gms | German Medical Science

64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

Early brain injury following subarachnoid hemorrhage in a murine injection model

Meeting Abstract

  • Marcel A. Kamp - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Institut für Neurophysiologie, Universitätsklinikum Köln
  • Maxine Dibué - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Institut für Neurophysiologie, Universitätsklinikum Köln; Zentrum für Molekulare Medizin, Köln
  • Hans-Jakob Steiger - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf
  • Toni Schneider - Institut für Neurophysiologie, Universitätsklinikum Köln; Zentrum für Molekulare Medizin, Köln
  • Daniel Hänggi - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocMO.09.03

doi: 10.3205/13dgnc073, urn:nbn:de:0183-13dgnc0730

Published: May 21, 2013

© 2013 Kamp et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Early brain injury (EBI) occurs within the first 72 hours after subarachnoid hemorrhage (SAH). Pathophysiology of EBI presents itself as complex, continuing to be poorly understood. To analyze the impact of EBI, we correlated early brain perfusion impairment with disturbances in cortical signalling.

Method: Totally, 80 C57BL/6J mice were analyzed. After induction of general anesthesia, 50 μl freshly-drawn blood obtained from the tail vein (or saline for the saline injection group or no injection but perforation of the atlanto-occipital membrane for the sham group) was injected in the cisterna magna. Relative rCBF and concentration of moving blood cells (Conc) was evaluated by Laser-Dopplermetry above the S1 and the cerebellar cortex and data were collected 30 minutes before and after SAH induction. Telemetric electrocorticograms from the S1 and cerebellar cortex recorded by implanted transmitters were continuously collected and were used to calculate absolute and relative power of frequency bands.

Results: Mortality rate group was 15.2% in the SAH. There were no deaths in the saline injection and the sham group. An acute impairment of regional cerebral perfusion was observed immediately after injection in the SAH group and in most animals of the saline injection group but not in sham operated animals. Quantification of acute hypoperfusion following injection revealed significant differences of cerebral and cerebellar rCBF and cerebellar Conc between the SAH and saline injection group (mean cerebral rCBF: 9.32±1.8 vs. 26.4±7.0; p=0.002; mean cerebellar rCBF: 25.6±4.9 vs. 61.3±13.8, p=0.006; mean cerebellar Conc: 83.2±10.6 vs. 168.5±17.3, p=0.00012). Injection of blood into the foramen magnum reduced total ECoG power by an average of 65%, whereas injection of saline (or sham injection) did not reduce total EcoG power (SAH vs Saline p=0.00017; SAH vs Sham p=0.02). SAH animals also displayed an instant reduction in absolute gamma power after injection compared to the two control groups (SAH vs Saline 22 μV2 vs. 69 µV2 p=0.033; SAH vs. Sham 22 μV2 vs. 52 µV2 p=0.002).

Conclusions: In response to subarachnoid blood, a cerebral hypoperfusion occurs parallel to an impairment of cortical signaling. The murine blood injection SAH model is suitable for a further pathophysiological analysis of EBI following SAH.