偏头痛导致脑卒中的机制研究进展

偏头痛和脑卒中是常见的神经系统疾病,都是严重致残的疾病,多项研究认为偏头痛尤其是先兆性偏头痛,与脑卒中风险增加有关。文中主要就偏头痛导致脑卒中的相关性及可能机制进行综述。     

偏头痛患者血清C-反应蛋白测定

偏头痛是一种常见病，其发病机制尚不完全清楚，许多证据表明偏头痛与免疫炎症反应有关，而C-反应蛋白(CRP)与免疫调节关系密切，此研究检测了52例偏头痛患者血清CRP水平，以有助于探讨偏头痛的发病机制。     

MUF对偏头痛诊断价值的研究

为了研究偏头痛样超声谱（ＭＵＦ）对偏头痛的诊断价值，使用ＴＣＤ对５３７例偏头痛患者和２３０例正常人进行检测，发现偏头痛组的ＭＵＦ明显高于对照组，且ＭＵＦ的发生与发作频度、病程有关，与是否有先兆无关，提示ＭＵＦ在偏头痛患者有一定普遍性，可作为偏头痛诊断的一个有用指标。     

偏头痛患者血浆内皮素和降钙素基因相关肽含量的变化与临床意义

目的：观察偏头痛患血装饰品中内皮素（ET）和降钙素基因相关肽（CGRP）含量的变化，并探讨其临床意义。方法：采用放射免疫的方法，测38例无先兆型偏头痛患及25例正常人血浆ET，CGRP含量。结果：均高于对照组偏头痛组的ET，CGRP含量，差异有显性意义（P＜0．01），ET和CGRP的比值升高（ET／CGRP）与偏头痛的严重程度有关，重度显高于轻中度。结论：偏头痛的发病可能与ET，CGRP水平失衡有关。     

偏头痛型脑卒中(附20例报告)

目的：探讨偏头痛型脑卒中的临床特征，以期引起对该病的认识与重视。方法：对20例偏头痛型脑卒中的临床资料进行分析，并结合文献讨论本病的可能发生机理。结果：20例患者平均年龄35.8岁，女性占95％，均有偏头痛史（平均15．6年），在偏头痛发作过程中发生脑梗塞（均经CT或MRI确诊）。主要临床表现以偏盲为最多；偏身感觉障碍，轻偏瘫次之。血液流变学均呈高凝状态。结论：本病是一种青年缺血性脑卒中，女性居多，均有偏头痛史，梗塞灶常发生在椎基底系统，以大脑后动脉受累为主。其发病机制可能与血管舒缩功能紊乱致严重的脑血管痉挛性狭窄及血液高凝状态有关。     

偏头痛的基因研究进展

偏头痛是一种遗传因素明显的原发性头痛，在过去的十多年里，偏头痛的遗传基础成为一个研究热点，其主要目标是鉴定易感基因。到目前为止，基因研究取得了突破性进展的一种偏头痛是家族偏瘫性偏头痛。影响无先兆偏头痛和先兆偏头痛等普通偏头痛的基因型及基因数量还不清楚。本文阐述了家族性偏瘫性偏头痛基因与普通偏头痛的关系，并从候选基因研究法与全基因扫描法两方面阐述与偏头痛相关的基因。     

癫痫,偏头痛与情感性障碍

癫痫、偏头痛与情感性障碍袁浩龙周蓓蓓癫痫、偏头痛与情感性障碍在其同病和治疗中相互重叠。有和无先兆偏头痛与忧郁症（ｄｙｓｔｈｙｍｉａ）、重性抑郁症、双相情感障碍（轻躁狂）躁狂发作及各类焦虑障碍均有关。与无先兆偏头痛相比，有先兆偏头痛病人的情感性障碍患病...     

幽门螺杆菌感染与偏头痛关系研究

幽门螺旋杆菌(Hp)感染是一种胃内持续性慢性感染，但近年来发现其与多种胃外疾病有关。其中研究较多的是与脑梗死、冠心病的关系，而与偏头痛关系的研究目前国内尚未见报道。我们测定了偏头痛组和健康对照组血清Hp特异性抗体IgG，同时偏头痛组38例行胃镜检查及Hp检测，探讨Hp感染与偏头痛的关系及其作用机制。     

硫酸镁联合氟桂利嗪治疗急性发作期偏头痛

偏头痛是一种常见且多发的神经科疾病，近年的国内研究资料表明，偏头痛发作与镁离子缺乏有关。我院2003年2月-2005年4月采用硫酸镁联合氟桂利嗪（西比灵）治疗急性发作期偏头痛患124例，取得满意疗效。     

抗心磷脂抗体与偏头痛关系的研究

用ＥＬＩＳＡ法分别对７５例偏头痛患者和正常人测定血清抗心磷脂抗体（ＡＣＡ），阳性率分别为３２％和２．６７％，差异显著（Ｐ＜０．０１）；另外还发现ＡＣＡ阳性的偏头痛患者无性别差异。结果说明ＡＣＡ与偏头痛有关，并对ＡＣＡ激发偏头痛的发病机制做了探讨。     

Is migraine a genetic illness? The various forms of migraine share a common genetic cause

Is migraine a genetic illness? This question was previously controversial, but today the answer yes is generally accepted. The scientific evidence is the significantly increased familial risk of migraine, and the significantly higher concordance rate of migraine in monozygotic than dizygotic twin pairs. Finally, the three identified ion-channel genes that can cause familial hemiplegic migraine provide very strong evidence of genetics. Mutations in these genes can also cause sporadic hemiplegic migraine. The next question is whether the different types of migraine, i.e. migraine without aura, migraine with aura, sporadic hemiplegic migraine and familial hemiplegic migraine share a common genetic cause. This question is at present controversial. However, the fact that all types of migraine are paroxystic in nature suggest that a common genetic cause could be mutations in ion channels, although a common mutation has not yet been identified in the more common types of migraine: migraine without aura and migraine with aura.

     

Rare and atypical forms of migraine

There are three categories of rare forms of migraine headache. Atypical aura can raise difficult diagnostic questions due to their clinical expression (visual or sensorial illusions and hallucinations), their mode of onset (sudden aura, developing in less than 4 minute), their duration (prolonged aura lasting more than 60 minutes), and the lack of an accompanying headache. Differential diagnostics include partial epilepsy or AIT, requiring careful search for the underlying cause. Rare migraine syndromes are separate clinical entities, most of which are recognized by the International Headache Society (IHS). These syndromes include basilar migraine, familial hemiplegic migraine, ophthalmoplegic migraine and the exceptional retinal migraine. Confusional migraine, usually observed in children, is no individualized by the IHS but can be included here. For secondary migraines there is a triggering factor leading to migraine in patients with no history of migraine previously. These include post-traumatic migraine and cervical migraine as well as migraine occurring with epileptic seizures and rare symptomatic migraine headache disclosing a general disease or an intracranial neurological lesion.     

When migraine progresses: transformed or chronic migraine

Migraine may be conceptualized, not just as an episodic disorder, but as a chronic recurrent and sometimes chronic progressive disorder. Transformed migraine, often referred to as chronic migraine is the result of migraine progression. This article will review the clinical features of transformed migraine, highlighting that its phenotype varies according to stage. Early in the process of transformation, attacks with migraine features are very common. As the disease evolves, most attacks lack the migraine features. The risk factors for migraine progression and the mechanisms for progression will be discussed. This review concludes with the prospects for treating transformed migraine and avoiding migraine progression.     

Migraine, suicidal ideation, and suicide attempts.

We examined the risk of suicide attempts and suicidal ideation separately in persons with (1) migraine with aura alone, (2) migraine with aura and coexisting major depression, (3) migraine without aura alone, and (4) migraine without aura and coexisting major depression. Persons with migraine with aura alone and migraine with aura and coexisting major depression had significantly higher rates of suicide attempts and suicidal ideation compared with persons with neither migraine nor major depression. The rates of suicide attempts and suicidal ideation in persons with migraine with aura and major depression were higher than the combined rates in persons with major depression alone and migraine with aura alone. In contrast, migraine without aura was not associated with an increased risk for suicide attempts and suicidal ideation.     

Platelet serotonin metabolism and ultrastructure in migraine

Biochemical and ultrastructural techniques were used to study the nature of platelet serotonin involvement in migraine. Serotonin levels were increased to a moderate degree in classic migraine, but not in common migraine. The platelet content of 5-hydroxyindoleacetic acid was equally reduced in both classic and common migraine. Platelet-dense bodies, the storage organelles for serotonin, were increased in both migraine groups, particularly in classic migraine. The results were interpreted as evidence for reduced platelet serotonin turnover combined with dense body hyposecretion in migraine sufferers. These findings are further supportive evidence for altered serotonergic function between attacks of migraine, and argue in favor of a role for serotonin in the mechanisms of a migraine attack.     

TOTAL 5-HYDROXYINDOLES IN BLOOD RELATED to MIGRAINE ATTACKS

The total 5-hydroxyindoles (5-HI) in whole blood were measured in 20 migraine patients during spontaneous migraine attacks and in headache-free periods. A statistically significant fall in blood 5-HI was found during headache in 17 patients suffering from classical and common migraine. In one patient with complicated migraine no change was found, and in two patients, one with common migraine and one with migraine and associated symptoms, there was a rise in total blood 5-HI during migraine attacks. the results are compared with previous findings in this field, and it is suggested that during migraine attacks there might be a rise in the plasma 5-HI. the possibility of using the 5-HI fall during spontaneous migraine attacks as a simple test for the diagnosis of migraine is discussed.     

Recent findings in headache genetics

PURPOSE OF REVIEW: The progress in headache genetics, especially migraine genetics, recently jumped ahead with some major discoveries. RECENT FINDINGS: Family and epidemiological studies further strengthen the genetic contribution to migraine and two recent observations gave new molecular insights in the disease. Studies on the genetics of familial hemiplegic migraine revealed, in addition to the previously identified familial hemiplegic migraine type 1 gene CACNA1A on chromosome 19, the familial hemiplegic migraine type 2 gene ATP1A2, encoding the alpha2-subunit of sodium/potassium pumps. Recent genome screens in families with migraine identified susceptibility loci on chromosomes 4, 6, 11 and 14. SUMMARY: The findings in familial hemiplegic migraine confirm that dysfunction in ion transport is a key factor in migraine pathophysiology and might help us in the elucidation of migraine molecular pathways. The identification of several migraine susceptibility loci underline its genetically complex nature.     

Genetics of migraine and migraine accompagneé: a study of eighty-one children and their families

Eighty-one patients suffering from childhood onset migraine and their families were investigated for familial prevalences of epileptic seizures and migraine. The incidence of epileptic seizures was not increased above the epidemiological risk. - In all, migraine is largely inherited from maternal ascendents, irrespective of the sex of the index case. Clinical subtypes of migraine ("non-focal migraine" and migraine accompagnée) are not accompanied by respectively increased familial prevalences. - Onset of migraine is earlier in patients with a higher familial impact. These findings are discussed in context with a proposed multifactorial pathogenesis of migraine.     

Migraine associated with head trauma

Migraine associated with head trauma i.e. onset of migraine in close temporal relation to a head trauma was analyzed in a large population based survey of 4000 forty-year-old males and females. Of the 29 people with migraine associated with head trauma, 20 had migraine without aura associated with head trauma, six had migrainous disorder without aura associated with head trauma and three had migraine with aura associated with head trauma. Eleven had a significant head trauma (loss of consciousness or posttraumatic amnesia lasting more than 10 minutes) and 18 had a minor head trauma. The overall lifetime prevalence of migraine associated with head trauma was 1.4% with a male-female ratio of 1:2.4. The symptomatology of migraine associated and unassociated with head trauma was not different. The first degree relatives of probands with migraine associated with head trauma were blindly interviewed by a physician. The first degree relatives of probands with migraine without aura associated with head trauma had a significantly lower risk of migraine without aura than first degree relatives of probands with migraine without aura unassociated with head trauma. We conclude that migraine without aura associated and unassociated with head trauma have a different aetiology. Thus, it is very likely that a head trauma may cause migraine without aura. The mechanisms involved in trauma induced migraine without aura are unknown.     

Most cases labeled as "retinal migraine" are not migraine.

BACKGROUND: Monocular visual loss has often been labeled "retinal migraine." Yet there is reason to believe that many such cases do not meet the criteria set out by the International Headache Society (IHS), which defines "retinal migraine" as attacks of fully reversible monocular visual disturbance associated with migraine headache and a normal neuro-ophthalmic examination between attacks. METHODS: We performed a literature search of articles mentioning "retinal migraine," "anterior visual pathway migraine," "monocular migraine," "ocular migraine," "retinal vasospasm," "transient monocular visual loss," and "retinal spreading depression" using Medline and older textbooks. We applied the IHS criteria for retinal migraine to all cases so labeled. To be included as definite retinal migraine, patients were required to have had at least two episodes of transient monocular visual loss associated with, or followed by, a headache with migrainous features. RESULTS: Only 16 patients with transient monocular visual loss had clinical manifestations consistent with retinal migraine. Only 5 of these patients met the IHS criteria for definite retinal migraine. No patient with permanent visual loss met the IHS criteria for retinal migraine. CONCLUSIONS: Definite retinal migraine, as defined by the IHS criteria, is an exceedingly rare cause of transient monocular visual loss. There are no convincing reports of permanent monocular visual loss associated with migraine. Most cases of transient monocular visual loss diagnosed as retinal migraine would more properly be diagnosed as "presumed retinal vasospasm."