Migraine and Stroke
2012; Lippincott Williams & Wilkins; Volume: 43; Issue: 12 Linguagem: Inglês
10.1161/strokeaha.112.656603
ISSN1524-4628
AutoresTobias Kurth, Hans‐Christoph Diener,
Tópico(s)Transcranial Magnetic Stimulation Studies
ResumoHomeStrokeVol. 43, No. 12Migraine and Stroke Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBMigraine and StrokePerspectives for Stroke Physicians Tobias Kurth, MD, ScD and Hans-Christoph Diener, MD, PhD Tobias KurthTobias Kurth From the Inserm Unit 708—Neuroepidemiology, Bordeaux, France (T.K.); the University of Bordeaux, Bordeaux, France (T.K.); the Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA (T.K.); and the Department of Neurology, University Hospital Essen, Essen, Germany (H.C.D.). and Hans-Christoph DienerHans-Christoph Diener From the Inserm Unit 708—Neuroepidemiology, Bordeaux, France (T.K.); the University of Bordeaux, Bordeaux, France (T.K.); the Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA (T.K.); and the Department of Neurology, University Hospital Essen, Essen, Germany (H.C.D.). Originally published20 Sep 2012https://doi.org/10.1161/STROKEAHA.112.656603Stroke. 2012;43:3421–3426Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 IntroductionMigraine and stroke have been linked by numerous individual studies1–4 and 3 meta-analyses.5–7 Advances in pathophysiology have increased our knowledge about potential mechanisms linking migraine with cerebral vascular events.8,9 Overall, there is consistent evidence that individuals with migraine are approximately 2 times more likely to develop an ischemic stroke6,7 and in most studies this association is limited to patients with migraine with aura (MA) and stronger among younger women, particularly if they smoke or/and use oral contraceptives.4,6It remains unclear, however, how important migraine is when a patient has a stroke. Because migraine is a very prevalent disease with approximately 20% of the general population being affected at least part of their lives,10 it is not surprising that many patients with a stroke have a history of migraine. However, often migraine is not directly linkable to the stroke event and uncertainties remain for the necessity of additional diagnostic workup and for potential therapeutic consequences. Moreover, the interrelationship between migraine and stroke is complicated by the fact that other distinct clinical conditions can trigger a migraine-like attack and that these conditions are stroke risk factors by themselves such as artery dissections.11In this review, we summarize the evidence linking migraine with stroke, highlight new aspects of this association, and discuss potential mechanisms that are of interest for the management of patients with stroke who have a history of migraine.Epidemiological Evidence Linking Migraine With StrokeIschemic StrokeResults of 3 meta-analyses of observational studies5–7 show that individuals with migraine have a 2-fold increased risk of ischemic stroke. In 26,7 this increased risk is limited to patients with MA. The risk seems to increase with increasing migraine attack frequency12,13 and women and younger age groups are particularly affected.6 With regard to potential modifying factors, smoking and oral contraceptive use have been linked with further increased risk.6 The combination of smoking and oral contraceptives among young female patients with MA has been shown to increase stroke risk by a factor of approximately 9 when compared with women without migraine.4,6Although migraine has been linked with increased prevalence of an unfavorable cardiovascular risk profile14,15 the association between MA and ischemic stroke is independent of traditional cardiovascular risk factors.5–7 Furthermore, the risk of ischemic stroke is most pronounced among individual with a low vascular risk profile,4,16–18 suggesting that other pathways play a role. With regard to functional outcome after ischemic stroke, a recent study showed that MA is only linked with ischemic strokes of good functional outcome.19Hemorrhagic StrokeOnly very few studies have evaluated the role of migraine in hemorrhagic stroke occurrence. One case–control study found an increased risk of hemorrhagic stroke for subjects with a family history of migraine (OR, 2.30; 95% CI, 1.35–3.90).2 Another study showed increased risk of hemorrhagic stroke (OR, 1.8; 95% CI, 1.2–2.7) for migraineurs, which was most consistent for women with migraine who also took oral contraceptives.1Results from a prospective cohort study among women indicate that the association between migraine and hemorrhagic stroke is limited to the subgroup of women with MA (relative risk, 2.25; 95% CI, 1.11–4.54).20 The risk was stronger for fatal hemorrhagic strokes and appeared to be limited to women aged ≥55 years. In a large, population-based inpatient sample, International Classification of Diseases, 9th Revision coding for migraine in the peripartum was associated with various vascular events, including intracerebral hemorrhage (OR, 9.1; 95% CI, 3.0–27.8).21MRI Structural Brain LesionsThere is increasing evidence that migraine is associated with higher prevalence of white matter hyperintensities (Figure 1)22,23 and silent infarcts.23–25 These pathologies are also relevant for stroke physicians because they may be found in MR imaging of patients with stroke with a history of migraine. In 2 studies the infarct lesions among patients with migraine are located in the posterior circulation territory (Figure 2),23,24 which is consistent with the location of strokes among young patients with migraine.16 In a study of individuals aged ≥65 years, infarct lesions were more likely outside the brain stem and cerebellum.25 A recent study of 34 patients with migraine and 35 matched control subjects suggested that the cerebellar predilection of ischemic lesions in migraine with aura might be a combination of altered autoregulation and additional factors such as the end artery cerebellar angioarchitecture.26Download figureDownload PowerPointFigure 1. Multiple deep white matter hyperintensities in a patient with migraine. Reprinted with permission from the investigators from Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis23 (CAMERA) Study.Download figureDownload PowerPointFigure 2. Cerebellar infarct-like lesion in a patient with migraine with aura. Corresponding T2-weighted (left) and fluid-attenuated inversion recovery images (right). Reprinted with permission from the investigators from Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis23 (CAMERA) Study.Despite the association between MA and structural brain lesions, the mechanisms and practical consequences remain unclear. In particular, it remains unclear whether presence of these lesions increases the likelihood of a subsequent stroke event among patients with MA. Thus, there is currently no evidence that the presence of these lesions would require different treatment or prophylactic strategies for patients with migraine and stroke.Role of Migraine-Specific Medication on Stroke RiskTwo effective migraine acute treatments, ergot alkaloids and triptans, have vasoconstrictive effects raising concerns about potential cardiovascular side effects including stroke. Although ergotamine overuse has been linked with increased risk of vascular disease,27 results of a large population-based study do not suggest a link of triptans with stroke.28 In addition, the fact that the migraine–stroke association is limited to MA argues against a strong influence of migraine treatment in stroke occurrence as all patients with migraine receive treatment not just patients with MA.Absolute Importance of Migraine Among Patients With StrokeDespite clear evidence from epidemiological studies that MA increase the risk of ischemic stroke by approximately 2-fold, one has to take into consideration that a stroke is still a rare event among patients with MA. Data from the Women's Health Study, which included women aged ≥45 years, suggest that there are 4 additional ischemic stroke cases per 10 000 women per year attributable to MA, when it is assumed that MA causes stroke.More relevant data about the role of migraine among patients with stroke may come from stroke registries. Of 3502 patients with first ischemic stroke from the Lausanne Stroke Registry, 130 (3.7%) had active migraine.16 In patients with ischemic stroke who were aged <45 years, active migraine was seen in 23% of women and 8.2% of men, which is consistent with the prevalence of active migraine in that age group in the general population. Although in these patients common causes for stroke (ie, large artery disease, embolic stroke, patent foramen ovale) was noted in approximately half of the cases, 35 of 66 (53%) had other, mostly undetermined causes. In 24 patients the migraine attack was present at the time of the stroke event and 11 had rare causes such as venous cerebral thrombosis, dolichoectasia, or fibromuscular dysplasia. In the population-based stroke registry of the city of Dijon, which included 2389 patients with stroke, only 49 (2%) had a history of migraine.29 With regard to the distribution of stroke subtypes, there was a suggestion of higher migraine prevalence among hemorrhagic stroke cases compared with other subtypes.In the Italian Project on Stroke in Young Adults, 981 patients 60 minutes and with neuroimaging signs of an infarct in a relevant area and provided that the stroke is not attributed to another disorder. Applying these criteria makes a migrainous infarct a very rare event. In the Lausanne Stroke Registry, 9 of 3502 (0.3%) ischemic strokes were classified as migrainous stroke16; in the Dijon Stroke Registry, there were 12 of 2389 (0.5%) cases.29 The presence of a prolonged aura in a patient with MA, however, does not necessarily mean this patient has a manifest stroke event.31Ischemic Stroke Triggering a MigraineThe association between migraine and ischemic stroke is complicated by the fact that an ischemic cerebral event can trigger a migraine-like attack,32 which may lead to misinterpretation of the stroke event as "complicated migraine." Many patients with stroke report having a headache. In a study of >2000 patients with stroke, 27% reported a headache at the time of stroke onset.33Distinct Clinical Conditions Linked to Migraine and StrokeThere are several clinical conditions that have been linked to migraine and by themselves increase the likelihood of stroke. The identification of this group of patients may be the most important aspect for stroke clinicians because it involves a somewhat different diagnostic workup and therapeutic considerations (Table).Table. Practical Considerations in Patients With a Stroke Who Have Migraine or a History of MigraineCommentConsiderations for the Acute PhaseConsiderations for Secondary PreventionPatients with ischemic stroke and Migraine with aura at the time of stroke onsetMigrainous stroke: patient with migraine with prolonged aura (>60 min), with for that patient typical aura symptoms, with neuroimaging signs of an infarct in a relevant area and the stroke is not attributed to another disorder; very rare eventMigraine attack triggered by ischemic vascular event (or nonmigrainecauses for that event)• The diagnostic workup and the treatment options for stroke in patients who have migraine at the time of stroke do not differ to other patients with stroke• In the absence of an obvious vascular or cardiac cause (atherosclerosis, atrial fibrillation, etc):- Cervical artery dissection?- Patent foramen ovale or other cardiac pathology allowing for microemboli?- Evidence for blood disorders? (ie, antiphospholipid antibody syndrome, systemic lupus erythematosus, essential thrombocythemia)- Evidence for rare disorders affecting brain vessel walls (ie, CADASIL, MELAS, Sneddon syndrome)?- Hypercoagulability?• Antithrombotic agents: use of dipyridamole can lead to headache; aspirin or clopidogrel may have beneficial effects on migraine• Migraine treatment after stroke: ergotamine or triptan use is contraindicated• Other: reduction of vascular risk factors, particularly smoking; among women: stop of oral contraceptive or postmenopausal hormone usePatient with active migraine with aura but not in close proximity to the stroke eventAs active migraine is common among younger individuals in whom stroke evens are uncommon=rare eventSame as aboveSame as abovePatient with history or active migraine without auraNot linked with increased risk of strokeNo additional workup necessarySame as abovePatient with history of migraine with aura but no active migraineCommon situation as the lifetime prevalence of migraine is approximately 20%No additional diagnostic workup due to migraineNo specific consideration because of history of migraine; if migraine reoccurs, see aboveCADASIL indicates cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy; MELAS, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.Cervical Artery DissectionA recent meta-analysis summarized the association between migraine and cervical artery dissection.11 In pooled analysis, migraine doubled the risk of cervical artery dissection (OR, 2.06; 95% CI, 1.33–3.19). The risk further increased for multiple dissections. Although the association was somewhat stronger for MA, there was no significant difference according to aura status.11 The reason for this link remains unclear. Shared genetic susceptibility34 and increased serum elastase in migraine35 might be involved. Cases of carotid artery dissections triggering migraine attacks have also been described.36Patent Foramen OvaleThe association between migraine and patent foramen ovale (PFO) has gained enormous attention over the past years. Initial evidence from case–control studies showed that PFO is more prevalent among patients with migraine and migraine more prevalent among patients with a PFO.37 The negative results of the Migraine Intervention With STARFlex Technology (MIST) trial38 have put unrealistic hopes that migraine can be cured by PFO closure in perspective. The lack of association between migraine and PFO in a large population-based study among elderly individuals39 and in a hospital-based case–control study40 further question whether PFO plays a causal part in patients with migraine in general. However, because it has been shown that small particles and air bubbles can trigger cortical spreading depression,41 the likely pathophysiological correlate of the migraine aura,8 it is plausible that PFO can trigger migraine aura in some patients.For young patients with a stroke of unknown origin, an examination of an existing PFO is part of routine causative diagnostics. The decision of PFO closure, however, should be based on stroke prevention and not on potential beneficial effects on migraine.Markers of Hypercoagulability and InflammationMigraine has been associated with endothelial dysfunction42 of which hypercoagulability is a well-established consequence. In a young, relatively healthy cohort of women, strong associations between biomarkers of endothelial activation and migraine were found.43 These include von Willebrand factor activity, C-reactive protein, tissue-type plasminogen activator antigen, and total nitrite/nitrate concentration and the association was generally stronger for MA. Particularly the role of von Willebrand factor in the migraine–stroke association has been investigated. In a study of 63 patients with migraine, 11 patients with a history of migraine and stroke, and 35 control subjects, von Willebrand factor antigen and activity was highest in the group of patients with migraine and stroke.44 In another study, carriers of factor V Leiden mutation, the G20210A mutation in the prothrombin gene, or both of the prothrombotic genotypes had 2-fold increased risk for MA (OR, 2.21; 95% CI, 1.05–4.68) as compared with patients with stroke without migraine.18Rare Clinical SyndromesThere are very rare and clinically distinct syndromes and vascular pathologies that have been linked with MA.9 These include cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), arteriovenous malformations, leptomeningeal angiomatosis, Sneddon syndrome, Moyamoya syndrome, right-to-left shunts, antiphospholipid antibody syndrome, cardiac myxoma, essential thrombocythemia, and mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). However, in most patients with stroke of unknown origin, a typical diagnostic workup will unveil most of these conditions.Genetic FactorsMigraine is determined by the interplay of environmental45 and genetic factors.46,47 However, only few studies could evaluate whether specific genetic factors further increase stroke risk among patients with MA. The strongest evidence links a polymorphism in the methylenetetrahydrofolate reductase gene with further increased ischemic stroke risk.48,49 However, practical consequences remain uncertain because patients with migraine do not have increased levels of homocysteine.43,50Results of a recent genomewide association study suggest that 2 single nucleotide polymorphisms are involved in the MA–ischemic stroke association,51 but further studies are needed to unveil involved mechanisms. Thus, genetic testing among patients with stroke and migraine is currently not indicated.The Clinical Challenge: Migraine Aura Versus Transient Ischemic AttackEven for experienced neurologists, a differentiation between migraine aura and transient ischemic attacks is often challenging. This is particularly true for patients aged ≥60 years among whom transient ischemic attack occurrence increases, whereas attacks of MA are more likely to become more atypical because they are not always followed by a migraine headache.52 The sudden onset of transient ischemic attack symptoms paired with the presence of vascular risk factors is the strongest difference from MA, which has a more gradual-progressing occurrence of symptoms. The presence of a headache after transient neurological symptoms does not necessarily mean that these symptoms are consistent with a diagnosis of MA, because a migraine-like attack can be triggered by ischemic vascular events.32Another problem may occur if a patient with known MA has a rapid onset of transient neurological symptoms, because the diagnosis of an ischemic cerebral event, or risk factors for it such as artery dissection,36 may be missed by discounting these symptoms as MA. A more detailed clinical workup is recommended for patients with known MA in whom their aura symptoms differ, are atypical, or are accompanied with clinical signs of involvement of the basilar artery.Practical ConsequencesTreatment and Secondary PreventionIn general, the acute treatment and secondary prevention of a patient with stroke who has a history of migraine does not differ from other patients with stroke (Table). Some aspects should be considered, however. Use of dipyridamole in the secondary prevention of recurrent stroke can lead to headache,53 which can be severe and patients may need to be switched to another antithrombotic treatment. There is some initial evidence that aspirin54 or clopidogrel55 have beneficial effects on migraine.Recommendations to reduce the presence of cardiovascular risk factors such as hypertension, hyperlipidemia, or obesityalso apply to patients with migraine who have a stroke. Patients with MA should strongly be advised to quit smoking and among women, oral contraceptives or postmenopausal hormone intake should be stopped.Migraine Treatment After StrokeThe treatment of acute migraine attacks (with or without aura) may have to be adjusted after an ischemic vascular event, including transient ischemic attack. Ergotamine or triptan use is contraindicated in patients who had any ischemic vascular event because of their potential to narrow arteries.There is currently no direct evidence to support that a migraine prophylactic treatment will reduce future stroke risk. If a patient has hypertension, some antihypertensive medications have migraine prophylactic characteristics. These include particularly β-blockers (propranolol, metoprolol, atenolol, bisoprolol) and angiotensin-converting enzyme or angiotensin receptor blockers.56SummaryAlthough MA has been consistently linked with increased risk of stroke, MA plays only a small role when managing and treating patients with stroke. In very few cases migraine can be directly linked to a stroke event. Even if a patient has no other risk factors for a stroke than MA, this does not necessarily imply that the migraine caused the stroke because the mechanisms of such a link are still unclear. Distinguishing MA from a transient ischemic attack remains challenging in some patients and migraine-like attacks can be triggered by ischemic events. The role of migraine-like attacks that are secondary to comorbidities that increase stroke risk such as cervical artery dissection should be considered in the clinical management. The acute treatment of patients with stroke who have a migraine does not differ from any other patient with stroke but secondary prevention and migraine acute treatment may need to be adjusted.DisclosuresDr Kurth has received investigator-initiated research funding from the French National Research Agency (ANR), the US National Institutes of Health, the Migraine Research Foundation, and the Parkinson's Research Foundation. He has received honoraria from Allergan, the American Academy of Neurology and Merck for educational lectures, the BMJ for editorial work, and from MAP Pharmaceutical for contributing to a scientific advisory panel. Dr Diener has received honoraria for participation in clinical trials and contribution to advisory boards or oral presentations from Addex Pharma, Allergan, Almirall, AstraZeneca, Bayer Vital, Berlin Chemie, Coherex, CoLucid, Böhringer Ingelheim, Bristol-Myers Squibb, GlaxoSmithKline, Grünenthal, Janssen-Cilag, Lilly, La Roche, 3M Medica, MAP Pharmaceuticals, Medtronic, Minster, MSD, Novartis, Johnson & Johnson, Pierre Fabre, Pfizer, Schaper and Brümmer, SanofiAventis, and Weber & Weber. Financial support for research projects was provided by Allergan, Almirall, AstraZeneca, Bayer, GSK, Janssen-Cilag, and Pfizer. Headache research at the Department of Neurology in Essen is supported by the German Research Council (DFG), the German Ministry of Education and Research (BMBF), and the European Union. He has no ownership interest and does not own stocks of any pharmaceutical company.FootnotesCorrespondence to Tobias Kurth, MD, ScD, Inserm Unit 708—Neuroepidemiology, Université Bordeaux Segalen, 146 rue Léo Saignat, case 11, 33076 Bordeaux, France. E-mail [email protected]References1. Collaborative Group for the Study of Stroke in Young Women.Oral contraceptives and stroke in young women: associated risk factors.JAMA. 1975; 231:718–722.CrossrefMedlineGoogle Scholar2. Chang CL, Donaghy M, Poulter N. Migraine and stroke in young women: case–control study.The World Health Organisation collaborative study of cardiovascular disease and steroid hormone contraception.BMJ. 1999; 318:13–18.Google Scholar3. Stang PE, Carson AP, Rose KM, Mo J, Ephross SA, Shahar E, et al. Headache, cerebrovascular symptoms, and stroke: the Atherosclerosis Risk In Communities Study.Neurology. 2005; 64:1573–1577.CrossrefMedlineGoogle Scholar4. MacClellan LR, Giles WH, Cole J, Wozniak MA, Stern B, Mtichell B, et al. Probable migraine with visual aura and risk of ischemic stroke: the Stroke Prevention in Young Women Study.Stroke. 2007; 38:2438–2445.LinkGoogle Scholar5. Etminan M, Takkouche B, Isorna FC, Samii A. Risk of ischaemic stroke in people with migraine: systematic review and meta-analysis of observational studies.BMJ. 2005; 330:63.CrossrefMedlineGoogle Scholar6. Schurks M, Rist PM, Bigal ME, Buring JE, Lipton RB, Kurth T. Migraine and cardiovascular disease: systematic review and meta-analysis.BMJ. 2009; 339:b3914.CrossrefMedlineGoogle Scholar7. Spector JT, Kahn SR, Jones MR, Jayakumar M, Dalal D, Nazarian S. Migraine headache and ischemic stroke risk: an updated meta-analysis.Am J Med. 2010; 123:612–624.CrossrefMedlineGoogle Scholar8. Dreier JP. The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease.Nat Med. 2011; 17:439–447.CrossrefMedlineGoogle Scholar9. Kurth T, Chabriat H, Bousser MG. Migraine and stroke: a complex association with clinical implications.Lancet Neurol. 2012; 11:92–100.CrossrefMedlineGoogle Scholar10. Lipton RB, Bigal ME. The epidemiology of migraine.Am J Med. 2005; 118(suppl 1):3S–10S.MedlineGoogle Scholar11. Rist PM, Diener HC, Kurth T, Schurks M. Migraine, migraine aura, and cervical artery dissection: a systematic review and meta-analysis.Cephalalgia. 2011; 31:886–896.CrossrefMedlineGoogle Scholar12. Kurth T, Schurks M, Logroscino G, Buring JE. Migraine frequency and risk of cardiovascular disease in women.Neurology. 2009; 73:581–588.CrossrefMedlineGoogle Scholar13. Donaghy M, Chang CL, Poulter N. Duration, frequency, recency, and type of migraine and the risk of ischaemic stroke in women of childbearing age.J Neurol Neurosurg Psychiatry. 2002; 73:747–750.CrossrefMedlineGoogle Scholar14. Scher AI, Terwindt GM, Picavet HS, Verschuren WM, Ferrari MD, Launer LJ. Cardiovascular risk factors and migraine: the GEM population-based study.Neurology. 2005; 64:614–620.CrossrefMedlineGoogle Scholar15. Bigal ME, Kurth T, Santanello N, Buse D, Golden W, Robbins M, et al. Migraine and cardiovascular disease: a population-based study.Neurology. 2010; 74:628–635.CrossrefMedlineGoogle Scholar16. Milhaud D, Bogousslavsky J, van Melle G, Liot P. Ischemic stroke and active migraine.Neurology. 2001; 57:1805–1811.CrossrefMedlineGoogle Scholar17. Kurth T, Schurks M, Logroscino G, Gaziano JM, Buring JE. Migraine, vascular risk, and cardiovascular events in women: prospective cohort study.BMJ. 2008; 337:a636.CrossrefMedlineGoogle Scholar18. Pezzini A, Grassi M, Lodigiani C, Patella R, Gandolfo C, Casoni F, et al. Predictors of migraine subtypes in young adults with ischemic stroke: the Italian project on stroke in young adults.Stroke. 2011; 42:17–21.LinkGoogle Scholar19. Rist PM, Buring JE, Kase CS, Schurks M, Kurth T. Migraine and functional outcome from ischemic cerebral events in women.Circulation. 2010; 122:2551–2557.LinkGoogle Scholar20. Kurth T, Kase CS, Schurks M, Tzourio C, Buring JE. Migraine and risk of haemorrhagic stroke in women: prospective cohort study.BMJ. 2010; 341:c3659.CrossrefMedlineGoogle Scholar21. Bushnell CD, Jamison M, James AH. Migraines during pregnancy linked to stroke and vascular diseases: US population based case–control study.BMJ. 2009; 338:b664.CrossrefMedlineGoogle Scholar22. Swartz RH, Kern RZ. Migraine is associated with magnetic resonance imaging white matter abnormalities: a meta-analysis.Arch Neurol. 2004; 61:1366–1368.CrossrefMedlineGoogle Scholar23. Kruit MC, van Buchem MA, Hofman PA, Bakkers JT, Terwindt GM, Ferrari MD, et al. Migraine as a risk factor for subclinical brain lesions.JAMA. 2004; 291:427–434.CrossrefMedlineGoogle Scholar24. Scher AI, Gudmundsson LS, Sigurdsson S, Ghambaryan A, Aspelund T, Eiriksdottir G, et al. Migraine headache in middle age and late-life brain infarcts.JAMA. 2009; 301:2563–2570.CrossrefMedlineGoogle Scholar25. Kurth T, Mohamed S, Maillard P, Zhu YC, Chabriat H, Mazoyer B, et al. Headache, migraine, and structural brain lesions and function: population based Epidemiology of Vascular Ageing-MRI study.BMJ. 2011; 342:c7357.CrossrefMedlineGoogle Scholar26. Reinhard M, Schork J, Allignol A, Weiller C, Kaube H. Cerebellar and cerebral autoregulation in migraine.Stroke. 2012; 43:987–993.LinkGoogle Scholar27. Wammes-van der Heijden EA, Rahimtoola H, Leufkens HG, Tijssen CC, Egberts AC. Risk of ischemic complications related to the intensity of triptan and ergotamine use.Neurology. 2006; 67:1128–1134.CrossrefMedlineGoogle Scholar28. Hall GC, Brown MM, Mo J, MacRae KD. Triptans in migraine: the risks of stroke, cardiovascular disease, and death in practice.Neurology. 2004; 62:563–568.CrossrefMedlineGoogle Scholar29. Sochurkova D, Moreau T, Lemesle M, Menassa M, Giroud M, Dumas R. Migraine history and migraine-induced stroke in the Dijon stroke registry.Neuroepidemiology. 1999; 18:85–91.CrossrefMedlineGoogle Scholar30. Olesen J, Bousser M-G, Diener H, Dodick D, First M, Goadsby P, et al. The International Classification of Headache Disorders: II Edition.Cephalalgia. 2004; 24(suppl 1):9–160.CrossrefMedlineGoogle Scholar31. Vroomen PC, Buddingh MK, Luijckx GJ, De Keyser J. The incidence of stroke mimics among stroke department admissions in relation to age group.J Stroke Cerebrovasc Dis. 2008; 17:418–422.CrossrefMedlineGoogle Scholar32. Olesen J, Friberg L, Olsen TS, Andersen AR, Lassen NA, Hansen PE, et al. Ischaemia-induced (symptomatic) migraine attacks may be more frequent than migraine-induced ischaemic insults.Brain. 1993; 116:187–202.CrossrefMedlineGoogle Scholar33. Tentschert S, Wimmer R, Greisenegger S, Lang W, Lalouschek W. Headache at stroke onset in 2196 patients with ischemic stroke or transient ischemic attack.Stroke. 2005; 36:e1–e3.LinkGoo
Referência(s)