偏头痛前驱症状的生物学内涵

近年来,偏头痛前驱期因其可能的头痛预测作用及早期头痛干预机会为人所重视.打呵欠、疲乏、颈强直、感知觉超敏症状(畏光、畏声、畏嗅)均是常见的偏头痛前驱症状.然而,关于偏头痛前驱症状的预测效能及其可能机制,目前结论尚未统一.偏头痛前驱症状可分为感知觉超敏症状、睡眠及认知相关症状、自主神经症状和其他症状.前驱症状与触发因素及偏头痛伴随症状的准确区分,目前仍未达成统一.疲乏、情绪变化、颈强直是青少年期患者常见的前驱症状.目前对偏头痛前驱症状的病理生理机制研究仍处于初步阶段.打呵欠是偏头痛具有预测意义的前驱症状之一,通常认为与多巴胺能神经元改变密切相关,在偏头痛病理生理中,可由多巴胺能D1、D2、D3受体介导.颈强直是偏头痛常见前驱症状,与多巴胺、5-羟色胺能神经元激活有关.下丘脑在偏头痛前驱期激活,可能是导致前驱期颈强直的重要原因.恶心作为偏头痛患者常见前驱症状,其病理生理学起源仍存在争议.目前的研究表明,前驱期恶心与5-羟色胺代谢改变有关.感知觉超敏症状包括皮肤异常性疼痛和畏光、畏声、畏嗅,在前驱期中丘脑激活已被证实与皮肤异常性疼痛和畏光相关.     

偏头痛前驱期影像学研究进展

偏头痛是一种具有高度致残性的原发性头痛,严重影响患者日常功能.偏头痛的头痛发作通常为中至重度的搏动性疼痛,常存在恶心、呕吐、畏光和畏声等伴随症状,给患者带来不同程度的痛苦体验.近年来,前驱期(Premonitory phase;Prodromal phase)一段最长可持续48 h的、发生在有先兆偏头痛先兆出现前和无先...     

偏头痛遗传学研究进展

根据2004年国际头痛协会(International Headache Society,HIS)分类标准,偏头痛分为有先兆偏头痛(migraine with aura,MA)和无先兆偏头痛(migraine without aura,MO).MO临床表现为中重度、单侧、搏动性头痛,并伴有恶心、呕吐、畏声、畏光等症状,持续几小时至几天;MA在临床上的表现除具有以上症状外,还会在偏头痛发生之前出现神经系统的症状,如,视野缺损,构音障碍,一侧的轻偏瘫,面部或四肢末梢的感觉麻木等先兆症状[1].另外,偏头痛患者不存在神经系统的阳性体征,并且辅助检查无阳性结果.通过流行病学研究得出,在普通人群中偏头痛的发病率约为15%,其中,女性患病率约为男性的3倍[2],40岁之后患病率逐渐降低.     

偏头痛发病与Willis环不完整性的相关性研究

目的通过分析偏头痛患者Willis环不完整性的发生率,探讨偏头痛发病的可能机制。方法收集自2014年1月至2019年2月南京脑科医院神经内科诊治的偏头痛患者191例,其中先兆偏头痛(MA)患者58例(男20/女38),无先兆偏头痛(MOA)患者133例(男43/女90),同时纳入年龄性别相匹配的健康体检者85名(男29/女56),采集所有受试者头颅MRA资料,对各组间Willis环的不完整性发生率进行比较。结果偏头痛组Willis环的不完整性发生率(56.54%)显著高于对照组(40.00%),MA组(60.34%)与MOA(54.14%)组Willis环的不完整性发生率比较无统计学差异;亚组分析发现,偏头痛组Willis环前部不完整性发生率(16.23%)与对照组(15.29%)相比无统计学差异,Willis环后部不完整性发生率(47.64%)较对照组(32.94%)显著增高(P0.05),MA组Willis环前部不完整性发生率(18.97%)与MOA组(15.04%)及对照组(15.29%)比较均无统计学差异,MA组(51.72%)及MOA组(46.61%)Willis环后部不完整性发生率较对照组(32.94%)均显著增高(均P0.05),MA组Willis环后部不完整性与MOA组相比无统计学差异。结论 Willis环的不完整性与偏头痛的发病存在一定相关性,是偏头痛发病可能病因。     

卵圆孔未闭伴房间隔膨出瘤与先兆偏头痛关系的超声心动图研究

目的 应用经食管超声心动图(transesophageal echocardiograghy,TEE)联合右心声学造影评估卵圆孔未闭(patent foramen ovale,PFO)伴房间隔膨出瘤(atrial septal aneurysm,ASA)与先兆偏头痛(migraine with aura,MA)的关系.方法 回顾性分析郑州大学第一附属医院2018-01—2021-05接受经食道超声心动图联合右心声学造影的988例患者的检查图像及临床资料.超声检查前,采用经过验证的头痛问卷,由两位神经科医生根据国际头痛标准诊断是否有先兆偏头痛,由超声医生在不知患者是否有偏头痛的前提下进行超声心动图检查,进行RLS分级,对无FPO和ASA组、PFO组、ASA组和PFO伴ASA组进行偏头痛及先兆偏头痛的单因素分析,并对有无先兆偏头痛患者的RLS分级进行比较.结果 孤立的PFO占15.38％,孤立的ASA占3.04％,PFO合并ASA占7.29％.偏头痛发生率19.03％,MA发生率8.20％.与无PFO和ASA组比较,PFO伴ASA组无先兆偏头痛(OR=2.324,95％CI:1.225～4.41,P=0.008)及有先兆偏头痛(OR=5.533,95％CI:3.031～10.1,P<0.001)患病率显著增高.偏头痛患者中,PFO伴ASA组有先兆发生的患病率显著增高(OR=2.381,95％CI:1.095～5.176).在RLS分级中,2级和3级分流在MA及MA—患者之间差异有统计学意义(χ2=7.912,P=0.005);PFO伴ASA组2级和3级分流显著高于PFO组(χ2=7.023,P=0.008).结论 PFO合并ASA与MA显著相关,且出现右向左分流的程度增高,PFO引起的偏头痛研究应集中于这种特殊的心房异常.     

偏头痛并发焦虑抑郁等精神心理症状的相关因素分析

目的探讨偏头痛并发焦虑、抑郁等精神心理症状的相关危险因素。方法选择我院2010-03—2013-05收治的180例偏头痛患者作为研究对象,对伴焦虑、抑郁等精神心理症状患者进行相关危险因素分析。结果观察组偏头痛伴随焦虑、抑郁和睡眠障碍的发生率分别为42.2%、60.5%,均明显高于对照组(P0.05)。长期慢性发作、头痛程度重、持续时间长、发作频率高、睡眠质量差、生活满意度差等均为偏头痛伴焦虑抑郁患者的相关危险因素,且伴焦、抑郁、睡眠障碍患者的MIDAS分值均明显高于无精神心理症状患者,差异有统计学意义(P0.05)。结论偏头痛患者多伴较高的焦虑、抑郁以及睡眠障碍等,相关危险因素较多,对其生活质量有较大影响。临床医生应考虑患者伴随的相关精神心理状况,及时予以心理疏导,改善患者的睡眠质量,促进患者预后。     

偏头痛与睡眠质量关系的研究

目的:探讨偏头痛与睡眠质量的关系.方法:采用阿森斯睡眠量表(AIS)对112例偏头痛患者(偏头痛组)及112名健康体检者(正常对照组)的睡眠质量进行评分,比较两组间失眠的发生率.对偏头痛组中无睡眠障碍亚组、可疑失眠亚组和失眠亚组先兆发作率及疼痛程度进行比较,分析睡眠质量与偏头痛的关系.结果:偏头痛组失眠的发生率(58.9%)明显高于正常对照组(24.1%)(P<0.001).偏头痛各亚组间先兆发作率的差异无统计学意义;失眠亚组中、重度头痛的比例(53.0%,37.9%)明显高于无睡眠障碍亚组(23.8%,19.1%)和可疑失眠亚组(40.0%,16.0%)(均P<0.001).相关性分析显示,偏头痛组睡眠质量与头痛程度呈负相关(P<0.001).结论:偏头痛患者睡眠质量较差,且睡眠质量越差的患者头痛程度越重,改善睡眠质量有可能减轻头痛程度.     

原发性头痛的发病机制研究进展

原发性头痛包括紧张型头痛(TTH)、偏头痛、丛集性头痛、其他三叉神经自发性头痛和其他头痛.其中,紧张型头痛为人群中最常见的头痛类型,几乎不包含神经血管因素.偏头痛属于神经血管性疾病,全世界有8%～15%的患者受其困扰,仅在欧洲,每年约损失600×103个工作日[1,2].偏头痛多为中至重度头痛,可持续4～72 h,常为单侧的搏动性疼痛,并伴有畏光、畏声和(或)恶心、呕吐.有先兆的偏头痛,多于头痛发生之前出现短暂的对侧神经系统症状.     

偏头痛遗传机制的研究进展

偏头痛(migraine)是一种反复发作的具有明显家族聚集性的神经血管性疾病.根据世界头痛协会(HIS)的分类[1],偏头痛分为有先兆的偏头痛(migraine with aura,MA)和无先兆的偏头痛(migraine without aura,MOA),其中MOA约占2/3.在欧洲国家,偏头痛的患病率约14%,男女比例约为1:3.家族聚集现象和双胞胎研究表明,偏头痛存在着明显的遗传机制.     

偏头痛相关性脑梗死的发病机制与诊断治疗

偏头痛作为原发性头痛,是一种常见的发作性神经血管紊乱疾病,临床表现为发作性头痛,部分患者在头痛前有眼前闪光或视野缺损、麻木等先兆症状,多数无先兆,常伴有恶心、呕吐、畏光、怕声等症状。     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.