Department of Neurology, Columbia University, New York, New York.
Department of Neurosurgery, Columbia University, New York, New York.
JAMA Neurol. 2017 Mar 1;74(3):301-309. doi: 10.1001/jamaneurol.2016.5325.
Periodic discharges (PDs) that do not meet seizure criteria, also termed the ictal interictal continuum, are pervasive on electroencephalographic (EEG) recordings after acute brain injury. However, their association with brain homeostasis and the need for clinical intervention remain unknown.
To determine whether distinct PD patterns can be identified that, similar to electrographic seizures, cause brain tissue hypoxia, a measure of ongoing brain injury.
DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study included 90 comatose patients with high-grade spontaneous subarachnoid hemorrhage who underwent continuous surface (scalp) EEG (sEEG) recording and multimodality monitoring, including invasive measurements of intracortical (depth) EEG (dEEG), partial pressure of oxygen in interstitial brain tissue (Pbto2), and regional cerebral blood flow (CBF). Patient data were collected from June 1, 2006, to September 1, 2014, at a single tertiary care center. The retrospective analysis was performed from September 1, 2014, to May 1, 2016, with a hypothesis that the effect on brain tissue oxygenation was primarily dependent on the discharge frequency.
Electroencephalographic recordings were visually classified based on PD frequency and spatial distribution of discharges. Correlations between mean multimodality monitoring data and change-point analyses were performed to characterize electrophysiological changes by applying bootstrapping.
Of the 90 patients included in the study (26 men and 64 women; mean [SD] age, 55 [15] years), 32 (36%) had PDs on sEEG and dEEG recordings and 21 (23%) on dEEG recordings only. Frequencies of PDs ranged from 0.5 to 2.5 Hz. Median Pbto2 was 23 mm Hg without PDs compared with 16 mm Hg at 2.0 Hz and 14 mm Hg at 2.5 Hz (differences were significant for 0 vs 2.5 Hz based on bootstrapping). Change-point analysis confirmed a temporal association of high-frequency PD onset (≥2.0 Hz) and Pbto2 reduction (median normalized Pbto2 decreased by 25% 5-10 minutes after onset). Increased regional CBF of 21.0 mL/100 g/min for 0 Hz, 25.9 mL/100 g/min for 1.0 Hz, 27.5 mL/100 g/min for 1.5 Hz, and 34.7 mL/100 g/min for 2.0 Hz and increased global cerebral perfusion pressure of 91 mm Hg for 0 Hz, 100.5 mm Hg for 0.5 Hz, 95.5 mm Hg for 1.0 Hz, 97.0 mm Hg for 2.0 Hz, 98.0 mm Hg for 2.5 Hz, 95.0 mm Hg for 2.5 Hz, and 67.8 mm Hg for 3.0 Hz were seen for higher PD frequencies.
These data give some support to consider redefining the continuum between seizures and PDs, suggesting that additional damage after acute brain injury may be reflected by frequency changes in electrocerebral recordings. Similar to seizures, cerebral blood flow increases in patients with PDs to compensate for the increased metabolic demand but higher-frequency PDs (>2 per second) may be inadequately compensated without an additional rise in CBF and associated with brain tissue hypoxia, or higher-frequency PDs may reflect inadequacies in brain compensatory mechanisms.
在急性脑损伤后，脑电图（EEG）记录中普遍存在不符合癫痫发作标准的周期性放电（PDs），也称为发作间连续体。然而，其与脑内稳态的关系以及是否需要临床干预仍然未知。
确定是否可以识别出与电发作相似的不同 PD 模式，这些模式会导致脑组织缺氧，从而衡量持续的脑损伤。
设计、设置和参与者：这项前瞻性队列研究纳入了 90 名患有高分级自发性蛛网膜下腔出血且处于昏迷状态的患者，这些患者接受了连续的表面（头皮）脑电图（sEEG）记录和多模态监测，包括皮层内（深度）脑电图（dEEG）、脑间质氧分压（Pbto2）和局部脑血流（CBF）的侵入性测量。患者数据于 2006 年 6 月 1 日至 2014 年 9 月 1 日在一家三级护理中心收集。回顾性分析于 2014 年 9 月 1 日至 2016 年 5 月 1 日进行，假设脑氧合的影响主要取决于放电频率。
根据 PD 频率和放电的空间分布，对脑电图记录进行了视觉分类。通过应用自举法进行变点分析，对多模态监测数据和变化点分析之间的相关性进行了研究，以描述电生理变化。
在纳入研究的 90 例患者中（男 26 例，女 64 例；平均[SD]年龄，55[15]岁），32 例（36%）在 sEEG 和 dEEG 记录上有 PDs，21 例（23%）仅在 dEEG 记录上有 PDs。PDs 的频率范围为 0.5 至 2.5 Hz。无 PDs 时中位数 Pbto2 为 23 mmHg，而 2.0 Hz 时为 16 mmHg，2.5 Hz 时为 14 mmHg（基于自举法，0 与 2.5 Hz 之间的差异有统计学意义）。变点分析证实了高频 PD 发作（≥2.0 Hz）和 Pbto2 降低（发作后 5-10 分钟，归一化 Pbto2 中位数降低 25%）之间存在时间关联。0 Hz 时局部脑血流增加 21.0 mL/100 g/min，1.0 Hz 时增加 25.9 mL/100 g/min，1.5 Hz 时增加 27.5 mL/100 g/min，2.0 Hz 时增加 34.7 mL/100 g/min，0 Hz 时全局脑灌注压增加 91.0 mm Hg，0.5 Hz 时增加 100.5 mm Hg，1.0 Hz 时增加 95.5 mm Hg，2.0 Hz 时增加 97.0 mm Hg，2.5 Hz 时增加 98.0 mm Hg，2.5 Hz 时增加 95.0 mm Hg，3.0 Hz 时增加 67.8 mm Hg，这些都是由于 PD 频率升高所致。
这些数据为重新定义发作和 PDs 之间的连续体提供了一些支持，表明急性脑损伤后可能会反映在电脑记录中的频率变化上出现额外的损伤。与癫痫发作相似，PD 患者的脑血流增加以补偿增加的代谢需求，但如果没有额外的 CBF 增加和相关的脑组织缺氧，高频 PDs（>2 次/秒）可能无法得到充分补偿，或者高频 PDs 可能反映了脑补偿机制的不足。
