gms | German Medical Science

68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

Occurrence of Spreading depolarization and impact on delayed infarct progression after malignant hemispheric stroke in C57/bl6 mice

Meeting Abstract

  • Anna Zdunczyk - Charité Berlin, Klinik für Neurochirurgie, Berlin, Deutschland
  • Leonie Schumm - Berlin, Deutschland
  • XI Bai - Berlin, Deutschland
  • Sebastian Major - Center for Stroke Research Berlin, Charité University Medicine Berlin, Berlin, Germany , Berlin, Deutschland
  • Peter Vajkoczy - Charité - Universitätsmedizin Berlin, Campus Mitte, Neurochirurgische Klinik, Berlin, Deutschland
  • Johannes Woitzik - Charité – Universitätsmedizin Berlin, Campus Benjamin Franklin, Neurochirurgische Klinik, Berlin, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocDI.27.03

doi: 10.3205/17dgnc340, urn:nbn:de:0183-17dgnc3406

Published: June 9, 2017

© 2017 Zdunczyk et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objective: Spreading depolarization (SD) occurs in high frequency in patients with malignant hemispheric stroke (MHS) and is coupled either to hyperaemic or hypoaemic blood flow responses. After experimental focal ischaemia SD is a significant cause for secondary stroke progression during the initial period of infarct maturation. Due to the need of surgery SD is typically monitored 48 to 120 hours after stroke onset under clinical conditions. Currently it is not known by what extent SD contributes to stroke progression during this delayed period. In this current study we analyze neurovascular coupling and occurrence of SD in a later phase of experimental cerebral ischemia.

Methods: Permanent focal ischemia was induced by distal occlusion of the left middle cerebral artery in male C57/bl6 mice. 24h after MCA occlusion, spreading depolarization was induced with potassium chloride. The neurovascular response was measured by laser speckle contrast analysis. Infarct progression was evaluated by sequential MRI. Three study groups were analyzed: control group without SD induction, SD induction with potassium chloride and SD induction and Ketamine administration (25 mg/kg body weight i.p.).

Results: 24 hours after stroke onset we observed 0.2 ± 0.2 SD/hour. The mean duration was 1.6 ± 1.0 minutes. During potassium application the frequency and duration increased to 3.3 ± 0.7 SD/hour and 3.2 ± 3.5 minutes, respectively. Ketamin treatment reduced the number and duration to 2.4 ± 0.8 SD/hour and 1.36 ± 0.95 minutes, respectively. Neurovascular coupling was dependent on the distance from the ischemic region but did not differ between individual groups. Induction of SD significantly increased stroke volume even 24 hours after stroke onset, which could be prevented by additional ketamine treatment.

Conclusion: Induction of SD with potassium was significantly associated with stroke progression even 24 hours after stroke onset. Therefore, SD might be a significant contributor for delayed stroke progression. Ketamine might be a possible drug to prevent SD induced stroke progression.