Plasma levels of inflammatory mediators in vestibular migraine.


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

The International journal of neuroscience, cilt.130, sa.4, ss.330-335, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 130 Sayı: 4
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1080/00207454.2019.1681994
  • Dergi Adı: The International journal of neuroscience
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, EMBASE, MEDLINE, Psycinfo
  • Sayfa Sayıları: ss.330-335
  • Anahtar Kelimeler: Vestibular migraine, inflammatory mediators, inflammasome, vascular neuropeptides, cytokine, headache, VERTIGO, NEUROPEPTIDES, PREVALENCE, CONTRIBUTE, CYTOKINE, GLIA
  • İstanbul Üniversitesi Adresli: Evet

Özet

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.