Department of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Harvard Medical School, Boston, MA, USA.
Epilepsia. 2018 Jul;59(7):1398-1409. doi: 10.1111/epi.14449. Epub 2018 Jun 13.
The treatment of focal epilepsies is largely predicated on the concept that there is a "focus" from which the seizure emanates. Yet, the physiological context that determines if and how ictal activity starts and propagates remains poorly understood. To delineate these phenomena more completely, we studied activity outside the seizure-onset zone prior to and during seizure initiation.
Stereotactic depth electrodes were implanted in 17 patients with longstanding pharmacoresistant epilepsy for lateralization and localization of the seizure-onset zone. Only seizures with focal onset in mesial temporal structures were used for analysis. Spectral analyses were used to quantify changes in delta, theta, alpha, beta, gamma, and high gamma frequency power, in regions inside and outside the area of seizure onset during both preictal and seizure initiation periods.
In the 78 seizures examined, an average of 9.26% of the electrode contacts outside of the seizure focus demonstrated changes in power at seizure onset. Of interest, seizures that were secondarily generalized, on average, showed power changes in a greater number of extrafocus electrode contacts at seizure onset (16.7%) compared to seizures that remained focal (3.8%). The majority of these extrafocus changes occupied the delta and theta bands in electrodes placed in the ipsilateral, lateral temporal lobe. Preictally, we observed extrafocal high-frequency power decrements, which also correlated with seizure spread.
This widespread activity at and prior to the seizure-onset time further extends the notion of the ictogenic focus and its relationship to seizure spread. Further understanding of these extrafocus, periictal changes might help identify the neuronal dynamics underlying the initiation of seizures and how therapies can be devised to control seizure activity.
局灶性癫痫的治疗主要基于这样一种概念，即存在一个“病灶”，癫痫发作即由此起源。然而，决定发作起始和传播的生理背景仍知之甚少。为了更全面地描绘这些现象，我们在发作起始前和起始时研究了发作起始区以外的活动。
17 例药物难治性癫痫患者植入立体定向深部电极，以进行发作起始区的定位和定位。仅分析起源于内侧颞叶结构的局灶性发作。在发作前和发作起始期间，使用频谱分析来量化在发作起始区内外区域中δ、θ、α、β、γ和高γ频带功率的变化。
在检查的 78 次发作中，平均有 9.26%的发作焦点以外的电极接触点在发作起始时显示功率变化。有趣的是，平均而言，继发性全身性发作在发作起始时在更多的额外焦点电极接触点显示功率变化（16.7%），而保持局灶性的发作则显示（3.8%）。这些额外焦点变化中的大多数发生在同侧外侧颞叶放置的电极的δ和θ频段中。在发作前，我们观察到额外焦点的高频功率下降，这也与发作传播相关。
在发作起始时间及其前后的这种广泛的活动进一步扩展了致痫灶及其与发作传播的关系。进一步了解这些额外焦点、发作前的变化可能有助于确定发作起始的神经元动力学以及如何设计治疗方法来控制发作活动。
