An increase in extracellular glutamate is a sensitive method of detecting ischaemic neuronal damage during cranial base and cerebrovascular surgery. An in vivo microdialysis study.
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.
Mendelowitsch
A
A
Department of Neurosurgery, George Washington University Medical Center, Washington, DC, USA.
Sekhar
L N
LN
Wright
D C
DC
Nadel
A
A
Miyashita
H
H
Richardson
R
R
Kent
M
M
Shuaib
A
A
D000328:Adult; D000368:Aged; D001925:Brain Damage, Chronic / Q000175:diagnosis*; D002545:Brain Ischemia / Q000175:diagnosis*; D002548:Cerebral Revascularization; D002813:Chondrosarcoma / Q000601:surgery; D004569:Electroencephalography; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D005110:Extracellular Space / Q000737:chemistry*; D005260:Female; D018698:Glutamic Acid / Q000032:analysis*; D006801:Humans; D002532:Intracranial Aneurysm / Q000601:surgery*; D007431:Intraoperative Complications / Q000175:diagnosis*; D008297:Male; D008577:Meningeal Neoplasms / Q000601:surgery; D008579:Meningioma / Q000601:surgery; D017551:Microdialysis; D008875:Middle Aged; D009455:Neurofibroma / Q000601:surgery; D009460:Neurologic Examination; D019292:Skull Base Neoplasms / Q000601:surgery*
D018698:Glutamic Acid