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Relationship Between Migraine and Epilepsy in Pediatric Age
Author(s) -
Piccinelli Paolo,
Borgatti Renato,
Nicoli Francesca,
Calcagno Patrizia,
Bassi Maria Teresa,
Quadrelli Marta,
Rossi Giorgio,
Lanzi Giovanni,
Balottin Umberto
Publication year - 2006
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.2006.00373.x
Subject(s) - migraine , aura , ictal , epilepsy , electroencephalography , pathological , medicine , migraine with aura , pediatrics , anesthesia , neuroscience , psychology , psychiatry
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.