gms | German Medical Science

65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

11. - 14. Mai 2014, Dresden

Elevated levels of Calcitonin-Gene related Peptide in serum and cerebrospinal fluid after spontaneous subarachnoid hemorrhage

Meeting Abstract

  • Karl-Michael Schebesch - Klinik und Poliklinik für Neurochirurgie am Universitätsklinikum Regensburg
  • Petra Schödel - Klinik und Poliklinik für Neurochirurgie am Universitätsklinikum Regensburg
  • Andreas Hochreiter - Klinik und Poliklinik für Neurochirurgie am Universitätsklinikum Regensburg
  • Judith Scheitzach - Klinik und Poliklinik für Neurochirurgie am Universitätsklinikum Regensburg
  • Alexander Brawanski - Klinik und Poliklinik für Neurochirurgie am Universitätsklinikum Regensburg
  • Elisabeth Bründl - Klinik und Poliklinik für Neurochirurgie am Universitätsklinikum Regensburg

Deutsche Gesellschaft für Neurochirurgie. 65. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Dresden, 11.-14.05.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. DocP 157

doi: 10.3205/14dgnc551, urn:nbn:de:0183-14dgnc5512

Veröffentlicht: 13. Mai 2014

© 2014 Schebesch et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: The endogenous, vasodilatatory Calcitonin-Gene related Peptide (CGRP) is stored in perivascular nerve fibres around cerebral arteries and regulates cerebral blood flow under physiologic conditions. Increased levels of CGRP are consistently reported in migraine patients but the role of CGRP in the pathophysiology of subarachnoid hemorrhage has not been evaluated yet.

Method: Prospectively, we collected cerebrospinal fluid (CSF) and serum over ten days in 24 patients (11 female, 13 male) who received a ventricular drainage within 24 hours after onset of the SAH. All patients were graded 3 or 4 according to Fisher. The levels of CGRP in serum and in CSF were determined using an enzyme-immunosorbent assay (EIA). 29 patients without any neurological disease served as control. The rate of ischemia (unrelated to clipping or coiling) was determined by computed tomography (CT).

Results: CGRP was released excessively into CSF and serum in all patients with SAH compared to the control group (p<0.05). The levels of CGRP constantly increased over the ten days after SAH while the serum levels reached maximum levels on days 4-7. Thirteen patients developed ischemic lesions. In these patients, the serum levels of CGRP ranged significantly higher than in those patients without ischemia (p<0.001).

Conclusions: We encountered an excessive release of CGRP in serum and in CSF due to SAH. In patients with vasospasm-related ischemia, extreme levels of CGRP in serum were found. This finding may add to the thesis that endogenous vasodilatatory neuropeptides are produced and released excessively to counteract cerebral vasospasm and consecutive ischemia. Thus, CGRP should be evaluated as potential biomarker for cerebral ischemia after SAH.