Evidence for Cortical Functional Changes in Patients With Migraine and White Matter Abnormalities on Conventional and Diffusion Tensor Magnetic Resonance Imaging

M. A. Rocca, B. Colombo, E. Pagani, A. Falini, M. Codella, G. Scotti, G. Comi, M. Filippi
2003 Stroke  
Background-In this study, we used functional MRI (fMRI) to investigate the pattern of cortical activations after a simple motor task in patients with migraine and white matter (WM) abnormalities on conventional MRI scans of the brain. We also investigated whether the extent of brain activations was correlated with WM structural pathology measured using diffusion tensor (DT) MRI. Methods-From 15 right-handed patients with migraine and 15 sex-and age-matched, right-handed healthy volunteers, we
more » ... tained the following: (1) fMRI (repetitive flexion-extension of the last 4 fingers of the right hand), (2) dual-echo turbo spin echo scans, and (3) pulsed-gradient spin-echo echo-planar sequence to calculate DT-MRI maps. fMRI analysis was performed using SPM99 and cluster detection. We measured the volume, the average mean diffusivity (D ), and the average fractional anisotropy of all lesions seen on the dual-echo scans. D histograms of the normal-appearing WM were also produced. Results-Compared with healthy volunteers, migraine patients had a larger relative activation of the contralateral primary sensorimotor cortex (Pϭ0.01) and a rostral displacement of the supplementary motor area (Pϭ0.03). The shapes of the curves reflecting the time course for fMRI signal intensity changes were similar between migraine patients and controls for all of the cortical areas we studied. Compared with healthy subjects, migraine patients had significantly lower D histogram peak height of the normal-appearing WM histogram (Pϭ0.02), which was found to be correlated with the extent of displacement of the supplementary motor area (rϭϪ0.80, PϽ0.001). Conclusions-This study suggests that functional cortical changes occur in patients with migraine and brain MRI abnormalities and that they might be secondary to the extent of subcortical structural damage. (Stroke. 2003;34:665-670.)
doi:10.1161/01.str.0000057977.06681.11 pmid:12624289 fatcat:vtxrlt6abvfmbb2mrmdsgfcvpm