Migraine is a recurrent neurological disorder characterised by headache and variable combinations of nausea, photophobia, phonophobia, and focal neurological symptoms. The International Classification of Headache Disorders, third edition (ICHD-3), provides standard diagnostic criteria and distinguishes migraine from secondary headache disorders [1]. Migraine is a major cause of years lived with disability worldwide and is particularly burdensome in women and adults of working age [2]. Contemporary models describe migraine as a disorder of sensory processing and homeostatic regulation involving trigeminovascular pathways, neuropeptide signalling, cortical spreading depolarisation, and altered processing of visual, auditory, and somatosensory input [3,4].

Refractive errors arise when the optical system does not focus images accurately on the retina. They are among the most common ocular conditions and a major source of avoidable visual impairment [5]. Myopia alone is projected to affect approximately half of the global population by 2050 [6]. Uncorrected or inadequately corrected hypermetropia, astigmatism, and anisometropia can increase accommodative and vergence demand, degrade retinal image quality, and contribute to asthenopia. These mechanisms make refractive error a plausible modifier of headache symptoms, although ocular strain and migraine are not interchangeable clinical entities. Evidence on migraine and refraction is mixed. Masked case-control work found greater astigmatic components among people with migraine [7], while a later prospective case-control study reported higher astigmatism, spherical equivalent, and anisometropia in migraine patients than controls [8]. Migraineurs also report greater pattern glare and visually triggered discomfort [9], and subtle binocular-vision anomalies have been described [10]. Conversely, population and clinical studies have cautioned that headache is common in people with and without refractive error and that the causal role of refraction may be overestimated [11,12]. Ocular causes of headache remain clinically relevant, especially when symptoms are frontal, occur after sustained near work, or coexist with blurred vision or diplopia [13,14]. A large contemporary optometry-clinic study also found that low spherical and cylindrical errors, hyperopia, and against-the-rule astigmatism were more frequent among patients reporting headache [15]. Digital-device use adds another layer of exposure. Digital eye strain encompasses ocular discomfort, blurred vision, dryness, and headache related to sustained screen tasks. Uncorrected refractive error, accommodative or vergence abnormalities, reduced blinking, small working distances, and prolonged near work may contribute [17–20]. Visual-pattern sensitivity and cortical hyper-responsiveness provide a potential neurological link, although evidence for tinted lenses or spectral filters remains limited and should not be generalised to all migraine patients [21,22]. Evidence from Pakistan is sparse. A Karachi ophthalmology study identified refractive error and asthenopia among common ocular findings in patients presenting with headache, but it did not specifically quantify migraine frequency using ICHD-3 criteria [16]. The present study therefore examined whether the presence, type, severity, and correction status of refractive errors were associated with monthly migraine-attack frequency among patients attending DHQ Hospital Mardan. We hypothesised that refractive errors—particularly astigmatism and hypermetropia—would remain associated with attack frequency after adjustment for demographic and clinical covariates, and that the association would be stronger with prolonged screen exposure and uncorrected refractive error.

Study design and setting

A hospital-based analytical cross-sectional study was conducted in the Neurology and Ophthalmology outpatient departments of District Headquarter (DHQ) Hospital Mardan, Khyber Pakhtunkhwa, Pakistan, from January through April 2026. Reporting was structured in accordance with the STROBE recommendations for cross-sectional studies [23].

Participants and sampling

Patients were recruited using non-probability consecutive sampling. Eligible participants were aged 12 years or older and had migraine confirmed by a neurologist according to ICHD-3 criteria [1]. Exclusion criteria were secondary headache, known intracranial pathology, active ocular inflammation or other ocular disease likely to cause pain, ocular surgery within the preceding six months, pregnancy, cognitive impairment precluding reliable history, or inability to complete refraction. For participants younger than 18 years, parental or guardian consent and participant assent were obtained.

Sample size

A target of 200 participants was set using the WHO sample-size approach for a single proportion, assuming an anticipated refractive-error prevalence of 30%, 95% confidence, approximately 6.5% absolute precision, and a small allowance for incomplete observations.

Migraine assessment

A structured proforma recorded age, sex, body mass index, migraine duration, aura status, family history, prophylactic medication use, and average daily screen time. Migraine-attack frequency was defined as the participant-reported number of discrete attacks during the preceding 30 days. Attack intensity was recorded using a 0–10 visual analogue scale. The primary outcome was monthly attack frequency. A secondary binary outcome, frequent attacks, was prespecified as five or more attacks per month.

Ophthalmic assessment

Each participant underwent monocular uncorrected and best-corrected visual-acuity testing, objective and subjective refraction, slit-lamp biomicroscopy, fundus examination, and binocular-vision assessment. Cycloplegic refraction was performed in participants younger than 40 years when latent hypermetropia or unreliable accommodation was suspected. Myopia was defined as spherical equivalent ≤−0.50 dioptres (D), hypermetropia as ≥+0.50 D, astigmatism as cylinder magnitude ≥0.75 D, and anisometropia as an interocular spherical-equivalent difference ≥1.00 D. Where more than one category was present, each type was retained for descriptive assessment; regression coding used mutually exclusive primary refractive-error categories based on the dominant refractive component. Correction status was classified as corrected when the participant’s habitual prescription was clinically appropriate at examination and uncorrected/undercorrected otherwise.

Severity classification

Severity was determined from the dominant refractive component: mild (myopia 0.50–2.99 D; hypermetropia 0.50–1.99 D; astigmatism 0.75–1.49 D; anisometropia 1.00–1.99 D), moderate (myopia 3.00–5.99 D; hypermetropia 2.00–4.99 D; astigmatism 1.50–2.99 D; anisometropia 2.00–2.99 D), and severe (values at or above the remaining category-specific thresholds).

Statistical analysis

Data were analysed in IBM SPSS Statistics version 25. Continuous variables are reported as mean±standard deviation and categorical variables as frequency and percentage. Group differences were assessed with Welch independent-samples t tests or Pearson chi-square tests, as appropriate. Multivariable linear regression estimated adjusted differences in monthly attack frequency. Logistic regression estimated adjusted odds ratios (aORs) for frequent attacks. Covariates were selected a priori: age, sex, daily screen time, migraine duration, aura, and prophylactic medication use. Variance inflation factors assessed collinearity; values below 2 indicated no important multicollinearity. Two-sided p<0.05 was considered statistically significant. Interaction terms were used for prespecified subgroup analyses.

Ethics

The institutional review process of DHQ Hospital Mardan approved the study. Written informed consent was obtained before enrolment, confidentiality was maintained through coded records, and participation was voluntary. The study was conducted in accordance with the Declaration of Helsinki.

The analysis included 200 participants, of whom 130 (65.0%) had at least one refractive error and 70 (35.0%) had no refractive error. Mean age was 32.4±11.6 years, and 145 participants (72.5%) were female. The refractive-error and no-error groups were similar in age, body mass index, migraine duration, aura, family history, and prophylactic medication use. Daily screen time was higher in the refractive-error group (7.5±3.6 vs 5.5±2.8 hours/day; p<0.001). The difference in sex distribution did not reach conventional statistical significance after recalculation from the supplied counts (p=0.056) (Table 1). In unadjusted analysis, the presence of any refractive error was associated with 2.45 additional migraine attacks per month (95% CI 1.70–3.20; p<0.001). The association changed little after adjustment for age and sex. In the fully adjusted model, refractive error remained associated with 1.92 additional attacks per month (95% CI 1.21–2.63; p<0.001). Female sex, daily screen time, and longer migraine duration were also independently associated with attack frequency. Aura and prophylactic medication use were not statistically significant in the model. All variance inflation factors were below 2 (Table 2). Type-specific analysis showed the largest adjusted association for astigmatism (β=3.22 attacks/month; 95% CI 2.23–4.21), followed by hypermetropia (β=2.85; 95% CI 1.77–3.93), anisometropia (β=1.88; 95% CI 0.46–3.30), and myopia (β=1.12; 95% CI 0.17–2.07) (Figure 1). The type-specific model explained 42% of variance in attack frequency (adjusted R²=0.42).

The refractive-error association was stronger among women than men (interaction p=0.041), among participants with at least six hours of screen exposure per day (interaction p=0.008), and among participants with uncorrected or undercorrected refractive error (interaction p=0.001). No statistically significant interaction was reported for age group, aura status, or migraine duration (Table 3). In logistic regression, any refractive error was associated with frequent attacks (aOR=3.65; 95% CI 2.42–5.50; p<0.001). Astigmatism had the largest type-specific odds ratio (aOR=4.15; 95% CI 2.48–6.95), and the odds increased across mild, moderate, and severe refractive-error categories. Uncorrected or undercorrected error, greater screen time, female sex, and longer migraine duration were independently associated with frequent attacks. The model showed adequate calibration (Hosmer–Lemeshow p=0.411) and good discrimination (AUC=0.84, 95% CI 0.78–0.90) (Table 4; Figure 2).

Table 1. Baseline demographic and clinical characteristics by refractive-error status (N=200)

Values are mean±SD or n (%). Continuous variables: Welch t test; categorical variables: Pearson χ² test. All p values are two-sided.

Table 2. Linear regression models for monthly migraine-attack frequency

*Reference category: no refractive error. Type-specific model adjusted for age, sex, screen time, migraine duration, aura, and prophylactic medication. β is the adjusted difference in attacks/month.

Table 3. Prespecified subgroup analysis of the refractive-error association

β values are from fully adjusted models within each subgroup. Interaction p values test effect modification by the listed subgroup variable.

Table 4. Multivariable logistic regression for frequent migraine attacks (≥5/month)

All estimates are mutually adjusted. Hosmer–Lemeshow χ²=8.24, df=8, p=0.411; AUC=0.84 (95% CI 0.78–0.90). Odds ratios are associations and should not be interpreted as risk ratios or causal effects.

In this hospital-based sample, refractive errors were common and independently associated with monthly migraine-attack frequency. The association persisted after adjustment for age, sex, screen time, migraine duration, aura, and prophylactic medication. Astigmatism and hypermetropia showed the largest type-specific coefficients, while uncorrected or undercorrected refractive error and prolonged daily screen exposure identified groups with stronger associations. These findings are clinically relevant, but the cross-sectional design means they cannot demonstrate that refractive error causes migraine or that correction will prevent attacks. The direction of the findings is consistent with several earlier studies. Harle and Evans found greater astigmatic components in a masked case-control comparison of migraine patients and controls [7].

Gunes and colleagues similarly reported higher astigmatism, spherical equivalent, and anisometropia among migraine patients [8]. More recent clinic-based evidence suggests that low spherical and cylindrical errors, hyperopia, and against-the-rule astigmatism may be more frequent among patients with headache [15]. However, other work has shown that overall headache prevalence may be similar in people with and without refractive error and that headache specifically attributable to refraction is relatively uncommon [11]. A systematic critique also highlighted limitations in exposure definition, outcome classification, masking, and causal inference in this literature [12]. Our results therefore add evidence of association, not proof of an ocular cause of migraine. Several mechanisms could explain the stronger associations observed for astigmatism and hypermetropia. Astigmatism degrades image quality across orientations and may require sustained optical and neural compensation. Hypermetropia can increase accommodative demand, particularly during near work. Both may contribute to asthenopia, blurred vision, or discomfort that co-occurs with migraine. Migraine itself involves altered sensory gain and impaired habituation, and visual-pattern sensitivity is well documented [3,4,9]. Subtle binocular-vision anomalies have also been reported in migraine [10].

These pathways could interact without implying that refractive error is the primary neurological cause of migraine. Screen exposure was independently associated with attack frequency and modified the refractive-error association. Digital eye strain is multifactorial: sustained accommodation and vergence, reduced blink rate, tear-film disturbance, small viewing distances, glare, and uncorrected refractive error may all contribute [17–20]. The present results support asking patients about device use and visual symptoms, but they do not validate specific commercial interventions such as blue-light-blocking lenses. Evidence for precision tints is mechanistically interesting—selected filters may reduce pattern discomfort or visual cortical hyperactivation in selected visually sensitive patients [21,22]—yet the clinical evidence remains small and heterogeneous. The correction-status finding should be interpreted cautiously. Participants whose prescription was judged appropriate had fewer reported attacks than those with uncorrected or undercorrected error, and the interaction was statistically significant. This is compatible with the improvement reported after adequate correction in earlier work [11], but reverse causation and confounding are possible. Patients with more frequent migraine may use screens differently, delay eye care, or perceive visual symptoms more intensely. A randomised or prospective before-and-after study with headache diaries is required to determine whether prescribing or updating optical correction reduces migraine frequency.

The study has practical implications. Neurologists should ask about blurred vision, near-work discomfort, diplopia, spectacle use, and recent eye examination, particularly when attacks are visually triggered or accompanied by marked asthenopia. Eye-care professionals should distinguish migraine from ocular and secondary headache causes and avoid attributing severe or atypical headache to minor refractive error without appropriate medical evaluation [13,14]. In Pakistan, where refractive services and specialist headache care may be unevenly accessible, coordinated referral between neurology and ophthalmology could identify treatable visual problems while reducing inappropriate reassurance or unnecessary investigations. The Karachi evidence that refractive error and asthenopia are common among ophthalmology patients with headache reinforces the relevance of this multidisciplinary approach [16]. Strengths include ICHD-3-based migraine diagnosis, comprehensive ophthalmic assessment, analysis of refractive-error type and correction status, and multivariable adjustment.

The study also evaluated screen time and prespecified effect modification. Limitations include the single-centre referral sample, consecutive non-probability sampling, cross-sectional design, reliance on 30-day recall rather than prospective diaries, and possible residual confounding by sleep, stress, caffeine, analgesic overuse, dry eye, accommodative dysfunction, and socioeconomic factors. The threshold of five attacks per month is a study-specific binary outcome and is not equivalent to the standard classification of high-frequency episodic migraine based on migraine days. Multiple subgroup tests increase the possibility of chance findings. Finally, the reported models should be independently reproduced from the raw dataset before journal submission. Future research should use prospective headache diaries, standardised accommodative and binocular testing, and clearly documented optical prescriptions. A pragmatic intervention trial could compare immediate correction with delayed correction among migraine patients with clinically meaningful uncorrected error, while maintaining standard neurological care. Outcomes should include migraine days, attack frequency, acute medication use, disability, visual symptoms, adherence, and cost-effectiveness.

Among patients with migraine attending DHQ Hospital Mardan, refractive errors—especially astigmatism and hypermetropia—were independently associated with greater monthly attack frequency. The association was stronger with prolonged screen exposure and uncorrected or undercorrected error. These results support routine ophthalmic assessment as part of selected patients’ multidisciplinary care, while prospective intervention studies are needed before refractive correction can be recommended specifically as a migraine-prevention strategy.

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