Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortex.
Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortex.
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DOI：
10.1002/ana.21943
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发表时间：
2010-05
影响因子：
11.2
通讯作者：
Woitzik, Johannes
中科院分区：
文献类型：
--
作者：
Bosche, Bert;Graf, Rudolf;Ernestus, Ralf-Ingo;Dohmen, Christian;Reithmeier, Thomas;Brinker, Gerrit;Strong, Anthony J.;Dreier, Jens P.;Woitzik, Johannes
延迟性缺血性神经功能缺损（DIND）导致蛛网膜下腔出血（SAH）患者预后不良。由于大脑近端动脉血管痉挛是否是DIND的唯一原因仍不确定，因此应考虑其他过程。一个潜在的候选是皮质扩张性去极化（CSD）引起的缺氧。我们假设复发性CSDs会影响皮质氧的可用性。脑损伤去极化合作研究中心（COSBID）招募了9例接受开放性神经外科手术的严重SAH患者。我们同时使用了皮质电图和组织氧压（ptiO2）在人类大脑皮层的定位记录。我们通过顺序脑成像筛查延迟性皮质梗死，并通过血管造影或飞行时间磁共振成像研究脑血管痉挛。在850小时的总记录时间内，9例患者中有8例出现120例csd。55个CSDs（约46%）仅在9例患者中的2例中发现，这些患者后来发展为DIND。89例（约75%）的CSD发生在SAH后的第5天至第7天，96例（80%）发生在复发性CSD的时间集群中。CSD簇同时发生，主要是双相CSD相关的ptiO2反应，包括初级缺氧期和次级高氧期。CSD频率与缺氧期持续时间呈正相关，与高氧期持续时间呈负相关。低氧相在CSD集群内逐渐增加；特别是在DIND患者中，在这些簇中，双相ptiO2反应变为单相ptiO2反应。单相缺氧ptiO2对CSD的反应主要见于DIND患者。我们将这些临床ptiO2发现主要归因于皮质微循环局部血流的变化，但也归因于代谢增强。除了脑血管近端痉挛等经典诱因外，CSD集群还可能减少氧供应，增加氧消耗，从而促进DIND。神经网络学报，2010；67:607 - 617
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 (ptiO2) 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 (∼46%) were found in only 2 of 9 patients, who later developed DIND. Eighty-nine (∼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 ptiO2 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 ptiO2 responses changed to monophasic ptiO2 decreases within these clusters. Monophasic hypoxic ptiO2 responses to CSD were found predominantly in DIND patients. We attribute these clinical ptiO2 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 O2 supply and increase O2 consumption, and thereby promote DIND. ANN NEUROL 2010;67:607–617
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影响因子：
14.5
作者：
Dreier, Jens P.;Woitzik, Johannes;Strong, Anthony J.
通讯作者：
Strong, Anthony J.
影响因子：
9.9
作者：
KISTLER, JP;CROWELL, RM;FISHER, CM
通讯作者：
FISHER, CM
影响因子：
2.4
作者：
Jaeger, M;Soehle, M;Meixensberger, J
通讯作者：
Meixensberger, J
影响因子：
6.3
作者：
Hashemi, Parastoo;Bhatia, Robin;Boutelle, Martyn G.
通讯作者：
Boutelle, Martyn G.
影响因子：
1.7
作者：
MIES, G;IIJIMA, T;HOSSMANN, KA
通讯作者：
HOSSMANN, KA