The Role of Inflammation in Migraine Headaches: A Review

炎症在偏头痛中的作用:综述

阅读:1

Abstract

Migraine is a chronic pulsating primary headache affecting billions of individuals worldwide. The condition is associated with neuroinflammation and is listed as the second most common form of headache disorders and the leading cause of disabilities. Migraineurs are susceptible to various pathological conditions ranging from mood and emotional dysregulation to neuronal disorders. Consequently, they often experience a higher rate of depression compared to non-migraineurs. Some migraineurs do not respond effectively to conventional drugs. As a result, there is a need for more alternative, effective treatment plans. Understanding the role of inflammation in migraine headache conditions could potentially bring solutions. The aim of the review is to outline the role of inflammation, focusing on neuronal excitability, pain, and inflammatory pathways involved in the context of migraine headaches. With the use of various academic and research databases, articles linked to inflammation and neuroinflammation were considered. Data were collected and analyzed surrounding inflammatory biomarkers and their link to migraine pathophysiology and current treatment plans. Studies highlight the impact of inflammatory mediators and neurotransmitters like interleukins (IL-1β,6,8,10), tumor necrosis factor-alpha (TNF-α), transforming growth-factor-beta (TNF-β), glutamate, and chemokines in the onset and severity of migraine headaches with and without aura, eliciting pain and inflammatory responses in the central nervous system. Studies also linked migraines and mood disorders, contributing to the increase in comorbidity prevalence. Further research is needed to address the increasing burden and gaps in existing treatments surrounding the inadequate relief and side effects reported with some migraine treatments. In addition, the use of medicinal plants for inflammation-targeted therapy needs to be further explored for more viable alternative treatments.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。