Page 40 - Migraine, the heart and the brain

Chapter 2
matter hyperintensity progression (P = .06). Interaction terms for hypertension (P = .90) and diabetes (P = .60) were not signi cant. Further exploratory analyses showed no association of the number of migraine attacks, migraine attack duration, migraine frequency, type of attack, or migraine therapy with lesion progression (eTable 2).
The increase in total deep white matter hyperintensity volume among women with migraine was related to an increased number of new lesions rather than intensities at follow-up did not differ between groups (P = .97). Participants in the migraine group had a higher incidence of 10 or more new lesions among 43 of 145 participants (30%) vs 5 of 57 in the control group (9%) (adjusted OR, 3.5; 95% CI, 1.3-9.6;P=.01). Among women with migraine , deep white matter hyperintensities were more diffusely distributed in the deep white matter than among controls (Figure 2).
Periventricular White Matter Hyperintensities
Progression of periventricular white matter hyperintensities did not differ between participants with migraine and controls. There was no association of sex, aura status, or migraine frequency with progression.
Infratentorial Hyperintensities
The prevalence of infratentorial hyperintensities at follow-up was 21% among women with migraine and 4% among controls (adjusted OR, 6.5; 95% CI, 1.5-28.3; P = .01; Table 3). Progression of infratentorial hyperintensities was not signi cantly higher among women with migraine (15%) than women in the control group (2%; adjusted OR, 7.7; 95% CI, 1.0-59.5; P=.05; Table 3). There was no relationship between migraine aura and number or frequency of migraine attacks with progression of infratentorial hyperintensities. Among men there were no differences in infratentorial hyperintensity prevalence or progression.
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