Helbok Raimund, Schiefecker Alois Josef, Friberg Christian, Beer Ronny, Kofler Mario, Rhomberg Paul, Unterberger Iris, Gizewski Elke, Hauerberg John, Möller Kirsten, Lackner Peter, Broessner Gregor, Pfausler Bettina, Ortler Martin, Thome Claudius, Schmutzhard Erich, Fabricius Martin
1 Department of Neurology, Neurocritical Care Unit, Medical University Innsbruck, Austria.
2 Department of Clinical Neurophysiology, Rigshospitalet, Copenhagen, Denmark.
J Cereb Blood Flow Metab. 2017 May;37(5):1871-1882. doi: 10.1177/0271678X16651269. Epub 2016 Jan 1.
Pathophysiologic mechanisms of secondary brain injury after intracerebral hemorrhage and in particular mechanisms of perihematomal-edema progression remain incompletely understood. Recently, the role of spreading depolarizations in secondary brain injury was established in ischemic stroke, subarachnoid hemorrhage and traumatic brain injury patients. Its role in intracerebral hemorrhage patients and in particular the association with perihematomal-edema is not known. A total of 27 comatose intracerebral hemorrhage patients in whom hematoma evacuation and subdural electrocorticography was performed were studied prospectively. Hematoma evacuation and subdural strip electrode placement was performed within the first 24 h in 18 patients (67%). Electrocorticography recordings started 3 h after surgery (IQR, 3-5 h) and lasted 157 h (median) per patient and 4876 h in all 27 patients. In 18 patients (67%), a total of 650 spreading depolarizations were observed. Spreading depolarizations were more common in the initial days with a peak incidence on day 2. Median electrocorticography depression time was longer than previously reported (14.7 min, IQR, 9-22 min). Postoperative perihematomal-edema progression (85% of patients) was significantly associated with occurrence of isolated and clustered spreading depolarizations. Monitoring of spreading depolarizations may help to better understand pathophysiologic mechanisms of secondary insults after intracerebral hemorrhage. Whether they may serve as target in the treatment of intracerebral hemorrhage deserves further research.
脑出血后继发性脑损伤的病理生理机制,尤其是血肿周围水肿进展的机制仍未完全明确。最近,去极化扩散在缺血性中风、蛛网膜下腔出血和创伤性脑损伤患者继发性脑损伤中的作用已得到证实。其在脑出血患者中的作用,尤其是与血肿周围水肿的关系尚不清楚。我们对27例接受血肿清除术和硬膜下皮质脑电图监测的昏迷脑出血患者进行了前瞻性研究。18例患者(67%)在24小时内进行了血肿清除术和硬膜下条形电极置入。皮质脑电图记录在术后3小时(四分位间距,3 - 5小时)开始,每位患者持续157小时(中位数),27例患者共持续4876小时。18例患者(67%)共观察到650次去极化扩散。去极化扩散在最初几天更为常见,第2天发生率最高。皮质脑电图抑制的中位时间比之前报道的更长(14.7分钟,四分位间距,9 - 22分钟)。术后血肿周围水肿进展(85%的患者)与孤立性和簇状去极化扩散的发生显著相关。监测去极化扩散可能有助于更好地理解脑出血后继发性损伤的病理生理机制。它们是否可作为脑出血治疗的靶点值得进一步研究。