偏头痛与卒中

偏头痛与卒中的关系是目前神经科领域引人关注的课题。许多研究表明,偏头痛与卒中存在复杂的相互关系,包括偏头痛是卒中的病因、偏头痛作为脑梗死的危险因素或后果以及偏头痛与脑梗死是共同病因所致。文章对偏头痛与卒中的关系做了综述。     

有先兆型偏头痛女性的卒中后转归更好

有先兆型偏头痛史的女性卒中风险增高。然而，美国Circulation报道的一项新研究表明，与无偏头痛的女性相比，有先兆型偏头痛女性的卒中事件更可能仅遗留轻微残疾或无残疾。     

偏头痛与卒中的关系

偏头痛与脑卒中之间的关系十分复杂。有些偏头痛可能增加其发生脑卒中的危险;有些脑卒中与偏头痛的发生可能无关系,表现为两者共存。有些患者的偏头痛在发作时酷似脑卒中,但少数患者在头痛发作期间可能诱发脑卒中。此外,偏头痛也可能是脑卒中的一种临床表现,称之为症状性偏头痛。尽管两者的临床特征和疾病过程存在明显差异,但在神经功能缺损、脑血流改变和病因方面的确存在复杂的相互关系。偏头痛与卒中的关系已引起广泛关注,并获得了一些相当重要的研究结果。     

偏头痛与脑卒中关系的研究进展

偏头痛严重影响人类的日常生活质量，偏头痛与脑血管病常共同发生。偏头痛不仅与缺血性卒中相关，而且可增加出血性卒中的风险，与亚临床脑病如脑白质病变、无症状的脑梗死样病变有关。偏头痛和脑血管疾病可能存在共同的危险因素或病理生理机制，如皮层扩布抑制、卵圆孔未闭等。     

卵圆孔未闭的封堵治疗是先兆性偏头痛的选择吗？

卵圆孔未闭与缺血性卒中和先兆性偏头痛相关,且可能为两者的发病原因。有几项研究表明经皮卵圆孔未闭封堵可能改善先兆性偏头痛的症状,但均存在不同的方法学问题。目前对于先兆性偏头痛患者仍推荐首选药物治疗,需要更多的前瞻性、随机、对照研究寻找卵圆孔未闭封堵治疗先兆性偏头痛的证据。     

卒中相关头痛的研究进展

卒中相关头痛即与卒中发生相关联的头痛,可出现于卒中当时、之前或之后,发生率为３％－５７％。年龄,性别,既往偏头痛史,无吸烟史、缺血性心脏病等因素可能与之有关。     

偏头痛与脑卒中

本文综述了近几年国外对偏头痛相关卒中的研究进展。肯定了偏头痛与脑卒中的发病关系,对不同类型的偏头痛相关卒中提出了各自分类标准,并总结现代这一领域的研究结果来阐述偏头痛诱发卒中的发病机理。     

卵圆孔未闭介入封堵治疗相关新进展

卵圆孔未闭(PFO)是目前成年人中最为常见的先天性心脏病之一,通常认为PFO不会干扰到心脏的血流动力学,但近年来许多研究表明,PFO与不明原因卒中、偏头痛之间存在着密切联系。随着心导管技术的发展,经皮介入封堵PFO安全有效,可有效预防PFO合并不明原因卒中患者再次卒中事件的发生;可以改善PFO合并偏头痛患者头痛症状,部分患者偏头痛症状完全消失,PFO介入封堵治疗不明原因卒中及偏头痛疗效得到初步验证。现针对介入封堵PFO治疗不明原因卒中和偏头痛的研究进展做出综述。     

女性偏头痛、头痛与卒中的风险

通常认为,偏头痛和普通头痛与以后的卒中风险有关,但这主要是回顾性病例对照研究得出的结论。而评价特定的头痛类型与卒中联系的前瞻性资料还不多见。美国波士顿布莱根妇女医院预防医学科的Kurth等在39754名年龄≥45岁参加妇女健康研究的卫生专业人员中进行了一项前瞻性队列研究,平均随访9年。自行报告卒中,并通过查阅病历证实。结果共发生了385例卒中(缺血性309例,出血性72例,原因不明4例)。与非偏头痛患者相比,报告偏头痛的全部参试者或报告无先兆型偏头痛的参试者任何类型卒中的风险均未增加;而报告有先兆型偏头痛的参试者经过校正的全…     

不明原因偏头痛合并卵圆孔未闭研究进展

正偏头痛是世界上最常见的原发性头痛综合征,它是一种复杂的疾病,有反复发作、搏动性、单侧痛等特点,与心血管和脑血管事件的长期风险增加有关,这种效应是由于卒中(缺血和出血热)和心肌梗死的风险增加所致,部分原因是先兆的存在。其中,先兆偏头痛(MA)与脑灌注不足、全身血管病变、内皮功能障碍和高凝状态也有关,这些因素都可能1     

Headache and the risk of stroke

Several studies have suggested that migraine is a risk factor for stroke. The association between migraine and the risk of stroke has been observed most often among premenopausal women but also in some studies among men. The association may be stronger among women who smoke and among women using oral contraceptives compared with nonsmokers and nonusers. Classic migraine with aura may be a more powerful predictor of stroke than common migraine without aura. Findings of a recent population-based study suggest that subclinical brain lesions are more common among migraine patients, particularly among those with aura, than among the control subjects. Two cohort studies have shown that chronic non-specific headache also is related to increased stroke risk. The effect of treatment of migraine and other types of headache on the risk of stroke is not known. Even though the relative risk of stroke may be fairly high among migraine patients, the absolute risk is usually low due to low baseline risk among young people.     

Migraine and the Risk for Stroke and Cardiovascular Disease

Numerous data have pointed to an association between migraine and cardiovascular diseases. The majority of the available data have indicated that migraine with aura can be considered a risk factor for ischemic stroke, whereas migraine without aura cannot be reliably considered as such. High frequency of attacks and a recent onset of migraine have been related to an increased ischemic stroke risk. In addition, in young subjects with ischemic stroke migraine with aura represents an independent risk factor of overall recurrent vascular events and of recurrent ischemic stroke. Also the risk of transient ischemic attack seems to be increased in migraineurs, although this issue has not been extensively investigated. Several studies have also addressed the possible association between migraine and hemorrhagic stroke. Although the results of these individual studies were conflicting, their meta-analysis showed that migraine is associated with a 1.5-fold increase in the risk of hemorrhagic stroke (including intracerebral and subarachnoid hemorrhage). Some studies have identified migraine also as a possible risk factor for cardiac vascular events while others have yielded negative results. A meta-analysis did not show an increased risk of myocardial infarction in subjects with any migraine vs no migraine but subsequently, data has pointed to an association between any migraine with cardiac ischemic disease. Migraine has also been associated by some studies with vascular mortality and with vascular diseases in regions other than the brain and the heart. Several studies have also indicated that compared with nonmigraineurs, migraineurs have a higher burden of asymptomatic white matter brain lesions and, according to some studies, also infarct-like lesions at brain magnetic resonance. The mechanisms underlying the relationship between migraine and cardiovascular disease are still unclear. The possible explanation may rely on a peculiar vascular vulnerability of migraineurs that may contribute to the pathogenesis of migraine and, in the presence of some other unknown factors may also contribute, over time, to the development of cardiovascular disease. At the moment, there are no reliable features that may indicate which subjects, across the overall migraine population, will develop vascular events and so far, no drugs are recommended for the vascular prevention in migraineurs unless other clear indications are present. In general, the acute treatment and the secondary prevention measures of a patient with stroke who has a history of migraine do not differ from that of other stroke patients. There is currently no direct evidence to support that a migraine prophylactic treatment will reduce future stroke risk in secondary prevention.     

Early post-procedural migraine attack predicts migraine resolution after patent foramen ovale transcatheter closure

AIM: In patients with patent foramen ovale-related migraine, the procedure of transcatheter closure itself is likely to cause a migraine attack. Our study is aimed to evaluate the incidence of migraine attacks immediately after closure procedure and their clinical and potential prognostic significance. METHODS: We reviewed our database from January 2005 to April 2007 searching for patients with severe disabling migraine despite anti-headache therapy who were submitted to transcatheter closure of patent foramen ovale (PFO). Medical records of these patients were carefully reviewed in order to record migraine episodes immediately (0 to 6 h) after closure procedure. RESULTS: Twenty-one patients with previous stroke and migraine underwent PFO closure: the procedure was successful in all of the patients with no perioperative and in-hospital complications. Ten patients (47.6%) experienced a migraine attack of mean duration 3.5+/-2.4 h immediately after the closure procedure. Those patients had the same procedure time compared with other patients, but had larger PFO: patients with migraine attack immediately after closure had higher rate of complete abolition of migraine in the follow-up. CONCLUSION: Although more larger studies are needed to evaluate the exact relationships between migraine and PFO, in patients with a tight correlation between migraine and PFO, a prolonged opening of the PFO, as during closure procedure, may cause a migraine attack immediately after the closure. This fact can be considered a positive prognostic factor for migraine abolishment in the follow-up.     

Patent foramen ovale and cerebrovascular diseases

Patent foramen ovale (PFO) has been linked to ischemic strokes of undetermined cause (cryptogenic strokes). PFO-a remnant of fetal circulation when the foramen ovale does not seal after birth-can permit microemboli to escape the pulmonary filter into the intracranial circulation, causing stroke. Coexistent atrial septal aneurysm, pelvic deep vein thrombosis and inherited clotting factor deficiencies could potentiate stroke risk in patients with PFO. Transcatheter PFO closure, a minimally invasive procedure, is one technique used to prevent recurrent cerebrovascular events. A connection between PFO and migraine headache has been conceptualized from retrospective evidence of reduced migraine frequency and severity after PFO closure; however, prospective randomized trials are needed to verify the efficacy of PFO closure on migraine prevention. In this review we discuss embryologic origins, diagnostic techniques and treatment options for prevention of paradoxical embolism thought to be related to PFO, and the relation of PFO to cryptogenic stroke and migraine.     

Neurologic symptoms as a feature of the antiphospholipid syndrome

Antiphospholipid antibodies may cause various neurologic diseases by vascular and immune mechanisms. Ischemic stroke and transient ischemic attacks are the most common neurologic complications in patients with antiphospholipid antibodies but migraine, epilepsy, chorea, or multiple sclerosis also may occur. Although the neurologic presentation of patients with the antiphospholipid syndrome may vary, many patients have striking similarities, such as initial memory loss, aphasia, cognitive dysfunction with progressive cerebral deterioration, and even dementia. In conclusion, antiphospholipid syndrome may constitute a treatable cause of neurologic diseases, and the measurement of antiphospholipid antibodies should be routinely performed in patients with neurologic disorders.     

Stroke and migraine

Young patients with migraine are at increased risk for stroke, particularly patients with an aura of focal neurologic deficits. Other causes of ischemia are often identified in patients with migraine, including patent foramen ovale, lupus anticoagulant, cervical carotid dissection, arteriovenous malformation, and hyperactivity of the clotting system. Migrainous stroke is only diagnosed when all other possible causes of stroke have been eliminated and the patient has irreversibility of the usual aura, associated with an ischemic infarct in the appropriate brain territory. Prophylactic therapy of migraine with aura may be beneficial in preventing migrainous stroke.     

Stroke and migraine

Young patients with migraine are at increased risk for stroke, particularly patients with an aura of focal neurologic deficits. Other causes of ischemia are often identified in patients with migraine, including patent foramen ovale, lupus anticoagulant, cervical carotid dissection, arteriovenous malformation, and hyperactivity of the clotting system. Migrainous stroke is only diagnosed when all other possible causes of stroke have been eliminated and the patient has irreversibility of the usual aura, associated with an ischemic infarct in the appropriate brain territory. Prophylactic therapy of migraine with aura may be beneficial in preventing migrainous stroke.     

The association between migraine and cerebral vascular events: an analytical review

This paper explores the uncertain relationship between migraine headache and thromboembolic stroke. In reviewing the literature that links migraine with thromboembolic cerebral vascular events, a distinction is made between two stroke events that occur in migraine patients: stroke associated with a migraine attack (a migrainous stroke) and stroke unrelated to a migraine attack (a non-migrainous stroke). In a recent community-based stroke register, migrainous strokes occurred at a rate of 3.4 per 100,000 per annum. Prevalence rates for migraine in young stroke populations (11-28%) are similar to those in the general population and do not support an additional long-term risk of non-migrainous stroke in migraine patients. The only study providing a controlled estimate of long-term thromboembolic stroke risk (odds ratio = 1.7; 95% CI 1.3, 2.2) included only women and has not been independently confirmed. The contribution of migraine to other known risk factors for thromboembolic stroke needs to be examined further by controlled studies.     

Relation of atrial shunts to migraine in patients with ischemic stroke and peripheral emboli

This study investigated whether the increased incidence of stroke in young subjects with migraine is because they have an increased prevalence of atrial right-to-left shunts. The investigators report the prevalence of clinically relevant atrial shunts in those with stroke and migraine compared with those with stroke but without migraine and also in historic control groups of subjects who had migraine with aura but no stroke and in population controls. Of 60 consecutive stroke patients, 42 (70%) had large- or medium-sized atrial shunts. Transcatheter shunt closure was performed in 39 patients, of whom 35 had patent foramen ovales (mean diameter 9.8 +/- 4.1 mm) and 4 had atrial septal defects. If atrial shunts were unrelated to stroke in patients with migraines, shunt prevalence in those with migraine and stroke would be the same as in those with migraine but without stroke. However, a much greater shunt prevalence was found in those with stroke and migraine with aura (84%) than in those with migraine with aura but no stroke (38.1%, p <0.001), population controls (12.2%, p <0.001), and those with stroke but no migraine (55.6%, p <0.05). Shunt prevalence was also significantly greater in patients who had stroke and migraine without aura (75%) than in population controls (p <0.001) and in those with migraine with aura but no stroke (p <0.05). In conclusion, the increased incidence of stroke in subjects with migraine compared with the general population is because they have a higher prevalence of large atrial shunts and hence an increased risk for paradoxic embolism.