Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Tadahiro Mihara.
Clinical Neurophysiology | 2000
Shinji Ohara; Takashi Nagamine; Akio Ikeda; Takeharu Kunieda; Riki Matsumoto; Waro Taki; Nobuo Hashimoto; Koichi Baba; Tadahiro Mihara; Stephan Salenius; Hiroshi Shibasaki
OBJECTIVE To clarify how the primary sensorimotor and supplementary motor areas are involved in the generation of the rhythmicity of electromyogram (EMG) activity during continuous muscle contraction. METHOD We analyzed the coherence between subdurally recorded cortical electroencephalograms (EEG) and EMGs of the contralateral wrist extensor muscle during continuous isometric contraction in 8 patients with medically intractable epilepsy. RESULTS In all subjects, a significant coherence between the primary motor area (M1) and EMG was observed at the peak frequency of 15+/-3 Hz (means+/-SD). In the primary somatosensory area (S1) of 7 subjects and the supplementary motor area proper (SMA proper) of 4 subjects, significant coherence with EMG was observed at 12+/-5 and 15+/-4 Hz, respectively. The time lags revealed by cross-correlogram were 10+/-3, 7+/-1 and 22+/-8 ms in the M1, S1 and SMA proper, respectively, with the EMG lagging in all areas. CONCLUSION These findings suggest that the rhythmic activity in the SMA proper, as well as in the S1 and M1, is related to the generation of the rhythmicity of EMG activity.
Epilepsy Research | 2011
Chigusa Shimizu-Okabe; Masaki Tanaka; Kazumi Matsuda; Tadahiro Mihara; Akihito Okabe; Kohji Sato; Yushi Inoue; Tateki Fujiwara; Kazuichi Yagi; Atsuo Fukuda
Focal cortical dysplasia (FCD), which is characterized histologically by disorganized cortical lamination and large abnormal cells, is one of the major causes of intractable epilepsies. γ-aminobutyric acid (GABA)(A) receptor-mediated synchronous depolarizing potentials have been observed in FCD tissue. Since alterations in Cl(-) homeostasis might underlie these depolarizing actions of GABA, cation-Cl(-) cotransporters could play critical roles in the generation of these abnormal actions. We examined the expression patterns of NKCC1 and KCC2 by in situ hybridization histochemistry and immunohistochemistry in FCD tissue obtained by surgery from patients with intractable epilepsy. KCC2 mRNA and protein were expressed not only in non-dysplastic neurons in histologically normal portions located in the periphery of the excised cortex, but also in dysplastic cells in FCD tissue. The levels of KCC2 mRNA and protein were significantly decreased in the neurons around large abnormal neurons (giant neurons), but not in giant neurons, compared with non-dysplastic neurons. The neurons localized only around giant neurons significantly smaller than non-dysplastic neurons. However NKCC1 expression did not differ among these cell types. These results suggest that the intracellular Cl(-) concentration ([Cl(-)](i)) of small neurons might increase, so that depolarizing GABA actions could occur in the FCD tissue of epileptic foci.
Experimental Brain Research | 2004
Takeharu Kunieda; Akio Ikeda; Shinji Ohara; Riki Matsumoto; Waro Taki; Nobuo Hashimoto; Koichi Baba; Yushi Ioue; Tadahiro Mihara; Kazuichi Yagi; Hiroshi Shibasaki
In order to clarify the role of the lateral non-primary motor area in the control of voluntary movements, we studied movement-related cortical potentials (MRCPs) by direct epicortical recording from the lateral frontal lobe in nine patients with intractable partial epilepsy as a part of presurgical evaluation. We adopted movement tasks involving different body sites: eye closing, lip pursing, shoulder abduction, middle finger extension, thumb abduction, and foot dorsiflexion. We found that one or two small areas on the caudal lateral convexity of the frontal lobe generated pre-movement potential shifts regardless of the sites of movement (omni-Bereitschaftspotential; “omni-BP”). Such regions were located at or just rostral to the primary motor face area in six subjects, and at or rostral to the primary motor upper extremity area in three. Moreover, half of those areas were identified just adjacent (either rostral or caudal) to the primary negative motor area (PNMA), a cortical area of the lateral frontal lobe where negative motor responses were elicited by electric cortical stimulation. In conclusion, it is suggested that the lateral non-primary motor area plays a significant role, and has a close and direct relationship with other cortical areas in the frontal lobe, just like its counterpart on the mesial frontal cortex (supplementary negative motor area, SNMA).
Neuroscience Letters | 2006
Shinji Ohara; Akio Ikeda; Masao Matsuhashi; Takeshi Satow; Takeharu Kunieda; Nobuhiro Mikuni; Koichi Baba; Tadahiro Mihara; Susumu Miyamoto; Hiroshi Shibasaki
To demonstrate the Bereitschaftspotentials (BPs) over the high lateral convexity in the superior frontal gyrus, movement-related cortical potentials with respect to the middle finger extension were recorded in seven patients with refractory epilepsy who underwent subdural implantation of platinum electrode grids and/or strips covering the high lateral frontal convexity. In two out of the seven patients, BPs were recorded from the electrodes placed on the superior frontal gyrus in the vicinity of the border between the medial and lateral frontal lobes, which were distinct from those recorded from the primary sensorimotor cortex. The results suggest the possible contribution of either the lateral dorsal non-primary motor area or the SMA to the generation of the BPs.
Clinical Neurophysiology | 2010
L. Ren; K. Teraoka; Kouichi Baba; Naotaka Usui; Kazumi Matsuda; Takayasu Tottori; Fumihiro Nakamura; Tadahiro Mihara; Yushi Inoue
M. Kinoshita1, T. Mitsueda-Ono2, T. Hitomi2, J. Taki3, K. Usui4, M. Matsuhashi4, R. Matsumoto2, N. Mikuni3, H. Fukuyama4, R. Takahashi2, A. Ikeda2 1Department of Neurology, Utano National Hospital, Kyoto, Japan, 2Department of Neurology, Graduate School of Medicine, Kyoto University, Japan, 3Department of Neurosurgery, Graduate School of Medicine, Kyoto University, Japan, 4Human Brain Research Center, Kyoto University, Japan
Brain | 2000
Shinji Ohara; Akio Ikeda; Takeharu Kunieda; Shogo Yazawa; Koichi Baba; Takashi Nagamine; Waro Taki; Nobuo Hashimoto; Tadahiro Mihara; Hiroshi Shibasaki
The Journal of Neuroscience | 2001
Shinji Ohara; Tatsuya Mima; Koichi Baba; Akio Ikeda; Takeharu Kunieda; Riki Matsumoto; Junichi Yamamoto; Masao Matsuhashi; Takashi Nagamine; Kenichi Hirasawa; Tomokatsu Hori; Tadahiro Mihara; Nobuo Hashimoto; Stephan Salenius; Hiroshi Shibasaki
Brain | 2004
Junichi Yamamoto; Akio Ikeda; Takeshi Satow; Masao Matsuhashi; Koichi Baba; Fumitaka Yamane; Susumu Miyamoto; Tadahiro Mihara; Tomokatsu Hori; Waro Taki; Nobuo Hashimoto; Hiroshi Shibasaki
American Journal of Physiology-gastrointestinal and Liver Physiology | 2004
Takeshi Satow; Akio Ikeda; Junichi Yamamoto; Tahamina Begum; Dinh Ha Duy Thuy; Masao Matsuhashi; Tatsuya Mima; Takashi Nagamine; Koichi Baba; Tadahiro Mihara; Yushi Inoue; Susumu Miyamoto; Nobuo Hashimoto; Hiroshi Shibasaki
Clinical Neurophysiology | 2003
Riki Matsumoto; Akio Ikeda; Shinji Ohara; Masao Matsuhashi; Kouichi Baba; Fumitaka Yamane; Tomokatsu Hori; Tadahiro Mihara; Takashi Nagamine; Hiroshi Shibasaki