Concurrent monitoring of cerebral electrophysiology and metabolism after traumatic brain injury: an experimental and clinical study.
Multiparameter cerebral monitoring has been widely applied in traumatic brain injury to study posttraumatic pathophysiology and to manage head-injured patients (e.g., combining O(2) and pH sensors with cerebral microdialysis). Because a comprehensive approach towards understanding injury processes will also require functional measures, we have added electrophysiology to these monitoring modalities by attaching a recording electrode to the microdialysis probe. These dual-function (microdialysis/electrophysiology) probes were placed in rats following experimental fluid percussion brain injuries, and in a series of severely head-injured human patients. Electrical activity (cell firing, EEG) was monitored concurrently with microdialysis sampling of extracellular glutamate, glucose and lactate. Electrophysiological parameters (firing rate, serial correlation, field potential occurrences) were analyzed offline and compared to dialysate concentrations. In rats, these probes demonstrated an injury-induced suppression of neuronal firing (from a control level of 2.87 to 0.41 spikes/sec postinjury), which was associated with increases in extracellular glutamate and lactate, and decreases in glucose levels. When placed in human patients, the probes detected sparse and slowly firing cells (mean = 0.21 spike/sec), with most units (70%) exhibiting a lack of serial correlation in the spike train. In some patients, spontaneous field potentials were observed, suggesting synchronously firing neuronal populations. In both the experimental and clinical application, the addition of the recording electrode did not appreciably affect the performance of the microdialysis probe. The results suggest that this technique provides a functional monitoring capability which cannot be obtained when electrophysiology is measured with surface or epidural EEG alone.
Alves
Oscar L
OL
Department of Neurosurgery, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, 23298, USA. tmreeves@hsc.vcu.edu
Bullock
Ross
R
Clausen
Tobias
T
Reinert
Michael
M
Reeves
Thomas M
TM
D000200:Action Potentials / Q000502:physiology; D000328:Adult; D000818:Animals; D001928:Brain Diseases, Metabolic / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology; D001930:Brain Injuries / Q000175:diagnosis* / Q000378:metabolism / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000293:injuries / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000295:instrumentation / Q000379:methods*; D004594:Electrophysiology; D045604:Extracellular Fluid / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D017551:Microdialysis / Q000295:instrumentation / Q000379:methods*; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000379:methods; D009474:Neurons / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D019344:Lactic Acid; D018698:Glutamic Acid; D005947:Glucose