Functional Changes of the Brainstem Triggering Diffuse 3 Hz Spike‐and‐Wave Complexes 111
Authors: Kohsaka Shinobu , Sakai Tacko , Mizukami Susumu , Uetake Kimiaki , Kohsaka Masako 
Published: August 2005

Purpose: In the previous studies (1 and 11), we had disclosed 2 types of functional changc in the lower brainstem beforc and during diffuse 3 Hz spike‐and‐wave complexes (SWC) in human primary generalized epilepsy (PGE): a long‐range biphasic fluctuation and rhythmic oscillations imposing on the descending limb of the former. Both were found to precede the onset of 3 H7. SWC. The results agreed with the “centrencephalic system” hypothesis for thc generating mcchanism 01 human PGE. In this study, we furthcr investigated the time coursc of development of rhythmic oscillations during the progrcssion of 3 Hz SWC. Methods: Six paticnts with typical absence scizure (TA) werc selected for this study. Six‐channel EEGs (Cz‐AI, Cz‐A2, T3‐C3, C3‐Cz, C Z ‐C and C4‐T4; band‐pass filter, I .S Hz ‐ I .5 kHz) were recorded together with 1 channel of acoustic trigger signal (SO dB hinaurally applied clicks, 20 times/sec) and stored on a magnetic tape. Thc data were replayed and sampled (sampling frequency, 10 kHz) through a personal computer, then spontaneous 3 Hz SWC was selected for the investigation. From the onset of SWC, 24 spike components were located with a pair of 3 segments (segment, 512‐point EEG data triggered by 1 trial of acoustic signal). As the averaging area composed of 3x24 segments was shifted forward by 1 segment, a series of 9 sequential brainstem auditory evoked potentials (BAEPs) were calculated in each shift using Cz‐A I and Cz‐A2. These sequential averaging procedures were repeated as the averaging area was shifted forward by 2 cycles of SWC until the first pair of segments reached the 17‐th SWC. The EEG trends were effectively subtracted by fitting a 7‐order polynomial curve before the average. Following these procedures, functional changes of the brainstem were investigated in 9 series composed of 9 sequential tracings of BAEPs from the onset of 3 Hz SWC. The sequence of BAEPs in a series corresponded to I cycle of SWC. Amplitude and area of both wave‐I11 and wave‐V were measured then tested for the differences within a cycle of SWC by 1‐way repeated measures of ANOVA in each series among the patients. One cycle of background EEGs was also averaged by reducing the data points to correlate the results of BAEPs. Results: Wave‐111 amplitude exhibited significant oscillatory changes synchronizing with I cycle of SWC: it gradually increased during the wave component, and then abruptly decreased predicting the next spike component. Both wave‐V parameters showed no significant changes. The oscillatory changes of wave‐I11 amplitude lasted from the onset to the middle stage of 3 Hz SWC development, They temporarily disappeared as the seizure progressed and then reappeared while background EEGs continued to exhibit 3 HZ SWC. Therefore, they were not considered as secondary phenomena generated by the cortical SWC. The phase of the reappearing oscillation was different from that of the preceding oscillations: the phase delayed so as to maintain its excitability during the spike component. Conclusion: The results confirm the previous conclusion that functional oscillations in the lower brainstem act pacemaker for cortical SWC, however they occur only during the early stage of SWC development. The results further suggest that the lower brainstem participates in the cessation of the seizure by changing the oscillatory phase against the cortical SWC.