"It has been suggested that recurrent migraine attacks may affect vulnerable deep tissues penetrating arteries and contributing to local critical hypoperfusion leading to minor brain injury observed as white matter abnormalities. Other proposed mechanisms have been suggested including atherosclerotic insults associated with the presence of cardiovascular risk factors [55, 56], endothelial dysfunction (e.g., both endothelial activation and impaired vascular reactivity) [57–59], genetic risk factors which are common in migraine and stroke , drugs commonly used to treat headache, having vasoconstrictor activity , and cardiac dysfunctions such as patent foramen ovale. In addition, irrespective of whether endothelial dysfunction is linked to platelet aggregation, recurrent endothelial insults may lead to microvascular brain damage contributing to white matter lesions . "
[Show abstract][Hide abstract] ABSTRACT: White matter hyperintensities (WMH) have been associated with mood disorders in psychiatric patients. In the present study, we aimed to assess whether WMHs are associated with depressive symptoms and different sensitivity of the behavioral inhibition (BIS), and activation (BAS) systems in patients with chronic headache. Participants were 85 adult outpatients (16 men and 69 women) with a diagnosis of chronic headache. All of the patients underwent brain magnetic resonance imaging (MRI) and were administered the BIS/BAS scales and the Center for Epidemiologic Studies Depression Scale. Above 40 % of patients had periventricular WMHs (PWMHs) and almost 98 % had deep WMHs (DWMHs). Patients with PWMHs reported fewer depressive symptoms than patients without PWMHs. Patients with more severe DWMHs (compared with patients with mild or without DWMH lesions) were older and reported lower scores on the drive dimension of the BIS/BAS scales. In multivariate analyses, patients with PWMHs were 1.06 times more likely to report fewer depressive symptoms than patients without PWMHs. WMH lesions in patients with chronic headache were associated with less depression severity.
The Journal of Headache and Pain 10/2012; 13(8). DOI:10.1007/s10194-012-0493-y · 2.80 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The purpose of this article is to review the latest concepts regarding migraine and ischemic stroke. In addition, focal neurological deficits and MRI changes in migraine patients will be reviewed.
A PubMed search of neurological literature pertaining to this study was conducted using specific keyword search terms pertaining to migraine and ischemic stroke.
Migraine, especially with aura, is a relative risk factor for stroke. Neuroimaging demonstrates the posterior circulation as being most vulnerable, although the reason for this distribution is unclear. Factors that may contribute to stroke in migraine include changes during cortical spreading depression with hyper- or hypoperfusion of neural tissue, vasospasm and endothelial dysfunction. Estrogen affects migraine expression as well as cerebral circulation, yet most women with migraine without aura are not at increased risk. Co-morbidity with patent foramen ovale can be mechanism of both disorders via presumed lack of filtration of microemboli or toxic substances; however, closure with reversal of right to left shunt seems to be more beneficial for cryptogenic stroke than migraine. Migraine and stroke are found in specific genetic disorders such as CADASIL, HERNS and MELAS giving clues to genetic factors. Stroke associated with migraine treatments such as ergots or triptans is rare, and usually associated with special circumstances such as overuse or concomitant thrombogenic conditions.
Although true migrainous infarction is rare, our understanding of the subtle associations between migraine and cerebrovascular behavior is expanding.
Neurological Research 11/2008; 30(8):801-12. DOI:10.1179/174313208X341049 · 1.44 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: CONTEXT: Migraine is considered to be an episodic condition with no long-term consequences. However, recent studies suggest that migraine attacks may be associated with pathologic changes in the brain, particularly in the cerebellum. OBJECTIVE: To determine whether individuals not reporting headache compared with individuals reporting migraine symptoms, particularly aura, in midlife are at increased risk of late-life infarct-like lesions found on magnetic resonance imaging (MRI) without consideration of clinical symptoms. DESIGN, SETTING, AND PARTICIPANTS: A population-based study of men and women in Reykjavik, Iceland (cohort born 1907-1935; n = 4689; 57% women) were followed up since 1967, examined, and interviewed about migraine symptoms in midlife (mean age, 51 years; range, 33-65 years). Between 2002 and 2006, more than 26 years later, brain MRIs were performed. Participants reporting headaches once or more per month were asked about migraine symptoms including nausea, unilateral location, photophobia, visual disturbance, and numbness. These individuals with headache were classified as having migraine without aura, migraine with aura, or nonmigraine headache. A comprehensive cardiovascular risk assessment was performed at both examinations. MAIN OUTCOME MEASURE: Presence of infarct-like lesions (total) and specifically located in the cortical, subcortical, and cerebellar regions. RESULTS: Infarct-like lesions were present in 39.3% of men and 24.6% of women. After adjusting for age, sex, and follow-up time, compared with those not reporting headaches once or more per month (n = 3243), those with midlife migraine with aura (n = 361) had an increased risk of late-life infarct-like lesions (adjusted odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.8) that specifically reflected an association with cerebellar lesions in women (prevalence of infarcts 23.0% for women with migraine with aura vs 14.5% for women not reporting headaches; adjusted OR, 1.9; 95% CI, 1.4-2.6 vs a 19.3% prevalence of infarcts for men with migraine with aura vs 21.3% for men not reporting headaches; adjusted OR, 1.0; 95% CI, 0.6-1.8; P<.04 for interaction by sex). Migraine without aura and nonmigraine headache were not associated with an increased risk. CONCLUSIONS: Migraine with aura in midlife was associated with late-life prevalence of cerebellar infarct-like lesions on MRI. This association was statistically significant only for women. This is consistent with the hypothesis that migraine with aura in midlife is associated with late-life vascular disease in the cerebellum and in women.
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