases risk of cerebral palsy.
Ontology highlight
ABSTRACT:
SUBMITTER: Al-Salam Z
PROVIDER: S-EPMC3761983 | biostudies-literature | 2012 Jan
REPOSITORIES: biostudies-literature
Publications
Antenatal magnesium sulfate decreases risk of cerebral palsy.
Journal of clinical neonatology 20120101 1
Similar Datasets
Project description:OBJECTIVE:To evaluate the relationship of maternal antenatal magnesium sulfate (MgSO4) with neonatal cranial ultrasound abnormalities and cerebral palsy (CP). STUDY DESIGN:In a randomized trial of MgSO4 or placebo in women at high risk of preterm delivery, up to 3 cranial ultrasounds were obtained in the neonatal period. Images were reviewed by at least 2 pediatric radiologists masked to treatment and other clinical conditions. Diagnoses were predefined for intraventricular hemorrhage, periventricular leukomalacia, intracerebral echolucency or echodensity, and ventriculomegaly. CP was diagnosed at 2 years of age by standardized neurologic examination. RESULTS:Intraventricular hemorrhage, periventricular leukomalacia, intracerebral echolucency or echodensity, and ventriculomegaly were all strongly associated with an increased risk of CP. MgSO4 administration did not affect the risk of cranial ultrasound abnormality observed at 35 weeks postmenstrual age or later. However, for the 82% of infants born at <32 weeks gestation, MgSO4 was associated with a reduction in risk of echolucency or echodensity. The reduction in risk for echolucency explained 21% of the effect of MgSO4 on CP (P = .04), and for echodensity explained 20% of the effect (P = .02). CONCLUSIONS:MgSO4 given prior to preterm delivery was associated with decreased risk of developing echodensities and echolucencies at <32 weeks gestation. However, this effect can only partially explain the effect of MgSO4 on CP at 2 years of age. TRIAL REGISTRATION:ClinicalTrials.gov: NCT00014989.
| S-EPMC4587284 | biostudies-literature
Project description:BackgroundResearch suggests that fetal exposure to magnesium sulfate before preterm birth might reduce the risk of cerebral palsy.MethodsIn this multicenter, placebo-controlled, double-blind trial, we randomly assigned women at imminent risk for delivery between 24 and 31 weeks of gestation to receive magnesium sulfate, administered intravenously as a 6-g bolus followed by a constant infusion of 2 g per hour, or matching placebo. The primary outcome was the composite of stillbirth or infant death by 1 year of corrected age or moderate or severe cerebral palsy at or beyond 2 years of corrected age.ResultsA total of 2241 women underwent randomization. The baseline characteristics were similar in the two groups. Follow-up was achieved for 95.6% of the children. The rate of the primary outcome was not significantly different in the magnesium sulfate group and the placebo group (11.3% and 11.7%, respectively; relative risk, 0.97; 95% confidence interval [CI], 0.77 to 1.23). However, in a prespecified secondary analysis, moderate or severe cerebral palsy occurred significantly less frequently in the magnesium sulfate group (1.9% vs. 3.5%; relative risk, 0.55; 95% CI, 0.32 to 0.95). The risk of death did not differ significantly between the groups (9.5% vs. 8.5%; relative risk, 1.12; 95% CI, 0.85 to 1.47). No woman had a life-threatening event.ConclusionsFetal exposure to magnesium sulfate before anticipated early preterm delivery did not reduce the combined risk of moderate or severe cerebral palsy or death, although the rate of cerebral palsy was reduced among survivors. (ClinicalTrials.gov number, NCT00014989.)
| S-EPMC2803083 | biostudies-literature
Project description:ObjectivesTo investigate known and suggested risk factors associated with cerebral palsy in a Swedish birth cohort, stratified by gestational age.SettingInformation on all births between 1995 and 2014 in Skåne, the southernmost region in Sweden, was extracted from the national birth register.ParticipantsThe cohort comprised a total of 215 217 children. Information on confirmed cerebral palsy and subtype was collected from the national quality register for cerebral palsy (Cerebral Palsy Follow-up Surveillance Programme).Primary and secondary outcome measuresWe calculated the prevalence of risk factors suggested to be associated with cerebral palsy and used logistic regression models to investigate the associations between potential risk factors and cerebral palsy. All analyses were stratified by gestational age; term (≥37 weeks), moderately or late preterm (32-36 weeks) and very preterm (<32 weeks).ResultsIn all, 381 (0.2 %) children were assigned a cerebral palsy diagnosis. Among term children, maternal preobesity/obesity, small for gestational age, malformations, induction, elective and emergency caesarian section, Apgar <7 at 5 min and admission to neonatal care were significantly associated with cerebral palsy (all p values<0.05). Among children born moderately or late preterm, small for gestational age, malformations, elective and emergency caesarian section and admission to neonatal care were all associated with cerebral palsy (all p values <0.05), whereas among children born very preterm no factors were significantly associated with the outcome (all p values>0.05).ConclusionOur results support and strengthen previous findings on factors associated with cerebral palsy. The complete lack of significant associations among children born very preterm probably depends on to the small number of children with cerebral palsy in this group.
| S-EPMC7418660 | biostudies-literature
Project description:The Beneficial Effects of Antenatal Magnesium clinical trial was conducted between 1997 and 2007, and demonstrated a significant reduction in cerebral palsy (CP) in preterm infants who were exposed to peripartum magnesium sulfate (MgSO4). However, the mechanism by which MgSO4 confers neuroprotection remains incompletely understood. Cord blood samples from this study were interrogated during an era when next-generation sequencing was not widely accessible and few gene expression differences or biomarkers were identified between treatment groups. Our goal was to use bulk RNA deep sequencing to identify differentially expressed genes comparing the following four groups: newborns who ultimately developed CP treated with MgSO4 or placebo, and controls (newborns who ultimately did not develop CP) treated with MgSO4 or placebo. Those who died after birth were excluded. We found that MgSO4 upregulated expression of SCN5A only in the control group, with no change in gene expression in cord blood of newborns who ultimately developed CP. Regardless of MgSO4 exposure, expression of NPBWR1 and FTO was upregulated in cord blood of newborns who ultimately developed CP compared with controls. These data support that MgSO4 may not exert its neuroprotective effect through changes in gene expression. Moreover, NPBWR1 and FTO may be useful as biomarkers and may suggest new mechanistic pathways to pursue in understanding the pathogenesis of CP. The small number of cases ultimately available for this secondary analysis, with male predominance and mild CP phenotype, is a limitation of the study. In addition, differentially expressed genes were not validated by qRT-PCR.
| S-EPMC9474611 | biostudies-literature
Project description:Objective This study aims to examine the relationship between antenatal magnesium sulfate (MgSO4) and neonatal death and/or severe necrotizing enterocolitis (NEC) among infants < 28 weeks. Methods Secondary analysis of a multicenter randomized trial of antenatal MgSO4 versus placebo administered to women to prevent death and cerebral palsy. Neonates < 28 weeks were included. The primary outcome was neonatal death before NICU discharge, and/or severe NEC (Bell criteria stage II/III). Neonates with and without death/severe NEC were compared. Results A total of 697 neonates met the criteria. Out of which 150 (21.5%) died and/or were diagnosed with severe NEC. Antenatal MgSO4 exposure was not associated with death/severe NEC in infants < 28 weeks. In a subgroup analysis of neonates < 26 weeks, treatment group assignment to antenatal MgSO4 was associated with an increased odds of death/severe NEC (adjusted odds ratio: 1.90, 95% confidence interval: 1.12-3.22, p = 0.017). Conclusions Among neonates < 26 weeks, antenatal MgSO4 was associated with death and severe NEC. Further prospective study in larger populations is needed.
| S-EPMC4816636 | biostudies-other
Project description:The aim of our study was to assess the feasibility of implementing a protocol for the use of magnesium sulfate to prevent cerebral palsy. This retrospective single-center study included all women with fetuses of gestational age <33 weeks of gestation whose birth was planned or expected within 24 hours from September 2011 to December 2012. They were to receive magnesium sulfate, administered intravenously as a 4-g bolus followed by a constant infusion of 1 g per hour. If delivery had not occurred after 12 hours and was no longer considered imminent, the infusion was to be discontinued. The study included 119 women, 81 (68.1%) of whom received magnesium sulfate. Among the latter, 71 (87.5%) gave birth within 24 hours. The reasons treatment was not given were: omission by medical team (19/38, 50%), urgent delivery (18/38, 47.4%), and contraindication to treatment (1/38, 2.6%). The mean gestational age at protocol implementation was 29.6 +/- 2.1 weeks. Maternal monitoring, especially at the onset of infusion, appeared suboptimal. No major maternal side effects were observed. Our study shows that implementing a protocol for prevention of cerebral palsy by magnesium sulfate is feasible in a tertiary obstetric center.
| S-EPMC4586759 | biostudies-literature
Project description:Antenatal brain hypoxia-ischemia, which occurs in cerebral palsy, is considered a significant cause of motor impairments in children. The mechanisms by which antenatal hypoxia-ischemia causes brain injury and motor deficits still need to be elucidated. Tetrahydrobiopterin is an important enzyme cofactor that is necessary to produce neurotransmitters and to maintain the redox status of the brain. A genetic deficiency of this cofactor from mutations of biosynthetic or recycling enzymes is a well-recognized factor in the development of childhood neurological disorders characterized by motor impairments, developmental delay, and encephalopathy. Experimental hypoxia-ischemia causes a decline in the availability of tetrahydrobiopterin in the immature brain. This decline coincides with the loss of brain function, suggesting this occurrence contributes to neuronal dysfunction and motor impairments. One possible mechanism linking tetrahydrobiopterin deficiency, hypoxia-ischemia, and neuronal injury is oxidative injury. Evidence of the central role of the developmental biology of tetrahydrobiopterin in response to hypoxic ischemic brain injury, especially the development of motor deficits, is discussed.
| S-EPMC5554922 | biostudies-other
Project description:We hypothesized that a deficiency in the descending serotonergic input to spinal cord may underlie postnatal muscle hypertonia after global antenatal hypoxic-ischemic injury in a rabbit model of cerebral palsy. Neurotransmitter content was determined by HPLC in the spinal cord of newborns with and without muscle hypertonia after fetal global hypoxic-ischemic brain injury and naïve controls. Contrary to our hypothesis, serotonin levels in both cervical and lumbar expansions and norepinephrine in cervical expansion were increased in hypertonic kits relative to non-hypertonic kits and controls, with unchanged number of serotonergic cells in caudal raphe by stereological count. Serotonergic fiber length per unit of volume was also increased in hypertonic kits' cervical and lumbar spinal cord, both in dorsal and ventral horns. Gene expression of serotonin transporter was increased and 5-HTR2 receptors were decreased in hypertonic kits relative to controls in cervical and lumbar cord. Intrathecal administration of non-selective serotonin receptor inhibitor methysergide decreased muscle tone in hypertonic kits only. Conversely, intrathecal administration of serotonin solution increased muscle tone only in non-hypertonic kits. We speculate that maturation of serotonergic system in spinal cord may be directly affected by decreased corticospinal connectivity after antenatal hypoxic-ischemic brain injury. Following prenatal hypoxia-ischemia, newborn rabbits exhibit elevated levels of serotonin in the spinal cord that were linked to muscle hypertonia. Serotonergic terminal density was also increased in hypertonic newborns' spinal cord. Intrathecal administration of the non-selective serotonin receptor inhibitor methysergide decreased muscle tone in hypertonic newborns only. Elevated spinal serotonin thus suggests a novel pathophysiological mechanism of hypertonia in cerebral palsy.
| S-EPMC4329027 | biostudies-literature
Project description:ObjectiveTo test the primary hypothesis that extremely preterm children antenatally exposed to both magnesium sulfate and antenatal corticosteroids have a lower rate of severe neurodevelopmental impairment or death compared with those exposed to antenatal corticosteroids alone.MethodsThis was a prospective observational study of children born at 22 0/7-26 6/7 weeks of gestation from 2011 to 2014 at Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network hospitals (N=3,093). The primary outcome was severe neurodevelopmental impairment or death at 18-26 months of corrected age follow-up based on exposure to antenatal corticosteroids and magnesium sulfate or antenatal corticosteroids alone. Secondary outcomes included components of severe neurodevelopmental impairment by exposure group and comparisons of severe neurodevelopmental impairment or death between children exposed to both antenatal corticosteroids and magnesium sulfate with those exposed to magnesium sulfate alone or to neither antenatal corticosteroids nor magnesium sulfate. Logistic regression models adjusted for background characteristics.ResultsChildren exposed to both antenatal corticosteroids and magnesium sulfate had a lower rate of severe neurodevelopmental impairment or death (813/2,239, 36.3%) compared with those exposed to antenatal corticosteroids alone (225/508, 44.3%; adjusted odds ratio [aOR] 0.73; 95% CI 0.58-0.91), magnesium sulfate alone (47/89, 53%; aOR 0.49; 95% CI 0.29-0.82), or neither therapy (121/251; 48.2%; aOR 0.66, 95% CI 0.49-0.89). Similarly, children exposed to both antenatal corticosteroids and magnesium sulfate had a lower rate of death compared with either or neither therapy, but the rate of severe neurodevelopmental impairment among survivors did not differ between exposure groups.ConclusionIn children born between 22 0/7 and 26 6/7 weeks of gestation, exposure to both antenatal corticosteroids and magnesium sulfate was associated with lower rates of severe neurodevelopmental impairment or death and death compared with exposure to antenatal corticosteroids alone.Clinical trial registrationClinicalTrials.gov, NCT00063063.
| S-EPMC7278037 | biostudies-literature
Project description:ObjectiveGenes associated with cardiovascular disease may also be risk factors for congenital cerebral palsy (CP) and these associations may be modified by sex, since there is an increased risk of CP in male children. We investigated the association between CP of the child with cardiovascular disease in parents, taking sex of the child into consideration.MethodsAll parents of non-adopted singletons born in Denmark between 1973 and 2003 were included. Parents of a child with CP, confirmed by the Danish National CP registry, were considered exposed. Cox proportional hazards regressions were used to model risk of cardiovascular outcomes for exposed parents compared to all other parents beginning at the child's 10(th) birthday.ResultsWe identified 733,730 mothers and 666,652 fathers among whom 1,592 and 1,484, respectively, had a child with CP. The mean age for mothers at end of follow up was 50 ± 8 years. After adjustment for maternal age, parental education, child's sex, child's residence, child being small for gestational age and maternal hypertensive disorder during pregnancy, mothers of CP male children had an excess risk of cardiovascular disease (HR: 1.52, 95% CI: 1.16-2.00), attributable mostly to an increased incidence of hypertension and cerebrovascular disease. After additional adjustment for preterm birth, the association was markedly attenuated for cardiovascular disease (1.34, 95%CI: 1.02 - 1.76), became nonsignificant for hypertension, but remained significant for cerebrovascular disease (HR: 2.73, 95% CI: 1.45- 5.12). There was no increased risk of cardiovascular events in mothers of female CP children, or fathers of CP children of any sex.ConclusionsWomen that have a male child with CP are at increased risk for premature cardiovascular disease. Part of this association may be related to risk factors for preterm births.
| S-EPMC3815096 | biostudies-literature