AN INCREASE IN EXTRACELLULAR GLUTAMATE IS A SENSITIVE METHOD OF DETECTING ISCHEMIC NEURONAL DAMAGE DURING CRANIAL BASE AND CEREBROVASCULAR SURGERY - AN IN-VIVO MICRODIALYSIS STUDY

All patients undergoing neurological surgery are at risk for serious c omplications. Ischaemic damage presenting with hemiparesis or speech d ifficulties occurs in up to 6% of patients undergoing cerebral bypass procedures and other complicated neurosurgical procedures. Currently a vailable methods for detection of such damage include the use of somat osensory evoked potentials (SSEPs) and electroencephalography (EEG). U nfortunately, these techniques have false positives and may remain nor mal in the presence of severe focal neurological deficits. Early detec tion of potential deficits may prevent or minimize damage through a ch ange in operative or anaesthetic strategy. With the availability of se veral potential neuroprotective compounds, it is also possible to trea t patients at risk of developing ischaemic complications if the indivi duals are identified early. The excitatory neurotransmitter glutamate is not only a metabolic product, but is also thought to promote ischae mia induced cell injury if released into the extracellular space. It m ay 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 intraoperative monit oring (IOM) as well as intra-operative in-vivo microdialysis measureme nt of glutamate. Our aim was to compare intra-operative microdialytic findings and IOM findings with respect to patients' early postoperativ e clinical courses. Three patients had significant intra-operative glu tamate increases indicating ischaemia. Two of these patients awoke wit h a new neurological deficit (hemiparesis). Routine IOM findings were either normal or showed only transient changes during the time the glu tamate levels were high. Our study shows that an increase in extracell ular glutamate, as monitored by in-vivo microdialysis, is an excellent early market of neuronal damage. While our glutamate measurements wer e done off-line, it may be possible to get in future continuous err-li ne measurements to serve as an early warning system for potential isch aemic damage.