PEDIATRICS Vol. 119 No. 3 March 2007, pp. e554-e561 (doi:10.1542/peds.2006-1308)
ARTICLE |
Postterm Delivery and Risk for Epilepsy in Childhood
a Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts
b Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark
c Departments of Paediatrics
d Gynaecology and Obstetrics, Aalborg Hospital, Aalborg, Denmark
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONCONCLUSIONREFERENCES |
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OBJECTIVE. Postterm delivery is a risk factor for perinatal complications, some of which increase risk for neurologic morbidity. We aimed to examine the association between postterm delivery and risk for epilepsy in childhood.
METHODS. We conducted a cohort study of singleton children who were born in 3 Danish counties from 1980 to 2001. Birth registry data were linked with hospital records to identify cases of epilepsy in the first 12 years of life. We included children who were born at 
39 gestational weeks and computed crude, age-specific, and birth weight standardized incidence rates of epilepsy. We estimated adjusted incidence rate ratios according to mode of delivery by Poisson regression.
RESULTS. Among the 277435 nonpreterm births, 32557 were at 42 weeks, including 3396 at 43 weeks. Nearly one fourth of the 2805 epilepsy cases occurred in the first year of life. In that period, birth weight standardized incidence rate ratios for epilepsy were 1.3 for birth at 42 weeks and 2.0 for birth at 43 weeks, compared with birth at 39 to 41 weeks. Among children who were delivered by cesarean section, incidence rate ratios adjusted for birth weight, presentation, malformations, and county were 1.4 for birth at 42 completed weeks and 4.9 for birth at 43 weeks, compared with term vaginal births. There was a similar tendency among children who were delivered with the assistance of instruments. We found no evidence for the association between postterm delivery and risk for epilepsy beyond the first year of life.
CONCLUSIONS. Prolonged gestation is a risk factor for early epilepsy; the added increase in risk for instrument-assisted and cesarean deliveries could be attributable to factors that are related to both birth complications and epilepsy.
Key Words: epidemiology • postterm delivery • epilepsy • prolonged pregnancy • child
Abbreviations: LMP—last menstrual period • CNS—central nervous system • ICD—International Classification of Diseases • CI—confidence interval • IRR—incidence rate ratio
Postterm delivery, defined as delivery at or after 42 completed weeks (294 days) after the first day of the last menstrual period1 (LMP), occurs with a reported prevalence of 2% to 14% of deliveries.2 (Other terms, such as "postdate," and "postmature," and "dysmature" sometimes have been used interchangeably with "postterm," but "postterm" currently is preferred.2) Predictors of postterm delivery include anencephaly, hormonal disturbances, nulliparity, young maternal age, and history of prolonged pregnancy.3,4 The biological mechanisms that lead to postterm delivery are poorly understood and remain "a challenge for epidemiologic research."2
Children who are born postterm have higher perinatal mortality than term children.5–10 Population-based studies in Denmark6 and Sweden7 report a 25% increase in risks for stillbirth and neonatal death in infants who are born after 42 weeks of gestation, with mortality increase being even greater when postterm infants are growth restricted,7,8,11 malformed,7 or first born.10
The risks for labor complications, including induction, instrument or cesarean delivery,2,3,6,12 and macrosomia,2,3,6 all are increased after a prolonged pregnancy. For the newborn, there is a greater risk for a low Apgar score,6,13 distress,5,14 deteriorating cardiac function,15 meconium aspiration,2,6,7 asphyxia,6 infection,3,6 and NICU admission.2,3 Reported neurologic complications include peripheral nerve paralysis,6 trauma of central nervous system (CNS),6 and convulsions.6,7 Previously, we13 and others16 found an association between depressed Apgar score and risk for childhood epilepsy; we noted that postterm delivery exacerbated the increase in risk.
Most studies of postterm delivery have focused on perinatal outcomes.3,6–8 Few studies have addressed long-term neurologic morbidity,17,18 and, to our knowledge, no formal epidemiologic study has examined the association between postterm delivery and risk for childhood epilepsy. Epilepsy is the most common serious neurologic disorder, with a heterogeneous and poorly understood etiology. The perinatal period is thought to play an important role in causing some cases of the disease.19,20 We examined the association between postterm delivery and the risk for epilepsy during the first 12 years of life.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONREFERENCES |
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We used electronic medical databases to conduct a cohort study within the Danish counties of Aarhus, North Jutland, and Viborg. From the Danish National Birth Registry,21,22 we retrieved records of all live singleton births that occurred between January 1, 1980, and December 31, 2001. In Denmark, nearly all children with epilepsy are hospitalized. To identify cases of epilepsy, we used computerized local hospital discharge registries, which record, for each hospital admission, up to 20 discharge diagnoses and, starting in 1994, also contain data on outpatient and emergency visits. The discharge diagnoses were coded according to the International Classification of Diseases, Eighth Revision (ICD-8) through the end of 1993 and according to the ICD-10 thereafter. The codes for epilepsy were 345.xx in ICD-8 and G40.0 to G41.9 in ICD-10. Clinically, epilepsy is diagnosed according to the International League Against Epilepsy guidelines, which define epilepsy as either
2 unprovoked seizure episodes, relevant electroencephalography findings, or both.23 We defined the outcome of epilepsy as the first-time hospitalization or outpatient visit recorded in the hospital discharge registry with a diagnosis of epilepsy within the first 12 years of life. The date of diagnosis was considered to be the date of epilepsy onset. Data on emigration and death were retrieved from the Danish Civil Registration System, which after being created in 1968, covers the entire Danish population and is updated daily.24,25 We linked records from the different registries by the civil registration number, which is a unique administrative identifier that is assigned at birth to Danish residents.
In the birth registry, gestational age was recorded in completed weeks through 1996 and in fractional weeks (based on days) thereafter. We defined postterm delivery, according to the World Health Organization guidelines, as delivery at 42 completed weeks of gestation.1 We calculated incidence rates of epilepsy and 95% confidence intervals (CI) by gestational age. For the main analysis, we included nonpreterm (39 weeks) births and computed crude and birth weight standardized incidence rates of epilepsy (using the person-time distribution in 500-g birth weight categories of the study cohort as the standard). We then calculated incidence rates of epilepsy in categories of completed gestational weeks (39-41, 42, and 43) according to the recorded age of onset. Within each gestational age category, we used Poisson regression26 to obtain fitted values of age-specific incidence rates, with age in completed years, age squared, and the square root of age as predictors. We created an indicator variable for each combination of mode of delivery (unassisted vaginal, forceps/vacuum-assisted, and cesarean) and gestational age category and used them in a Poisson model to examine variation of the gestational age-epilepsy incidence rate ratio (IRR) by mode of delivery.
Because idiopathic epilepsies tend to have genetic determinants and therefore may be unrelated to prolonged gestation,19,20,27 we did a subanalysis restricting the case definition to epilepsy cases that were not listed as idiopathic (censored when ICD-10 codes were G40.0 or G40.3). We did this subanalysis in the cohort of children who were born in 1994-2001, because their diagnoses were recorded using the ICD-10, in which idiopathic epilepsies are listed specifically.
There was little confounding by any of the variables that were available for analysis. For the adjusted analyses, we retained fetal presentation as a potential risk factor for neurologic morbidity, county of birth as a marker for coding practices, and an indicator for birth defects diagnosed at birth because having such a birth defect was a strong predictor of epilepsy in our data and affected the magnitude and the precision of IRR estimates for forceps-assisted deliveries. (In addition, a recent study found maternal use of antiepileptic medication to be a risk factor for birth defects, making the latter a correlate of maternal epilepsy.28) Birth weight may be a correlate of traits that causally link prolonged gestation and risk for epilepsy (eg, malnutrition in overly small infants, trauma as a result of large size in overly heavy infants), which is an argument against using birth weight for adjustment in this analysis. Removing birth weight from any of the analyses had little effect on the results. We retained birth weight for the standardization and adjustment, because it may be a marker of antenatal hormonal or metabolic perturbations that may affect both the size and the susceptibility to disease.29 Variables for infant's gender and birth order; confidence of the LMP; and mother's age, smoking, and cohabiting with the partner were not used in the final analytic models because in these data they were not associated with epilepsy risk and their inclusion did not change the results. We analyzed the data with SAS 9.01 software (SAS Institute, Cary, NC) and used Episheet30 to calculate standardized estimates.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONREFERENCES |
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During the study period, 338633 single live births were recorded in the 3 counties. We excluded 336 (0.1%) records with missing gestational age. Among the remainder, 277435 (82%) births occurred at 39 completed weeks of gestation or later. Of these, 32557 (12%) infants were delivered postterm, including 3396 (1%) delivered at 43 weeks or later.
Compared with term newborns, postterm infants were less likely to weigh 
2500 g and more likely weigh >4000 g, to undergo cesarean or instrument delivery, to be first born, or to have a 5-minute Apgar score <7. Compared with mothers who delivered at term, mothers who delivered postterm were somewhat more likely to cohabit with a partner and less likely to have smoked during pregnancy (Table 1).
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Across the full range of gestational age, the crude incidence rate of epilepsy decreased with increasing gestational age through week 41, after which it increased again, although the precision of estimates was low at both extremes of gestational age distribution (Fig 1). Overall, 2805 epilepsy cases were recorded among the members of the cohort during the follow-up period. Regardless of gestational age, incidence rates of epilepsy were the greatest in the first year of life, with 657 (23%) of the cases recorded with the onset during this period (Table 2; Fig 2). In year 2 after birth, there were 357 (13%) cases; in year 3, there were 283 (10%); in year 4, there were 240 (8%); in year 5, there were 197 (7%); in year 6, there were 204 (7%); in year 7, there were 170 (6%); in year 8, there were 163 (6%); in year 9, there were 157 (6%), in year 10, there were 158 (6%); in year 11, there were 117 (4%); and in year 12, there were 102 (4%). The first year of life was the period when the differences in the epilepsy rates according to gestational age were most pronounced (Fig 2). We therefore focused subsequent analysis on epilepsy that occurred before age 1.
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Of the epilepsy cases with the recorded onset during the first year of life, the proportion of girls with the diagnosis was
48% regardless of gestational age at birth. Table 3 shows crude and birth weight standardized incidence rates and rate ratios. The standardized IRR was 1.3 (95% CI: 1.0–1.7) for 42 completed weeks of gestation and 2.0 (95% CI: 1.2–3.5) for gestation of 43 weeks or longer.
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The magnitude of the IRR varied according to delivery mode (Table 4). For children who were delivered vaginally without help of vacuum or forceps, postterm gestation of any length was associated with 1.3-fold increase in epilepsy risk in the first year of life. Among children who were born by cesarean section, delivery at 42 weeks was not related to an increase in risk beyond that associated with cesarean section itself, but delivery at 43 weeks or later was associated with a 3.5-fold increase in risk compared with term cesarean births and a nearly fivefold increase in risk compared with term unassisted vaginal births. For vacuum- or forceps-assisted deliveries, our point estimates showed a dose–response pattern, with longer postterm gestation conferring greater epilepsy risk. When mode of delivery was added as a covariate to the other variables that were used in the adjusted analysis, adjusted IRR was 1.3 (95% CI: 1.0–1.6) for birth at 42 weeks and 1.9 (95% CI: 1.1–3.1) for birth at 43 weeks onward. In this analysis, adjusted IRR were 1.4 (95% CI: 1.0–1.8) for cesarean delivery and 1.1 (95% CI: 0.8–1.4) for vacuum/forceps-assisted delivery, compared with unassisted vaginal delivery.
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Of the 202 epilepsy cases recorded in the first year of life among children who were born in 1994–2001, 36 (18%) were recorded as idiopathic. Rates of epilepsy excluding these cases (per 10 000) were 15 (95% CI: 12–17) for children who were born during weeks 39 to 41 of gestation and 23 (95% CI: 15–33) for children who were born at 42 weeks or later; crude rate ratio was 1.6 (95% CI: 1.0–2.3). An analysis of a "low-risk" subgroup (restricted to children with optimal birth weight for gestational age [between 10th and 90th percentiles], no malformation at birth, Apgar score >6 at 5 minutes, and vaginal delivery in cephalic presentation without assistance of forceps or vacuum) yielded IRR of 1.4 (95% CI: 0.9–1.9) for delivery at 42 completed weeks and 1.7 (95% CI: 0.6–3.7) for delivery at 43 weeks or later.
We were able to access data on labor induction for the small subset of the most recent (1997–2001) births in our study cohort. Restricting this subcohort to vaginal deliveries, we calculated incidence rates of epilepsy in the first year of life, according to labor induction and postterm delivery (Table 5). Although all of the CIs overlap and the data are sparse, the point estimates suggest that the effect of prolonged gestation on the risk for epilepsy may be more pronounced in the absence of labor induction.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONREFERENCES |
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In this large, population-based cohort study, we found delivery at
42 weeks of gestation to be associated with an increased risk for epilepsy in the first year of life. The magnitude of the risk increase depended on the duration of prolonged gestation. Little evidence for an association in subsequent years lends support to the conjecture that perinatal causes and postterm delivery in particular play a greater role in determining early-life neurologic susceptibility. During the first year of life 42 (6%) of 657 children with epilepsy also had a diagnosis of cerebral palsy: 36 among term infants (incidence: 1.5 in 10 000) and 6 among infants who were born at 42 completed weeks (incidence: 2.0 in 10 000). These findings suggest that prolonged gestation may be a risk factor for other neurologic disability.
The overall prevalence of postterm deliveries did not change substantially with the year of birth in our cohort, but the prevalence of deliveries at 43 weeks or more decreased from 2% in the 1980s to <0.5% in 2000–2001. Thus, over time, very late deliveries have accounted for a decreasing proportion of postterm births. This could be caused either by a true decrease of prevalence resulting from more routine labor induction before 43 weeks or by better pregnancy dating. We calculated IRRs for epilepsy in the first year of life in 3 strata of birth year (with comparable prevalence of delivery at 43+ weeks): 1980–1990, 1991–1993, and 1994–2001. The respective periods' IRRs were 1.0 (95% CI: 0.7–1.5), 1.3 (95% CI: 0.8–2.0), and 1.5 (95% CI: 1.0–2.2) for delivery at 42 completed weeks and 1.8 (95% CI: 0.9–3.2), 1.9 (95% CI: 0.5–5.1), and 2.0 (0.3–6.4) for delivery at 43 completed weeks or later. The slight upward trend of the point estimates is consistent with the conjecture of better pregnancy dating, resulting in diminished misclassification of gestational age over time.
Postterm delivery may precipitate or accelerate epilepsy through increasing risk for infectious, hypoxic, or mechanical injury to the developing brain. A potential causal mechanism for the observed association could involve intrauterine exposure to meconium, occurring in up to 30% of postterm births.31 Meconium passage is associated with impaired fetal oxygenation and may increase risk for fetal bacterial invasion, leading to inflammatory brain damage.31,32 Prolonged pregnancy also is associated with up to a 33% decrease in amniotic fluid volume,33,34 which can lead to fetal distress15,34,35 and cause early CNS damage.
Increased likelihood of labor induction and instrument deliveries after prolonged pregnancy,3 coupled with greater fetal size, set the stage for mechanical injuries during labor and delivery. Approximately 24% of deliveries that occur after the 42nd week of gestation in Denmark are induced.6 Induced contractions may be forceful and prolonged, causing extended occlusion of the umbilical cord, reduced oxygenation, and fetal acidosis, all of which may contribute to neurologic damage.36 Labor induction could be a confounder in this study if contraindications for labor induction, such as breech presentation or maternal severe hypertension, also were markers of a fetus's neurologic susceptibility.37 At the same time, the analysis of the recent births with available induction data suggests that, at least for vaginal deliveries, the effect of prolonged gestation on the risk for epilepsy may be more pronounced when the labor is not induced.
In a study of singleton infants who weighed 2500 to 4000 g and were born in cephalic presentation to nulliparous mothers, Towner et al38 found that birth that was assisted by vacuum or forceps, compared with unassisted vaginal birth, was associated with up to a threefold increased risk for cerebral hemorrhage and CNS depression and nearly a twofold increased risk for convulsions; the increase in risk was doubled or tripled when a failed vacuum extraction necessitated the use of forceps (which occurs in 9% to 14% of vacuum-assisted deliveries39). In our cohort, instrument delivery at term alone was associated with only a slight increase in epilepsy risk, as was postterm delivery alone (Table 4). The 2 conditions together, however, were more likely to produce a more substantial increase in risk. This observation also is consistent with the current view that some cases of epilepsy are a result of accumulated CNS insults.19,20 A limitation of our study is the inability to distinguish between emergency and elective cesarean sections and between forceps deliveries with and without attempted vacuum extraction.
Although, until now, no study specifically assessed the association of prolonged gestation with epilepsy risk, large population-based studies in Nordic countries report an association between birth after week 42 and increased incidence of convulsions, which are symptoms of epilepsy.19 A Danish study of 110000 nonpreterm births found an adjusted relative risk for convulsions to be 1.4 (95% CI: 0.90- 2.1),6 and in a Swedish study of >500000 nonpreterm births, the relative risk estimate for convulsions was 1.5 (95% CI: 1.2–2.0).7 These estimates are similar to the birth weight standardized IRRs for epilepsy in our study.
Lack of detailed clinical data is a limitation of our study. For example, because ICD-8, which was used to code diagnoses through 1993, does not have a special code for infantile spasms, it is possible that this common early-life epilepsy type was underascertained for children who were born before 1994. (ICD-10, used from 1994 onward, lists infantile spasms under the heading G40.4, which was included in our case definition.) We noted that more than half of the epilepsy cases in the first year of life received a code of "unspecified" or "other," precluding valid inferences about distribution of epilepsy types on the basis of routine registration data. At the same time, the abbreviated nature of computerized records may be only partially to blame for this drawback. As Korff and Nordli40 noted in their 2006 review, many infants with epilepsy "do not fit in any of the currently used subcategories."
The validity of our results depends on accurate classification of gestational age. Postterm deliveries accounted for 9.1% of all births in our cohort. As reviewed by Shea et al,2 studies that used combined early ultrasonography/LMP dating method place the prevalence of postterm delivery between 4% and 7%. From published tables of a Danish nationwide study, we back-calculated the prevalence of postterm deliveries in 1978–1993 to be 7.6% of all births.6 Reported prevalence depends to a large extent on the definition of postterm (as many as 8 different definitions are cited in studies2). In our data, excluding children who were born with gestational age recorded at exactly 42 weeks reduced the prevalence to 2.3% of all births. We included week 42 in our definition of postterm in accordance with current guidelines. Increased risk for some outcomes has been reported for births as early as week 41 of gestation. The present definition, although undoubtedly subject to misclassification, is a compromise between over- and underascertainment of true postterm deliveries.
Prevalence of postterm delivery also depends on the method of gestational age determination and on variations in menstrual cycle length (the LMP-based gestational age dating assumes a 28-day menstrual cycle1). Midwives in Denmark record gestational age in completed weeks after LMP and, whenever necessary, make corrections after ultrasound examination.41 The use of ultrasound in Denmark increased during our study period.41 Nevertheless, the prevalence of postterm births in our cohort decreased only slightly over time, suggesting that increased use of ultrasound did not affect pregnancy dating profoundly, at least at the upper extreme of gestational age distribution. Although a good general agreement has been reported between LMP- and ultrasound-based gestation estimation,42 misclassification tends to occur at the extremes of the distribution. According to some studies, LMP-based dating tends to overestimate the prevalence of postterm delivery by 9%,43 whereas ultrasound dating, in some cases, may underestimate the relative risk for postterm delivery by >10%.44
Nondifferential misclassification of gestational age would be expected to cause attenuation of relative effects.45 Also, the incidence rate of epilepsy in this study is slightly higher than other reports from developed countries,19 which may reflect overascertainment of epilepsy in electronic discharge records.13 Any errors regarding the ascertainment of epilepsy are likely to be independent of the child's gestational age and therefore also would result in underestimation of the effect. The relative effect could be overestimated if misclassification of febrile seizures as epilepsy were more likely to occur among children who are born postterm. At the same time, children with febrile seizures are more likely to develop some types of epilepsy later in life.46
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CONCLUSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONREFERENCES |
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We offer evidence that prolonged gestation is a risk factor for epilepsy in the first year of life.
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ACKNOWLEDGMENTS |
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This study was funded by the Western Danish Research Forum for Health Sciences. Ms Ehrenstein is supported by the Ruth L. Kirschstein Individual Predoctoral Fellowship from the National Institute of Neurological Disorders and Stroke.
We thank the reviewers for the excellent comments that helped improve this article.
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FOOTNOTES |
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Accepted Sep 20, 2006.
Address correspondence to Vera Ehrenstein, MPH, Department of Clinical Epidemiology, Aarhus University Hospital, Ole Worms Allë 1150, 8000 Arhus C, Denmark. E-mail: verad{at}bu.edu
The authors have indicated they have no financial relationships relevant to this article to disclose.
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