Steiner L A, Coles J P, Czosnyka M, Minhas P S, Fryer T D, Aigbirhio F I, Clark J C, Smielewski P, Chatfield D A, Donovan T, Pickard J D, Menon D K
Wolfson Brain Imaging Centre, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
J Neurol Neurosurg Psychiatry. 2003 Jun;74(6):765-70. doi: 10.1136/jnnp.74.6.765.
After head injury, impaired cerebrovascular autoregulation has been associated with abnormally high or low cerebral blood flow. The physiological relevance of cerebral blood flow levels is difficult to assess in these patients, whose cerebral metabolic rate for oxygen (CMRO(2)) is known to be abnormal. Investigation of these relations requires quantitative measures of cerebral blood flow and CMRO(2), to allow assessment of oxygen supply and demand relations.
To investigate the relation between dysautoregulation and global cerebral oxygen metabolism following head injury.
Using positron emission tomography, global cerebral blood flow, CMRO(2), and oxygen extraction fraction were determined in 22 patients who were investigated in 26 examinations on days 1 to 11 (mean (SD), 3.5 (2.3)) after head injury. Cerebrovascular pressure reactivity was assessed using a pressure reactivity index, calculated as the moving linear correlation coefficient between mean arterial blood pressure and intracranial pressure. Outcome was assessed six months after injury using the Glasgow outcome scale.
Low CMRO(2) was associated with disturbed pressure reactivity (inverse function, R(2) = 0.21, p = 0.018) and there was a correlation between disturbed pressure reactivity and oxygen extraction fraction (quadratic function, R(2) = 0.55, p = 0.0001). There was no significant relation between pressure reactivity and cerebral blood flow. An unfavourable outcome was associated with disturbed pressure reactivity. There was no significant relation between outcome and CMRO(2) or oxygen extraction fraction.
There is a close relation between dysautoregulation and abnormal cerebral metabolism but not blood flow. Further studies are needed to determine whether metabolic dysfunction is a result of or a cause of disturbed pressure reactivity, and to establish if there is a relation between cerebral oxygen metabolism and outcome.
头部受伤后,脑血管自动调节功能受损与脑血流量异常增高或降低有关。在这些已知脑氧代谢率(CMRO₂)异常的患者中,很难评估脑血流量水平的生理相关性。研究这些关系需要对脑血流量和CMRO₂进行定量测量,以便评估氧供需关系。
研究头部受伤后自动调节功能障碍与全脑氧代谢之间的关系。
使用正电子发射断层扫描,对22例头部受伤后第1至11天(平均(标准差),3.5(2.3))接受26次检查的患者测定全脑血流量、CMRO₂和氧摄取分数。使用压力反应性指数评估脑血管压力反应性,该指数计算为平均动脉血压与颅内压之间的移动线性相关系数。受伤6个月后使用格拉斯哥预后量表评估预后。
低CMRO₂与压力反应性紊乱相关(反比函数,R² = 0.21,p = 0.018),压力反应性紊乱与氧摄取分数之间存在相关性(二次函数,R² = 0.55,p = 0.0001)。压力反应性与脑血流量之间无显著关系。不良预后与压力反应性紊乱相关。预后与CMRO₂或氧摄取分数之间无显著关系。
自动调节功能障碍与脑代谢异常密切相关,但与脑血流量无关。需要进一步研究以确定代谢功能障碍是压力反应性紊乱的结果还是原因,并确定脑氧代谢与预后之间是否存在关系。