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61st Annual Meeting of the German Society of Neurosurgery (DGNC) as part of the Neurowoche 2010
Joint Meeting with the Brazilian Society of Neurosurgery on the 20 September 2010

German Society of Neurosurgery (DGNC)

21 - 25 September 2010, Mannheim

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Evidence of cortical spreading depressions in a cortical intracerebral hemorrhage swine model – impact on cerebral blood flow and metabolism

Meeting Abstract

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  • Berk Orakcioglu - Neurochirurgische Klinik und Poliklinik Heidelberg, Universitätsklinikum Heidelberg, Deutschland
  • Yoichi Uozumi - Neurochirurgische Klinik und Poliklinik Heidelberg, Universitätsklinikum Heidelberg, Deutschland; Department of Neurosurgery, National Defense Medical College, Tokorozawa, Japan
  • M. Modar Kentar - Neurochirurgische Klinik und Poliklinik Heidelberg, Universitätsklinikum Heidelberg, Deutschland
  • Edgar Santos - Neurochirurgische Klinik und Poliklinik Heidelberg, Universitätsklinikum Heidelberg, Deutschland
  • Andreas Unterberg - Neurochirurgische Klinik und Poliklinik Heidelberg, Universitätsklinikum Heidelberg, Deutschland
  • Oliver W. Sakowitz - Neurochirurgische Klinik und Poliklinik Heidelberg, Universitätsklinikum Heidelberg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocV1590

doi: 10.3205/10dgnc065, urn:nbn:de:0183-10dgnc0655

Published: September 16, 2010

© 2010 Orakcioglu 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

Text

Objective: The pathophysiology of the perihemorrhagic zone (PHZ) following intracerebral hemorrhage (ICH) remains unclear. With the aim of characterising perihemorrhagic changes we established an experimental electrocorticographic (ECoG) monitoring in swine. The description of the model will be presented and preliminary data suggesting the existence of spreading depolarisations (SD) related to ICH.

Methods: Eight male swine (30–35kg) were sedated, mechanically ventilated and 8/16 channel unipolar EcoG monitoring (Wyler grid electrodes, GEOMETRY, STEEL/PLATINUM, Ad-Tech, Racine, WI) was placed onto the healthy cortical surface. A thermodiffusion-CBF and a microdialysis probe were additionally placed in cerebral white matter. After equilibration of the recordings a frontal lobar ICH was induced. Online monitoring of all relevant physiological parameters, thermodiffusion-CBF (td-CBF) and ECoG was continuously obtained for up to 18 hours post ICH.

Results: Within the hyperacute phase of ICH (<3hrs) no pathological electrocorticographical changes were detected. In the remaining time SDs occurred as early as 6 hours after ICH induction. Once SDs were present immediate perfusion changes (both hypoperfusion and hyperperfusion) and metabolic deterioration were observed in 6 out of 8 animals.

Conclusions: We established an experimental, ICH model in swine applying multiparametric neuromonitoring and ECoG. Spreading depolarizations are not likely to occur in the hyperacute phase after ICH but will subsequently be present past 6 hours. These findings frequently go along with alteration of cortical perfusion and metabolic deterioration. Our findings support the theory that SDs may contribute to secondary injury in the PHZ of ICH. This model may serve as a basis for further study of SDs after cortical ICH.