• Kimberly A Leiken, Jing Xiang, Emily Curry, Hisako Fujiwara, Douglas F Rose, Janelle R Allen, Joanne E Kacperski, Hope L O'Brien, Marielle A Kabbouche, Scott W Powers, and Andrew D Hershey.
• Division of Neurology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, MLC 2015, Cincinnati, OH, 45220, USA. Kimberly.leiken@cchmc.org.
• J Headache Pain. 2016 Jan 1; 17: 46.

BackgroundReports have suggested that abnormal cortical excitability may be associated with acute migraines. The present study quantitatively assesses the degree of cortical excitability in chronic migraine as compared to acute migraine and healthy controls within the pediatric population.MethodsWe investigated 27 children suffering from chronic migraine, 27 children suffering from acute migraine, and 27 healthy controls using a magnetoencephalography (MEG) system, recording at a sampling rate of 6000 Hz. All groups were age-matched and gender-matched. Neuromagnetic brain activation was elicited by a finger-tapping motor task. The spatiotemporal and spectral signatures of MEG data within a 5-2884 Hz range were analyzed using Morlet wavelet transform and beamformer analyses.ResultsCompared with controls, the chronic migraine group showed (1) significantly prolonged latencies of movement-elicited magnetic fields (MEFs) between 5 and 100 Hz; (2) increased spectral power between 100 and 200 Hz, and between 2200 and 2800 Hz; and (3) a higher likelihood of neuromagnetic activation in the ipsilateral sensorimotor cortices, supplementary motor area, and occipital regions. Compared with acute migraine group, chronic migraine patients showed (1) significantly higher odds of having strong MEFs after 150 ms; and (2) significantly higher odds of having neuromagnetic activation from the deep brain areas.ConclusionsResults demonstrated that chronic migraine subjects were not only different from the healthy controls, but also different from acute migraine subjects. The chronification of migraines may be associated with elevated cortical excitability, delayed and spread neural response, as well as aberrant activation from deep brain areas.

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