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. 2026 Sep 28;30(9):e70367. doi: 10.1002/ejp.70367

De Novo Pain in Pregnancy: The Mediating Roles of Depression and Maternal‐Fetal Attachment in De Novo Chronic Pain

Bruna H Micheletti 1, Mariana Tassi 2, Samantha K Millard 3, Duana S Jimenez 2, Mariana M Komatsu 2, Thaís L Matuki 2, Ricardo Iglesio 4, T S Arenholt Louise 5, Peter D C Leutscher 5, Daniel C de Andrade 3,4, Lisandra S Bernardes 2,5,6,7,✉
PMCID: PMC13617512  PMID: 42803132

ABSTRACT

Background

Chronic pain affects up to 30% of pregnant individuals globally and substantially impairs maternal well‐being. The prevalence and contributing factors of de novo chronic pain in pregnancy (DNPAP) remain poorly studied, with previous chronic pain rarely distinguished from newly arising pain. We examined the prevalence and characteristics of DNPAP and its association with foetal and maternal factors, including dysmenorrhea, depressive symptoms and maternal‐foetal attachment.

Methods

This cross‐sectional study included 207 pregnant women between 30 and 34 weeks of gestation. Assessments comprised pain measures (Douleur Neuropathique‐4, McGill Pain Questionnaire, Brief Pain Inventory and Pain Catastrophizing Scale) and maternal well‐being measures (Edinburgh Postnatal Depression Scale, Maternal‐Foetal Attachment Scale and Prenatal Psychosocial Profile). Women with DNPAP were compared with those without chronic pain to identify associated factors.

Results

De novo pain was reported by 20.7% of participants, with 59.6% describing it as moderate to severe. DNPAP was significantly associated with higher depressive symptoms, lower maternal‐foetal attachment and a history of dysmenorrhea. Mediation analyses identified depressive symptoms as a key factor linking foetal malformations and gestational diseases to de novo pain.

Conclusion

Depression, reduced maternal‐foetal attachment and a history of dysmenorrhea were significantly associated with de novo pain during pregnancy. Depressive symptom severity mediated the relationship between foetal malformations or gestational diseases and DNPAP. Clear characterization of pregnancy‐related pain can inform preventive and therapeutic strategies to improve maternal health outcomes.

Significance Statement

This study is the first to report the prevalence of de novo chronic pain during pregnancy, which was found to be high affecting 20.7% of the pregnant women. De novo chronic pain in pregnancy is directly associated with depressive symptoms and is mediated by depressive symptoms in cases involving foetal malformation diagnosis and the presence of gestational diseases. A history of dysmenorrhea is significantly associated with the development of de novo chronic pain in pregnancy, suggesting potential shared underlying mechanisms that open possibilities for testing new early‐detection, therapeutic, and prognostication approaches to pain across women's life‐cycle.

1. Introduction

Chronic pain affects approximately one‐fourth of the general population, with a reported prevalence in 2022 of 20% in the United States (Yong et al. 2022), 18% in developing countries in 2019 (Sá et al. 2019) and a prevalence of 33% reported worldwide in 2015 (Jackson et al. 2015). Chronic pain frequently persists during pregnancy, with tension‐type headache, migraines and non‐specific low back pain being the most common conditions (Casagrande et al. 2015; Sabino and Grauer 2008). For example, dysmenorrhea (pain during the menstrual period and usually presents as cyclic low abdominal cramps, that can radiate to the low back or legs) impacts non‐pregnant women's well‐being and has multifactorial mechanisms, being present in 16%–91% of women in reproductive age (Ju et al. 2014). It is associated with a family history of dysmenorrhea and high levels of stress and is a risk factor for developing general chronic pain (R. Li et al. 2020). It has been hypothesized that women with a history of dysmenorrhea are more susceptible to developing de novo pain when pregnant, but there are no studies showing this association. Indeed, pregnancy is associated with de novo chronic pain, defined as chronic pain arising for the first time during gestation. The true prevalence of de novo pain associated with pregnancy (DNPAP), and its clinical characteristics, contributing factors, and potential consequences remain largely unknown.

The mechanisms underlying chronic pain in pregnancy are multifactorial, involving mechanical, hormonal and psychosocial influences (Sabino and Grauer 2008) and its impact on maternal well‐being is substantial (Elden et al. 2016). Chronic pain during pregnancy can severely impair daily activities such as sitting, standing, walking and even turning in bed, with some women requiring mobility aids (Arnow et al. 2006; Bakker et al. 2013; Lagadec et al. 2018; Vermani et al. 2010). In addition to physical disability, sexual activity, emotional health, and partner relationships may also be compromised. (Ray‐Griffith et al. 2018; Yenişehir et al. 2024).

Mood disorders, particularly depression and anxiety, also intersect with chronic pain. Approximately 10% of pregnant women are affected by major depressive disorder, though underdiagnosis is common (Vigod et al. 2016). Women experiencing chronic pain are significantly more likely to present with mood disorders (Virgara et al. 2018). Furthermore, maternal complications such as gestational diabetes, hypertension, and preeclampsia, as well as the diagnosis of foetal abnormalities, have been linked to increased risk of depression and anxiety during pregnancy (Bansil et al. 2010; Kozhimannil 2009; Kurki 2000; Rona et al. 1998). These psychological and medical comorbidities may contribute to the development or persistence of pain, yet their relationship with DNPAP has not been systematically investigated.

Additionally, chronic pain may affect maternal‐foetal attachment, the emotional bond between mother and foetus, which is crucial for postnatal relationships (McNamara et al. 2019). Untreated pain could potentially disrupt this attachment, which influences maternal mental health and child development (Bergman et al. 2010). Early identification and management of chronic pain may help strengthen this bond and improve maternal psychological outcomes, but research on this topic remains sparse.

Despite the high burden of chronic pain in pregnancy, most studies do not differentiate between pre‐existing chronic pain and DNPAP, limiting the understanding of whether de novo pain has distinct characteristics or risk factors. This knowledge gap hinders the advancement of targeted prevention and management strategies. A better understanding of DNPAP could enable earlier identification of women at risk, support the design of preventive and therapeutic interventions, and mitigate the long‐term consequences of pain chronification.

The aim of this study was to investigate the prevalence of DNPAP, describe its clinical characteristics, examine its association with maternal and foetal condition, and assess its potential relationship with depressive symptoms and maternal‐foetal attachment.

2. Methods

2.1. Study Design

This was a case–control study that evaluated pregnant women who had scheduled consultations at the Hospital das Clínicas of the University of São Paulo, from August 2014 to August 2016.

2.2. Participants

The inclusion criteria consisted of adult women with a singleton pregnancy between the 30th and 34th weeks of gestation who were able to give consent and complete the questionnaires and scales. Patients attending outpatient consultations were invited to participate. After informed consent, participants were asked two questions: During this pregnancy, have you experienced persistent pain for more than 3 months, present most of the time? If yes, did you already have this pain before pregnancy? Women answering ‘yes’ to the first question were classified as having chronic pain. Those who also answered ‘no’ to the second question were classified as having de novo chronic pain in pregnancy (DNPAP). Accordingly, participants were divided into three groups: NP (no pain), DNPAP (de novo pain) and CPBDP (chronic pain before and during pregnancy). All participants completed the Assessment Pack 1 questionnaires (Figure 1). Women with DNPAP and with CPBDP also completed the Assessment Pack 2 questionnaires (Figure 1).

FIGURE 1.

FIGURE 1

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Study Flow Diagram.

Maternal and pregnancy‐related variables were retrieved from hospital records (Table 1).

TABLE 1.

Frequency and mean of the variables compared between the three groups.

De novo pain N = 43 (20.7%) Without pain N = 150 (72.4%) Pain before and during pregnancy N = 14 (6.7%)
With a current partner 36 (83.7%) 125 (83.3%) 13 (92.8%)
First pregnancy 18 (41.9%) 77 (51.3%) 4 (28.6%)
Number of consultations during pregnancy 6.88 ± 2.86 (1–13) 6.95 ± 3.11 (1–25) 7.54 ± 2.30 (4–11)
Physical activity 2 (4.6%) 15 (10%) 2 (14.3%)
Previous abdominal surgery 7 (16.3%) 18 (12%) 2 (14.3%)
Dysmenorrhea 28 (65.1%)** 74 (49.3%) 6 (42.8%)
BMI 26.60 ± 4.82 (18.40–42.20)* 25.20 ± 4.68 (16.60–44.50) 25.90 ± 2.93 (21.90–30.10)
Previous mood disorders 6 (14%) 15 (10%) 3 (21.4%)
Alcohol intake 1 (0.3%) 2 (1.3%) 0 (0%)
Current smoker 2 (4.7%) 7 (4.7%) 1 (7.1%)
Presence of gestational disease 3 (7%) 11 (7.3%) 3 (21.4%)
Fetal malformation 20 (46.5%) 86 (57.3%) 8 (57.1%)
EPDS
Total 10.50 ± 5.17 (2–21)** 8.35 ± 5.25 (0–23) 11.40 ± 7.37 (3–25)
MFAS
Total 83.20 ± 22.20 (27–115)* 89 ± 20.5 (26–116) 83.10 ± 21.90 (42–111)
PPP
Stress 20.60 ± 6.10 (13–43)** 18.10 ± 4.93 (11–34) 22.90 ± 6.34 (15–33)
Companion support 53.70 ± 15.60 (11–66) 56.70 ± 14.20 (11–66) 53 ± 16 (18–66)
Support from other people 54.80 ± 12.10 (21–66) 55.40 ± 12.60 (11–66) 48.80 ± 17.50 (11–66)
Self‐esteem 32.60 ± 5.33 (23–44) 33.70 ± 4.49 (22–44) 32.80 ± 5.97 (20–40)
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Note: The values are presented as mean ± SD, minimum and maximum. *p < 0.2 and **p < 0.05 (comparison between ‘without pain’ and de novo pain groups). Bold indicates the statistical significance of p values.

2.3. Assessment Tools

All patients completed the Assessment Pack 1. It evaluated psychological aspects and included the Edinburgh Postnatal Depression Scale (EPDS), the Maternal‐Foetal Attachment Scale (MFAS), and the Prenatal Psychosocial Profile (PPP).

The EPDS is used to screen for depression during pregnancy and postpartum. In the questionnaire, the patient responds to each of the 10 statements on a scale from 0 to 3. The total score is the sum of all responses, ranging from 0 to 30. Higher scores indicate a greater risk of depression (Cox et al. 1987; Matijasevich et al. 2014).

The MFAS is used to quantify maternal attachment to the foetus. The scale consists of 24 items, with responses provided on a likert scale ranging from ‘always’ to ‘never’ with responses scored from 5 to 1, respectively. The total score ranges from 25 to 125. Higher scores indicate a stronger attachment between the mother and foetus (Baldisserotto and Theme Filha 2023; Cranley 1981).

The PPP consists of four categories of likert‐scale questions designed to objectively measure perceived stress, partner support, support from others and self‐esteem. Higher scores indicate a greater level of each category (Curry et al. 1994, 1998; Weissheimer and Mamede 2015).

Patients with chronic pain (Groups DNPAP and CPBDP) completed Assessment Pack 2, which included questionnaires on the presence of chronic pain according to the International Association for the Study of Pain definitions, pain location, and characteristics, such as the Douleur Neuropathique‐4 (DN4), the short form of the McGill Pain Questionnaire (sf‐MPQ), the Brief Pain Inventory (BPI) and the Pain Catastrophizing Scale (PCS).

The DN‐4 questionnaire is a screening tool for neuropathic pain based in a brief physical examination and on the presence of specific pain descriptors (Bouhassira et al. 2005; Santos et al. 2010; Truini et al. 2023). It is composed of 10 items, including 7 symptoms and 3 sensorial tests; a score of 4 or higher indicates a likely neuropathic pain.

The sf‐MPQ is a multidimensional instrument comprising 15 descriptors (8 sensory, 5 affective and 2 evaluative), used to evaluate the different qualities of pain. Each descriptor is marked by the patient as present or absent, and sensory, affective, evaluative and total scores are obtained by counting the descriptors chosen (Ferreira et al. 2013; Melzack 1987).

The BPI is a questionnaire divided in two parts: Pain Intensity Index (PII) and Pain Interference in Daily Activities (PIDA). These two categories are evaluated on a rate of 0 to 10, considering the last 24 h. The result is calculated by the mean. It also evaluates the pain location, treatments and use of pain relief medications (Cleeland and Ryan 1994; Ferreira et al. 2011). For descriptive visualization, the BPI body diagram was transposed onto a standardized schematic mannequin divided into predefined anatomical regions. To facilitate visualization of the relative distribution of pain locations, the regional frequencies were standardized as z‐scores across all mapped regions and indicated through shading intensity in a figure.

The PCS evaluates catastrophism, which represents the suffering caused by the pain and the excessive attention that the patient draws into this symptom. Each item of the questionnaire is evaluated in a rate varying from 0 (never) to 4 (always). The scale comprises 13 items, yielding a total score ranging from 0 to 52. Results are divided into a total score, a rumination score, a magnification score and a helplessness score, and higher scores indicate a higher level of catastrophizing (Sehn et al. 2012; Sullivan et al. 1995).

2.4. Ethics

The study was approved by the ethics review board of University of de São Paulo (USP), − CAAE 26298614.0.0000.0068. All patients were informed about the objectives and method of the study, as well as its risks. Confidentiality about the collected information was guaranteed and participants provided both oral and written consent to participate.

2.5. Statistical Analysis

Quantitative variables were described using mean and standard deviation (SD), while qualitative variables were represented as frequencies (%). Baseline characteristics were analysed across the three patient groups. Pain location, prevalence and characteristics, as assessed by pain questionnaires, were described and compared between Groups DNPAP and CPBDP. Variables associated with de novo pain were investigated by comparing descriptive variables between Groups NP and DNPAP.

Univariable logistic regression analysis was used for initial screening of candidate predictors associated with the occurrence of de novo chronic pain. Variables with significant associations with DNPAP at p < 0.2 were selected for bivariate analysis and multivariable logistic regression. To provide unadjusted effect‐size estimates, bivariate association analysis was performed between DNPAP status and the predictor variables. Point‐biserial correlation coefficients were calculated for continuous variables, and phi coefficients were calculated for binary variables. Collinearity among candidate predictors was assessed using Pearson correlations and variance inflation factors. Variables with conceptual overlap and higher correlation were evaluated for model parsimony, and the final model retained predictors with stronger association with DNPAP for clearer clinical interpretability.

A multivariable generalized linear model with a binomial distribution was then employed to assess the impact of each variable on de novo pain. Statistical significance was set at p < 0.05. Additionally, correlations between the Maternal‐Foetal Attachment (MFAS) score, Edinburgh Postnatal Depression Scale (EPDS) score, and various components of the Prenatal Psychosocial Profile (PPP) score were examined, considering potential relationships among variables such as stress and depression.

2.6. Mediation Analysis

After univariate analysis, several exploratory mediation analyses were conducted to assess whether depression and attachment could mediate the association between dysmenorrhea, foetal malformation, or gestational diseases and de novo chronic pain. These models were guided by the findings identified during the primary analysis and are therefore exploratory in nature. Linear regression assumptions were met, and mediation was assessed using indirect effects (total indirect, depression‐only and attachment‐only), direct effects and total effects. Effect sizes and significance were determined using bootstrapped β‐coefficients and 95% confidence intervals (1000 samples). Mediation analysis was conducted in R (version 4.4.0) using PROCESS (version 4.3.1), Model 4 (Hayes 2022). These models were interpreted as exploratory statistical indirect‐effect models rather than evidence of causal mediation.

3. Results

A total of 210 women were screened and met the inclusion criteria (Figure 1). Off these, 3 declined participations due to personal time constraints, resulting in 207 women being enrolled in the study. Forty‐three women (20.77%) described de novo chronic pain in pregnancy and fourteen women (6.76%) chronic pain during pregnancy that was already present before pregnancy.

3.1. Pain Descriptors in Patients With Pain During Pregnancy

Table 2 presents the prevalence of pain, as well as the results of the DN4, PCS, MPQ and BPI pain questionnaires in patients that reported chronic pain during pregnancy.

TABLE 2.

Pain measures compared between the groups de novo pain, pain before and during pregnancy, and total patients with pain (de novo pain and pain before and during pregnancy).

Total patients with pain N = 57 (27.5%) De novo pain N = 43 (20.7%) Pain before and during pregnancy N = 14 (6.7%)
Positive DN‐4 10 (17.5%) 6 (14%) 4 (28.6%)
PCS
Total 27.30 ± 13.60 (1–49) 26 ± 14.40 (1–49) 31.40 ± 10.30 (7–49)
Rumination 11 ± 4.90 (1–21) 10.40 ± 4.96 (1–17) 12.60 ± 4.48 (4–21)
Magnification 6.45 ± 3.78 (0–13) 6.36 ± 3.94 (0–13) 6.71 ± 3.36 (0–12)
Helplessness 13.10 ± 14.90 (0–113) 13.20 ± 17 (0–113) 12.90 ± 5.22 (3–22)
MPQ (descriptors)
Sensory 5.89 ± 2.89 (1–10) 5.86 ± 3.06 (1–10) 6 ± 2.39 (1–10)
Affective 2.45 ± 1.56 (0–5) 2.45 ± 1.60 (0–5) 2.43 ± 1.50 (0–5)
Evaluative 0.946 ± 0.227 (0–1) 0.976 ± 0.154 (0–1) 0.857 ± 0.363 (0–1)
Miscellany 1.86 ± 1.46 (0–4) 1.83 ± 1.46 (0–4) 1.93 ± 1.49 (0–4)
TOTAL 11.10 ± 5.31 (1–20) 11.10 ± 5.66 (1–20) 11.20 ± 4.28 (2–18)
MPQ (pain intensity)
Sensory 13.70 ± 6.45 (1–28) 13.40 ± 6.91 (1–28) 14.40 ± 4.99 (4–23)
Affective 4.30 ± 3.16 (0–11) 4.07 ± 3.04 (0–10) 5 ± 3.53 (0–11)
Evaluative 2.98 ± 2.21 (0–15) 2.69 ± 1.47 (0–6) 3.86 ± 3.57 (0–15)
Miscellany 2.26 ± 4.14 (0–17) 4.43 ± 4.13 (0–14) 4.57 ± 4.35 (0–17)
TOTAL 26.10 ± 13.40 (4–52) 25.20 ± 13.50 (4–47) 28.90 ± 13 (8–52)
BPI—pain intensity index 3.94 ± 2.14 (0–7.75) 3.92 ± 2.11 (0–7.25) 4 ± 2.33 (0.5–7.75)
BIDA—pain interference in daily activities 5.25 ± 2.86 (0–9.86) 5.18 ± 2.71 (0–9.86) 5.46 ± 3.37 (0–9.43)
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The DN4 was positive in 14% of those with DNPAP. Besides that, the intensity of pain, evaluated by MPQ, had a mean of 25.2 and the BPI showed a considerable variation in pain intensity, varying from 0 to 7.25, with a mean of 3.92 in DNPAP.

Figure 2 illustrates the localization of pain of the patients with de novo pain based on the BPI score self‐rated pain drawing on a mannequin. The most affected areas are the pelvic and lumbar regions.

FIGURE 2.

FIGURE 2

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Diagram with pain location and intensity in patients with de novo pain, based on the Brief Pain Inventory.

3.2. Variables Associated With De Novo Pain in Pregnancy

Baseline characteristics are described in Table 1. When comparing patients without pain (NP) to those with de novo pain (DNPAP), univariable analysis showed that the patients with de novo chronic pain in pregnancy had a significant higher prevalence of dysmenorrhea (65.1% vs. 49.3%), this history increased the risk of developing de novo pain in 3.86 times. Patients with DNPAP also showed higher BMI 26.6 kg/m2 (18.4–42.2) vs. 25.2 kg/m2 (16.6–44.5) in patients without pain. The Edinburgh Postnatal Depression Scale (EPDS), Maternal‐Foetal attachment Scale (MFAS) and the stress component of the Prenatal Psychosocial Scale (PPP) also showed statistically significant association with DNPAP.

In the bivariate correlation analyses, DNPAP status was positively associated with PPP stress score (r = 0.191, 95% CI 0.044 to 0.329, p = 0.011) and EPDS total score (r = 0.162, 95% CI 0.016 to 0.300, p = 0.030). History of dysmenorrhea showed a positive but non‐significant association with DNPAP (φ = 0.129, 95% CI −0.017 to 0.270, p = 0.083). (Table 3).

TABLE 3.

Bivariate association analysis between de novo pain status (DNPAP) and candidate predictors.

coef p CI
Dysmenorrhea 0.129 0.083 ‐0.017 0.270
BMI 0.123 0.110 −0.028 0.268
EPDS 0.162 0.030 0.016 0.300
MFA −0.109 0.153 −0.253 0.040
PPP stress score 0.191 0.011 0.044 0.329
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Note: Bold indicates the statistical significance of p values.

Collinearity diagnostics did not indicate problematic multicollinearity among candidate predictors, with variance inflation factors ranging from 1.030 to 1.412. Table 4 presents the Pearson correlations among the psychological variables.

TABLE 4.

Pearson correlations among the psychological variables.

r 95% CI p
PPP stress PPP partner support −0.244 −0.381 to −0.097 0.001
PPP stress PPP support from others −0.132 −0.276 to 0.018 0.085
PPP stress PPP self‐esteem −0.344 −0.469 to −0.205 < 0.001
PPP stress MFAS total −0.156 −0.299 to −0.006 0.042
PPP stress EPDS total 0.492 0.371 to 0.596 < 0.001
PPP partner support PPP support from others 0.406 0.270 to 0.526 < 0.001
PPP partner support PPP self‐esteem 0.209 0.059 to 0.350 0.007
PPP partner support MFAS total 0.032 −0.122 to 0.185 0.684
PPP partner support EPDS total −0.252 −0.388 to −0.105 0.001
PPP support from others PPP self‐esteem 0.164 0.015 to 0.307 0.032
PPP support from others MFAS total −0.054 −0.204 to 0.100 0.493
PPP support from others EPDS total −0.130 −0.274 to 0.021 0.090
PPP self‐esteem MFAS total 0.294 0.149 to 0.426 < 0.001
PPP self‐esteem EPDS total −0.205 −0.343 to −0.058 0.007
MFAS total EPDS total 0.060 −0.089 to 0.206 0.432
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Both the PPP stress score and the EPDS had p < 0.2 in the univariable analysis and were moderately correlated (Pearson r = 0.492, 95% CI 0.371 to 0.596, p < 0.001). Because PPP stress was not associated with DNPAP in the multivariable model, whereas EPDS was, we chose to include only EPDS in the final model. In the multivariable logistic regression model, history of dysmenorrhea (OR = 3.86, 95% CI 1.46–10.24, p = 0.007), higher EPDS total score (OR = 1.11, 95% CI 1.02–1.20, p = 0.011) and lower MFAS total score (OR = 0.97, 95% CI 0.95–1.00, p = 0.019) were associated with de novo chronic pain in pregnancy. BMI was not associated with DNPAP. (Table 5).

TABLE 5.

Multivariable logistic regression model.

coef standard error OR 95% CI for OR p
Dysmenorrhea 1.351 0.497 3.86 1.46 10.24 0.007
BMI 0.071 0.043 1.07 0.99 1.17 0.096
EPDS total 0.105 0.041 1.11 1.02 1.20 0.011
MFA total −0.026 0.011 0.97 0.95 1.00 0.019
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Note: Bold indicates the statistical significance of p values.

3.3. Mediation Analysis

The study of mediation showed that there was no direct effect of the presence of foetal malformations on de novo chronic pain in pregnancy and no indirect effect via attachment. However, depression (b = 0.18, 95% CI: [0.02, 0.49]) significantly mediated the correlation between the presence of foetal malformations and de novo pain (Figure 3A).

FIGURE 3.

FIGURE 3

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(A) Mediation analysis model (n = 187) assessing the total and direct effects of presence of foetal malformations on de novo pain, assessment of indirect effects via depression and attachment. Blue arrows highlight the indirect effects (a and b‐paths), and the orange arrow highlights the direct effect (c'‐path). Coefficients and bootstrapped (1000) lower and upper limit 95% confidence intervals. (B) Mediation analysis model (n = 187) assessing the total and direct effects of presence of gestational disease on de novo pain, assessment of indirect effects via depression and attachment. Blue arrows highlight the indirect effects (a and b‐paths), and the orange arrow highlights the direct effect (c'‐path). Coefficients and bootstrapped (1000) lower and upper limit 95% confidence intervals.

Similarly, there was no direct effect of gestational disease on de novo chronic pain in pregnancy and no indirect effect via attachment. Here too, depressive scores mediated (b = 0.50, 95% CI: [0.11, 1.09]) the correlation between presence of gestational diseases and de novo pain (Figure 3B).

There were no total or direct effects of dysmenorrhea on de novo chronic pain and no indirect effects via depression, attachment, or overall mediation (Figure 4).

FIGURE 4.

FIGURE 4

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Mediation analysis model (n = 187) assessing the total and direct effects of previous presence of dysmenorrhea on de novo pain, with assessment of indirect effects via depression and attachment. Blue arrows highlight the indirect effects (a and b‐paths), and the orange arrow highlights the direct effect (c'‐path). Coefficients and bootstrapped (1000) lower and upper limit 95% confidence intervals.

The only significant effect was the b1 path, indicating that higher depression levels were associated with de novo pain (b = 0.096, 95% CI: [0.03, 0.18]). In summary, the mediation analysis showed that depressive symptoms mediated the impact of both the presence of foetal malformation and gestational diseases in the appearance of de novo chronic pain in pregnancy.

4. Discussion

Here we reported that among the 27.5% of women reporting pain during pregnancy, 75% had de novo pain (DNPAP). To the best of our knowledge, the specific prevalence of DNPAP has not yet been reported. Compared to patients without pain, patients with de novo pain in pregnancy reported a significantly higher frequency of dysmenorrhea before pregnancy (65.1% vs. 49.3%), higher scores on the postnatal depression and lower maternal‐foetal attachment scores.

A history of dysmenorrhea was the most significant predictor of de novo pain during pregnancy, increasing its likelihood by 3.86 times. Previous research has demonstrated a direct correlation between dysmenorrhea and chronic pain in non‐pregnant women, linked to allodynia and central sensitization (Gagnon and Elgendy 2020; Jarrell and Arendt‐Nielsen 2016). Our study is the first to establish the association between dysmenorrhea and de novo pain in pregnancy, supporting the hypothesis that dysmenorrhea may be a marker of vulnerability for developing new pain syndromes, potentially due to higher sensitivity to nociceptive stimulus (Iacovides et al. 2015). This is particularly relevant during pregnancy, a period marked by hormonal and anatomical changes, in which pain is a frequent complaint.

Depression was also correlated with de novo pain, consistent with findings in both non‐pregnant individuals (Bair et al. 2003; Sheng et al. 2017; Zis et al. 2017) and pregnant women (Long et al. 2020). While our findings do not establish causality, depression may contribute to the development of chronic pain in pregnancy. Interventions to treat depression, such as improving social support and promoting healthy habits, have also been shown to prevent chronic pain (Aktas and Calik 2015; Zuckerman et al. 1989). Additional factors, such as binge eating and poor sleep quality, which are linked to psychiatric disorders, have also been implicated in the development of chronic pain (Y. Li et al. 2023). The interaction between dysmenorrhea and depression is noteworthy, as both conditions are associated with emotional suppression and anxiety, further increasing the risk of DNPAP (Payne et al. 2013). Given that depression affects more than 10% of pregnant women and chronic pain affects over 25%, future longitudinal studies should examine the longitudinal development of these associations from early pregnancy, which will provide insights into preventive or early therapeutic measures to lessen their burden.

Although foetal malformations and the presence of other gestational diseases have been linked to higher depression rates, they were not directly associated with de novo chronic pain in our study. This suggests that the psychological response to pregnancy complications may be the primary factor influencing pain, as not all women respond similarly to the diagnosis of high‐risk in pregnancy or foetal malformation. Not only are depressive symptoms more severe in those with de novo pain, but it was also mediated by the impact of both foetal malformations and the presence of gestational diseases on the report of de novo chronic pain during pregnancy. Specifically, foetal malformations and gestational diseases were found to indirectly increase the risk of chronic pain through their association with higher depression levels, which in turn contributed to the onset of pain. This suggests that psychological factors, rather than the physical conditions themselves, play an important role in the appearance of chronic pain in pregnancy.

Maternal‐foetal attachment was negatively correlated with de novo pain, with patients experiencing more intense pain experiencing lower attachment scores. This was the first report on the relationship of maternal‐foetal attachment and chronic pain during pregnancy. Previous research has shown that pain during labour and the use of epidural analgesia are associated with lower maternal attachment (Alhusen 2008; Eitenmüller et al. 2022; Makeen et al. 2022; Smorti, Ponti, Ghinassi, et al. 2020; Smorti, Ponti, Simoncini, et al. 2020) likely due to depression, which is negatively correlated with attachment in general (Alhusen 2008; Eitenmüller et al. 2022; Lindgren 2001; McFarland et al. 2011; Ohara et al. 2018; Pisoni et al. 2014). The emotional state of pregnant women may hinder their attachment to the foetus, as observed in women with hyperemesis gravidarum (McCormack et al. 2011). Future studies should explore the temporal and causal relationships between these variables.

Only 6.7% of participants reported chronic pain prior to pregnancy, yet 35.6% experienced a worsening of pain after pregnancy, indicating that pregnancy may exacerbate pre‐existing pain or precipitate new pain states. The pelvic region was the most affected site, with higher pain intensity than other body regions, consistent with previous literature (Röst et al. 2006; Vermani et al. 2010).

Given our findings, future research should focus on preventing depression, dysmenorrhea, and low maternal‐foetal attachment as potential strategies to mitigate de novo pain during pregnancy. Interventions such as cognitive‐behavioural therapy, mindfulness, and strengthening social support have been shown to effectively prevent depression and improve maternal‐foetal bonding (Gheibi et al. 2020; Lindgren 2001; Ohara et al. 2018; Smorti, Ponti, Ghinassi, et al. 2020; Smorti, Ponti, Simoncini, et al. 2020; Toosi et al. 2017), and they may also reduce dysmenorrhea and pain during pregnancy.

5. Limitations

A limitation of this study is the inherent nature of dysmenorrhea report in cross‐sectional studies, which may introduce recall bias since this condition was experienced months before the assessment, before pregnancy started. Additionally, dysmenorrhea was not quantified by severity, which could provide valuable insights into its relationship with de novo pain. Future studies should investigate the correlation between dysmenorrhea intensity and disability, measured by tools such as The World Health Organization Disability Assessment Schedule (de Arruda et al. 2023), and the development of chronic pain during pregnancy. Again, the cross‐sectional design of our study also limits our ability to establish causal relationships, but it offers valuable insights into the complex interplay between emotional factors, maternal‐foetal attachment and pain in pregnancy. Another limitation is that no formal a priori power calculation was performed. Because the prevalence of DNPAP had not been previously established, the study was exploratory in nature and primarily aimed to estimate prevalence and identify candidate associated factors in a convenience sample of pregnant women. It is possible that the number of women with DNPAP was modest and the study was likely underpowered to detect small associations.

6. Conclusion

One in five women developed new chronic pain developing during pregnancy (de novo chronic pain). Its occurrence was associated with a history of dysmenorrhea, higher depression intensity and lower maternal‐foetal attachment, with a strong mediation of depression on the emergence of chronic pain in pregnancy. These findings highlight the importance of pain history and psychological factors in pregnancy‐related pain. Future research should incorporate these variables into risk screening and preventive strategies to mitigate chronic pain during pregnancy, potentially improving maternal health and reducing the social and economic burden of chronic pain.

Author Contributions

This study was designed by Lisandra Bernardes and Daniel C. de Andrade. Data analysis was performed by Lisandra Bernardes, Daniel C. de Andrade, Bruna Micheletti, Ricardo Iglesio, Mariana Tassi, Samantha Millard, Duana Jimenez, Mariana Komatsu and Thais Matuki. The statistical analysis was made by Samantha Millard, Ricardo Iglesio and Bruna Micheletti. The figures and tables were designed by Bruna Micheletti and Ricardo Iglesio. The results were critically examined by all authors. Bruna Micheletti had a primary role in preparing the manuscript, which was edited by Lisandra Bernardes, Ricardo Iglesio, Daniel C. de Andrade, Peter Leutscher and Louise Arenholt. All authors have read and approved the final version of the manuscript and agree to be accountable for all aspects of the work.

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