Engelhorn T, Dörfler A, Egelhof T, Schwab S, Heiland S, Sartor K, Forsting M
Abteilung Neuroradiologie, Universitätsklinik Heidelberg.
Zentralbl Neurochir. 1998;59(3):157-65.
Acute ischemia in the complete territory of the carotid or the middle cerebral artery may lead to cerebral edema with raised intracranial pressure and progression to coma and death. Although clinical data suggest benefit for patients undergoing decompressive surgery for massive space occupying hemispheric stroke, little data about the effects of this procedure on morbidity and outcome is available. The experimental data support an early surgical approach. For early and probably most effective treatment of severe, space-occupying cerebral ischemia, the "malignant" character of the brain edema has to be recognized early after onset of vessel occlusion. Hereby magnetic resonance imaging (MRI) may allow to determine the clinical significance of brain edema early after onset, simultaneously allowing to monitor the evolution of ischemia. We performed serial SE-MRI in rats with acute hemispheric infarctions treated by decompressive craniectomy. Focal cerebral ischemia was induced in 36 rats using an endovascular occlusion technique. Decompressive craniectomy was performed 4 and 24 hours after vessel occlusion in groups of 12 animals each. Twelve animals were not treated by decompressive craniectomy (control group). Four, 24, 48, 72 and 168 hours after MCAO all animals were examined with conventional T1- and T2-weighted SE-MRI. Shift of the midline structures and compression of the ventricles were scored. Changes in weight and neurological performance were measured daily. The infarction volume was calculated by triphenyltetrazolium chloride staining 168 hours after MCAO. While mortality in the untreated group was 33.3%, none of the animals treated by a decompressive craniectomy died (mortality 0%). Neurological behaviour, weight loss and infarction volume were significantly better in the animals treated by early decompressive craniectomy (p < 0.05). Four hours after MCAO all untreated animals showed a massive shift of the midline structures and a massive compression of the ventricles; only 7 of 12 animals treated early by craniectomy showed mild mass effects. Correlation of the histological brain damage with T2-weighted MRI 4 hours after MCAO was poor (r = 0.41); later than 24 hours there was a good correlation (r > 0.7). Our results suggest that decompressive craniectomy in malignant cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. In the acute phase of hemispheric infarction conventional SE-MRI is not sensitive in estimation of infarction size. Later than 24 hours, conventinal SE-MRI proved to be useful in monitoring brain edema and infarction size in this rat model of malignant hemispheric stroke.
颈动脉或大脑中动脉整个供血区域的急性缺血可能导致脑水肿,颅内压升高,并进而发展为昏迷和死亡。尽管临床数据表明,对于因大面积占位性半球性卒中而接受减压手术的患者有益,但关于该手术对发病率和预后影响的数据却很少。实验数据支持早期手术治疗。为了对严重的、占位性脑缺血进行早期且可能最有效的治疗,必须在血管闭塞发作后尽早认识到脑水肿的“恶性”特征。在此,磁共振成像(MRI)可能有助于在发作后早期确定脑水肿的临床意义,同时能够监测缺血的进展情况。我们对接受减压颅骨切除术治疗的急性半球梗死大鼠进行了系列自旋回波MRI(SE-MRI)检查。采用血管内闭塞技术在36只大鼠中诱导局灶性脑缺血。在血管闭塞后4小时和24小时,分别对每组12只动物进行减压颅骨切除术。12只动物未接受减压颅骨切除术(对照组)。在大脑中动脉闭塞(MCAO)后4、24、48、72和168小时,对所有动物进行常规T1加权和T2加权SE-MRI检查。对中线结构的移位和脑室受压情况进行评分。每天测量体重和神经功能的变化。在MCAO后168小时,通过氯化三苯基四氮唑染色计算梗死体积。未治疗组的死亡率为33.3%,而接受减压颅骨切除术治疗的动物无一死亡(死亡率为0%)。早期接受减压颅骨切除术治疗的动物在神经行为、体重减轻和梗死体积方面均明显更好(p<0.05)。MCAO后4小时,所有未治疗的动物均出现中线结构的大量移位和脑室的大量受压;早期接受颅骨切除术治疗的12只动物中只有7只表现出轻度的占位效应。MCAO后4小时,组织学脑损伤与T2加权MRI的相关性较差(r = 0.41);24小时后则有良好的相关性(r>0.7)。我们的结果表明,恶性脑缺血中的减压颅骨切除术可降低死亡率并显著改善预后。如果在血管闭塞后早期进行,还可显著减小梗死面积。在半球梗死急性期,常规SE-MRI对梗死面积的估计不敏感。在24小时之后,在这种恶性半球性卒中大鼠模型中,常规SE-MRI被证明可用于监测脑水肿和梗死面积。