Masaki Yoshimura1, Shouwen Zhang2, Yuki Ueda3, Kazumi Matsuda4, Katsumi Imai5, Yukitoshi Takahashi6, Yushi Inoue7. 1. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: yosimura@szec.hosp.go.jp. 2. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: george12188@126.com. 3. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: ueda.de.yuki@gmail.com. 4. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: matsuda-1@hosp.go.jp. 5. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: imaik-1@hosp.go.jp. 6. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: takahashi-ped@umin.ac.jp. 7. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku 420-8688, Shizuoka, Japan. Electronic address: yinoue-jes@umin.net.
Abstract
PURPOSE: To clarify the neurophysiologic mechanism of epileptic negative myoclonus (ENM), we analyzed the magnetoencephalography (MEG) of a patient with ENM. METHODS: The 52-year-old right-handed male had frequent ENM in the right upper limb during awake and monthly seizures with sudden tonic stiffening of the right forearm during sleep. MRI demonstrated a focal cortical dysplasia in the cortex of the posterior portion of the left superior frontal sulcus. Whole-head type MEG, electroencephalography and electromyography were simultaneously recorded during ENM. Single equivalent currents dipoles (ECDs) were calculated for each spike component followed by silent period (SP) in the right deltoid muscle. These MEG spike components were averaged with respect to their peaks, and single ECD was also calculated for the averaged spike component. Furthermore, we analyzed the MEG with the silent-period-locked-averaging (SPLA) method. Twenty MEG signal data were averaged with respect to the onset of SP. Twenty epochs in each of five separate periods of recording were repeatedly averaged. ECDs were calculated for spike components observed in each averaged epoch. RESULTS: ECDs of each spike followed by SP were clustered near the cortex of the left central sulcus. In MEG spike averaging and SPLA method, ECDs at the peak of spike components were located near the right shoulder division of the primary sensorimotor cortex reproducibly. ECDs on the ascending phase before the peak were located lateral to the above ECD location in MEG spike averaging method. CONCLUSIONS: ENM was produced by an inhibitory action on the primary sensorimotor cortex corresponding to the body segment in which ENM occurs.
PURPOSE: To clarify the neurophysiologic mechanism of epileptic negative myoclonus (ENM), we analyzed the magnetoencephalography (MEG) of a patient with ENM. METHODS: The 52-year-old right-handed male had frequent ENM in the right upper limb during awake and monthly seizures with sudden tonic stiffening of the right forearm during sleep. MRI demonstrated a focal cortical dysplasia in the cortex of the posterior portion of the left superior frontal sulcus. Whole-head type MEG, electroencephalography and electromyography were simultaneously recorded during ENM. Single equivalent currents dipoles (ECDs) were calculated for each spike component followed by silent period (SP) in the right deltoid muscle. These MEG spike components were averaged with respect to their peaks, and single ECD was also calculated for the averaged spike component. Furthermore, we analyzed the MEG with the silent-period-locked-averaging (SPLA) method. Twenty MEG signal data were averaged with respect to the onset of SP. Twenty epochs in each of five separate periods of recording were repeatedly averaged. ECDs were calculated for spike components observed in each averaged epoch. RESULTS:ECDs of each spike followed by SP were clustered near the cortex of the left central sulcus. In MEG spike averaging and SPLA method, ECDs at the peak of spike components were located near the right shoulder division of the primary sensorimotor cortex reproducibly. ECDs on the ascending phase before the peak were located lateral to the above ECD location in MEG spike averaging method. CONCLUSIONS: ENM was produced by an inhibitory action on the primary sensorimotor cortex corresponding to the body segment in which ENM occurs.
Authors: Li Yang; Quanping Su; Na Xu; Liyun Xu; Juan Zhao; Chao Fan; Yufen Li; Baomin Li Journal: Medicine (Baltimore) Date: 2020-10-30 Impact factor: 1.817