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Updated: Jan 22, 2026

Investigating Migraine-Like Behavior Using Light Aversion in Mice
Published on: August 11, 2021
Does inflammation have a role in migraine?
Lars Edvinsson1,2, Kristian Agmund Haanes3, Karin Warfvinge4,3
1Department of Clinical Sciences, Division of Experimental Vascular Research, Lund University, Lund, Sweden. lars.edvinsson@med.lu.se.
Abstract:
Migraine is a prevalent disorder, affecting 15.1% of the world's population. In most cases, the migraine attacks are sporadic; however, some individuals experience a gradual increase in attack frequency over time, and up to 2% of the general population develop chronic migraine. The mechanisms underlying this chronicity are unresolved but are hypothesized to involve a degree of inflammation. In this article, we review the relevant literature related to inflammation and migraine, from the initiation of attacks to chronification. We propose that the increase in migraine frequency leading to chronic migraine involves neurogenic neuroinflammation, possibly entailing increased expression of cytokines via activation of protein kinases in neurons and glial cells of the trigeminovascular system. We present evidence from preclinical research that supports this view and discuss the implications for migraine therapy.
Insights
Migraine attacks can worsen over time, potentially leading to chronic migraine. This progression may involve neurogenic neuroinflammation, a process linked to increased cytokines and protein kinase activation.
Area of Science:
- Neurology
- Neuroscience
- Inflammation Research
Background:
- Migraine affects 15.1% globally, with 2% developing chronic migraine.
- Mechanisms of migraine chronification remain unclear, but inflammation is a suspected factor.
- Understanding inflammation's role is crucial for developing effective migraine therapies.
Purpose of the Study:
- To review the literature on inflammation and migraine, from attack initiation to chronification.
- To propose a hypothesis involving neurogenic neuroinflammation in migraine progression.
- To discuss therapeutic implications based on preclinical evidence.
Main Methods:
- Literature review of studies on inflammation and migraine.
- Analysis of preclinical research data.
- Synthesis of evidence regarding neuroinflammation in the trigeminovascular system.
Main Results:
- Neurogenic neuroinflammation is proposed as a key mechanism in migraine chronification.
- Increased cytokine expression via protein kinase activation in neurons and glial cells is implicated.
- Preclinical evidence supports the role of neuroinflammation in migraine progression.
Conclusions:
- Neuroinflammation, particularly involving cytokines and protein kinases in the trigeminovascular system, is a plausible driver of migraine chronification.
- Further research into neuroinflammatory pathways may reveal novel therapeutic targets for chronic migraine.
- Targeting neuroinflammation could offer new strategies for managing migraine frequency and severity.
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