Migraine as an inflammatory disorder with microglial activation as a prime candidate

ABSTRACT

Background

The lower threshold of neuronal hyperexcitability has been correlated with migraines for decades but as technology has progressed, it has now become conceivable to learn more about the migraine disease. Apart from the “cortical spreading depression” and “activation of the trigeminovascular system”, inflammation has been increasingly recognized as a possible pathogenic process that may have the possibility to regulate the disease severity. Microglial cells, the prime candidate of the innate immune cells of central nervous tissue, has been associated with numerous diseases; including cancer, neurodegenerative disorders, and inflammatory disorders.

Aim

In this review, we have attempted to link the dot of various microglial activation signaling pathways to enlighten the correlation between microglial involvement and the progression of migraine conditions.

Method

A structured survey of research articles and review of the literature was done in the electronic databases of Google Scholar, PubMed, Springer, and Elsevier until 31 December 2021.

Result & Conclusion

Of 1136 articles found initially and screening of 1047 records, 47 studies were included for the final review. This review concluded that inflammation and microglial overexpression as the prime candidate, plays an important role in the modulation of migraine and are responsible for the progression toward chronification. Therefore, this increases the possibility of preventing migraine development and chronification by blocking microglia overexpression.

KEYWORDS:

• Migraine
• microglial cells
• neurogenic neuroinflammation
• neuronal hyperexcitability

Acknowledgments

Authors are thankful to the Institute of Human Genetics & Department of Zoology, University of Jammu, for their invaluable support.

Author Contributions

P.K. & A.S. contribute to the study design, A.S. & M.Y. drafted the manuscript, A.S. & S.S. edited the pictures and table. P.K. & M.Y. edited the manuscript, P.K. finalize the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.