Alexander M J, Martin N A, Khanna R, Caron M, Becker D P
Division of Neurosurgery, U.C.L.A. Medical Center.
Acta Neurochir Suppl (Wien). 1994;60:479-81. doi: 10.1007/978-3-7091-9334-1_131.
Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.
头部受伤后的局灶性挫伤可能与局灶性或弥漫性脑水肿相关。早期的全脑充血和挫伤灶周围充血可能在脑水肿中起作用,尽管因果关系尚未明确界定。我们研究了27例因头部受伤导致局灶性挫伤的患者(入院时格拉斯哥昏迷评分3 - 12分)(CT检查未发现蛛网膜下腔、脑室内或脑实质内出血)。在受伤后的几天内,连续使用颅内压监测仪、头部CT以及静脉注射133氙进行局部脑灌注研究对患者进行观察。受伤当天可见皮质血流降低以及平均CBF15血流降低。此外,F1分析表明,在受伤当天,挫伤灶周围脑区的皮质血流(平均60 cc/100 g/min)显著高于挫伤区(平均43 cc/100 g/min)(p < 0.05)。挫伤区的平均局部脑血流仍低于正常水平(CBF15 < 35 cc/100 g/min),然而,受伤后的头几天皮质血流增加(第3天F1峰值 = 95 cc/100 g/min),随后降至低于正常的水平。受伤当天挫伤灶周围脑区的平均脑血流较低(CBF15 = 29 cc/100 g/min),尽管高于挫伤区,且在创伤后第3天增加至峰值45 cc/1009/min。然而,挫伤灶周围脑区的皮质血流呈现出不同的趋势。创伤当天平均F1较低,创伤后一天显著升高(平均105 cc/100 g/min)。27例局灶性挫伤患者中只有15例有脑水肿的证据。其中11例表现为局灶性水肿,4例表现为弥漫性水肿。如随访CT所见,局灶性水肿在创伤后的头几天内出现,而弥漫性水肿患者在入院CT时即显示有水肿。挫伤区最初的血流减少与随后挫伤灶周围的充血边缘有关。41%的患者中,局灶性充血与局灶性水肿相关,而弥漫性水肿似乎与挫伤的充血反应无关。