OBJECTIVE/BACKGROUND: The aim of this longitudinal study was to investigate changes
of migraine-related brain white matter hyperintensities 3 years after an initial study.
Baseline quantitative magnetic resonance imaging (MRI) studies of migraine patients
with hemispheric white matter hyperintensities performed in 2009 demonstrated signs
of tissue damage within the hyperintensities. The hyperintensities appeared most frequently
in the deep white matter of the frontal lobe with a similar average hyperintensity
size in all hemispheric lobes. Since in this patient group the repeated migraine attacks
were the only known risk factors for the development of white matter hyperintensities,
the remeasurements of migraineurs after a 3-year long follow-up may show changes in
the status of these structural abnormalities as the effects of the repeated headaches.
METHODS: The same patient group was reinvestigated in 2012 using the same MRI scanner
and acquisition protocol. MR measurements were performed on a 3.0-Tesla clinical MRI
scanner. Beyond the routine T1-, T2-weighted, and fluid-attenuated inversion recovery
imaging, diffusion and perfusion-weighted imaging, proton magnetic resonance spectroscopy,
and T1 and T2 relaxation time measurements were also performed. Findings of the baseline
and follow-up studies were compared with each other. RESULTS: The follow-up proton
magnetic resonance spectroscopy studies of white matter hyperintensities showed significantly
decreased N-acetyl-aspartate (median values 8.133 vs 7.153 mmol/L, P = .009) and creatine/phosphocreatine
(median values 4.970 vs 4.641 mmol/L, P = .015) concentrations compared to the baseline,
indicating a more severe axonal loss and glial hypocellularity with decreased intracellular
energy production. The diffusion values, the T1 and T2 relaxation times, and the cerebral
blood flow and volume measurements presented only mild changes between the studies.
The number (median values 21 vs 25, P < .001) and volume (median values 0.896 vs 1.140
mL, P < .001) of hyperintensities were significantly higher in the follow-up study.
No changes were found in the hemispheric and lobar distribution of hyperintensities.
An increase in the hyperintensity size of preexisting lesions was much more common
than a decrease (median values 14 vs 5, P = .004). A higher number of newly developed
hyperintensities were detected than disappeared ones (130 vs 22), and most of them
were small (<.034 mL). Small white matter hyperintensities in patients with a low
migraine attack frequency had a higher chance to disappear than large white matter
hyperintensities or white matter hyperintensities in patients with a high attack frequency
(coefficient: -0.517, P = .034). CONCLUSIONS: This longitudinal MRI study found clinically
silent brain white matter hyperintensities to be predominantly progressive in nature.
The absence of a control group precludes definitive conclusions about the nature of
these changes or if their degree is beyond normal aging.