Evidence of shared genetic risk factors for migraine and rolandic epilepsy

Authors

  • Tara Clarke,

    1. Department of Epidemiology, Mailman School of Public Health, Columbia University Medical Center, New York City, New York, U.S.A.
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  • Zeynep Baskurt,

    1. Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Ontario, Canada
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  • Lisa J. Strug,

    1. Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Ontario, Canada
    2. Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada
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  • Deb K. Pal

    1. Department of Epidemiology, Mailman School of Public Health, Columbia University Medical Center, New York City, New York, U.S.A.
    2. Epidemiology Division, Department of Psychiatry, Columbia University Medical Center, New York City, New York, U.S.A.
    3. Division of Statistical Genetics, Mailman School of Public Health, Columbia University Medical Center, New York City, New York, U.S.A.
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Address correspondence to Dr. Deb K. Pal, Department of Clinical Neuroscience, Institute of Psychiatry, King’s College London, London SE5 8AF, U.K. E-mail: Deb.Pal@iop.kcl.ac.uk

Summary

Purpose: Evidence for a specific association between migraine and rolandic epilepsy (RE) has been conflicting. Children with migraine frequently have electroencephalographic (EEG) abnormalities, including rolandic discharges, and approximately 50% of siblings of patients with RE exhibit rolandic discharges. We assessed migraine risk in RE probands and their siblings.

Methods: We used cohort and reconstructed cohort designs to respectively assess the relative risk of migraine in 72 children with RE and their 88 siblings using International Classification of Headache Disorders (ICHD-2) criteria. Incidences were compared in 150 age and geographically matched nonepilepsy probands and their 188 siblings. We used a Cox proportional hazards model, using age as the time base, adjusting hazard ratios (HRs) for sex in the proband analysis, and for sex and proband migraine status in the sibling analysis.

Results: Prevalence of migraine in RE probands was 15% versus 7% in nonepilepsy probands, and in siblings of RE probands prevalence was 14% versus 4% in nonepilepsy siblings. The sex-adjusted HR of migraine for an RE proband was 2.46 [95% confidence interval (CI) 1.06–5.70]. The adjusted HR of having ≥1 sibling with migraine in an RE family was 3.35 (95% CI 1.20–9.33), whereas the HR of any one sibling of a RE proband was 2.86 (95% CI 1.10–7.43).

Discussion: Migraine is strongly comorbid in RE and independently clusters in their siblings. These results suggest shared susceptibility to migraine and RE that is not directly mediated by epileptic seizures. Susceptibility gene variants for RE may be tested as risk factors for migraine.

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