TL;DR: High-field functional MRI with near-continuous recording during visual aura in three subjects observed blood oxygenation level-dependent signal changes that strongly suggest that an electrophysiological event such as CSD generates the aura in human visual cortex.
Abstract: Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Using high-field functional MRI with near-continuous recording during visual aura in three subjects, we observed blood oxygenation level-dependent (BOLD) signal changes that demonstrated at least eight characteristics of CSD, time-locked to percept/onset of the aura. Initially, a focal increase in BOLD signal (possibly reflecting vasodilation), developed within extrastriate cortex (area V3A). This BOLD change progressed contiguously and slowly (3.5 ± 1.1 mm/min) over occipital cortex, congruent with the retinotopy of the visual percept. Following the same retinotopic progression, the BOLD signal then diminished (possibly reflecting vasoconstriction after the initial vasodilation), as did the BOLD response to visual activation. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retinotopic progression of the visual percept. These data strongly suggest that an electrophysiological event such as CSD generates the aura in human visual cortex.
TL;DR: These population-based findings suggest that some patients with migraine with and without aura are at increased risk for subclinical lesions in certain brain areas.
Abstract: ContextClinical series have suggested an increased prevalence of cerebral infarction
and white matter lesions (WMLs) in migraine patients. It is not known whether
these lesions are prevalent in the general migraine population.ObjectivesTo compare the prevalence of brain infarcts and WMLs in migraine cases
and controls from the general population and to identify migraine characteristics
associated with these lesions.DesignCross-sectional, prevalence study of population-based sample of Dutch
adults aged 30 to 60 years.ParticipantsRandomly selected patients with migraine with aura (n = 161), patients
with migraine without aura (n = 134), and controls (n = 140), who were frequency
matched to cases for age, sex, and place of residence. Nearly 50% of the cases
had not been previously diagnosed by a physician.Main Outcome MeasuresBrain magnetic resonance images were evaluated for infarcts, by location
and vascular supply territory, and for periventricular WMLs (PVWMLs) and deep
WMLs (DWMLs). The odds ratios (ORs) and 95% confidence intervals (CIs) of
these brain lesions compared with controls were examined by migraine subtype
(with or without aura) and monthly attack frequency (<1 attack, ≥1 attack),
controlling for cardiovascular risk factors and use of vasoconstrictor migraine
agents. All participants underwent a standard neurological examination.ResultsNo participants reported a history of stroke or transient ischemic attack
or had relevant abnormalities at standard neurological examination. We found
no significant difference between patients with migraine and controls in overall
infarct prevalence (8.1% vs 5.0%). However, in the cerebellar region of the
posterior circulation territory, patients with migraine had a higher prevalence
of infarct than controls (5.4% vs 0.7%; P = .02;
adjusted OR, 7.1; 95% CI, 0.9-55). The adjusted OR for posterior infarct varied
by migraine subtype and attack frequency. The adjusted OR was 13.7 (95% CI,
1.7-112) for patients with migraine with aura compared with controls. In patients
with migraine with a frequency of attacks of 1 or more per month, the adjusted
OR was 9.3 (95% CI, 1.1-76). The highest risk was in patients with migraine
with aura with 1 attack or more per month (OR, 15.8; 95% CI, 1.8-140). Among
women, the risk for high DWML load (top 20th percentile of the distribution
of DWML load vs lower 80th percentile) was increased in patients with migraine
compared with controls (OR, 2.1; 95% CI, 1.0-4.1); this risk increased with
attack frequency (highest in those with ≥1 attack per month: OR, 2.6; 95%
CI, 1.2-5.7) but was similar in patients with migraine with or without aura.
In men, controls and patients with migraine did not differ in the prevalence
of DWMLs. There was no association between severity of PVWMLs and migraine,
irrespective of sex or migraine frequency or subtype.ConclusionsThese population-based findings suggest that some patients with migraine
with and without aura are at increased risk for subclinical lesions in certain
brain areas.
TL;DR: Migraine is associated with a twofold increased risk of ischaemic stroke, which is only apparent among people who have migraine with aura, and the results suggest a higher risk among women and risk was further magnified for people with migraine who were aged less than 45, smokers, and women who used oral contraceptives.
Abstract: Objective To evaluate the association between migraine and cardiovascular disease, including stroke, myocardial infarction, and death due to cardiovascular disease. Design Systematic review and meta-analysis. Data sources Electronic databases (PubMed, Embase, Cochrane Library) and reference lists of included studies and reviews published until January 2009. Selection criteria Case-control and cohort studies investigating the association between any migraine or specific migraine subtypes and cardiovascular disease. Review methods Two investigators independently assessed eligibility of identified studies in a two step approach. Disagreements were resolved by consensus. Studies were grouped according to a priori categories on migraine and cardiovascular disease. Data extraction Two investigators extracted data. Pooled relative risks and 95% confidence intervals were calculated. Results Studies were heterogeneous for participant characteristics and definition of cardiovascular disease. Nine studies investigated the association between any migraine and ischaemic stroke (pooled relative risk 1.73, 95% confidence interval 1.31 to 2.29). Additional analyses indicated a significantly higher risk among people who had migraine with aura (2.16, 1.53 to 3.03) compared with people who had migraine without aura (1.23, 0.90 to 1.69; meta-regression for aura status P=0.02). Furthermore, results suggested a greater risk among women (2.08, 1.13 to 3.84) compared with men (1.37, 0.89 to 2.11). Age less than 45 years, smoking, and oral contraceptive use further increased the risk. Eight studies investigated the association between migraine and myocardial infarction (1.12, 0.95 to 1.32) and five between migraine and death due to cardiovascular disease (1.03, 0.79 to 1.34). Only one study investigated the association between women who had migraine with aura and myocardial infarction and death due to cardiovascular disease, showing a twofold increased risk. Conclusion Migraine is associated with a twofold increased risk of ischaemic stroke, which is only apparent among people who have migraine with aura. Our results also suggest a higher risk among women and risk was further magnified for people with migraine who were aged less than 45, smokers, and women who used oral contraceptives. We did not find an overall association between any migraine and myocardial infarction or death due to cardiovascular disease. Too few studies are available to reliably evaluate the impact of modifying factors, such as migraine aura, on these associations.
TL;DR: The present findings suggest that MA and MO share the pain phase, and headache was, however, less severe and shorter lasting in MA than in MO.
Abstract: In a cross-sectional study of headache disorders in a representative general population of 1,000 persons the epidemiology of migraine with aura (MA) and migraine without aura (MO) was analysed in relation to sex and age distribution, symptomatology and precipitants. The headache disorders were classified on the basis of a clinical interview as well as a physical and a neurological examination using the operational diagnostic criteria of the International Headache Society (IHS). Lifetime prevalence of MA was 5%, male:female ratio 1:2. Lifetime prevalence of MO was 8%, M:F ratio 1:7. Women, but not men, were significantly more likely to have MO than MA. Neither MA nor MO showed correlation to age in the studied age interval (25-64 years). Premonitory symptoms occurred in 16% of subjects with MA and in 12% with MO. One or more precipitating factor was present in 61% with MA and in 90% with MO. In both MA and MO the most conspicuous precipitating factor was stress and mental tension. Visual disturbances were the most common aura phenomenon occurring in 90% of subjects with MA. Aura symptoms of sensory, motor or speech disturbances rarely occurred without coexisting visual disturbances. The pain phase of MA fulfilled the criteria for MO of the IHS. Headache was, however, less severe and shorter lasting in MA than in MO. Onset at menarche, menstrual precipitation, menstrual problems, influence of pregnancy and use of oral contraceptives all showed some relationship with the presence of MO and less with MA. The present findings suggest that MA and MO share the pain phase.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: A simple model for migraine attacks is suggested: A pathological disturbance in one cerebral hemisphere causes the aura symptoms and after a time delay, it also causes the headache by stimulating local vascular nociceptors.
Abstract: Ten years of study has resulted in considerable but fragmented knowledge about regional cerebral blood flow in migraine with aura (classic migraine). In the present study, the number of repeatedly studied patients (n = 63) was large enough to determine statistically significant sequences of events and statistically significant spatial relations. The first observable event was a decrease of regional cerebral blood flow posteriorly in one cerebral hemisphere. Further development of this pathological process was accompanied by the aura symptoms. Thereafter headache occurred while regional cerebral blood flow remained decreased. During the headache phase, regional cerebral blood flow gradually changed from abnormally low to abnormally high without apparent change in headache. In some patients headache disappeared while regional cerebral blood flow remained increased. Although regional cerebral blood flow reduction and aura symptoms in the great majority of patients were unilateral, one-third had bilateral headache. Unilateral headache usually localized to the side on which regional cerebral blood flow was reduced and from which the aura symptoms originated (i.e., aura symptoms were perceived to occur contralaterally but presumably originated in the hypoperfused hemisphere). Our results suggest a simple model for migraine attacks: A pathological disturbance in one cerebral hemisphere causes the aura symptoms and after a time delay, it also causes the headache by stimulating local vascular nociceptors. Bilateral headache caused by a unilateral cerebral disturbance may be explained by recent neuroanatomical and neurophysiological findings.