Plasma levels of inflammatory mediators in vestibular migraine.

Karaaslan Z., Ozcelik P., Ulukan Ç., Ulusoy C. A., Orhan K. S., Orhan E., ...More

The International journal of neuroscience, vol.130, no.4, pp.330-335, 2020 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 130 Issue: 4
  • Publication Date: 2020
  • Doi Number: 10.1080/00207454.2019.1681994
  • Journal Name: The International journal of neuroscience
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, EMBASE, MEDLINE, Psycinfo
  • Page Numbers: pp.330-335
  • Keywords: Vestibular migraine, inflammatory mediators, inflammasome, vascular neuropeptides, cytokine, headache, VERTIGO, NEUROPEPTIDES, PREVALENCE, CONTRIBUTE, CYTOKINE, GLIA
  • Istanbul University Affiliated: Yes


Objectives: Vestibular migraine (VM) is an under-recognized entity with substantial burden for the individual and society. The underlying mechanism of VM and its distinction from other migraine mechanisms still remain unclear. Inflammatory pathways have been suggested to contribute to vestibular migraine. Our aim was to further investigate the possible role of inflammation in the pathophysiology of VM. Methods: We recruited 30 patients with VM diagnosed according to ICHD-3 criteria and 50 gender- and age-matched controls. Blood samples were obtained from 11 VM patients during an attack and from 13 VM patients under prophylactic treatment. Plasma levels of calcitonin gene related peptide (CGRP), neurokinin A (NKA), substance P (SP), NLRP1, NLRP3, caspase-1, IL-1 beta, IL-6, TNF-alpha and NF kappa B were measured by ELISA. Results: IL-6 levels were significantly reduced in VM patients, whereas levels of other inflammation parameters were comparable to those of healthy controls. Levels of inflammatory mediators were not correlated with clinical parameters. Likewise, there were no significant differences among VM patients with and without headache attack and prophylactic treatment. Conclusion: Our results argue against involvement of systemic inflammation in the pathophysiology of VM.