Epilepsy and postpartum depression


Address correspondence to Dr. Katherine Turner, A.O. St. Paolo, Centro Regionale per l’Epilessia, Via A. di Rudinì, 8, 20142 Milan, Italy. E-mail: katherine.turner@ao-sanpaolo.it


Purpose: Postpartum depression occurs in 10–20% of women who have recently given birth, but less than half of cases are recognized. The purpose of this study was to examine whether there was a difference in the rate of postpartum depression between patients with epilepsy and healthy controls, and to determine the relationship between epilepsy and postpartum depression.

Methods: The sample consisted of 55 patients with epilepsy and 55 patients without epilepsy. All patients were recruited at the Regional Epilepsy Center and at the Department of Obstetrics and Gynecology, University of Milan, St. Paolo Hospital (Italy). Every woman was assessed with the Edinburgh Postnatal Depression Scale and a clinical interview to screen for postpartum depression.

Results: We found a statistically significant higher rate of postpartum depression in patients with epilepsy compared with controls (p < 0.05).

Discussion: These findings highlight the importance of screening for postpartum depression; it can improve the recognition of the disorder and can provide adequate treatment and follow-up.

Postpartum depression (PPD), as defined by the World Health Organization (WHO), is similar to the symptomatology in non–postpartum mood episodes and may include psychotic features. Although the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) specifies that the symptoms of PPD must begin within 4 weeks after delivery, many authors believe that women remain at increased risk for PPD for up to 1 year after delivery (DSM-IV-TR, 2000).

PPD affects approximately 10%–20% of women in the first year following delivery (Verkerk et al., 2003). Several investigations reported that up to 50% of all cases go undetected (Hearn et al., 1998; Beck, 2006). This finding emphasizes the need for early diagnosis and treatment of PPD. For this reason, the purpose of the present study was to investigate and analyze the relationship between epilepsy and PPD in depth, because no other study has examined this topic, with the exception of our previous investigation (Turner et al., 2006). We conducted this study to obtain more valid and accurate estimates of PPD in women with epilepsy based on a larger and more representative patient cohort with comprehensive assessment.

More precisely, we decided to verify whether there was a difference in the rate of PPD between women with epilepsy and healthy controls, and to correlate PPD rates with demographic and clinical variables in the epilepsy sample.


All patients and controls gave their written informed consent before the psychological session. The study protocol was approved by the ethics committee of St. Paolo Hospital.

Fifty-five consecutive women with epilepsy, treated at the Regional Epilepsy Centre of St. Paolo Hospital, University of Milan, Italy, were enrolled in the study according to the following inclusion criteria: diagnosis of focal or generalized epilepsy (Commission on Classification and Terminology of the International League Against Epilepsy–ILAE, Engel, 2001); at least 18 years of age; between 5 and 8 weeks of gestation; and an education level equal to or higher than 8 years. Patients receiving medications other than antiepileptic drugs (AEDs) and patients with a psychiatric background were excluded.

Table 1 provides the demographic and clinical characteristics of the patients with epilepsy and controls.

Table 1.   Demographic and clinical characteristics of women with epilepsy
 Epilepsy patients (N = 55)Controls (N = 55)Statistical testp-value
  1. Values are mean ± SD. SD, standard deviation; CBZ, carbamazepine; VPA, valproic acid; PB, phenobarbital; LTG, lamotrigine; TPM, topiramate; CLB, clobazam; DPG, depamag; ESM, ethosuximide; PHT, phenytoin.

  2. Values within parentheses represent percentage.

Age (years)33.0 ± 4.331.8 ± 4.5U = 1,412.50.549
Education (years)12.5 ± 3.113.4 ± 2.9U = 1,275.50.133
Marital status
 Married49 (89)45 (82)U = 1,102.51.000
 With partner6 (11)8 (14)U = 21.000.090
 Divorced02 (4)  
Country of origin Italy55 (100)55 (100)  
Nulliparous37 (67)47 (85)U = 0.7960.526
EPDS score7.6 ± 5.14.0 ± 3.8t = 4.1490.000
Vaginal delivery40 (73)50 (91)U = 1,000.0 1.000
Type of epilepsy
 Generalized epilepsy 25 (45)   
 Focal epilepsy30 (55)   
 Probably symptomatic7 (13)   
 Symptomatic18 (33)   
 Idiopathic30 (54)   
Seizure frequency (monthly)1.4 ± 4.6   
Duration of epilepsy (years)17.4 ± 8.6   
Onset of epilepsy (years)15.6 ± 7.9   
Monotherapy47 (85)   
CBZ22 (47)   
VPA12 (26)   
PB5 (11)   
LTG2 (4)   
TPM2 (4)   
CLB1 (2)   
DPG1 (2)   
ESM1 (2)   
PHT1 (2)   

Fifty-five women without epilepsy were recruited at the Department of Obstetrics and Gynecology. The control group was chosen to match the patients group with respect to age and education. The inclusion criteria for the women without epilepsy were: at least 18 years of age; between 5 and 8 weeks of gestation; and an education level equal to or higher than 8 years. Women receiving medications and those with a psychiatric history were excluded.

A first clinical interview was performed to exclude patients with a psychiatric background.

Five weeks to 8 weeks postpartum all women completed the Edinburgh Postnatal Depression Scale (EPDS) and were assessed with a second clinical interview.


Edinburgh Postnatal Depression Scale (EPDS)

EPDS is a 10-item (scored on a scale of 0–3) self-reported scale assessing the symptoms of PPD. Women were asked to think about how they had felt over the preceding 7 days (Cox et al., 1987). EPDS has been validated in Italy (Benvenuti et al., 1999). In our study, we used a 9/10 cut-off.

Clinical interview

We used a semistructured clinical interview administered by a trained clinician and we included the major axis I and II diagnostic classes (DSM-IV-TR). In the first clinical interview we assessed for DSM IV-TR criteria clinical syndromes and personality disorders of Axis II. The interview comprised past and current medical history and details on drugs taken by the women.

In the second assessment, we evaluated PPD. The diagnosis of PPD was performed by an interviewer using the EPDS score with a 9/10 cut-off and a clinical interview according to the DSM IV-TR.


Statistical analyses were performed using the “Statistical Package for Social Sciences” for Windows (SPSS 13.0, Chicago, IL, U.S.A.).

Data are presented as mean ± SD (standard deviation). Sociodemographic characteristics in women with and without epilepsy were compared with the Mann-Whitney test. EPDS scores were analyzed with the two-tailed Student’s t-test for unpaired samples. A multiple linear regression analysis was performed to determine the interaction between the demographic and clinical variables (age, education, type of epilepsy, duration and age at onset of epilepsy, seizure frequency, etiology, number of AEDs) and the EPDS scores, used as a dependent variable. A stepwise selection procedure was used with the α to enter set at 0.05 and to remove set at 0.10. Significance was set at a p < 0.05.


Fifty-five women with epilepsy had a mean EPDS score of 7.6 ± 5.1, whereas the mean EPDS score in the women without epilepsy was 4.0 ± 3.8 (p < 0.05). PPD was present in 39% of the patients with epilepsy and in 12% of the controls. There were no significant differences in age (p > 0.05), education (p > 0.05), marital status (p > 0.05), or parity (p > 0.05) between the patients with epilepsy and controls. The multiple linear regression analysis performed in women with epilepsy showed that no demographic or clinical variable was associated with PPD score (p > 0.05).

None of our patients with and without epilepsy had premature births, intrauterine growth impairments, operative deliveries, or admissions to neonatal intensive care units. No children of the women with and without epilepsy presented malformations or minor anomalies. AEDs that are implicated in causing depression are phenobarbital (PB), topiramate (TPM), and levetiracetam (LEV). We didn’t find any statistical difference in EPDS scores between patients who were taking AEDs with negative psychotropic effects (TPM and PB, N = 7, 15%) versus women who were treated with AEDs without negative psychotropic properties (p < 0.05).


Our results provided evidence that women with epilepsy had a higher rate of PPD compared to controls (p < 0.05). No demographic and epilepsy-related variables were associated with PPD in our group of women with epilepsy (p > 0.05). The specific etiology of PPD remains unclear (Cooper & Murray, 1998). In the literature, no single causative factor has been identified, but a multifactorial etiology has been suggested. However, many authors have reported the importance of clinical (premature births, intrauterine growth impairment, operative deliveries, admission to neonatal care units), biological (deregulation of neurotransmitters, serotonin, hormonal factors) and psychological variables (stressful life events, marital conflict, and low social support) (O’Hara, 1995; Cooper & Murray, 1997; Segre et al., 2007). Women with a previous history of depression have a 25% risk of recurrent depression after delivery (Dennis, 2005). None of our patients had such a history.

The impact of depression on the epilepsy population is significant, with a reported prevalence rate of up to 50%. Its etiology is complex and it has a multifactorial origin: clinical factors (such as, side of seizure focus, seizure frequency, AEDs, genetic vulnerability, history of depressive disorder) are presented as well as psychological and social factors (social stigmatization, adverse life events, low quality of life, vocational difficulties, socioeconomic problems) (Hermann et al., 2000; Piazzini et al., 2001). In particular, phenomenology of depression in women is still a major debate. The general epidemiologic data consistently reported a greater prevalence of depressive mood disorders in women, about twice that for men in the population without epilepsy (Kohler et al., 1999; Scheibe et al., 2003). However, this difference seems to be less powerful in the population with epilepsy (Kanner, 2003).

There are a number of studies on the pharmacologic and psychological treatment of PPD (Glangeaud-Freudenthal & Boyce, 2003; Ross et al., 2006). Women are often reluctant to take an antidepressant medication because of concern about breast milk transmission during breast-feeding and potential side effects, in particular women with epilepsy, who are already treated with AEDs, although there is some evidence that antidepressant pharmacotherapy is relatively safe for the baby (Misri & Kendrick, 2007). However, many patients benefit from concomitant treatment with both these approaches. PPD demands the same pharmacologic treatment as major depression does.

PPD can be related to adverse cognitive and socioemotional outcome in children. Women with PPD display less affectionate behavior, are less responsive to their infants, and are withdrawn with flatness of affect compared with mothers who are not depressed (Grace et al., 2003; Luoma et al., 2004).

In summary, a strong aspect of the present research is the sample examined: To our knowledge this is only the second work regarding women with epilepsy who have PPD. Our findings offer a starting point for further investigations based on a larger sample, to determine reliably to the link between epilepsy and PPD and to provide professional and qualified support to women who have such symptoms. On the basis of these results, we started a psychoeducation support group to help women with PPD.


We would like to thank all the mothers who generously and enthusiastically participated in the study.

We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

Disclosure: None of the authors has any conflict of interest to disclose.