Department of Neurosurgery, University of Cologne, Cologne, Germany.
Ann Neurol. 2010 May;67(5):607-17. doi: 10.1002/ana.21943.
Delayed ischemic neurological deficit (DIND) contributes to poor outcome in subarachnoid hemorrhage (SAH) patients. Because there is continuing uncertainty as to whether proximal cerebral artery vasospasm is the only cause of DIND, other processes should be considered. A potential candidate is cortical spreading depolarization (CSD)-induced hypoxia. We hypothesized that recurrent CSDs influence cortical oxygen availability.
Centers in the Cooperative Study of Brain Injury Depolarizations (COSBID) recruited 9 patients with severe SAH, who underwent open neurosurgery. We used simultaneous, colocalized recordings of electrocorticography and tissue oxygen pressure (p(ti)O(2)) in human cerebral cortex. We screened for delayed cortical infarcts by using sequential brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magnetic resonance imaging.
In a total recording time of 850 hours, 120 CSDs were found in 8 of 9 patients. Fifty-five CSDs ( approximately 46%) were found in only 2 of 9 patients, who later developed DIND. Eighty-nine ( approximately 75%) of all CSDs occurred between the 5th and 7th day after SAH, and 96 (80%) arose within temporal clusters of recurrent CSD. Clusters of CSD occurred simultaneously, with mainly biphasic CSD-associated p(ti)O(2) responses comprising a primary hypoxic and a secondary hyperoxic phase. The frequency of CSD correlated positively with the duration of the hypoxic phase and negatively with that of the hyperoxic phase. Hypoxic phases significantly increased stepwise within CSD clusters; particularly in DIND patients, biphasic p(ti)O(2) responses changed to monophasic p(ti)O(2) decreases within these clusters. Monophasic hypoxic p(ti)O(2) responses to CSD were found predominantly in DIND patients.
We attribute these clinical p(ti)O(2) findings mainly to changes in local blood flow in the cortical microcirculation but also to augmented metabolism. Besides classical contributors like proximal cerebral vasospasm, CSD clusters may reduce O(2) supply and increase O(2) consumption, and thereby promote DIND.
迟发性缺血性神经功能缺损（DIND）是蛛网膜下腔出血（SAH）患者预后不良的原因。由于目前仍不确定近端大脑动脉血管痉挛是否是 DIND 的唯一原因，因此应考虑其他因素。皮质扩散性去极化（CSD）诱导的缺氧是一个潜在的候选因素。我们假设反复出现的 CSD 会影响皮质氧合。
合作性脑损伤去极化研究中心（COSBID）的多个中心招募了 9 名接受开颅手术的严重 SAH 患者。我们使用皮层脑电图和组织氧分压（p（ti）O（2））的同步、局灶性记录。我们通过连续的脑成像筛查延迟性皮质梗死，并通过血管造影或时间飞越磁共振成像检查脑血管痉挛。
在 850 小时的总记录时间内，在 9 名患者中的 8 名患者中发现了 120 次 CSD。在后来发生 DIND 的 2 名患者中，仅发现了 55 次 CSD（约 46%）。所有 CSD 中有 89 次（约 75%）发生在 SAH 后第 5 至 7 天，96 次（80%）发生在 CSD 反复出现的时间簇中。CSD 簇同时发生，主要是双相 CSD 相关的 p（ti）O（2）反应，包括原发性缺氧和继发性缺氧。CSD 的频率与缺氧期的持续时间呈正相关，与超氧期的持续时间呈负相关。缺氧期在 CSD 簇内逐渐增加；特别是在 DIND 患者中，双相 p（ti）O（2）反应在这些簇内转变为单相 p（ti）O（2）下降。CSD 引起的单相缺氧 p（ti）O（2）反应主要发生在 DIND 患者中。
我们将这些临床 p（ti）O（2）发现主要归因于皮质微循环中局部血流的变化，但也归因于代谢增加。除了近端大脑动脉血管痉挛等经典因素外，CSD 簇还可能降低 O（2）供应并增加 O（2）消耗，从而促进 DIND。
