Abstract
Background and purpose
Cerebral microdialysis is an invasive monitoring tool allowing analysis of various substances derived from the extracellular space in brain tissue such as glutamate, glycerol, lactate, and pyruvate. In order to assess the potential effects of hemicraniectomy, hypothermia and conservative therapy on these substances, we used neurochemical monitoring with microdialysis in large human stroke patients.
Methods
This is an open, prospective observational study in 24 patients with large MCA infarction undergoing either hypothermia (33°C), hemicraniectomy, or maximum conservative therapy. Microdialysis probe placement was aimed at the peri-infarct tissue within 24 h after stroke onset. Glutamate, glycerol, pyruvate, and lactate were analyzed every 60 min. Measurements of two consecutive days were pooled for statistical analysis.
Results
Average glutamate concentrations in patients treated with hemicraniectomy (5.3 ± 0.5 μmol/l, P < 0.0001; n = 6) and hypothermia (14.5 ± 3.6 μmol/l, P < 0.0001; n = 14) were significantly lower than in conservatively treated patients (68.3 ± 5.2 μmol/l; n = 4). Glycerol concentration was significantly lower in patients treated by hypothermia (111 ± 17 μmol/l; P < 0.0001) and hemicraniectomy (138 ± 8 μmol/l; P < 0.0001) as compared to conservatively treated patients with 612 ± 27 μmol/l. The lactate–pyruvate ratio was significantly lower both in the hypothermia (16.2 ± 3.3) and hemicraniectomy groups (31.3 ± 1.5) than in the conservative treatment group (56 ± 2.9).
Conclusion
Microdialysis allows bed-side monitoring of neuroprotective effects of stroke rescue therapies such as hypothermia and hemicraniectomy. Rescue of peri-infarct tissue and/or prevention of secondary ischemic injury could be associated with a lower mortality in invasively treated patients.
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Acknowledgment
This study was sponsored by the “Bundesministerium fuer Bildung und Forschung” (BmBF) as part of the “Kompetenznetz Schlaganfall.”
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Berger, C., Kiening, K. & Schwab, S. Neurochemical Monitoring of Therapeutic Effects in Large Human MCA Infarction. Neurocrit Care 9, 352–356 (2008). https://doi.org/10.1007/s12028-008-9093-8
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DOI: https://doi.org/10.1007/s12028-008-9093-8