Cerebral circulation after head injury. Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury?
Cerebral circulation after head injury. Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury?
复制标题
头部受伤后的脑循环。
DOI：
10.3171/jns.1981.55.1.0063
复制
发表时间：
1981
影响因子：
4.1
通讯作者：
W. Tweed
中科院分区：
文献类型：
--
作者：
J. Overgaard;C. Mosdal;W. Tweed
~/本文报道了一系列头部损伤的昏迷年轻患者，其中早期区域脑血流量（rCBF）与神经功能预后相关，并估计了rCBF与环境反应性交流互动恢复相容的临界阈值。在损伤后1周内，63例患者通过颈动脉内注射技术和35通道外计数，用放射性氙进行rCBF研究。将该组患者的2724个rCBF值与9个对照组的381个rCBF值进行比较。对存活的患者进行了2年的随访，以确定其最终的神经预后。当检查rCBF值频率分布的直方图时，很明显，在所有结果组中，rCBF的分布范围更广，并且向左移动。在清醒的对照组中，rCBF值没有低于40 ml/100 gm/min，而在昏迷患者中，交流脑功能恢复的阈值（有或没有神经功能缺陷）在17至20 ml/100 gm/min之间。然而，恢复交流脑功能（有或没有神经功能缺陷）的患者与没有恢复交流脑功能的患者（死亡或持续植物人状态）之间存在明显差异。在后两个结果组中，14.5%的rCBF值小于20 ml/100 gm/min，在受伤后最初几个小时内检查的发生率最高。缺血性rCBF主要分布在额叶和顶叶。这些研究证实了先前的死后病理学研究，揭示了死前额顶叶“分水岭”区域的脑缺血是导致头部损伤后早期端脑性脑死亡的主要因素。脑损伤患者局部缺血的病理生理机制尚不清楚，但颅内压升高引起的血流动力学改变可能是一个主要因素。皮层功能存活的临界阈值似乎与正常大脑相似，约为17至20 ml/100 gm/min。
~/ A series of comatose young patients with head injuries is presented in whom early regional cerebral blood flow (rCBF) is correlated with neurological outcome, and the critical threshold of rCBF compatible with recovery of responsive communicative interaction with the environment is estimated. Within the 1st week following injury, 63 patients had rCBF studies performed with radioactive xenon by the intracarotid bolus-injection technique and 35-channel external counting. A comparison was made between 2724 rCBF values from this group of patients with 381 from nine controls. Surviving patients were followed for 2 years to determine their eventual neurological outcome. When histograms of the frequency distribution of rCBF values were examined, it was evident that there was both a wider spread of rCBF and a shift to the left in all outcome groups. In awake controls, no rCBF values were less than 40 ml/100 gm/min, whereas in comatose patients the threshold for recovery of communicative brain function (with or without neurological deficits) was between 17 and 20 ml/100 gm/ min. There was a clear difference, however, between patients who recovered communicative brain function (with or without neurological deficit) and those who did not (dying or surviving in a persistent vegetative state). In the latter two outcome groups, 14.5% of rCBF values were less than 20 ml/100 gm/min, with the highest incidence in those examined within the first few hours of injury. The distribution of ischemic rCBF was mainly in the frontal and parietal lobes. These investigations confirm previous postmortem pathological studies in revealing that cerebral ischemia in the frontoparietal "watershed" areas antemortem is a major factor leading to telencephalic brain death in the early hours after head injury. The pathophysiological mechanisms of this localized ischemia in patients with head injury are not well understood, but probably hemodynamic alterations resulting from increased intracranial pressure are a major factor. The critical threshold for survival of cortical function seems to be similar to that of normal brain, about 17 to 20 ml/100 gm/min.