gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

Clusters of spreading depression is an electrophysiological correlate of delayed neurological deterioration after subarachnoid hemorrhage

Spreading-Depression-Clusters sind elektrophysiologische Korrelate für verzögerte neurologische Defizite nach Subarachnoidalblutung

Meeting Abstract

  • corresponding author J.P. Dreier - Charité-Berlin, Klinik für Neurologie, Berlin
  • J. Woitzik - Universitätsklinikum Mannheim, Klinik für Neurochirurgie, Mannheim
  • M. Fabricius - University of Copenhagen, Department of Neurophysiology, Copenhagen, Denmark
  • R. Bhatia - King’s College, London, UK
  • S. Major - Charité-Berlin, Klinik für Neurologie, Berlin
  • C. Drenckhahn - Charité-Berlin, Klinik für Neurologie, Berlin
  • T.N. Lehmann - Charité–Berlin, Klinik für Neurochirurgie, Berlin
  • A. Sarrafzadeh - Charité–Berlin, Klinik für Neurochirurgie, Berlin
  • COSBID study group
  • M. Lauritzen - University of Copenhagen, Department of Neurophysiology, Copenhagen, Denmark
  • A.J. Strong - King’s College, London, UK

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocFR.10.09

The electronic version of this article is the complete one and can be found online at:

Published: May 8, 2006

© 2006 Dreier 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: Aneurysmal subarachnoid hemorrhage (SAH) has a mortality rate around 45%. Delayed ischemic neurological deficit (DIND) is the predominant in-hospital complication. In animal experiments it was found that products of hemolysis in the subarachnoid space induced prolonged cortical spreading depressions (SD) which triggered waves of severe vaso-constriction. This process led to widespread cortical necrosis similar to the predominant infarct pattern of DIND in human autopsy studies. Therefore, we prospectively studied the occurrence of SD in patients with SAH.

Methods: 18 patients were consecutively recruited by four centers, members of the Co-operative Study on Brain Injury Depolarizations (COSBID) study group. Research consents were obtained after clinical decision for surgical treatment. A linear, 6-contact electrocorticography (ECoG) recording strip (Wyler) was placed on the cortex accessible through the craniotomy. Thereafter, the electrocorticogram was continuously monitored for periods up to 10 days. SD was defined by the sequential onset of a rapidly developing reduction of the power of ECoG amplitude of at least 50% associated with a propagating, polyphasic slow potential shift.

Results: During a recording period of 2265.5 hours 13 of 18 patients developed a total of 298 SD. Six patients showed a delayed decrease of consciousness (GCS, fall from GCS 14 (12, 15) to 9 (8, 11), P<0.05, Wilcoxon test). This correlated significantly with the occurrence of new clusters of SD. Evolution of new CT-proven brain infarcts was characterized by a pattern change of SD towards very prolonged depression.

Conclusions: 72% of patients with SAH in this study showed recurrent SD. Delayed neurological deterioration was associated with new clusters of SD. Brain infarcts were associated with a characteristic pattern change of SD.