Brain stem and cerebellar hyperintense lesions in migraine.
ABSTRACT Migraineurs are at increased risk of cerebellar infarcts and supratentorial white matter lesions. The prevalence, frequency, and distribution of infratentorial hyperintense lesions in migraine are unknown.
Migraineurs with aura (n=161), without aura (n=134), and controls (n=140) from a population-based sample of adults (30 to 60 years of age) were evaluated with MRI.
Infratentorial hyperintensities were identified in 13 of 295 (4.4%) migraineurs and in 1 of 140 (0.7%) controls (P=0.04). Twelve cases had hyperintensities, mostly bilaterally, in the dorsal basis pontis. Those with infratentorial hyperintensities also had supratentorial white matter lesions more often.
We found an increased prevalence of infratentorial (mostly pontine) hyperintensities in migraineurs from the general population. This extends the knowledge about vulnerable brain regions and type of lesions in migraine brains. A hemodynamic ischemic pathogenesis is likely, but further research is needed.
Full-textDOI: · Available from: Mark A van Buchem, Jun 02, 2015
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ABSTRACT: To compare the white matter lesions seen in multiple sclerosis and migraine using monoexponential and high b-value biexponential diffusion measurements. Diffusion-weighted images were acquired on a 3.0-Tesla magnetic resonance imaging system. Diffusion parameters were estimated using monoexponential (0-1000 s/mm(2) ) and biexponential (0-5000 s/mm(2) ) approaches from 15 multiple sclerosis patients, 15 patients with migraine and 15 healthy control subjects. The study was performed in accordance with the approval of the Regional Research Ethics Committee. The apparent diffusion coefficient (ADC) values were measured in the lesions and the normal-appearing white matter of patients and in the white matter of controls. High lesional ADCmono values were detected in both patient groups without significant differences between the groups (10.72 and 9.86 × 10(-4) mm(2) /s for MS and migraine respectively, P = 0.2134). The biexponential measurements showed significantly higher ADCfast , ADCslow , and Pslow values in the migraine lesions than in the multiple sclerosis lesions (16.47 versus 14.29, 1.41 versus 0.76, and 20.34 versus 12.01 all values in 10(-4) mm(2) /s; P = 0.0344, P = 0.0019, P = 0.0021, respectively). Biexponential diffusion analysis may help to differentiate multiple sclerosis-related white matter lesions from migraine-related ones.J. Magn. Reson. Imaging 2014. © 2014 Wiley Periodicals, Inc.Journal of Magnetic Resonance Imaging 03/2015; 41(3). DOI:10.1002/jmri.24580 · 2.79 Impact Factor
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ABSTRACT: Objective The objective of the current article is to review the shared pathophysiological mechanisms which may underlie the clinical association between headaches and sleep disorders. Background The association between sleep and headache is well documented in terms of clinical phenotypes. Disrupted sleep-wake patterns appear to predispose individuals to headache attacks and increase the risk of chronification, while sleep is one of the longest established abortive strategies. In agreement, narcoleptic patients show an increased prevalence of migraine compared to the general population and specific familial sleep disorders have been identified to be comorbid with migraine with aura. Conclusion The pathophysiology and pharmacology of headache and sleep disorders involves an array of neural networks which likely underlie their shared clinical association. While it is difficult to differentiate between cause and effect, or simply a spurious relationship the striking brainstem, hypothalamic and thalamic convergence would suggest a bidirectional influence.Cephalalgia 07/2014; 34(10). DOI:10.1177/0333102414541687 · 4.12 Impact Factor
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ABSTRACT: Background: Small cerebellar cavities (≤15 mm) are often observed coincidentally in ageing subjects and have also been associated with migraine. Although generally assumed to be of ischaemic origin, descriptive imaging studies are sparse and imaging findings have not been correlated with histopathology. We aimed to investigate whether small ischaemic cavities in the cerebellum show characteristic infarct patterns that might be helpful for diagnostic imaging. Methods: We examined 40 whole postmortem cerebella with 7-tesla MRI ex vivo for the presence of small ischaemic cavities. The scan protocol included a T2-, T2*- and fluid-attenuated inversion recovery-weighted sequence for all specimens. We investigated to which degree small ischaemic cavities affect the cortical, juxtacortical and/or deep subcortical regions of the cerebellum. In a subset of the cavities identified, we correlated the imaging data with histopathological findings. This was performed by cutting the particular cerebellar specimen into 5-mm-thick slices. Serial sections were performed if cavities remained unidentified macroscopically. Results: Twenty-two cavities were seen on ex vivo MRI in 8 out of 40 examined cerebella. Twenty out of 22 cerebellar cavities were located in the cortex, and only 2 in the deep white matter, with no cavities located in the juxtacortical white matter. None of the 20 cerebellar cortical cavities showed extension into the juxtacortical white matter on MRI, although in 1 cortical cavity some surrounding gliosis was seen to extend into the juxtacortical white matter. Nine out of 22 cavities were sampled for pathological correlation, including 7 cerebellar cortical cavities and both cavities or lacunes in the deep white matter. Three out of 7 cortical and both the deep cavities were histopathologically verified as cavities of ischaemic origin, while the remaining cortical cavities could not be retrieved upon histopathologic examination. Some microscopic gliosis was seen to extend into the juxtacortical white matter of all confirmed cortical cavities. Conclusion: Knowledge of typical infarct patterns may facilitate the detection and characterisation of cerebellar ischaemic cavities in vivo. Cerebellar cortical cavities appeared to be much more common than deep cavities and presented on imaging as a full-thickness defect in the cerebellar cortex without extension in the adjacent white matter. © 2014 S. Karger AG, Basel.Cerebrovascular Diseases 08/2014; 38(1):17-23. DOI:10.1159/000365411 · 3.70 Impact Factor