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

Cerebral energy failure after subarachnoid hemorrhage – the role of hyperglycolysis

Zerebrale Energiekrise nach Subarachnoidalblutung – die Rolle der Hyperglykolyse

Meeting Abstract

  • corresponding author M. Oertel - Universitätsklinikum Gießen-Marburg, Klinik für Neurochirurgie, Gießen
  • S. Kästner - Universitätsklinikum Gießen-Marburg, Klinik für Neurochirurgie, Gießen
  • W. Scharbrodt - Universitätsklinikum Gießen-Marburg, Klinik für Neurochirurgie, Gießen
  • D.K. Böker - Universitätsklinikum Gießen-Marburg, Klinik für Neurochirurgie, Gießen

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.10.07

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

Published: May 8, 2006

© 2006 Oertel 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: After subarachnoid hemorrhage (SAH) cerebral metabolism is significantly impaired. Hyperglycolysis describes the reduction of oxidative metabolism followed by a relative increase of anaerobic glycolysis to maintain the energy supply. This phenomenon is known in head injury but has not been shown after SAH, yet. This study was conducted to test the hypothesis that hyperglycolysis is present in patients with SAH and associated with vasospasm.

Methods: A total of 105 measurements were conducted on 21 SAH patients (age 49±15 years, median Hunt/Hess Grade 4) the first five days following admission. Arteriovenos differences were calculated for oxygen (avDO2) and glucose (avDGlc). Hyperglycolysis was defined as a Metabolic Ratio (MR=avDO2(Vol%)/avDGlc(mg/dl)) <0.58. Vasospasm was diagnosed by transcranial Doppler sonography (VMCA>120 cm/s and Lindegaard Ratio >3) in conjunction with neurological deterioration.

Results: All but one patient developed at least one episode of hyperglycolysis during the observation period. Those patients, who experienced hyperglycolysis in more than 50% (n=12) of the time were significantly older (45±13 vs. 52±16 years; p=0.004) with higher jugular-venous saturations (67.6±8.3 vs. 79.2±5.2%; p=0.002) All patients developed vasospasm after post-hemorrhage day 3. Before and after day 3 hyperglycolysis occurred in 45% and 55% of studies, respectively. (p=0.3)

Conclusions: Hyperglycolysis is a common event after SAH. It may be associated with relative hyperemia but is independent of the presence of vasospasm.