Miller J D, Bullock R, Graham D I, Chen M H, Teasdale G M
Department of Neurosurgery, University of Mississippi, Jackson.
Neurosurgery. 1990 Sep;27(3):433-9. doi: 10.1097/00006123-199009000-00016.
Ischemic brain damage is the most important neuropathological finding in humans who die after acute subdural hematoma; however, its causes are poorly understood. We have produced acute subdural hematoma in the rat by injecting 400 microliters of autologous blood (approximately 20% of intracranial volume) into the subdural space. Extensive areas of ischemic damage, involving 14 to 16% of the volume of the hemisphere, developed in this model at 4 and 24 hours after the lesion. The hematomas were associated with a brief peak in intracranial pressure (51 mm Hg), which remained at three times normal levels (14 mm Hg) for 3 hours. In this model, therefore, ischemic damage appears to be due to the local effects of blood overlying the cortex at 4 hours after the ictus, rather than to globally raised intracranial pressure. The implications for the pathophysiology of acute subdural hematomas in humans are discussed.
缺血性脑损伤是急性硬膜下血肿死亡患者最重要的神经病理学发现；然而，其病因尚不清楚。我们通过向大鼠硬膜下腔注射400微升自体血（约占颅内体积的20%）制造了急性硬膜下血肿。在该模型中，损伤后4小时和24小时出现了广泛的缺血损伤区域，占半球体积的14%至16%。血肿与颅内压短暂峰值（51毫米汞柱）相关，该峰值在3小时内维持在正常水平（14毫米汞柱）的三倍。因此，在该模型中，缺血性损伤似乎是由于发作后4小时覆盖皮质的血液的局部作用，而非颅内压整体升高所致。文中讨论了其对人类急性硬膜下血肿病理生理学的影响。
