Funding: This work was supported by grants from the EEA/Norwegian Financial Mechanism HU 0114 – “Save what can be saved” – applied neurological research using high-field magnetic resonance imaging and by TAMOP 4.2.1.B. A.S and N.K. were supported by the Bolyai Scholarship of the Hungarian Academy of Science. N.K. was supported by grants of University of Pécs (PTE_AOK_KA_2011) and OTKA PD 103964.
Quantitative MRI Studies of Chronic Brain White Matter Hyperintensities in Migraine Patients
Article first published online: 26 DEC 2012
© 2012 American Headache Society
Headache: The Journal of Head and Face Pain
Volume 53, Issue 5, pages 752–763, May 2013
How to Cite
Aradi, M., Schwarcz, A., Perlaki, G., Orsi, G., Kovács, N., Trauninger, A., Kamson, D. O., Erdélyi-Bótor, S., Nagy, F., Nagy, S. A., Dóczi, T., Komoly, S. and Pfund, Z. (2013), Quantitative MRI Studies of Chronic Brain White Matter Hyperintensities in Migraine Patients. Headache: The Journal of Head and Face Pain, 53: 752–763. doi: 10.1111/head.12013
Conflict of interest: The authors report no conflicts of interest.
- Issue published online: 24 APR 2013
- Article first published online: 26 DEC 2012
- Manuscript Accepted: 26 SEP 2012
- EEA/Norwegian Financial Mechanism HU 0114
- TAMOP 4.2.1.B
- Bolyai Scholarship of the Hungarian Academy of Science
- University of Pécs. Grant Number: PTE_AOK_KA_2011
- OTKA PD 103964
- brain white matter hyperintensity;
- quantitative 3.0-Tesla magnetic resonance imaging;
- repeated hemodynamic change
The aim of this study was to examine chronic brain white matter hyperintensities in migraine and to gain data on the characteristics of the lesions.
Migraine associates with a higher incidence of magnetic resonance imaging (MRI)-visible white matter signal abnormalities. Several attack-related pathomechanisms have been proposed in the lesion development, including the effect of repeated intracerebral hemodynamic changes.
Supratentorial white matter hyperintensities of 17 migraine patients were investigated interictally with quantitative MRI, including quantitative single voxel spectroscopy, diffusion, and perfusion MRI at 3.0-Tesla. The findings were compared with data measured in the contralateral, normal-appearing white matter of migraineurs and in the white matter of 17 healthy subjects.
Significantly higher apparent diffusion coefficient values, prolonged T2 relaxation times, and decreased N-acetyl-aspartate and creatine/phosphocreatine concentrations were found in the white matter hyperintensities. The cerebral blood flow and blood volume values were mildly decreased inside the hyperintensities. Differences were not present between the migraine patients' normal-appearing white matter and the white matter of healthy subjects.
The MRI measurements denote tissue damage with axonal loss, low glial cell density, and an enlarged extracellular space with an increased extracellular water fraction. These radiological features might be the consequences of microvascular ischemic changes during migraine attacks.