A Neuronal Hyper-responsiveness in PRVEPs of Migraine Patients.
- Author:
Woo Jung KIM
1
;
Jeong Ho HAN
;
Hyun Wook HA
;
Eun Hyang SONG
;
Jung Suk LEE
;
Doo Eung KIM
Author Information
1. Department of Neurology, Korea Veterans Hospital.
- Publication Type:Original Article
- Keywords:
Evoked potential;
Migraine;
Cortical response
- MeSH:
Brain;
Epilepsy;
Evoked Potentials;
Evoked Potentials, Visual;
Headache;
Healthy Volunteers;
Humans;
Migraine Disorders*;
Neurons*
- From:Journal of the Korean Neurological Association
2001;19(3):239-244
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Although a number of visual evoked potentials (VEPs) studies have been performed to elucidate the pathophysiology of migraines, their results have been controversial. We studied the pattern-reversal visual evoked potentials (PRVEPs) during long periods of stimulation to show whether or not PRVEPs in migraines are abnormal. METHODS: Patients were divided into two groups; Group 1 (migraine with aura; MWA, n=29) and Group 2 (migraine without aura ; MOA, n=32) according to the International Headache Society criteria. PRVEPs were performed in both groups and in healthy volunteers (n=62). PRVEPs were averaged in 100 responses for a total duration of 10 minutes after an initial 3 minutes during stimulation and were analysed in terms of latencies and peak to peak amplitudes of N1-P1 and P1-N2 peaks. RESULTS: Amplitudes of PRVEPs in migraines showed significant increases compared to normal subjects (p<0.001), and amplitudes of PRVEPs in MWA showed significant increases compared to those in MOA (p<0.05). CONCLUSIONS: These results are explained by cortical hypoexcitability and hyper-responsiveness in migraine and by additional cortical hyper-responsiveness (another hyper-responsiveness) in MWA compared to MOA. We suggest that serotonergic and noradrenergic hyperactivity could be responsible for cortical hypoexcitability and hyper-responsiveness in a migraine brain. Another hyper-responsiveness in MWA could also be thought of as some evidence for cortical neuronal abnormality in MWA in addition to serotonergic and noradrenergic hyperactivity in a migraine brain. (J Korean Neurol Assoc 19(3):239~244, 2001)
