gms | German Medical Science

63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

13. - 16. Juni 2012, Leipzig

Evaluation of CSF biomarkers for cerebral vasospasm and ischemia after subarachnoid hemorrhage

Meeting Abstract

Suche in Medline nach

  • C. Jung - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • A. Unterberg - Neurochirurgische Klinik, Universitätsklinikum Heidelberg
  • V. Seifert - Neurochirurgische Klinik, Universitätsklinikum Frankfurt a. Main

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocDO.07.02

doi: 10.3205/12dgnc058, urn:nbn:de:0183-12dgnc0583

Veröffentlicht: 4. Juni 2012

© 2012 Jung et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Objective: Delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) and delayed ischemic neurological deficits are still feared complications after subarachnoid hemorrhage (SAH). Although, microdialysis has been demonstrated to be a useful method for detection of brain ischemia, it remains a local indicator for intracerebral events. Therefore, we sought to determine, if alterations in NSE and S100B in serum or CSF levels of free amino acids (AA) including inhibitory and excitatory AA may be associated with cerebral vasospasm or ischemic lesions in patients after SAH.

Methods: Levels of free AA (including glutamate, aspartate, glycine and GABA) in CSF were analysed by HPLC in 20 patients after SAH and in 10 controls. Cerebral arteriograms were performed to assess cerebral vasospasm and follow-up CCT scans were performed to assess ischemic brain lesions.

Results: CSF glutamate, glutamine, glycine, serine and histidine significantly increased, while GABA decreased after SAH. CSF Glutamate (CC:0.48; p = 0.03), glutamine (CC:0.47; p = 0.04), glycine (CC:0.53; p = 0.02) and histidine (CC:0.66; p = 0.001) were associated with arteriographic cerebral vasospasm. Glutamate levels increased up to 13-times parallel to ischemic events. Serum S100B significantly correlated with ischemic lesions (CC = 0.85; p < 0.001), however, NSE did neither correlate with ischemia nor vasospasm.

Conclusions: This study shows that excitatory and inhibitory amino acids in CSF are altered after SAH, and might be useful as CSF-biomarkers for vasospasm and ischemia. Furthermore, S100B seems to be a good marker for ischemic cerebral events. However, further studies with larger number of cases are needed to validate these results.