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61st Annual Meeting of the German Society of Neurosurgery (DGNC) as part of the Neurowoche 2010
Joint Meeting with the Brazilian Society of Neurosurgery on the 20 September 2010

German Society of Neurosurgery (DGNC)

21 - 25 September 2010, Mannheim

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Expression of Neuropeptide Y in CSF in patients with subarachnoid hemorrhage – related vasospasm

Meeting Abstract

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  • Karl-Michael Schebesch - Klinik für Neurochirurgie, Universität Regensburg, Deutschland
  • Alexander Brawanski - Klinik für Neurochirurgie, Universität Regensburg, Deutschland
  • Simone Kagerbauer - Klinik für Anästhesiologie, Technische Universität München, Deutschland
  • Martin Proescholdt - Klinik für Neurochirurgie, Universität Regensburg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocV1597

doi: 10.3205/10dgnc072, urn:nbn:de:0183-10dgnc0723

Published: September 16, 2010

© 2010 Schebesch et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Objective: Among other function, the neurotransmitter polypeptide Neuropeptide Y (NPY) serves as a potent vasoconstrictor, physiologically. In the human brain, NPY is expressed in the hypothalamus, forebrain, hippocampus and brainstem and its role in the pathogenesis of SAH-related vasospasm has not been conclusively determined yet. In our series, we focused on the expression of NPY in CSF including 12 patients with and 11 patients without SAH-related vasospasm.

Methods: We evaluated a population of 23 patients with aneurysmal SAH (15 female, 8 male), mean age 53.9 yrs (range 34–80 yrs). In 12 patients, angiography and/or transcranial Doppler clearly revealed vasospasm. CSF was drawn daily from the ventricular tube and levels of NPY were determined on days 1, 4 and 10 after onset of SAH, utilizing a sandwich ELISA assay.

Results: Levels of NPY were significantly higher in patients with vasospasm compared to patients without vasospasm on day 1 (mean: 0.156±0.241 vs. 0.064±0.082 ng/ml, p<0.001); day 4 (mean: 0.216±0.245 vs. 0.043±0.044 ng/ml, p<0.001) and day 10 (mean: 0.141±0.182 vs. 0.020±0.040 ng/ml, p<0.001).

Conclusions: We could clearly show that the potent vasoconstrictor NPY is excessively expressed in CSF in patients with segmental vasoconstriction following SAH. As the time course (day 1 to 10) reveals, the neuronal re-uptake probably is inhibited. Our results justify the revival of research on NPY in patients suffering from aneurysmal SAH. NPY may play a major role in the multifactorial cascade of vasospasm due to aneurysmal SAH.