Association between maternal migraine and infantile colic: a narrative review

Abstract

Background

Infantile colic (IC) is a common and distressing condition characterized by excessive crying and fussiness in otherwise healthy infants, typically resolving by three to four months of age. The etiology of IC remains poorly understood, but shared mechanisms with maternal migraine, such as genetic predisposition, sensory hypersensitivity, and gastrointestinal dysregulation, suggest a potential association. This narrative review aims to explore the relationship between maternal migraine and IC, summarizing current evidence and potential underlying mechanisms.

Methods

A comprehensive search was conducted in electronic databases, including PubMed, Scopus, Web of Science, and Google Scholar, from 2010 up to August 22, 2024. Studies were included if they investigated the association between maternal migraine and IC, included human participants, and were published in English. Case-control and cross-sectional studies providing original data were narratively analyzed. Data extraction focused on study characteristics, maternal migraine and IC definitions, and key findings.

Results

Out of 792 screened studies, 8 met the inclusion criteria, including 5 case-control and 3 cross-sectional studies. Most studies demonstrated a significant association between maternal migraine and IC, with maternal migraine increasing the likelihood of IC by 2.6 to 5 times. Proposed mechanisms include dysregulation of the trigeminovascular system, sensory hypersensitivity, disrupted sleep-wake cycles, and shared genetic predisposition. Evidence for paternal migraine’s role in IC was inconsistent, with most studies reporting no significant association.

Conclusions

The findings suggest a strong and consistent association between maternal migraine and IC, potentially driven by shared genetic, neurological, and environmental factors. IC may represent an early-life manifestation of migraine-related syndromes. However, variability in study designs and methodologies limits the generalizability of these findings. Future longitudinal and mechanistic studies are needed to clarify the pathways linking maternal migraine to IC and to explore potential interventions for at-risk infants.

Introduction

Infantile colic, characterized by excessive crying and fussiness in otherwise healthy infants, is a common condition that affects up to 20% of infants during the first three months of life. This abdominal discomfort is presented with excessive high-pitch crying, irritability, and fussiness behaviour accompanied by clenched fists, drawn-up legs, and a red face because of an unknown cause. Symptoms usually resolve after three to four months of age [1–3]. There are so many definitions for colic but the most widely used one states colic as excessive crying that lasts more than three hours a day for more than three days a week for more than three weeks [4]. Despite its self-limiting nature, infantile colic can be highly distressing for caregivers and is often associated with significant parental stress, anxiety, and fatigue. Although the cause of colic is unknown, perhaps there is a relationship between the mode of feeding, neurodevelopmental, gastrointestinal, and psychosocial factors, and IC [5].

IC can have short and long-term outcomes. In a short time, it can cause early cessation of breastfeeding, and family anxiety and can be associated with severe outcomes like child abuse or shaken baby syndrome​ [5–9].​ In a long time, IC might lead to behavioral problems during childhood or adolescence, lower IQ scores, hyperactivity, and also sleeping. In addition, IC can lead to functional gastrointestinal disorders (FGIDS) during childhood or adolescence, it can increase the prevalence of childhood migraine, allergic rhinitis, asthma, atopic eczema, and food allergy [10–15].

Maternal health and its influence on infant outcomes have been the subject of increasing scientific interest [3]. Among maternal conditions, migraine is a prevalent neurological disorder affecting approximately 15–20% of women of reproductive age have been hypothesized as a potential contributor to infantile colic [4]. Migraines are characterized by recurrent attacks of severe headache, often accompanied by nausea, photophobia, and phonophobia, and are believed to involve complex interactions between genetic, hormonal, and environmental factors. Interestingly, both migraine and infantile colic share overlapping pathophysiological mechanisms, including dysregulation of the trigeminovascular system, hypersensitivity to sensory stimuli, and altered gastrointestinal function [1, 5, 16].

Emerging evidence suggests that maternal migraine may play a role in the development of infantile colic [6, 7]. Observational studies have indicated a potential link between these conditions, with infants of mothers who experience migraines appearing to have a higher risk of developing colic [8, 9]. This association may be explained by shared genetic predispositions, environmental exposures during pregnancy, or maternal stress responses that influence infant neurodevelopment. Additionally, alterations in maternal-infant interactions, influenced by maternal pain and psychological distress, may further contribute to the onset or exacerbation of colic symptoms [10, 11].

We propose that infantile colic (IC) may represent an early-life manifestation of migraine-related disorders, based on three key mechanistic links: (1) Trigeminovascular Dysregulation: Shared activation pathways between migraine and IC (e.g., CGRP-mediated signaling) [1, 5], (2) Sensory Hypersensitivity: Heightened response to stimuli in both conditions [17, 18] (3) Circadian Rhythm Disruption: Melatonin dysregulation in mothers with migraine may influence infant colic onset [19].

Despite the growing body of literature, the relationship between maternal migraine and infantile colic remains poorly understood, and no comprehensive review has synthesized the available evidence. To address this gap, this narrative review aims to explore the potential association between maternal migraine and infantile colic, highlighting proposed mechanisms, current evidence, and implications for clinical practice. By examining this relationship, we aim to contribute to a better understanding of the complex interplay between maternal health and infant outcomes, ultimately fostering more targeted approaches to prevent and manage infantile colic.

Methods

This narrative review was conducted to explore the potential association between maternal migraine and infantile colic. The methodology employed followed established guidelines for narrative reviews, emphasizing a comprehensive and structured approach to literature selection, analysis, and synthesis.

Literature search strategy

A systematic search of relevant articles was conducted across multiple electronic databases, including PubMed, Scopus, Web of Science, and Google Scholar, from 2010 to August 22, 2024. The search strategy included a combination of Medical Subject Headings (Mesh) terms and free-text keywords such as (“maternal migraine” OR “maternal headache” OR “maternal head pain” OR “maternal cephalalgia”) AND (“infantile colic” OR “baby colic” OR “infant colic” OR “excessive crying in infants” OR “paroxysmal fussing”) NOT (“animal” OR “rat” OR “mouse” OR “pediatric migraine”) were used to combine the search terms to ensure a broad yet focused retrieval of relevant studies. The reference lists of included articles and relevant reviews were also screened to identify additional studies that met the inclusion criteria.

Inclusion and exclusion criteria

Studies were included if they met ALL of:

1. Population:

• - Mothers with clinically diagnosed migraine (ICHD-3 criteria) OR self-reported migraine with ≥ 3 episodes.

• - Infants aged 0–6 months meeting Wessel’s criteria for colic (crying > 3 h/day, >3days/week).

• 2.Outcome Measures:

- Must report at least one quantitative measure:

Primary outcome: Odds ratio (OR) of colic in infants of migraineurs vs. non-migraineurs.

Secondary outcomes: Prevalence rates, risk ratios (RR), or raw data to calculate these measures.

Studies were excluded if they did not report:

Quantitative measures of association (e.g., OR, RR, mean difference), OR.

Sufficient data to calculate these measures (e.g., raw counts in case/control groups).

Study selection process

The initial search results were screened for relevance based on titles and abstracts. Full-text articles were then retrieved for further evaluation. Two reviewers independently assessed the eligibility of studies based on the inclusion and exclusion criteria. Discrepancies between the reviewers were resolved through discussion and consensus, and when necessary, a third reviewer was consulted. Of the initial 792 records identified through database searching, we excluded 742 studies during title/abstract screening based on our predefined criteria. Fifty full-text articles were thoroughly assessed for eligibility. After detailed evaluation, we excluded 42 studies for the following reasons: [1] 22 studies lacked quantitative outcome measures [2], 15 studies used non-standard definitions of either migraine or infantile colic, and [3] 5 studies involved ineligible populations. Ultimately, 8 studies met al.l inclusion criteria and were included in our narrative review. These selection details are clearly presented in the PRISMA flowchart (Fig. 1) in the manuscript.

Fig. 1.

Flow chart for study selection

Data extraction and synthesis

Data from the included studies were extracted using a pre-designed data extraction form. The extracted data included:

Study characteristics (authors, year of publication, country, and study design).

Sample characteristics (population size, maternal migraine characteristics, and infantile colic definitions).

Key findings related to the association between maternal migraine and infantile colic.

Proposed mechanisms linking maternal migraine to infantile colic.

The data were synthesized qualitatively, with a focus on identifying recurring themes, trends, and gaps in the literature. The results were organized thematically to address the objectives of this narrative review.

Ethical consideration

This study was based on published literature, and therefore, consent was not required. It was approved by Tehran University of Medical Sciences and assigned the ethics code IR.TUMS.CHMC.REC.1403.260.

Results

Association between maternal migraine and infantile colic

Two case-control studies highlighted a significant association between maternal migraine and infantile colic (IC). One study conducted in Iran (2022), investigated 154 infants younger than 4 months. Diagnostic criteria for migraine were the International Headache Society (IHS) criteria and Wessel criteria for IC. The prevalence of maternal migraine was notably higher in infants with IC compared to controls with an odds ratio (OR) of 6.17 (95% CI: 2.73–14.44), compared to the control group (53.2% vs. 15.6%, P < 0.001). The OR for IC in infants of mothers with migraine was 5.01 (95% CI: 2.26–11.10, P < 0.001) after adjusting for confounders. Also, a higher prevalence of a positive family history of migraine in the case group than in the control group (59.7% vs. 35.1%, P = 0.002) was reported [20]. Another case-control study in Turkey (2015) corroborated this finding. In this study, a total of 290 mothers participated, 143 of these were in the case group and 147 were in the control group. Diagnostic criteria for IC were Wessel criteria and for migraine were not mentioned. This study showed that maternal migraine prevalence significantly associated with IC (21.7% vs. 8.2%, p = 0.001) [21]. Both studies support the hypothesis that maternal migraine plays a significant role in the pathophysiology of IC.

Influence of parental migraine

The influence of both maternal and paternal migraines on IC has been investigated in multiple studies, with findings consistently pointing to a stronger association between maternal migraine and IC compared to paternal migraine. A prospective case-control study conducted in Turkey (2017–2020) explored the relationship between parental migraine and IC in 95 infants aged 6–8 weeks. Infants with IC, identified using Wessel’s criteria, were compared to healthy controls of the same age. The ID Migraine Diagnosis Scale was one proven reliable in Turkey. The study revealed that maternal migraine and headache frequencies were significantly higher in the colic group (59.2% vs. 23.9%, p = 0.001 for migraine; 71.4% vs. 34.8%, p < 0.001 for headache). In contrast, no significant differences were observed in the frequency of paternal migraine or headache between the colic and control groups (p = 0.736 for migraine; p = 0.634 for headache). These findings suggest that maternal migraine plays a more pronounced role in the development of IC, potentially due to maternal-infant interactions or prenatal influences [19].

A large cross-sectional study conducted in the United States (2017–2018) further supported this maternal link. Migraine was determined based on modified ICHD-3(International Classification of Headache Disorders 3rd edition criteria). IC queried from parents with the question, “Has your baby cried for at least three hours on at least three days in the last week?” The study assessed parental migraine and IC in 1,419 infants aged 4–8 weeks. Maternal migraine was associated with a significantly increased risk of IC (OR: 1.7; 95% CI: 1.3–2.4), with an even higher risk for mothers experiencing frequent migraines (≥ 15 headache days/month; OR: 2.5; 95% CI: 1.2–5.3). Interestingly, while paternal migraine was not significantly associated with IC (OR: 1.0; 95% CI: 0.7–1.5), paternal mental health conditions such as depression (OR: 2.4; 95% CI: 1.4–4.3) and anxiety (OR: 1.7; 95% CI: 1.1–2.7) were linked to an increased risk of IC in their infants. These results underscore the complexity of parental contributions to IC, with maternal migraine emerging as a key risk factor [22].

Further insights were provided by a cross-sectional study conducted in Iran in 2020, which examined 195 infants aged 4–12 weeks and their parents. Diagnostic criteria for IC were Wessel criteria and for migraine were not mentioned. Results showed a significant association between parental migraine and IC (58.5% vs. 41.5% in colicky infants and 6.9% vs. 93.1% in non-colicky infants, P = 0.001). Also, a robust association between maternal migraine and IC was demonstrated (47.7% vs. 0%, p = 0.001). Conversely, paternal migraine was only weakly associated with IC (10.8% vs. 4.6%, p = 0.10). This aligns with findings from other studies, emphasizing that the maternal impact on IC is more substantial than the paternal influence [23].

Overall, the evidence suggests a clear and significant relationship between maternal migraine and IC, while the link between paternal migraine and IC appears weaker or non-significant. The stronger maternal association may be explained by shared genetic factors, prenatal influences, or the effects of maternal stress and pain on infant development. The lack of a consistent relationship between paternal migraine and IC may reflect differences in the nature of father-infant interactions, as well as the reduced influence of paternal health on prenatal and perinatal conditions. These findings highlight the importance of further investigating maternal and paternal factors independently, as well as exploring the underlying mechanisms driving the maternal-migraine-IC association.

Familial history and IC

The role of familial migraine history in the development of infantile colic (IC) has been explored in several studies, with a particular focus on maternal and parental contributions. A retrospective case-control study conducted in Iran (2015–2016), investigated 164 children aged 5–15 years to assess whether IC might be an early-life expression of childhood migraine. The history of IC was identified by Wessel criteria and The history of migraine was noted by ICHD II criteria. This study found that children with migraine were significantly more likely to have a history of IC compared to those without migraine (41.46% vs. 35.7%, p = 0.049). Additionally, a positive family history of migraine was more common in children with IC (46.6% vs. 29.7%, p = 0.001), suggesting that genetic predisposition may play a key role in the link between IC and migraine. However, the study did not clearly define whether the family history of migraine referred specifically to maternal, paternal, or other relatives, which limits the ability to pinpoint the primary familial influence [24].

Further evidence comes from a cross-sectional study conducted in the United States (2010), which evaluated 154 two-month-old infants of mothers and fathers with migraines. Migraine was obtained by having a physician diagnosis or a positive screen on ID Migraine and IC was diagnosed via parental report using modified Wessel criteria. This study found that infants born to mothers with migraines were 2.6 times more likely to experience colic compared to those born to mothers without migraines (29% vs. 11%, prevalence ratio: 2.6; 95% CI: 1.2–5.5, p = 0.02). While data on paternal migraine were available for only 93 of the 154 infants, the study noted that the prevalence of colic was higher in infants with fathers who had migraines (22% vs. 10%). However, the prevalence ratio for paternal migraine and colic (2.3; 95% CI: 0.6–9.4) had wide confidence intervals, rendering the association statistically insignificant (p = 0.24). These findings suggest that familial migraine history, particularly maternal, has a more robust influence on the risk of IC than paternal history, although the role of paternal migraine cannot be entirely ruled out [18].

The connection between familial migraine and IC is further supported by studies emphasizing genetic and environmental contributions to both conditions. Genetic predisposition may increase the likelihood of infants inheriting traits associated with heightened sensory reactivity, dysregulation of the trigeminovascular system, and gastrointestinal hypersensitivity—shared mechanisms underlying both migraine and IC. Additionally, maternal stress, migraine-related hormonal changes during pregnancy, and prenatal exposures could influence the development of IC in infants [25].

Contradictory findings

While the majority of studies suggest a strong association between maternal migraine and IC, some research has produced contradictory findings, raising questions about the consistency and generalizability of these results. A prospective case-control study conducted in Egypt (2012) investigated the prevalence and risk factors for IC in 540 infants aged 3–16 weeks. This study found that 37% of infants met the Wessel criteria for IC. Although parental headache was reported more frequently in the parents of colicky infants compared to parents of non-colicky infants, the study concluded that there was no statistically significant relationship between parental headache and IC (55% vs. 33.8%, p = 0.05). Notably, this study did not differentiate between general headaches and migraines, which may have diluted the potential association between parental migraine and IC. Additionally, the lack of specific diagnostic criteria for migraine further complicates the interpretation of these findings and underscores the importance of using validated migraine assessment tools in future studies [26].

A summary of the studies is given in the Table 1.

Table 1.

The relationship between maternal migraine and colic

study	Country	Study design	Sample size	Sample population	Colic criteria	Migraine criteria	Results
[20]	Iran	Case-control	154	Hospital-based	Wessel’s	IHS	Maternal migraine in the IC group vs. control group: (53.2% vs. 15.6%), OR: 6.17 (95% CI: 2.73–14.44, P < 0.001)
[21]	Turkey	Case-control	290	Hospital-based	Wessel’s	Not mentioned	Maternal migraine in the IC group vs. control group: 21.7% vs. 8.2%, p = 0.001
[19]	Turkey	Prospective case-control	95	Hospital-based	Wessel’s	ID Migraine	Maternal/Paternal migraine and headache frequency in the IC group vs. control group: Maternal: 59.2% vs. 23.9%, p = 0.001 for migraine; 71.4% vs. 34.8%, p < 0.001 for headache Paternal: p = 0.736 for migraine; p = 0.634 for headache
[23]	Iran	Cross-sectional	195	Clinic-based	Wessel’s	Not mentioned	Parental/Maternal migraine: Parental: 58.5% vs. 41.5% in colicky infants and 6.9% vs. 93.1% in non-colicky infants, p = 0.001 Maternal: 47.7% vs. 0%, p = 0.001
[22]	USA	Cross-sectional	1419	Population-based	Parental report	ICHD-3	Maternal migraine: OR: 1.7 (95% CI: 1.3–2.4); maternal frequent migraines: OR: 2.5 (95% CI: 1.2–5.3); paternal migraine: OR: 1.0 (95% CI: 0.7–1.5); paternal depression: (OR: 2.4 (95% CI: 1.4–4.3); paternal anxiety: OR: 1.7 (95% CI: 1.1–2.7)
[24]	Iran	retrospective case-control	164	Hospital-based	Wessel’s	ICHD-2	IC in children with migraine vs. control group: 41.46% vs. 35.7%, p = 0.049 Family history of migraine in children with IC vs. healthy children: 46.6% vs. 29.7%, p = 0.001
[18]	USA	Cross-sectional	154	Clinic-based	Wessel’s	ID Migraine	Colicky infants in mothers with migraines: (29% vs. 11%), OR: 2.6 (95% CI: 1.2–5.5, P = 0.02) Colicky infants in fathers with migraines: (22% vs. 10%), OR: 2.3 (95% CI: 0.6–9.4, P = 0.24)
[26]	Egypt	Prospective case-control	540	Community-based	Wessel’s	Unspecified methods	Parental headache in the IC group: 55% vs. 33.8%, p = 0.05

Study participants

• Studies in infants

All included studies investigated infants, with sample sizes ranging from 95 to 1,419 participants. Case-control studies compared infants with colic to healthy controls [19–21, 24, 26]. Cross-sectional studies analyzed parental migraine prevalence in unselected infant populations [18, 22, 23]. Key demographic characteristics:

• Maternal age range: 22–35 years

• Infant age: 2–12 weeks

• Study in older children (5–15 years)

One retrospective study investigated whether a history of IC was more common in children with migraine [24].

Diagnostic criteria

• IC

All studies used Wessel’s criteria except:

• One study relied on parental report (cried ≥ 3 h on ≥ 3 days in the past week) [22].

• Migraine

• Gold-standard criteria: Three studies used ICHD-3 or IHS criteria [20, 22, 24].

• Screening tools: The ID Migraine scale was used in two studies [18, 19].

• Unspecified methods: Three studies did not report migraine criteria, limiting comparability [21, 23, 26].

Primary outcomes

• Maternal migraine associations.

• Positive association in 6 studies [18–23].

• No association in 1 study [26].

• Dose-response effect in 1 study [22].

• Paternal Migraine Association.

• No significant association in 5 studies [18, 19, 22, 23, 26].

• Borderline association in 1 study [24].

Notable covariates

• Maternal age [20–22], infant variables (age, sex, gestational age, gravidity, birth weight, birth order) [19, 20, 22–24, 26], and family history [18–20, 22, 23, 26].

• Breastfeeding status [20, 24, 26] and parental anxiety/depression [22].

Discussion

This review summarizes the findings of five case-control and three cross-sectional studies of the effect of maternal migraine in IC. The findings of this review indicate a significant association between maternal migraine and IC, suggesting that maternal migraine may play an important role in the development of colic symptoms in infants. This relationship was consistently demonstrated across multiple studies, with maternal migraine significantly increasing the likelihood of IC. The odds ratios in various studies suggest that infants of mothers with migraines are several times more likely to develop IC compared to infants of mothers without migraines. Such a robust association points to shared pathophysiological mechanisms and potential genetic and environmental influences.

One of the most plausible mechanisms linking maternal migraine and IC involves dysregulation of the trigeminovascular system. This system, which plays a central role in migraine pathophysiology, is also involved in gastrointestinal motility and sensitivity. In migraines, the activation of the trigeminal nerve can lead to neurogenic inflammation and altered pain processing. Similarly, infants with IC may exhibit heightened visceral sensitivity, which could be related to the same pathways, particularly during their early developmental stages when their nervous system is maturing. This shared dysregulation could explain why infants of mothers with migraines are more prone to colic [5, 25].

Another potential mechanism is sensory hypersensitivity, a hallmark of migraine that may also manifest in IC. Migraines are characterized by heightened sensitivity to light, sound, and other sensory inputs, which may have a genetic basis. Infants of migraineurs may inherit a predisposition to heightened sensory reactivity, making them more sensitive to stimuli such as noise, light, or gastrointestinal discomfort. This heightened sensitivity may result in prolonged crying episodes that characterize IC, particularly during the early months when infants are most vulnerable to external stimuli [17, 18, 25, 27–29].

Alterations in gastrointestinal function also provide a plausible explanation for the observed association. Migraines have been linked to gastrointestinal disorders, including irritable bowel syndrome, via shared mechanisms such as altered gut-brain axis signalling and gut microbiota imbalances. Similar mechanisms could play a role in IC [30, 31]. Infants with IC have been shown to exhibit altered gut microbiota composition and gastrointestinal hypersensitivity, which may be influenced by maternal factors during pregnancy. For instance, maternal migraines, often accompanied by stress, hormonal fluctuations, and changes in inflammatory cytokines, may disrupt fetal development and predispose infants to dysregulated gastrointestinal function, contributing to the development of IC [32].

Disruptions in the sleep-wake cycle are another factor that may underlie both migraine and IC. Migraines are often triggered by sleep disturbances, and IC frequently occurs during the evening hours, aligning with periods of increased infant wakefulness and overstimulation. The maturation of the circadian rhythm and melatonin production during the first few months of life is critical for regulating infant sleep and gastrointestinal motility. Infants of mothers with migraines may experience delayed or disrupted circadian rhythm development due to prenatal or postnatal influences, which could exacerbate colic symptoms. This disruption may partially explain why colic typically resolves around three to four months of age when the infant’s circadian system becomes more established [33–37].

The genetic predisposition to migraine may further contribute to the relationship with IC. Familial aggregation of migraines is well-documented, and genetic factors linked to migraine, such as mutations in ion channel or receptor genes, may predispose infants to both migraine-like symptoms and colic. This genetic susceptibility may manifest as early-life crying and fussiness in the form of IC, which could later develop into migraines or other related conditions as the child grows. This is consistent with the inclusion of IC among childhood periodic syndromes associated with migraines in the ICHD-III [38, 39].

While the relationship between maternal migraine and IC is well-supported, the evidence for paternal migraine is weaker. Most studies found no significant association between paternal migraine and IC, suggesting that maternal factors, including the intrauterine environment and maternal-infant interactions, may have a more direct impact on infant outcomes. However, the role of paternal migraine and broader familial migraine history should not be overlooked, as they may contribute to the genetic predisposition for IC. Additionally, environmental factors such as maternal stress, prenatal exposures, and parental coping strategies may interact with genetic predispositions to influence the risk of IC [22, 33].

The mechanisms underlying the observed association between maternal migraine and IC highlight the intricate interplay between genetic, neurological, and environmental factors. Understanding these mechanisms may pave the way for targeted interventions aimed at reducing the burden of IC in infants and improving maternal-infant health outcomes. Early identification of infants at risk for IC, particularly those born to mothers with migraines, could allow for proactive management strategies, including interventions to regulate sensory input, optimize infant sleep patterns, and support maternal well-being. Furthermore, exploring IC as a potential early-life indicator of migraine susceptibility may provide insights into the developmental trajectory of migraines and related conditions, enabling earlier diagnosis and treatment in later life.

Despite the strong association between maternal migraine and IC, several limitations in the existing literature should be acknowledged. Variability in study designs, sample sizes, population characteristics, and diagnostic criteria for both migraine and IC complicates direct comparisons across studies. For instance, differences in the methods used to identify IC and migraine, the timing of data collection, and the inclusion of potential confounders such as parental stress, infant feeding practices, and environmental factors may all contribute to inconsistent results. Some studies relied on self-reported data for parental headache or migraine history, which can introduce recall bias or misclassification, while others used validated diagnostic tools such as the International Classification of Headache Disorders (ICHD) criteria or the ID-Migraine screener, leading to more robust findings.

Moreover, cultural and regional differences in the perception and reporting of both migraine and IC could account for some discrepancies. For example, in the Egyptian study, the prevalence of colic was relatively high (37%), and it is unclear whether sociocultural factors influenced parental reporting or clinical diagnosis of IC. Similarly, differences in healthcare access, parental education, and awareness of migraine as a condition could influence how families report symptoms, potentially biasing results.

Despite these inconsistencies, it is important to recognize that the absence of a significant association in certain studies does not necessarily refute the link between maternal migraine and IC. Instead, it highlights the complexity of these conditions and the need for well-designed, large-scale studies that account for potential confounders and use standardized diagnostic criteria. Additionally, the influence of other factors, such as maternal anxiety, depression, and genetic predisposition, may interact with migraines to influence the risk of IC and should be further explored in future research.

Conclusion

In conclusion, this review underscores a significant and consistent association between maternal migraine and IC, supported by overlapping mechanisms that link these conditions. However, further research is needed to clarify the precise pathways involved and to explore the long-term implications of this association. By addressing these gaps, future studies could contribute to a more comprehensive understanding of the maternal-infant health continuum and improve outcomes for both mothers and their children.

Author contributions

All authors equally contributed significantly to the conception and design of the work, acquisition, analysis, interpretation of data, drafted the work, and final revised it.

Funding

None.

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

This study was based on published literature, and therefore, consent was not required. It was approved by Tehran University of Medical Sciences and assigned the ethics code IR.TUMS.CHMC.REC.1403.260.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.