Cerebral Taurine Levels are Associated with Brain Edema and Delayed Cerebral Infarction in Patients with Aneurysmal Suba
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ORIGINAL ARTICLE
Cerebral Taurine Levels are Associated with Brain Edema and Delayed Cerebral Infarction in Patients with Aneurysmal Subarachnoid Hemorrhage Mario Kofler1 • Alois Schiefecker1 • Boris Ferger2 • Ronny Beer1 • Florian Sohm3 Gregor Broessner1 • Werner Hackl4 • Paul Rhomberg5 • Peter Lackner1 • Bettina Pfausler1 • Claudius Thome´3 • Erich Schmutzhard1 • Raimund Helbok1
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Ó Springer Science+Business Media New York 2015
Abstract Background Cerebral edema and delayed cerebral infarction (DCI) are common complications after aneurysmal subarachnoid hemorrhage (aSAH) and associated with poor functional outcome. Experimental data suggest that the amino acid taurine is released into the brain extracellular space secondary to cytotoxic edema and brain tissue hypoxia, and therefore may serve as a biomarker for secondary brain injury after aSAH. On the other hand, neuroprotective mechanisms of taurine treatment have been described in the experimental setting. Methods We analyzed cerebral taurine levels using highperformance liquid chromatography in the brain extracellular fluid of 25 consecutive aSAH patients with
multimodal neuromonitoring including cerebral microdialysis (CMD). Patient characteristics and clinical course were prospectively recorded. Associations with CMD-taurine levels were analyzed using generalized estimating equations with an autoregressive process to handle repeated observations within subjects. Results CMD-taurine levels were highest in the first days after aSAH (11.2 ± 3.2 lM/l) and significantly decreased over time (p < 0.001). Patients with brain edema on admission or during hospitalization (N = 20; 80 %) and patients developing DCI (N = 5; 20 %) had higher brain extracellular taurine levels compared to those without (Wald = 7.3, df = 1, p < 0.01; Wald = 10.1, df = 1, p = 0.001, respectively) even after adjusting for disease
& Raimund Helbok [email protected]
Bettina Pfausler [email protected]
Mario Kofler [email protected]
Claudius Thome´ [email protected]
Alois Schiefecker [email protected]
Erich Schmutzhard [email protected]
Boris Ferger [email protected]
1
Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
2
CNS Diseases Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Birkendorfer Str. 65, 88397 Biberach an der Riss, Germany
Gregor Broessner [email protected]
3
Department of Neurosurgery, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
Werner Hackl [email protected]
4
UMIT – University for Health Sciences, Medical Informatics and Technology, Eduard-Wallno¨fer-Zentrum 1, 6060 Hall, Austria
5
Department of Radiology, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
Ronny Beer [email protected] Florian Sohm [email protected]
Paul Rhomberg [email protected] Peter Lackner [email protected]
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Neurocrit Care
severity and CMD-probe location. Th
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