increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury a microdialysis study object to determine the extent and duration of change in extracellular glutamate levels after human traumatic brain injury tbi 17 severely brain injured adults underwent implantation of a cerebral microdialysis probe and systematic sampling was conducted for 1 to 9 days postinjurymethods a total of 772 hourly microdialysis samples were obtained in 17 patients median glasgow coma scale score 525 mean age 394204 years the mean standard deviation glutamate levels in the dialysate were evaluated for 9 days during which the mean peak concentration reached 254137 microm on postinjury day 3 in each patient transient elevations in glutamate were seen each day however these elevations were most commonly seen on day 3 in all patients there was a mean of 4525 transient elevations in glutamate lasting a mean duration of 4449 hours these increases were seen in conjunction with seizure activity however in many seizurefree patients the increase in extracellular glutamate occurred when cerebral perfusion pressure was less than 70 mm hg p 0001 given the potential injuryinduced uncoupling of cerebral blood flow and metabolism after tbi these increases in extracellular glutamate may reflect a degree of enhanced cellular crisis which in severe head injury in humans appears to last up to 9 daysconclusions extracellular neurochemical measurements of excitatory amino acids may provide a marker for secondary insults that can compound human tbi