Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage.
Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage.
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DOI：
10.1093/brain/awp102
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发表时间：
2009-07
期刊：
影响因子：
--
通讯作者：
COSBID study group
中科院分区：
文献类型：
--
作者：
Dreier JP;Major S;Manning A;Woitzik J;Drenckhahn C;Steinbrink J;Tolias C;Oliveira-Ferreira AI;Fabricius M;Hartings JA;Vajkoczy P;Lauritzen M;Dirnagl U;Bohner G;Strong AJ;COSBID study group
皮层扩散去极化（CSD）是一种与阳离子和水的净流入相关的大量神经元去极化波。在人类皮质中，将时间锁定到进行性缺血性损伤，测量了延长的CSD簇。CSD诱导阻力血管的张力改变，导致健康组织中的短暂过度灌注（生理血液动力学反应）;或有进行性损伤风险的组织中的灌注不足[反向血液动力学反应=皮质扩散性缺血（CSI）]，这迄今为止仅在实验中得到证实。在此，我们对13例蛛网膜下腔出血患者进行了一项前瞻性、多中心研究，采用新型硬膜下光电电极技术同时进行激光多普勒血流仪（LDF）和直流皮质电描记术，并结合组织氧分压（ptiO 2）测量。同时记录417例CSD的局部脑血流量和皮质电图。12例患者发生孤立性CSD，与生理性、不存在或反向血液动力学反应相关。而生理血流动力学反应导致组织高氧，逆反应导致组织缺氧。通过神经影像学评估，在5名接近结构性脑损伤的患者中测量了延长的CSD簇。群集与CSD诱导的扩散性低灌注相关，其持续时间（长达144分钟）明显长于孤立的CSD。因此，由逆血流动力学反应引起的氧耗可能有助于建立延长的CSD簇和病变进展。结合皮质电图和灌注监测也显示了一个特征性的血管签名，可用于无创检测CSD。低频血管波动（LF-VF）（f < 0.1 Hz），可通过功能成像方法检测，由大脑的静息神经元活动确定。CSD提供静息活动的去极化阻滞，电生理学记录为高频皮层电图活动的扩散性抑制。因此，我们观察到LF-VF的扩散抑制，伴随着高频皮层电图活动的扩散抑制，独立于CSD是否与生理、缺失或逆血流动力学反应相关。因此，LF-VF的扩散性抑制可以区分进行性缺血和修复阶段，其方式类似于先前所示的高频皮层电图活动的扩散性抑制。总之，这表明：（i）CSI是一种新的人类疾病机制与病变发展和潜在的目标，治疗干预中风;和（ii）延长蔓延supplementation LF-VF是一种新的“功能性标志物”进行性缺血。
The term cortical spreading depolarization (CSD) describes a wave of mass neuronal depolarization associated with net influx of cations and water. Clusters of prolonged CSDs were measured time-locked to progressive ischaemic damage in human cortex. CSD induces tone alterations in resistance vessels, causing either transient hyperperfusion (physiological haemodynamic response) in healthy tissue; or hypoperfusion [inverse haemodynamic response = cortical spreading ischaemia (CSI)] in tissue at risk for progressive damage, which has so far only been shown experimentally. Here, we performed a prospective, multicentre study in 13 patients with aneurysmal subarachnoid haemorrhage, using novel subdural opto-electrode technology for simultaneous laser-Doppler flowmetry (LDF) and direct current-electrocorticography, combined with measurements of tissue partial pressure of oxygen (ptiO2). Regional cerebral blood flow and electrocorticography were simultaneously recorded in 417 CSDs. Isolated CSDs occurred in 12 patients and were associated with either physiological, absent or inverse haemodynamic responses. Whereas the physiological haemodynamic response caused tissue hyperoxia, the inverse response led to tissue hypoxia. Clusters of prolonged CSDs were measured in five patients in close proximity to structural brain damage as assessed by neuroimaging. Clusters were associated with CSD-induced spreading hypoperfusions, which were significantly longer in duration (up to 144 min) than those of isolated CSDs. Thus, oxygen depletion caused by the inverse haemodynamic response may contribute to the establishment of clusters of prolonged CSDs and lesion progression. Combined electrocorticography and perfusion monitoring also revealed a characteristic vascular signature that might be used for non-invasive detection of CSD. Low-frequency vascular fluctuations (LF-VF) (f < 0.1 Hz), detectable by functional imaging methods, are determined by the brain's resting neuronal activity. CSD provides a depolarization block of the resting activity, recorded electrophysiologically as spreading depression of high-frequency-electrocorticography activity. Accordingly, we observed a spreading suppression of LF-VF, which accompanied spreading depression of high-frequency-electrocorticography activity, independently of whether CSD was associated with a physiological, absent or inverse haemodynamic response. Spreading suppressions of LF-VF thus allow the differentiation of progressive ischaemia and repair phases in a fashion similar to that shown previously for spreading depressions of high-frequency-electrocorticography activity. In conclusion, it is suggested that (i) CSI is a novel human disease mechanism associated with lesion development and a potential target for therapeutic intervention in stroke; and that (ii) prolonged spreading suppressions of LF-VF are a novel ‘functional marker’ for progressive ischaemia.
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影响因子：
14.5
作者：
Dreier, Jens P.;Woitzik, Johannes;Strong, Anthony J.
通讯作者：
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影响因子：
48
作者：
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3.3
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作者：
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通讯作者：
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影响因子：
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作者：
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