gms | German Medical Science

60th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Benelux countries and Bulgaria

German Society of Neurosurgery (DGNC)

24 - 27 May 2009, Münster

Cerebral Interleukin-6 in aneurysmal subarachnoid haemorrhage (aSAH) patients

Meeting Abstract

  • D. Graetz - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • A. Nagel - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • C. Gericke - Biometrie und Medizinische Epidemiologie, Charité – Universitätsmedizin Berlin
  • P. Vajkoczy - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin
  • A. Sarrafzadeh - Neurochirurgische Klinik, Charité – Universitätsmedizin Berlin

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocDI.03-07

DOI: 10.3205/09dgnc124, URN: urn:nbn:de:0183-09dgnc1249

Published: May 20, 2009

© 2009 Graetz et al.
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Outline

Text

Objective: There is increasing evidence that inflammation may play a role in the etiology of secondary complications in aneurysmal aSAH patients. This study was to evaluate cerebral Interleukin-6 (IL-6) levels in aSAH patients in three different compartments: cerebrospinal fluid (CSF), extracellular fluid (ECF) and plasma.

Methods: Patients (n=30) were classified according to the presence of neurological symptoms on admission and the development of a secondary deterioration. A microdialysis (MD) catheter was placed into the vascular territory of interest after aneurysm clipping. Samples for IL-6 were collected daily in CSF, ECF and plasma. Receiver operating characteristic (ROC) analysis and nonparametric tests were performed.

Results: IL-6 levels were highest in CSF followed by ECF and plasma. 75% of the patients reached their maximum within 2 days (ECF, Plasma) and 5 days (CSF) after aSAH. In initially symptomatic patients (n=13; WFNS: Q1=2.5, median=4, Q3=5) IL-6 in CSF and ECF indicated a secondary deterioration (delayed ischemic neurological deficits) (AUC=0.88, p=0.001 and AUC=0.86, p=0.003) while in initially asymptomatic patients (n=17, WFNS: Q1=1, median=1, Q3=2.5) IL-6 had no predictive value. These high IL-6 levels were measured in metabolically compromised brain tissue with higher LPR indicating anaerobic metabolism.

Conclusions: Because MD IL-6 levels differed from CSF levels with lower CSF values in the acute phase, a different origin of IL-6 production is possible. In patients with acute focal neurological deficits on admission a secondary deterioration is related to the IL-6 production. IL-6 might be a target for new therapeutic options in this subgroup of aSAH patients.