Bouma G J, Muizelaar J P, Stringer W A, Choi S C, Fatouros P, Young H F
Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond.
J Neurosurg. 1992 Sep;77(3):360-8. doi: 10.3171/jns.1992.77.3.0360.
The role of cerebral ischemia in the pathophysiology of traumatic brain injury is unclear. Cerebral blood flow (CBF) measurements with 133Xe have thus far revealed ischemia in a substantial number of patients only when performed between 4 and 12 hours postinjury. But these studies cannot be performed sooner after injury, they cannot be done in patients with intracranial hematomas still in place, and they cannot detect focal ischemia. Therefore, the authors performed CBF measurements in 35 comatose head-injured patients using stable xenon-enhanced computerized tomography (CT), simultaneously with the initial CT scan (at a mean (+/- standard error of the mean) interval of 3.1 +/- 2.1 hours after injury). Seven patients with diffuse cerebral swelling had significantly lower flows in all brain regions measured as compared to patients without swelling or with focal contusions; in four of the seven, cerebral ischemia (CBF less than or equal to 18 ml/100 gm.min-1) was present. Acute intracranial hematomas were associated with decreased CBF and regional ischemia in the ipsilateral hemisphere, but did not disproportionately impair brain-stem blood flow. Overall, global or regional ischemia was found in 11 patients (31.4%). There was no correlation between the presence of hypoxia or hypertension before resuscitation and the occurrence of ischemia, neither could ischemia be attributed to low pCO2. Ischemia was significantly associated with early mortality (p less than 0.02), whereas normal or high CBF values were not predictive of favorable short-term outcome. These data support the hypothesis that ischemia is an important secondary injury mechanism after traumatic brain injury, and that trauma may share pathophysiological mechanisms with stroke in a large number of cases; this may have important implications for the use of hyperventilation and antihypertensive drugs in the acute management of severely head-injured patients, and may lead to testing of drugs that are effective or have shown promise in the treatment of ischemic stroke.
脑缺血在创伤性脑损伤病理生理学中的作用尚不清楚。迄今为止，使用氙 - 133进行脑血流量（CBF）测量时，仅在伤后4至12小时进行测量的情况下，才在相当数量的患者中发现缺血情况。但这些研究无法在伤后更早进行，无法在颅内血肿仍存在的患者中进行，也无法检测局灶性缺血。因此，作者使用稳定氙增强计算机断层扫描（CT）对35例昏迷的头部受伤患者进行了CBF测量，与初始CT扫描同时进行（伤后平均（±平均标准误差）间隔为3.1±2.1小时）。与无肿胀或有局灶性挫伤的患者相比，7例弥漫性脑肿胀患者在所有测量脑区的血流量均显著降低；在这7例患者中的4例中，存在脑缺血（CBF小于或等于18 ml/100 gm·min-1）。急性颅内血肿与同侧半球CBF降低和局部缺血相关，但对脑干血流的损害并不不成比例。总体而言，11例患者（31.4%）发现存在全脑或局部缺血。复苏前的缺氧或高血压的存在与缺血的发生之间没有相关性，缺血也不能归因于低二氧化碳分压。缺血与早期死亡率显著相关（p<0.02），而正常或高CBF值并不能预测良好的短期预后。这些数据支持以下假设：缺血是创伤性脑损伤后一种重要的继发性损伤机制，并且在许多情况下，创伤可能与中风共享病理生理机制；这可能对在严重头部受伤患者的急性管理中使用过度换气和抗高血压药物具有重要意义，并且可能导致对在缺血性中风治疗中有效或已显示出前景的药物进行测试。
