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Could Experimental Inflammation Provide Better Understanding of Migraines?
Philip Victor Reducha1,2, Lars Edvinsson1,3, Kristian Agmund Haanes1,2
1Department of Clinical Experimental Research, Glostrup Research Institute, Copenhagen University Hospital, Rigshospitalet Glostrup, 2600 Glostrup, Denmark.
Abstract:
Migraines constitute a common neurological and headache disorder affecting around 15% of the world's population. In addition to other mechanisms, neurogenic neuroinflammation has been proposed to play a part in migraine chronification, which includes peripheral and central sensitization. There is therefore considerable evidence suggesting that inflammation in the intracranial meninges could be a key element in addition to calcitonin gene-related peptide (CGRP), leading to sensitization of trigeminal meningeal nociceptors in migraines. There are several studies that have utilized this approach, with a strong focus on using inflammatory animal models. Data from these studies show that the inflammatory process involves sensitization of trigeminovascular afferent nerve terminals. Further, by applying a wide range of different pharmacological interventions, insight has been gained on the pathways involved. Importantly, we discuss how animal models should be used with care and that it is important to evaluate outcomes in the light of migraine pathology.
Insights
Neurogenic neuroinflammation and meningeal inflammation, involving calcitonin gene-related peptide (CGRP), are key in migraine chronification. Animal models show trigeminovascular afferent nerve sensitization, but outcomes require careful interpretation for migraine pathology.
Area of Science:
- Neurology
- Neuroscience
- Inflammation research
Background:
- Migraines are a prevalent neurological disorder affecting 15% of the global population.
- Neurogenic neuroinflammation and peripheral/central sensitization are implicated in migraine chronification.
- Inflammation in the intracranial meninges, alongside calcitonin gene-related peptide (CGRP), is a significant factor in migraine pathology.
Purpose of the Study:
- To explore the role of neurogenic neuroinflammation in migraine pathogenesis.
- To investigate the involvement of meningeal inflammation and CGRP in trigeminal sensitization.
- To review insights gained from pharmacological interventions in animal models of migraine.
Main Methods:
- Utilized inflammatory animal models to study migraine mechanisms.
- Applied various pharmacological interventions to identify involved pathways.
- Analyzed data on trigeminovascular afferent nerve terminal sensitization.
Main Results:
- Inflammatory processes in animal models demonstrate sensitization of trigeminovascular afferent nerve terminals.
- Pharmacological interventions provided insights into the pathways mediating neuroinflammation in migraines.
- Evidence suggests meningeal inflammation and CGRP contribute to trigeminal nociceptor sensitization.
Conclusions:
- Neurogenic neuroinflammation and meningeal inflammation are critical components in migraine chronification.
- Animal models are valuable but require careful interpretation in the context of human migraine pathology.
- Understanding these inflammatory pathways offers potential therapeutic targets for migraine treatment.
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