Disclosure: This project supported by Endo Pharmaceuticals, Inc.
Genomic Expression Patterns in Menstrual-Related Migraine in Adolescents
Article first published online: 6 JAN 2012
© 2011 American Headache Society
Headache: The Journal of Head and Face Pain
Volume 52, Issue 1, pages 68–79, January 2012
How to Cite
Hershey, A., Horn, P., Kabbouche, M., O'Brien, H. and Powers, S. (2012), Genomic Expression Patterns in Menstrual-Related Migraine in Adolescents. Headache: The Journal of Head and Face Pain, 52: 68–79. doi: 10.1111/j.1526-4610.2011.02049.x
Conflict of Interest: None
- Issue published online: 23 JAN 2012
- Article first published online: 6 JAN 2012
- Accepted for publication September 12, 2011.
- adolescent headache;
- gene expression;
Background.— Exacerbation of migraine with menses is common in adolescent girls and women with migraine, occurring in up to 60% of females with migraine. These migraines are oftentimes longer and more disabling and may be related to estrogen levels and hormonal fluctuations.
Objective.— This study identifies the unique genomic expression pattern of menstrual-related migraine (MRM) in comparison to migraine occurring outside the menstrual period and headache-free controls.
Methods.— Whole blood samples were obtained from female subjects having an acute migraine during their menstrual period (MRM) or outside of their menstrual period (non-MRM) and controls (C) – females having a menstrual period without any history of headache. The messenger RNA was isolated from these samples, and genomic profile was assessed. Affymetrix Human Exon ST 1.0 (Affymetrix, Santa Clara, CA, USA) arrays were used to examine the genomic expression pattern differences between these3 groups.
Results.— Blood genomic expression patterns were obtained on 56 subjects (MRM = 18, non-MRM = 18, and controls = 20). Unique genomic expression patterns were observed for both MRM and non-MRM. For MRM, 77 genes were identified that were unique to MRM, while 61 genes were commonly expressed for MRM and non-MRM, and 127 genes appeared to have a unique expression pattern for non-MRM. In addition, there were 279 genes that differentially expressed for MRM compared to non-MRM that were not differentially expressed for non-MRM. Gene ontology of these samples indicated many of these groups of genes were functionally related and included categories of immunomodulation/inflammation, mitochondrial function, and DNA homeostasis.
Conclusions.— Blood genomic patterns can accurately differentiate MRM from non-MRM. These results indicate that MRM involves a unique molecular biology pathway that can be identified with a specific biomarker and suggest that individuals with MRM have a different underlying genetic etiology.