Weiss Shennan A, Orosz Iren, Salamon Noriko, Moy Stephanie, Wei Linqing, Van't Klooster Maryse A, Knight Robert T, Harper Ronald M, Bragin Anatol, Fried Itzhak, Engel Jerome, Staba Richard J
Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A.
Epilepsia. 2016 Nov;57(11):1916-1930. doi: 10.1111/epi.13572. Epub 2016 Oct 10.
Ripples (80-150 Hz) recorded from clinical macroelectrodes have been shown to be an accurate biomarker of epileptogenic brain tissue. We investigated coupling between epileptiform spike phase and ripple amplitude to better understand the mechanisms that generate this type of pathologic ripple (pRipple) event.
We quantified phase amplitude coupling (PAC) between epileptiform electroencephalography (EEG) spike phase and ripple amplitude recorded from intracranial depth macroelectrodes during episodes of sleep in 12 patients with mesial temporal lobe epilepsy. PAC was determined by (1) a phasor transform that corresponds to the strength and rate of ripples coupled with spikes, and a (2) ripple-triggered average to measure the strength, morphology, and spectral frequency of the modulating and modulated signals. Coupling strength was evaluated in relation to recording sites within and outside the seizure-onset zone (SOZ).
Both the phasor transform and ripple-triggered averaging methods showed that ripple amplitude was often robustly coupled with epileptiform EEG spike phase. Coupling was found more regularly inside than outside the SOZ, and coupling strength correlated with the likelihood a macroelectrode's location was within the SOZ (p < 0.01). The ratio of the rate of ripples coupled with EEG spikes inside the SOZ to rates of coupled ripples in non-SOZ was greater than the ratio of rates of ripples on spikes detected irrespective of coupling (p < 0.05). Coupling strength correlated with an increase in mean normalized ripple amplitude (p < 0.01), and a decrease in mean ripple spectral frequency (p < 0.05).
Generation of low-frequency (80-150 Hz) pRipples in the SOZ involves coupling between epileptiform spike phase and ripple amplitude. The changes in excitability reflected as epileptiform spikes may also cause clusters of pathologically interconnected bursting neurons to grow and synchronize into aberrantly large neuronal assemblies.
临床宏观电极记录到的涟漪（80 - 150赫兹）已被证明是致痫脑组织的一种准确生物标志物。我们研究了癫痫样棘波相位与涟漪幅度之间的耦合，以更好地理解产生这种病理性涟漪（pRipple）事件的机制。
我们对12例内侧颞叶癫痫患者睡眠期间颅内深部宏观电极记录到的癫痫样脑电图（EEG）棘波相位与涟漪幅度之间的相位幅度耦合（PAC）进行了量化。PAC通过以下方式确定：（1）一种相量变换，它对应于与棘波耦合的涟漪的强度和速率，以及（2）涟漪触发平均法，以测量调制信号和被调制信号的强度、形态和频谱频率。耦合强度根据发作起始区（SOZ）内外的记录部位进行评估。
相量变换和涟漪触发平均法均显示，涟漪幅度常常与癫痫样EEG棘波相位强烈耦合。在SOZ内部比外部更常发现耦合，并且耦合强度与宏观电极位于SOZ内的可能性相关（p < 0.01）。SOZ内与EEG棘波耦合的涟漪速率与非SOZ中耦合涟漪速率的比值大于无论耦合情况检测到的棘波上的涟漪速率比值（p < 0.05）。耦合强度与平均归一化涟漪幅度的增加相关（p < 0.01），并且与平均涟漪频谱频率的降低相关（p < 0.05）。
SOZ中低频（80 - 150赫兹）pRipples的产生涉及癫痫样棘波相位与涟漪幅度之间的耦合。癫痫样棘波所反映的兴奋性变化也可能导致病理上相互连接的爆发性神经元簇生长并同步成异常大的神经元集合。
