重复经颅磁刺激治疗对精神分裂症认知功能影响的对照研究

目的观察和评价重复经颅磁刺激（rTMS）治疗对精神分裂症患者认知功能的影响。方法收集精神分裂症患者，并随机分为rTMS真刺激组和rTMS伪刺激组，进行4周治疗。应用注意网络测验（ANT）和威斯康星卡片分类测验（WCST），在rTMS治疗前后评估患者的注意和执行功能。共23例患者完成治疗，rTMS真刺激组12例，rTMS伪刺激组11例。结果rTMS干预前后，两组的注意网络测验各项指标没有显示明显差异（P〉0．05）。与rTMS干预前相比，rTMS干预结束时，rTMS真刺激组的WCST测试总时间缩短（干预前536S±217S，干预后405S±174S；t=2．69，P〈0．05），错误思考时间缩短（干预前335S±148S，干预后233S±128S；t=3．19，P〈0．01）和选择错误率降低（干预前58．1％±14．8％，干预后51．6％4-15．3％；t=2．16，P：0．05）；rTMS伪刺激组WCST测试的正确思考时间也有缩短（P〈0．01）。结论重复经颅磁刺激rTMS治疗没有引起精神分裂症患者的认知功能损害。同时，有改善患者部分认知功能损害倾向，值得进一步研究。     

重复经颅磁刺激对帕金森病运动功能及运动诱发电位的影响

目的:探讨低频重复经颅磁刺激(rTMS)对PD患者运动皮质兴奋性影响的持续效应。方法:对38例PD患者,予0.5Hz rTMS刺激其主要受累肢体对侧的M1Hand(20×80,100%RMT),连续7d。于首次干预前及末次干预后20min、1周及1个月分别评价其临床运动功能和运动诱发电位。结果:低频rTMS干预后,PD患者UPDRS Ⅲ、僵直、运动迟缓评分、计时运动试验及CSP均存在显著时间效应(P<0.001)。结论:低频rTMS可改善PD患者运动迟缓症状,其对运动功能的影响可持续到刺激停止后1个月,与运动皮质兴奋性的改变一致。     

低频重复经颅磁刺激治疗精神分裂症慢性幻听的疗效及随访研究

目的研究低频重复经颅磁刺激（rTMS）对精神分裂症难治性慢性幻听症状的疗效。方法将46例精神分裂症伴慢性幻听患者随机分为研究组（23例）和对照组（23例）。研究组在原有抗精神病药物种类及剂量不变的同时给予经左侧颞顶叶的2周共10次低频（1Hz）rTMS刺激,对照组采用假rTMS刺激。治疗前后对两组分别进行AHRS听幻觉量表及临床疗效总评量表（CGI）评定幻听症状的变化,并对治疗有效者于3个月后随访。结果研究组治疗前、后AHRS评分分别为（8．1±2．5）和（3．5±1．5）;对照组为（7．8±2．6）和（6．5±2．1）,研究组疗效明显优于对照组（F=20．3,P〈0．05）。所有患者均完成试验,未见有严重的副反应出现。结论低频rTMS治疗精神分裂症难治性慢性幻听症状,疗效肯定且安全性好。     

新发帕金森病的急性多巴反应性评价

目的：建立急性左旋多巴负荷试验用于鉴别新发帕金森病（PD）与新发帕金森综合征（PDS）患者,并筛选评价指标的临界值。方法：选择89例有PD样表现但未服用过左旋多巴的患者,根据临床诊断分为PD组（n=48）和PDS组（n=41）,进行了急性左旋多巴／卡比多巴（100／25mg）试验。根据两组患者统-PD评分运动分量表（UPDRS—Ⅲ）评分的平均最大改善率进行比较,并建立受试者工作特征（ROC）曲线,以该曲线上最大Youden指数对应的运动评分最大改善率作为临界值。结果：PD组在服用左旋多巴-卡比多巴后的平均UPDRS-Ⅲ评分平均最大改善率高于PDS组,差异有统计学意义（P〈0．01）。建立的ROC曲线在鉴别PD和PDS差异具有统计学意义,ROC曲线下面积为0．827（P〈0．01）,对应上网UPDRS运动评分改善率的最佳临界值为12．45％（Youden指数0．565,敏感度80．9％,特异度75．6％）。结论：急性左旋多巴-卡比多巴试验可作为PD疗效和诊断的一种辅助参考方法。     

双侧电刺激对脑卒中后康复的影响

目的探讨双侧电刺激治疗对脑卒中后神经功能康复的影响。方法150例急性脑卒中偏瘫患者随机分为两组。两组均采用常规药物和功能锻炼治疗,双侧治疗组加用双侧电刺激治疗,对照组加用单侧电刺激治疗。疗程1个月。采用临床神经功能缺损程度评分、简式Fugl-meyer运动功能评分（FMA）、改良Barthel指数（MBI）,于初期（治疗前）、末期（治疗后3个月）对两组患者进行评定神经功能。结果治疗后,双侧治疗组临床神经功能缺损程度评分明显减少（P〈0．01）;FMA、MBI明显提高（P〈0．01）。结论双侧电刺激治疗可明显促进患肢运动功能康复,降低致残率,提高日常生活能力。     

帕金森病患者运动皮质兴奋性的经颅磁刺激研究

目的:本研究拟应用低频重复性经颅磁刺激(rTMS)分别刺激帕金森病(PD)患者M1手代表区(M1Hand)及运动前区(PMC),探讨不同干预手段对运动皮质兴奋性的影响,以及M1与PMC间的联系。方法:对18名确诊PD患者先后进行4种不同干预,即口服美多芭、低频rTMS刺激M1Hand(0.5Hz,100%静息阈值,共1600次脉冲)、低频rTMS刺激PMC(0.5Hz,100%静息阈值,共1600次脉冲)以及假刺激。于每次干预前后各进行临床评价并测定运动诱发电位(MEP)相关指标。结果:①口服美多芭后UPDRSⅢ(P=0.001)以及其中有关僵直(P=0.001)、运动迟缓(P<0.001)的评分均较服药前显著改善。三种不同磁刺激干预产生结果不同,M1Hand组UPDRSⅢ减低(P=0.015),僵直(P=0.010)、运动迟缓(P=0.004)亦有所改善;PMC组UPDRSⅢ较干预前减低(P=0.046),僵直评分亦减低,但无显著性意义(P=0.163);②口服美多芭1h后MEP120减低(P=0.002),CSP延长(P=0.006);M1Hand组MEP120无著变,而CSP延长(P=0.015);PMC组MEP120减低(P=0.004),而CSP无著变;假刺激组则均无显著性改变。结论:低频rTMS对不同脑区产生的效应不同:刺激M1可使CSP延长;而刺激PMC可使MEP波幅减低。     

重复经颅磁刺激对产后抑郁症患者的疗效

目的观察重复经颅磁刺激（rTMS）对产后抑郁（PPD）患者的疗效。方法将49例PPD患者随机分为假刺激组25例和治疗组24例。两组患者均给予常规心理和抗抑郁药物治疗,治疗组在此基础上加用rTMS治疗,假刺激组采用同样刺激参数的假刺激线圈给予的rTMS治疗。于治疗前、治疗2,4周末采用汉密尔顿抑郁量表24项版（HAMD-24）评估患者抑郁程度。结果与治疗前比较,假刺激组患者治疗2周后HAMD评分有下降趋势,但差异无统计意义（P〉0．05）;治疗4周后HAMD评分明显下降,差异有统计学意义（P〈0．05）。与治疗前比较,治疗组患者治疗2,4周后HAMD评分均明显下降,差异均有统计学意义（P〈0．05）;与假刺激组比较,治疗组患者治疗2周及4周后HAMD评分降低更为显著,差异有统计学意义（P〈0．05）。结论在常规心理和抗抑郁药物治疗基础上加用rTMS可更迅速、有效地缓解PPD患者症状。     

高-低频交互rTMS对中期帕金森病患者SCOPA-AUT评分认知功能及运动功能的影响

目的 分析高-低频交互重复经颅刺激（rTMS）对中期帕金森（PD）患者自主神经症状量表（SCOPA-AUT）评分、认知功能和运动功能的影响。方法 选择2019-12—2022-12成都市第三人民医院收治的109例中期PD患者,采用简单随机化法分为观察组55例和对照组54例。所有患者均接受PD常规药物治疗,观察组另采用高-低频rTMS结合治疗,对照组给予rTMS假刺激干预,比较治疗前、治疗1个月后2组患者自主神经功能、认知功能、运动功能和日常生活能力。结果 2组治疗1个月后SCOPA-AUT评分分别为（20.08±3.44）分和（22.96±4.55）分,帕金森氏病综合评分量表（UPDRS-Ⅲ）评分分别为（24.15±3.22）分和（27.07±3.56）分,较治疗前均明显降低（P<0.05）,蒙特利尔认知评估量表（MoCA）评分分别为（27.40±2.08）分和（25.83±2.92）分,日常生活能力（ADL）评分分别为（47.03±3.34）分和（44.19±3.20）分,均较治疗前明显升高（P<0.05）,且观察组SCOPA-AUT评分、UPDRS-Ⅲ评分均低于对照组,...     

低频重复经颅磁刺激对脑梗死失语的治疗作用及机制研究

目的探讨低频重复经颅磁刺激（10w—rTMS）对急性期脑梗死运动性失语的治疗作用、安全性及相关机制。方法选取左半球脑梗死后运动性失语右利手的患者24例,经ABC失语检查表评定后随机分为对照组（n=12）和治疗组（n=12）。对照组给予常规药物和语言康复治疗;治疗组在对照组治疗基础上给予low—rTMS治疗。rTMS治疗方法：频率1Hz、强度为运动阈值的80％、部位为右侧大脑半球Broca区、每序列50次脉冲、每天10个序列、序列间隔120S,共10d。两组治疗前、疗程后2周、疗程后2月和疗程后6月均行汉语ABC失语检查表语言评分评价其语言功能。两组各选取8例患者在治疗前、疗程后2周行磁共振波谱（MRS）和单光子发射计算机断层摄影（SPECT）检查,分别检测脑代谢和脑血流改变。结果①ABC评分结果：疗程后2周、疗程后2月、疗程后6月治疗组其值均高于对照组和治疗前（P〈0．05）。@SPECT结果：两组治疗前和疗程后2周左额下回缺血灶明显大于对侧镜像区;疗程后2周治疗组左额下回缺血灶明显小于治疗前和对照组,其摄取值高于对照组（P〈0．05）。③MRS结果：治疗前两组Broca区出现明显的倒置双乳酸（Lac）峰,N．乙酰天门冬氨酸（NAA）和NAA／肌酸（cr）值均比对侧镜像区明显降低（均P〈0．05）,而胆碱（Cho）值则升高（P〈0．05）;疗程后2周治疗组的NAA和NAA／Cr值明显高于对照组（P〈0．05）;Cho值比对照组减低（P〈0．05）。结论1Hz、rTMS对急性脑梗死失语患者有一定的康复作用;且此治疗是安全的。语言功能改善,推测可能与低频rTMS刺激健侧语言区通过远隔效应增加了局部语言区的血流量和脑代谢,抑制右侧半球的兴奋性有关。     

不同频率重复经颅磁刺激对脑梗死患者运动功能影响的研究

目的 比较高频、低频重复经颅磁刺激(rTMS)在脑梗死患者运动功能康复中的作用. 方法 选取自2010年10月至2011年6月在珠江医院康复医学科治疗的60例脑梗死患者,按随机数字表法分成高频rTMS组(20例)、低频rTMS组(20例)和假刺激组(20例).在常规药物治疗及功能训练治疗相同的情况下,高频rTMS组、低频rTMS组给予每天1次、每次10 min的高频(3 Hz)或低频(1 Hz)rTMS治疗,连续14d;假刺激组给予假刺激.比较3组患者治疗前后的简易Fugl-Meyer(FMA)运动功能评分、Barthel指数、运动诱发电位(MEP)潜伏期及中枢运动传导时间(CMCT). 结果 治疗前,3组患者间FMA评分、Barthel指数、MEP潜伏期及CMCT比较差异无统计学意义(P＞0.05).治疗后,3组患者FMA评分、Barthel指数、MEP潜伏期及CMCT均较治疗前差异有统计学意义(P＜0.05);高频rTMS组、低频rTMS组的运动功能恢复明显优于假刺激组,FMA评分、Barthel指数、MEP潜伏期及CMCT与假刺激组比较差异均有统计学意义(P＜0.05),高频rTMS组与低频rTMS组间FMA评分、Barthel指数、MEP潜伏期及CMCT比较差异无统计学意义(P＞0.05). 结论 高频及低频rTMS均有利于脑梗死患者运动功能的康复,且两者间疗效无明显差异.     

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.     

Hepatic Considerations in the Use of Antiepileptic Drugs

Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.     

Vascular Malformations and Epilepsy: Clinical Considerations and Basic Mechanisms

Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.     

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.     

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 and Utilization in Children

Summary: Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmacokinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.     

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.