Schellinger Peter D, Fiebach Jochen B, Hoffmann Katrin, Becker Kristina, Orakcioglu Berk, Kollmar Rainer, Jüttler Eric, Schramm Peter, Schwab Stefan, Sartor Klaus, Hacke Werner
Department of Neurology, University of Heidelberg, Heidelberg, Germany.
Stroke. 2003 Jul;34(7):1674-9. doi: 10.1161/01.STR.0000076010.10696.55. Epub 2003 Jun 12.
Cerebral ischemia has been proposed as a contributing mechanism to secondary neuronal injury after intracerebral hemorrhage (ICH). The search for surrogate parameters that allow treatment stratification for spontaneous ICH continues. We sought to assess the presence and prognostic effect of perihemorrhagic ischemic changes and hypoperfusion in a prospective stroke MRI study.
We performed stroke MRI in 32 patients with hyperacute ICH (mean, 16.9+/-17.2 mL) within 6 hours after symptom onset (mean, 3.1+/-1.3 hours). Clinical data at baseline (National Institutes of Health Stroke Scale) and on day 90 (Barthel Index, modified Rankin Scale) were assessed. Perihemorrhagic perfusion- and diffusion-weighted imaging changes were assessed in a 1-cm-wide area around the clot.
Despite a mild perihemorrhagic mean transit time prolongation of 0.7+/-1.1 second, there were no significant perihemorrhagic apparent diffusion coefficient or mean transit time changes indicating irreversible ischemia or hypoperfusion. ICH size, time to imaging, or clinical severity at baseline or outcome were not reflected by changes of relative apparent diffusion coefficient or perfusion-weighted imaging. ICH size correlated with baseline clinical severity (r=0.51, P=0.005). There was a significant association (P=0.0494) and a significant negative correlation (r=-0.468, P=0.0103) of perihemorrhagic perfusion change with time from symptom onset not associated with ICH size.
Perihemorrhagic hypoperfusion probably is a consequence of reduced metabolic demand (diaschisis) rather than a sign of ischemia. We found no evidence for a perihemorrhagic and potentially salvageable ischemic penumbra in hyperacute ICH. Further studies should address metabolic, toxic, apoptotic, and microvascular aspects.
脑缺血被认为是脑出血（ICH）后继发性神经元损伤的一个促成机制。对于自发性ICH，寻找能够进行治疗分层的替代参数的工作仍在继续。我们试图在一项前瞻性卒中MRI研究中评估出血周围缺血性改变和灌注不足的存在情况及其预后影响。
我们对32例超急性ICH（平均体积16.9±17.2 mL）患者在症状发作后6小时内（平均3.1±1.3小时）进行了卒中MRI检查。评估了基线时（美国国立卫生研究院卒中量表）和第90天时（巴氏指数、改良Rankin量表）的临床数据。在血凝块周围1厘米宽的区域评估出血周围灌注加权成像和扩散加权成像的变化。
尽管出血周围平均通过时间轻度延长了0.7±1.1秒，但出血周围表观扩散系数或平均通过时间没有显著变化，表明不存在不可逆缺血或灌注不足。相对表观扩散系数或灌注加权成像的变化未反映出ICH大小、成像时间或基线时的临床严重程度或结局。ICH大小与基线临床严重程度相关（r=0.51，P=0.005）。出血周围灌注变化与症状发作后的时间存在显著关联（P=0.0494），且存在显著负相关（r=-0.468，P=0.0103），这与ICH大小无关。
出血周围灌注不足可能是代谢需求降低（交叉性小脑神经机能联系失联络）的结果，而非缺血的迹象。我们未发现超急性ICH存在出血周围且可能可挽救的缺血半暗带的证据。进一步的研究应关注代谢、毒性、凋亡和微血管方面。
