144 Ab stra c t / Po ste r: 2-6 C linic a l MEG : Pa in a nd so ma to se nso ry func tio n (range 130 to 190 ms). In all subjects, the left and right fusiform response was earlier in time and stronger in dipole moment in response to face compared to food stimuli with main effects for latency (faces 155.5 ms (SE 5.8 ms); foods 177.3 ms (SE 4.1 ms); both p < 0.01) and amplitude (faces 46.1 nAm (SE 5.4 nAm); foods 26.0 nAm (SE 4.7 nAm); both p < 0.01). No significant condition X hemisphere interaction was found. Present findings are in-line with previous studies indicating areas within the fusiform gyrus most sensitive to face-specific stimuli. The findings also demonstrate the robustness of this phenomenon since a delayed and weaker fusiform response to non-socially relevant stimuli was observed in 100% of the subjects. The magnitude of the latency advantage for faces versus food (approximately 20 ms in healthy subjects), along with the robustness of the observation, offers potential utility as a biomarker for social impairment (where, by hypothesis, it is reduced) and thereby as an index for quantitative monitoring of socialization therapy. Po ste r: 2- 6 C linic a l MEG : Pa in a nd so m a to se nso ry func tio n 2-6-1: Aberrant somatosensory evoked responses imply GABAergic dysfunction in Angelman syndrome *Kiyoshi Egawa 1 , Naoko Asahina 1 , Hideaki Shiraishi 1 , Kyousuke Kamada 2 , Fumiya Takeuchi 3 , Shingo Nakane 4 , Akira Sudo 1 , Shinobu Kohsaka 1 , Shinji Saitoh 1 1 Department of Pediatrics, Hokkaido University Graduate School of Medicine, Sapporo 2 Department of Neurosurgery, University of Tokyo Graduate School of Medicine, Tokyo 3 Department of Radiological Technology, Hokkaido University School of Medicine, Sapporo 4 Magnetoencephalographic laboratory, Hokkaido University Hospital, Sapporo, Japan A role for GABAergic inhibition in cortical sensory processing is one of the principle concerns of brain research. Angelman syndrome (AS) is thought to be one of the few neurodevelopmental disorders with GABAergic-related genetic involvement. AS results from a functional deficit of the imprinted UBE3A gene in 15q11-q13, resulting mainly from a 4-Mb deletion that includes GABA A receptor subunit genes. These genes are believed to affect the GABAergic system and modulate the clinical severity of AS. To understand the underlying cortical dysfunction, we have investigated the primary somatosensory-evoked responses in AS patients. Subjects included eleven AS patients with a 15q11-q13 deletion (AS Del), two AS patients without a 15q11-q13 deletion, but with a UBE3A mutation (AS non-Del), six epilepsy patients (non-AS) and eleven normal control subjects. Somatosensory evoked fields (SEFs) in response to median nerve stimulation were measured by magnetoencephalography. The N1m peak latency in AS Del patients was significantly longer (34.6 ±4.8 ms) than that in non-AS patients (19.5 ±1.2 ms, P < 0.001) or normal control subjects (18.4 ±1.8 ms, P < 0.001). The next component, P1m, was prolonged and ambiguous, and was only detected in patients taking clonazepam. In contrast, waveforms of AS non-Del were similar to that of control, rather than to AS Del. Thus, GABAergic dysfunction in AS Del patients is likely due to hemizygosity of GABA A receptor subunit genes, suggesting that GABAergic inhibition plays an important role in synchronous activity of human sensory cortex. 2-6-2: Somatosensory evoked magnetic fields in patients with tongue sensory deficits *Hitoshi Maezawa 1,2 , Kazuya Yoshida 2,3 , Kazuhisa Bessho 2 , Masao Matsuhashi 1,4 , Youhei Yokoyama 1,5 , Takashi Nagamine 1 , Hidenao Fukuyama 1 1 Human Brain Research Center, Graduate School of Medicine, Kyoto University, 2 Department of Oral and Maxillofacial Surgery, Graduate School of Medicine, Kyoto University, 3 Department of Oral and Maxillofacial Surgery, National Hospital Organization, Kyoto Medical Center, 4 Kyoto Institute of Technology, 5 Department of Neurosurgery, Graduate School of Medicine, Kyoto University Quantitative evaluation of the tongue sensory disturbances is important clinically. Somatosensory evoked fields following tongue stimulation was applied to overcome the difficulty of using electrophysiological approach to the peripheral nerve in the oral area. Six patients with unilateral tongue deficits were recruited (6 right side). Abnormal sensation area and its symmetric normal sensation area were stimulated electrically using pin electrodes non-invasively. The same stimulus intensity was used for both sites, which was adjusted to 4 times sensory thresholds in the normal area. 600 times were averaged. The signals recorded by 204-channel planar gradiometers out of whole-head 306 sensors were used for analysis. The band pass was 0.1 to 990 Hz and the sampling rate was 2997 Hz. The mean amplitude between 10 and 150 ms for the root mean square (RMS) was calculated from the 18-channel over the contralateral hemisphere (RMS[10, 150]). To estimate the activated cortical response, we calculated the difference of RMS[10, 150] and RMS[-50, -5] and termed it as aRMS. (aRMS = RMS[10, 150] - RMS[-50, -5]). Although normal area stimulation elicited 2 to 4 responses in all subjects, abnormal area stimulation showed smaller response in 4 patients. The across-subject average of the aRMS for the normal and abnormal side stimulation were 7.02 ± 1.92 and 1.72 ± 1.59 fT/cm, respectively. Significant difference of the aRMS was recognized between the sides of stimulation. The cortical activation evoked by abnormal side was significantly smaller than that after normal area in all patients.