Relationship Between Migraine and Epilepsy in Pediatric Age



  • Paolo Piccinelli MD,

  • Renato Borgatti MD,

  • Francesca Nicoli MD,

  • Patrizia Calcagno MD,

  • Maria Teresa Bassi PhD,

  • Marta Quadrelli MD,

  • Giorgio Rossi MD,

  • Giovanni Lanzi MD,

  • Umberto Balottin MD

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  • From the Child Neuropsychiatry Unit, University of Insubria, Macchi Foundation Hospital, Varese, Italy (Piccinelli, Nicoli, Calcagno, Quadrelli, and Dr. Balottin); Department of Child Neurorehabilitation, Scientific Institute “Eugenio Medea,” Bosisio Parini, Italy (Borgatti and Bassi); and Department of Child Neuropsychiatry, University of Pavia, IRCCS Fondazione C. Mondino, Pavia, Italy (Rossi, and Lanzi)

Address all correspondence to Dr. Umberto Balottin, Unità di Neuropsichiatria Infantile, Ospedale Filippo Del Ponte, 21100 Varese, Italy.


Objective.—Many studies have supported the hypothesis of alteration of cortical hyperexcitability as a possible pathological mechanism underlying the onset of migraine and epileptic attacks. Different biochemical pathways involving cellular structures may increase or decrease the excitability of neuronal membranes. The aim of this study was to identify a possible link between migraine and epilepsy from a clinical and neurophysiologic point of view.

Methods.—One-hundred thirty-seven children and adolescents consecutively diagnosed for tension-type headache and idiopathic migraine with and without aura were studied. Anamnestic, clinical, and instrumental data were collected by a neurological examination, a specific questionnaire, and awake electroencephalogram (EEG) registrations. EEG features of nonheadache and nonseizures control group were compared.

Results.—Fourteen cases (10.2%) had a positive history for seizures with fever, isolated seizures, or epilepsy. Distribution differed according to headache diagnosis; migraine with aura (MWA) was largely prevalent. Specific electroencephalographic abnormalities were present in 11.7% of the sample, with a significant different distribution across the groups of children with headache and the control group: specific interictal abnormalities were found in 10 of 23 (43.5%) children with MWA. Two factors, seizures and specific interictal electroencephalographic abnormalities, showed a different distribution in patients with MWA compared to other classes of headache and control group (P≤ .01).

Conclusion.—The present study supports the hypothesis of a possible clinical continuum between some types of MWA and epileptic syndromes as entities due to altered neuronal excitability with similar genetic substrates.