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Methyprednisolone i.v. alters levels of CGRP and melatonin in cluster headache patients
The Journal of Headache and Pain volume 14, Article number: P63 (2013)
Introduction
Treatment with steroids for short term cluster headache (CH) prophylaxis is a widely accepted therapy. However, the mechanism of action of steroids in CH prophylaxis is unknown. Various studies could show that the trigeminovascular system and the hypothalamus play probably a key role in CH pathophysiology. The neuropeptid calcitonin gene related peptide (CGRP) is released in an acute attack indicating activation of the trigeminovasclular system.[1] The hypothalamus regulates the circadian secretion of melatonin which is reduced in CH patients during a bout.[2]
Objective
The aim of this study was to assess if treatment with high dose methylprednisolone (MP) i.v. inhibits release of CGRP and influences secretion of melatonin in CH.
Methods
10 patients with episodic Cluster headache and 5 control patients with an acute episode of multiple sclerosis (MS) who should receive MP i.v. were included in the study. Patients were treated at the beginning of an episode (CH or MS) with a course of once daily 1g MP i.v. for three days followed by oral tapering. CGRP was assessed in plasma of the external jugular vein and the metabolite of melatonin in urine - 6-sulfatoxymelatonin – was collected separately during the day and night. Measurements were done before as well as one day, one and two weeks after start of treatment. Patients recorded the number and severity of headache attacks each day.
Results
Treatment with MP led to a transient and significant decline of headache frequency. Simultaneously, CGRP plasma levels were reduced up to one week after end of treatment. Secretion of melatonin increased one and two weeks after treatment significantly. No significant changes could be observed in the control group.
Conclusion
The results could point to a possible mechanism of action of steroids in cluster headache prophylaxis. The altered secretion pattern could be explained through a direct effect of MP on the trigeminovascular system and the hypothalamus but could also be a consequence of the reduced frequency of attacks.
References
Goadsby PJ, Edvinsson L: Human in vivo evidence for trigeminovascular activation in cluster headache. Neuropeptide changes and effects of acute attacks therapies. Brain 1994, 117(Pt 3):427–34.
Leone M, Lucini V, D'Amico D, Grazzi L, Moschiano F, Fraschini F, et al.: Abnormal 24-hour urinary excretory pattern of 6-sulphatoxymelatonin in both phases of cluster headache. Cephalalgia 1998, 18(10):664–7. 10.1046/j.1468-2982.1998.1810664.x
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Open Access This article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Neeb, L., Anders, L., Euskirchen, P. et al. Methyprednisolone i.v. alters levels of CGRP and melatonin in cluster headache patients. J Headache Pain 14 (Suppl 1), P63 (2013). https://doi.org/10.1186/1129-2377-14-S1-P63
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DOI: https://doi.org/10.1186/1129-2377-14-S1-P63