
Scoping Review Suggests Infantile Colic May Signal Early Migraine Susceptibility
Key Takeaways
- Twelve observational studies (1997–2025) demonstrated a bidirectional migraine–colic association, including both maternal migraine predicting infantile colic and infantile colic predicting later childhood migraine.
- Maternal migraine was repeatedly associated with higher colic prevalence, with adjusted effect sizes sometimes large but highly variable, reflecting heterogeneity in ascertainment and confounding control.
A review of 12 studies showed that maternal migraine was linked to a higher likelihood of infant colic, and that infant colic was in turn linked to a higher risk of migraine later in childhood.
A newly published review in Headache reported a consistent bidirectional association between migraine and infantile colic, with maternal migraine linked to a higher likelihood of colic in infancy and infantile colic linked to an elevated risk of migraine later in childhood.1
The findings, although based entirely on observational data, add to growing evidence that colic may represent an early behavioral marker of migraine predisposition rather than an unrelated, self-limited condition of infancy. The review, conducted by coauthor Ilari Kuitunen, MD, PhD, associate professor of pediatric epidemiology at University of Eastern Finland, summarized 12 observational studies published between 1997 and 2025 across 9 countries, including Italy, the United States, Japan, Iran, Turkey, the United Kingdom, France, Finland, and Israel.
Kuitunen told NeurologyLive® that while he sees the colic-migraine link as more suggestive than confirmed for now, he believes the findings could still reshape how clinicians talk with families and, eventually, how migraine itself gets diagnosed in children. "I'd say that it could give something to familiarize the parents with. It might provide more understanding towards the colic as a periodic symptom," he said.
As for whether colic points specifically toward migraine or reflects a broader sensitivity in some infants, Kuitunen was cautious about overstating the current evidence. "Currently I would suggest [it] to be an early sign of possible sensitivity. However, in the future I hope that genetic studies would also provide possible additional links between these," he added.
Looking ahead, he sees room for the science to sharpen this picture and for that precision to eventually reshape clinical practice. "I believe that it would make the diagnoses of migraine earlier, and as in many diseases the disease phenotypes have become more precise, it could further make a possibility to consider new treatment strategies," Kuitunen told NeurologyLive.
Study Overview
Using PRISMA-ScR guidance, the authors searched PubMed, Scopus, and Web of Science through September 30, 2025, and screened 159 records, ultimately including 12 studies with sample sizes ranging from 100 to 1057 participants. All told, 6 studies examined maternal migraine as an exposure and infantile colic as the outcome. The remaining 6 examined infantile colic as an exposure and later childhood migraine, diagnosed per International Headache Society criteria, as the outcome. Study designs ranged from case-control and cross-sectional studies to an 18-year prospective cohort follow-up. Colic was defined either by clinical criteria or by parental/survey report, and migraine diagnoses relied on author-defined criteria rather than a single standardized protocol.
Key Findings
Across the 6 studies linking maternal migraine to infant colic, colic prevalence was consistently higher among infants of mothers with migraine than among controls. For example, 38.4% versus 26.9% in 1 case-control study, and 32.3% versus 21.8% in a US cross-sectional survey. Odds ratios (ORs) ranged from 0.97 to 37.71 across analyses, with several adjusted estimates showing statistically significant associations, including an adjusted OR of 7.32 (95% CI, 1.08-49.82) for migraine without aura and colic in a Japanese cohort.
In the 6 studies addressing colic as a predictor of later migraine, associations were similarly consistent but heterogeneous in magnitude. One case-control study reported an adjusted OR of 6.61 (95% CI, 4.38-10.00) for a colic history among children with migraine versus controls. In an 18-year Finnish prospective cohort, children with a colic history had more than double the risk of subsequent migraine without aura (adjusted risk ratio, 2.4; 95% CI, 1.4-4.2), though risk for migraine with aura was not significantly elevated (adjusted risk ratio, 0.96; 95% CI, 0.5-1.9). An Iranian case-control study reported a markedly elevated but imprecise estimate (OR, 37.71; 95% CI, 13.28-107.14).
Clinical Context and Interpretation
Migraine is a highly heritable, polygenic neurological disorder that can impair quality of life in children through recurrent, disabling headache episodes.2,3 Infantile colic, by contrast, is typically transient, resolving by 3 to 4 months of age, but its pathophysiology remains incompletely understood. Prior work has proposed colic as an early-life expression of migraine, given shared features such as recurrent, intense episodes and possible common neurodevelopmental or genetic underpinnings.4 The current review's authors noted that trigeminovascular activation and neuronal hyperexcitability documented in pediatric migraine may have parallels in the sensory hypersensitivity seen in some infants with colic.
The authors concluded that the observed associations support a model of shared susceptibility or overlapping pathophysiology between colic and migraine, potentially reflecting a developmental continuum in which the same underlying predisposition manifests as colic in infancy and migraine later in childhood. They emphasized, however, that infantile colic should not be regarded as a migraine equivalent, but rather as a possible early marker of migraine predisposition that could inform clinical suspicion and family counseling.
Limitations and Future Research
All included studies were observational, precluding causal inference and leaving findings vulnerable to residual confounding. Substantial heterogeneity in colic and migraine definitions, study designs, and follow-up durations limits direct comparability of effect estimates. Data extraction was not performed independently in duplicate, and inclusion criteria were broadened mid-protocol to accept parent-reported colic, introducing potential misclassification.
The search also excluded Embase and PsycINFO and did not include gray literature, and most studies originated in high-income settings, limiting generalizability. The authors called for large, prospective cohort studies with standardized definitions of colic and migraine, detailed migraine subtype phenotyping, and longitudinal follow-up from infancy through adolescence to clarify whether colic represents an early manifestation of migraine, a risk marker, or a shared susceptibility driven by genetic or neurodevelopmental mechanisms.









