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dc.contributor.authorUlusoy, Canan Aysel
dc.contributor.authorKucukali, Cem Ismail
dc.contributor.authorOrhan, Kadir Serkan
dc.contributor.authorUlukan, Çağrı
dc.contributor.authorKaraaslan, Zerrin
dc.contributor.authorTuzun, Erdem
dc.contributor.authorOrhan, Elif
dc.contributor.authorOzcelik, Pinar
dc.contributor.authorAKDAL, GÜLDEN
dc.contributor.authorBaykan, Betul
dc.date.accessioned2021-03-02T19:14:29Z
dc.date.available2021-03-02T19:14:29Z
dc.date.issued2020
dc.identifier.citationKaraaslan Z., Ozcelik P., Ulukan Ç., Ulusoy C. A. , Orhan K. S. , Orhan E., Kucukali C. I. , Tuzun E., Baykan B., AKDAL G., "Plasma levels of inflammatory mediators in vestibular migraine.", The International journal of neuroscience, cilt.130, ss.330-335, 2020
dc.identifier.issn0020-7454
dc.identifier.othervv_1032021
dc.identifier.otherav_967133c0-4392-408f-b59a-477e1731efc4
dc.identifier.urihttp://hdl.handle.net/20.500.12627/5393
dc.identifier.urihttps://doi.org/10.1080/00207454.2019.1681994
dc.description.abstractObjectives: 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.
dc.language.isoeng
dc.subjectSinirbilim ve Davranış
dc.subjectNEUROSCIENCES
dc.subjectTemel Bilimler
dc.subjectYaşam Bilimleri
dc.subjectYaşam Bilimleri (LIFE)
dc.titlePlasma levels of inflammatory mediators in vestibular migraine.
dc.typeMakale
dc.relation.journalThe International journal of neuroscience
dc.contributor.departmentİstanbul Üniversitesi , Deneysel Tıp Araştırma Enstitüsü , Sinirbilim Ad
dc.identifier.volume130
dc.identifier.issue4
dc.identifier.startpage330
dc.identifier.endpage335
dc.contributor.firstauthorID268920


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