Frameless stereotactic aspiration and thrombolysis of deep intracerebral hemorrhage is associated with reduced levels of extracellular cerebral glutamate and unchanged lactate pyruvate ratios.
BACKGROUND
Intracerebral hemorrhage (ICH) is a devastating form of stroke commonly resulting in severe morbidity and high mortality. Secondary brain injury often occurs in the days following the initial hemorrhage and is associated with significant neurological deterioration. The neurochemistry associated with secondary injury is poorly understood. The purpose of this study is to characterize the neurochemical changes in perihematomal tissue during frameless minimally invasive evacuation of spontaneous hematomas.


METHODS
This is a nonrandomized prospective microdialysis study of 12 consecutive patients undergoing Frameless Stereotactic Aspiration and Thrombolysis (FAST) of deep ICHs. Hourly glucose, lactate, pyruvate, and glutamate were measured in the perihematomal tissue of patients undergoing minimally invasive hematoma evacuation. Analyte concentrations were compared to evaluate the natural history of perihematomal neurochemistry and to identify changes potentially related to secondary injury.


RESULTS
Brain hematoma volumes were reduced 87% during FAST and National Institute of Health Stroke Scale (NIHSS) scores were improved from an average of 19 at admission to 12.6 at time of discharge from the intensive care unit. Glutamate average values decreased from the first 24 hours of measurement (12 mmol/L +/- 6) to the final 24-hour epoch (5 mmol/L +/- 6). Glutamate reduction showed a significant linear (p = 0.0007) and quadratic (p <0.05) trend during hematoma drainage. Lactate pyruvate ratios (LPR), a common marker of ischemia, were unchanged.


CONCLUSIONS
This study reports that elevated levels of glutamate are found in the perihematomal region after ICH and are decreased during hematoma drainage. Conversely, ischemic LPRs are not found in perihematomal regions and were unchanged during hematoma drainage. These data suggest that excitotoxicity related to glutamate may have an important impact on secondary injury. The data failed to support the role of ischemia in secondary perihematomal damage.
Miller
Chad M
CM
Division of Neurosurgery, David Geffen School of Medicine at University of California-Los Angeles, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA. Chadmiller@mednet.ucla.edu
Vespa
Paul M
PM
McArthur
David L
DL
Hirt
Daniel
D
Etchepare
Maria
M
D001921:Brain / Q000000981:diagnostic imaging / Q000473:pathology; D002533:Cerebral Angiography; D002543:Cerebral Hemorrhage / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D002552:Cerebral Ventricles / Q000473:pathology; D005260:Female; D018698:Glutamic Acid / Q000097:blood*; D006801:Humans; D019344:Lactic Acid / Q000097:blood*; D008297:Male; D017551:Microdialysis / Q000379:methods; D011446:Prospective Studies; D019289:Pyruvic Acid / Q000097:blood*; D013238:Stereotaxic Techniques; D015912:Thrombolytic Therapy; D014057:Tomography, X-Ray Computed
D019344:Lactic Acid; D018698:Glutamic Acid; D019289:Pyruvic Acid