Mendelowitsch A, Sekhar L N, Wright D C, Nadel A, Miyashita H, Richardson R, Kent M, Shuaib A
Department of Neurosurgery, George Washington University Medical Center, Washington, DC, USA.
Acta Neurochir (Wien). 1998;140(4):349-55; discussion 356. doi: 10.1007/s007010050108.
All patients undergoing neurological surgery are at risk for serious complications. Ischaemic damage presenting with hemiparesis or speech difficulties occurs in up to 6% of patients undergoing cerebral bypass procedures and other complicated neurosurgical procedures. Currently available methods for detection of such damage include the use of somatosensory evoked potentials (SSEPs) and electro-encephalography (EEG). Unfortunately, these techniques have false positives and may remain normal in the presence of severe focal neurological deficits. Early detection of potential deficits may prevent or minimize damage through a change in operative or anaesthetic strategy. With the availability of several potential neuroprotective compounds, it is also possible to treat patients at risk of developing ischaemic complications if the individuals are identified early. The excitatory neurotransmitter glutamate is not only a metabolic product, but is also thought to promote ischaemia induced cell injury if released into the extracellular space. It may be a significant parameter for ischaemic brain metabolism. In this report we describe 10 patients who underwent extracranial-intracranial (EC-IC) high flow bypass procedures with routine intra-operative monitoring (IOM) as well as intra-operative in-vivo microdialysis measurement of glutamate. Our aim was to compare intra-operative microdialytic findings and IOM findings with respect to patients' early postoperative clinical courses. Three patients had significant intra-operative glutamate increases indicating ischaemia. Two of these patients awoke with a new neurological deficit (hemiparesis). Routine IOM findings were either normal or showed only transient changes during the time the glutamate levels were high. Our study shows that an increase in extracellular glutamate, as monitored by in-vivo microdialysis, is an excellent early market of neuronal damage. While our glutamate measurements were done off-line, it may be possible to get in future continuous on-line measurements to serve as an early warning system for potential ischaemic damage.
所有接受神经外科手术的患者都有发生严重并发症的风险。在接受脑搭桥手术和其他复杂神经外科手术的患者中，高达6%会出现伴有偏瘫或言语困难的缺血性损伤。目前用于检测此类损伤的方法包括使用体感诱发电位（SSEP）和脑电图（EEG）。不幸的是，这些技术存在假阳性，并且在存在严重局灶性神经功能缺损时可能仍保持正常。早期发现潜在的缺损可能通过改变手术或麻醉策略来预防或减少损伤。随着几种潜在神经保护化合物的出现，如果能早期识别个体，也有可能治疗有发生缺血性并发症风险的患者。兴奋性神经递质谷氨酸不仅是一种代谢产物，而且如果释放到细胞外空间，还被认为会促进缺血诱导的细胞损伤。它可能是缺血性脑代谢的一个重要参数。在本报告中，我们描述了10例接受颅外-颅内（EC-IC）高流量搭桥手术的患者，术中进行了常规监测（IOM）以及谷氨酸的术中活体微透析测量。我们的目的是比较术中微透析结果和IOM结果与患者术后早期临床病程的关系。3例患者术中谷氨酸显著升高，提示缺血。其中2例患者苏醒后出现新的神经功能缺损（偏瘫）。常规IOM结果要么正常，要么在谷氨酸水平升高期间仅显示短暂变化。我们的研究表明，通过活体微透析监测，细胞外谷氨酸的增加是神经元损伤的一个极好的早期指标。虽然我们的谷氨酸测量是离线进行的，但未来有可能进行连续在线测量，作为潜在缺血性损伤的早期预警系统。
