gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

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Spreading depolarizations in perilesional cortex of human ischemic stroke

'Spreading depolarizations' im periläsionalen Cortex von Patienten nach zerebrovaskulärem Insult

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  • corresponding author O. Sakowitz - Klinik für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
  • C. Dohmen - Klinik für Neurologie, Universität zu Köln, Deutschland
  • T. Reithmeier - Klinik für Neurochirurgie, Universität zu Köln, Deutschland
  • B. Bosche - Klinik für Neurochirurgie, Universität zu Köln, Deutschland
  • R. Ernestus - Klinik für Neurochirurgie, Universität zu Köln, Deutschland
  • G. Brinker - Klinik für Neurochirurgie, Universität zu Köln, Deutschland
  • J. Woitzik - Klinik für Neurochirurgie, Universität Heidelberg, Klinikum Mannheim, Mannheim, Deutschland
  • M. Fabricius - Department of Clinical Neurophysiology, Glostrup Hospital, University of Copenhagen, Denmark
  • K. Kiening - Klinik für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
  • J. Dreier - Klinik für Neurologie, Campus Mitte, Charité - Universitätsmedizin Berlin, Berlin, Deutschland
  • A. Strong - Department of Clinical Neurosciences, Kings College London, London, UK
  • R. Graf - Max-Planck-Institut für Neurologische Forschung, Köln, Deutschland
  • COSBID study group

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocDO.01.03

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2007/07dgnc003.shtml

Published: April 11, 2007

© 2007 Sakowitz et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Objective: Cortical spreading depression (CSD) and peri-infarct depolarisation (PID) are examples of spreading depolarisations (SD) in experimental models of stroke. SD are thought to cause infarct expansion and secondary neuronal damage. In human victims of stroke SD have never been shown, while in patients with subarachnoid hemorrhage and traumatic brain injury SD have been reported recently. In this study we investigated the occurrence of SD in perilesional cortex of patients following surgical decompression for malignant middle cerebral artery (MCA) infarction.

Methods: Twelve patients were recruited by centers of the Co-operative Study on Brain Injury Depolarisations (COSBID) after approval by the local ethics committees. Following decompressive hemicraniectomy for malignant MCA infarction, subdural electrode strips with 6 linear contacts (Wyler, 5/10 mm; Ad-Tech Medical Instrument Corp., Racine, WI) were placed adjacent to infarcted cortex in a centrifugal orientation. Postoperatively, perilesional localization of electrode strips was confirmed by computer tomography. Monitoring of the electrocorticogram (EcoG) was performed for up to 120 h following infarction.

Results: In all patients with perilesional location of EcoG recordings (n=9) spontaneously occurring SD were observed. In total, 147 episodes were recorded. Of these, 98 episodes were classified as CSD, characterized by slow potential changes spreading between channels with a gradually developing depression of ECoG activity and subsequent recovery. Forty-nine episodes were defined as PID with stereotyped spreading slow potential changes on channels with locally depressed spontaneous ECoG activity. In patients with recordings overlying infarcted tissue (n=3) no SD were observed.

Conclusions: In perilesional cortex of patients with malignant MCA infarction the incidence of SD was surprisingly high. Their absence in recordings of infarcted tissue suggests that SD are associated with the ongoing pathophysiology of human stroke. Future studies will have to show the potential value of SD for diagnostics and targeted therapy of stroke progression.