Migraine and white matter lesions: a mendelian randomization study

Abstract

Previous studies have found that migraine patients are associated with white matter lesions (WMLs), but the causal relationship between the two remains unclear. We intend to explore the bidirectional causal relationship between migraine and WMLs using a two-sample mendelian randomization (MR) method. We employed summary-level data from a recent large-scale genome-wide association study (GWAS) that characterized three white matter (WM) phenotypes: white matter hyperintensities (WMH, N = 18,381), fractional anisotropy (FA, N = 17,673), and mean diffusivity (MD, N = 17,467), as well as migraine (N = 589,356). The inverse variance-weighted (IVW) method was used as the main approach for analyzing causality. Weighted median analysis, simple median analysis, and MR-Egger regression served as complementary methods. The bidirectional MR study affords no support for causality between WMLs and migraine. In all MR methods, there was no obvious causal evidence between them. In our bidirectional MR study, we didn't reach this conclusion that WMLs can cause migraine, migraine wouldn't increase the risk of WMLs, either.

Figure 1

Design and main assumptions of our Mendelian randomization study.

Figure 2

The causal effects of white matter lesions on migraine using two-sample Mendelian randomization methods. IVW, inverse variance weighted; SNPs, single nucleotide polymorphisms; OR, odds ratios; CI, confidence interval; WMH, white matter hyperintensities; FA, fractioal anisotropy; MD, mean diffusivity.

Figure 3

The causal effects of migraine on white matter lesions using two-sample mendelian randomization methods. IVW, inverse variance weighted; SNPs, single nucleotide polymorphisms; OR, odds ratios; CI, confidence interval. WMH, white matter hyperintensities; FA, fractioal anisotropy; MD, mean diffusivity.