Hofmeijer Jeannette, van Kaam C R, van de Werff Babette, Vermeer Sarah E, Tjepkema-Cloostermans Marleen C, van Putten Michel J A M
Department of Clinical Neurophysiology, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, Netherlands.
Department of Neurology, Rijnstate Hospital, Arnhem, Netherlands.
Front Neurol. 2018 Jan 25;9:17. doi: 10.3389/fneur.2018.00017. eCollection 2018.
There is strong evidence suggesting detrimental effects of cortical spreading depolarization (CSD) in patients with acute ischemic stroke and severe traumatic brain injury. Previous studies implicated scalp electroencephalography (EEG) features to be correlates of CSD based on retrospective analysis of EEG epochs after having detected "CSD" in time aligned electrocorticography. We studied the feasibility of CSD detection in a prospective cohort study with continuous EEG in 18 patients with acute ischemic stroke and 18 with acute severe traumatic brain injury.
Full band EEG with 21 silver/silver chloride electrodes was started within 48 h since symptom onset. Five additional electrodes were used above the infarct. We visually analyzed all raw EEG data in epochs of 1 h. Inspection was directed at detection of the typical combination of CSD characteristics, i.e., (i) a large slow potential change (SPC) accompanied by a simultaneous amplitude depression of >1Hz activity, (ii) focal presentation, and (iii) spread reflected as appearance on neighboring electrodes with a delay.
In 3,035 one-hour EEG epochs, infraslow activity (ISA) was present in half to three quarters of the registration time. Typically, activity was intermittent with amplitudes of 40-220 µV, approximately half was oscillatory. There was no specific spatial distribution. Relevant changes of ISA were always visible in multiple electrodes, and not focal, as expected in CSD. ISA appearing as "SPC" was mostly associated with an amplitude increase of faster activities, and never with suppression. In all patients, depressions of spontaneous brain activity occurred. However, these were not accompanied by simultaneous SPC, occurred simultaneously on all channels, and were not focal, let alone spread, as expected in CSD.
With full band scalp EEG in patients with cortical ischemic stroke or traumatic brain injury, we observed various ISA, probably modulating cortical excitability. However, we were unable to identify unambiguous characteristics of CSD.
有强有力的证据表明，皮质扩散性去极化（CSD）对急性缺血性中风和重度创伤性脑损伤患者有有害影响。以往的研究基于在时间对齐的皮层脑电图中检测到“CSD”后对脑电图片段的回顾性分析，认为头皮脑电图（EEG）特征与CSD相关。我们在一项前瞻性队列研究中，对18例急性缺血性中风患者和18例急性重度创伤性脑损伤患者进行连续脑电图监测，研究CSD检测的可行性。
症状发作后48小时内开始使用21个银/氯化银电极进行全频段脑电图监测。在梗死灶上方额外使用了5个电极。我们对1小时片段的所有原始脑电图数据进行视觉分析。检查旨在检测CSD特征的典型组合，即：（i）伴有大于1Hz活动同时幅度降低的大慢电位变化（SPC），（ii）局灶性表现，以及（iii）以相邻电极上出现且有延迟为表现的扩散。
在3035个1小时的脑电图片段中，低频活动（ISA）在记录时间的一半至四分之三时间内出现。通常，活动是间歇性的，幅度为40 - 220µV，约一半是振荡性的。没有特定的空间分布。ISA的相关变化总是在多个电极上可见，并非如CSD预期的那样局灶性。表现为“SPC”的ISA大多与更快活动的幅度增加相关，从未与抑制相关。所有患者均出现自发性脑活动降低。然而，这些并未伴有同时的SPC，在所有通道上同时出现，并非局灶性，更不用说如CSD预期的那样扩散了。
对于皮质缺血性中风或创伤性脑损伤患者进行全频段头皮脑电图监测时，我们观察到了各种ISA，可能在调节皮质兴奋性。然而，我们未能识别出CSD的明确特征。
