• Arend M Hamming, Wermer Marieke J H MJH Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands., S Umesh Rudrapatna, Christian Lanier, Hine J A van Os, Walter M van den Bergh, Michel D Ferrari, Annette van der Toorn, van den Maagdenberg Arn M J M AMJM Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands Department of Human Genetics, Leiden University Medi, Ann M Stowe, and Rick M Dijkhuizen.
• Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Centre Utrecht, Utrecht, The Netherlands.
• J. Cereb. Blood Flow Metab. 2016 Jul 1; 36 (7): 1224-31.

AbstractSpreading depolarizations may contribute to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage, but the effect of spreading depolarizations on brain lesion progression after subarachnoid hemorrhage has not yet been assessed directly. Therefore, we tested the hypothesis that artificially induced spreading depolarizations increase brain tissue damage in a rat model of subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by endovascular puncture of the right internal carotid bifurcation. After one day, brain tissue damage was measured with T2-weighted MRI, followed by application of 1 M KCl (SD group, N = 16) or saline (no-SD group, N = 16) to the right cortex. Cortical laser-Doppler flowmetry was performed to record spreading depolarizations. MRI was repeated on day 3, after which brains were extracted for assessment of subarachnoid hemorrhage severity and histological damage. 5.0 ± 2.7 spreading depolarizations were recorded in the SD group. Subarachnoid hemorrhage severity and mortality were similar between the SD and no-SD groups. Subarachnoid hemorrhage-induced brain lesions expanded between days 1 and 3. This lesion growth was larger in the SD group (241 ± 233 mm(3)) than in the no-SD group (29 ± 54 mm(3)) (p = 0.001). We conclude that induction of spreading depolarizations significantly advances lesion growth after experimental subarachnoid hemorrhage. Our study underscores the pathophysiological consequence of spreading depolarizations in the development of delayed cerebral tissue injury after subarachnoid hemorrhage.© The Author(s) 2015.

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