Association between Bell's palsy in pregnancy and pre‐eclampsia
+ Author Affiliations
- From the Department of Medicine, Sunnybrook and Women's College Health Science Centre, Toronto, Ontario, Canada
- Received March 6, 2002.
- Revision received March 12, 2002.
Background: Previous published case series have suggested an association between the onset of Bell's palsy in pregnancy and the risk of pre‐eclampsia and gestational hypertension.
Aim: To evaluate the period of onset of Bell's palsy in pregnancy and the associated risk of adverse maternal and perinatal events, including the hypertensive disorders of pregnancy.
Study design: Case series study of consecutive female patients.
Methods: Women presenting with Bell's palsy during pregnancy or the puerperium were identified by a hospital record review at five Canadian centres over 11 years. Information was abstracted about each woman's medical and obstetrical history, period of onset of Bell's palsy, and associated maternal complications, including pre‐eclampsia and gestational hypertension as well as preterm delivery and low infant birth weight (<2500>
Results: Forty‐one patients were identified. Mean onset of Bell's palsy was 35.4 weeks gestation (SD 3.9). Nine (22.0%, 95%CI 10.8–35.7) were also diagnosed with pre‐eclampsia and three (7.3%, 95%CI 1.4–17.1) with gestational hypertension, together (29.3%, 95%CI 16.5–43.9) representing nearly a five‐fold increase over the expected provincial/national average. There were three twin births. The observed rates of Caesarean (43.6%) and preterm (25.6%) delivery, as well as low infant birth weight (22.7%), were also higher than expected, although the rate of congenital anomalies (4.5%) was not.
Conclusions: The onset of Bell's palsy during pregnancy or the puerperium is probably associated with the development of the hypertensive disorders of pregnancy. Pregnant women who develop Bell's palsy should be closely monitored for hypertension or pre‐eclampsia, and managed accordingly.
In 1830, Sir Charles Bell described the association between idiopathic facial palsy (Bell's palsy) and pregnancy.1 The prevalence rate of Bell's palsy in pregnancy is estimated at 45.1 cases per 100 000 women, considerably higher than in the non‐pregnant population.2 In a systematic review, we observed that almost all cases of Bell's palsy were confined to the third trimester of pregnancy and the immediate postpartum period.3 Furthermore, there was a significantly higher rate of gestational hypertension and pre‐eclampsia (22.2%, 95%CI 12.5–36.4) among these cases, more than four times that found in the general obstetrical population.4
A limitation to previously published research into Bell's palsy in pregnancy is the absence of any systematic evaluation of important obstetrical and perinatal outcomes.3 Accordingly, these studies may have been biased toward underreporting of such events. We undertook this multi‐centre retrospective case series study with three principal objectives. First, to evaluate the timing of onset of Bell's palsy in pregnancy; second, to investigate the association between Bell's palsy and the hypertensive disorders of pregnancy; and third, to determine the prevalence of peripartum and perinatal outcomes among women who developed Bell's palsy during or immediately after pregnancy.
We reviewed the hospital charts of women diagnosed with Bell's palsy in pregnancy between 1990 and July 2001. Participants were identified through the Medical Records Departments of five Ontario hospitals: the Hamilton Health Sciences Corporation and St Joseph's Hospital, both in Hamilton; and the Sunnybrook and Women's College Health Sciences Centre, University Health Network, and Mount Sinai Hospitals, all in Toronto. A search for these charts was made using the ICD‐9CM diagnostic codes related to Bell's palsy and any concurrent pregnancy within ±12 months of the diagnosis of Bell's palsy.
From each hospital chart, we abstracted information on maternal demographics, past medical history, maternal complications during the index pregnancy, and mode of delivery. Gestational hypertension was defined as a blood pressure >140/90 mmHg after 20 weeks gestation, and pre‐eclampsia was defined as a blood pressure >140/90 mmHg, with the additional presence of at least 2+ proteinuria on dipstick or >300 mg of proteinuria over a 24‐h period. Abstracted perinatal outcomes included neonatal gestational age at birth, birth weight and the presence of any fetal anomalies detected in utero or at birth. We attempted to corroborate the chart data by contacting each patient by telephone. Perinatal outcomes and delivery information for these women were compared to rates previously described for the province of Ontario or Canada.
Using the current study data, we updated our previous systematic review3 to better estimate the rate of gestational hypertension and pre‐eclampsia among women with Bell's palsy during pregnancy or the puerperium. The rates from all studies were pooled using a random effects model,5 and the presence of significant heterogeneity for the pooled estimate was defined at a p value <0.10 id="xref-ref-6-1" class="xref-bibr" href="http://qjmed.oxfordjournals.org/content/95/6/359.full#ref-6">6
All abstracted data were entered into Microsoft Excel version 5.0c. Calculation of the pooled estimate of pre‐eclampsia and gestational hypertension was done using Meta‐Analyst 0.988.7 Permission to conduct this study was obtained from the Ethics Review Board of each participating medical centre. Permission to contact the women was obtained from their family physicians or obstetricians, and once contacted, each woman provided informed consent before being administered the telephone questionnaire.
From the five hospitals, 41 women were diagnosed with unilateral Bell's palsy between 1990 and July 2001. The hospital charts were successfully reviewed for all 41 cases, and 19 women (46%) also had their information corroborated by telephone interview. For the remaining 22 women, either their telephone number was no longer in service, or written consent to contact them could not be obtained from their family physician or obstetrician.
The pre‐pregnancy characteristics of all 41 participants are listed in Table 1. The mean maternal age was 29.0 years (SD 6.0); the majority were nulliparous (36.6%) and there were three twin pregnancies. Few had a previous history of either chronic (one woman, 2.7%) or gestational hypertension (two women, 5.4%), and none (0%) had been diagnosed with pre‐eclampsia. One had experienced Bell's palsy previously, with a full recovery before the index pregnancy (Table 1).
The mean gestational age at the onset of Bell's palsy in the index pregnancy was 35.4 weeks gestation (SD 3.9). Only one woman (2.4%) presented before 27 weeks gestation, 33 (80.5%) between 27 and 42 weeks, four (9.8%) within the first week postpartum, while for three women (7.3%) the period of onset was not defined.
Nine women (22.0%, 95%CI 10.8–35.7) were diagnosed with pre‐eclampsia and three (7.3%, 95%CI 1.4–17.1) with isolated gestational hypertension. Thus, out of 41 women with Bell's palsy, 12 (29.3%, 95%CI 16.5–43.9) developed a hypertensive disorder, nearly five times the expected rate for Ontario/Canada (Table 2).
The overall mean neonatal birth weight was 3003.3 g (SD 873.8). The corresponding rates of Caesarean delivery (43.6%), preterm birth (25.6%) and low neonatal birth weight (22.7%) were comparably higher than expected (Table 2). Of the two neonates (4.5%) born with a detectable congenital anomaly, one had Down's syndrome and the other lethal fetal hydrops.
Using the current study data, in conjunction with those 11 studies included in our previous systematic review,3 the pooled rate of combined gestational hypertension or pre‐eclampsia was 25.0% (95%CI 8.3–55.2) among 203 women with Bell's palsy in pregnancy or the puerperium.
Of these 41 consecutive women, the majority presented with Bell's palsy during late pregnancy and the puerperium. They had an increased rate of the hypertensive disorders of pregnancy and operative delivery, while their infants experienced higher rates of preterm birth and low birth weight, compared to figures for the general population.
Study strengths and limitations
This study was probably biased by the retrospective collection of data, which was principally from the hospital charts of five large urban obstetrical centres. Since few clinicians were probably aware of the possible association between Bell's palsy and hypertension in pregnancy, it is unlikely that our estimates would have been much inflated by the presence of diagnostic suspicion bias, especially since we used objective definitions for the diagnosis of gestational hypertension and pre‐eclampsia. Although we included consecutive patients, and attempted to corroborate their chart data through telephone interviews, many could not be contacted, so some adverse perinatal events may have been missed or incorrectly recorded. In the absence of a concurrent control group, we had to rely upon national and provincial data to estimate the expected rates of adverse maternal and perinatal outcomes within the five participating centres. Such comparisons cannot account for possible differences between the women studied herein and those previously selected for large epidemiological studies. Finally, the presence of statistical heterogeneity for the pool estimate of pre‐eclampsia and gestational hypertension could be explained by the fact that previous investigators did not systematically assess for these events, or define them using standard criteria.3
Evidence for an association between Bell's palsy and pre‐eclampsia
Our results suggest that the vast majority of women who develop Bell's palsy in pregnancy had no known risk factors before pregnancy, including diabetes mellitus or chronic hypertension. As with previously published data, our findings support the hypothesis of an association between Bell's palsy and pre‐eclampsia.3 First, the observed rate of pre‐eclampsia was approximately five times higher than expected. Second, both disorders appeared late in pregnancy, and very rarely before the second trimester. Third, more women with Bell's palsy developed pre‐eclampsia (22%) than gestational hypertension (7.3%), suggesting that Bell's palsy and pre‐eclampsia may share a common pathway in their manifestation and pathogenesis, as outlined below.
Women in their third trimester of pregnancy may be predisposed to Bell's palsy due to the increase in maternal extracellular fluid volume during this period.12 Other nerve compression syndromes, including carpal tunnel syndrome,13 are also seen more commonly in the latter part of pregnancy.14 An increase in perineural oedema, resulting in facial nerve impingement, may form the underlying basis for facial nerve palsy.15 Pre‐eclampsia often manifests with considerable oedema within both subcutaneous and nervous system tissues,16 probably creating a neuro‐compressive effect. A second possible explanation may be the presence of a hypercoagulable state associated with pre‐eclampsia, resulting in thrombosis of the vasa nervorum, thereby leading to nerve ischemia and paralysis.15 Since the aetiology of Bell's palsy remains unknown, but is probably multifactorial,17 these and other mechanisms may provide insight into the treatment and recovery of ‘idiopathic’ facial palsy in pregnancy.
Clinical and research recommendations
Regardless of its aetiology, the notion that Bell's palsy in pregnancy may be associated with impending pre‐eclampsia cannot be overlooked. For these women, we recommend heightening maternal and fetal surveillance for the remainder of pregnancy. Although our data do not permit us to comment on the recovery of Bell's palsy after delivery, others have observed nearly 100% recovery in women with incomplete palsy, but only a 52% satisfactory outcome in the presence of a complete facial paralysis.18 Thus, research is needed to better characterize the association between Bell's palsy and pre‐eclampsia, and the relative rate of recovery of facial palsy in such cases. Investigators might also consider whether certain drugs used in the treatment of pre‐eclampsia (e.g. magnesium sulphate) can worsen the recovery of Bell's palsy,19 as well as the benefit of other therapies, including corticosteroids.20
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