帕金森病患者丘脑底核脑深部电刺激术后心率变异性的Meta分析

目的系统评价丘脑底核脑深部电刺激术对帕金森病患者心率变异性的影响。方法以subthalamic nucleus、deep brain stimulation、DBS、STN、electrical stimulation、Parkinson disease、heart rate variability和帕金森病、脑深部电刺激、心率变异性等中英文检索词计算机检索2000年1月1日-2017年12月1日美国国立医学图书馆生物医学信息检索系统(Pub Med)、荷兰医学文摘(EMBASE/SCOPUS)、Cochrane图书馆、中国知网中国知识基础设施工程(CNKI)、万方数据库、维普数据库(VIP)等收录的关于帕金森病患者丘脑底核脑深部电刺激术后心率变异性变化的队列研究,采用心率变异性的高频部分(HF)、低频部分(LF)和低频部分/高频部分(LF/HF)作为评价指标,采用Newcastle-Ottawa量表(NOS)和Rev Man 5.3统计软件进行文献质量评价和Meta分析。结果共获得28篇英文文献,经剔除重复和不符合纳入标准者,最终纳入6项高质量(NOS评分7分)临床研究共101例行丘脑底核脑深部电刺激术的帕金森病患者。Meta分析显示,帕金森病患者丘脑底核脑深部电刺激术前后心率变异性之LF值(SMD=0.050,95%CI:-0.230~0.330;P=0.740)、HF值(SMD=0.160,95%CI:-0.120~0.430;P=0.270)和LF/HF比值(SMD=0.110,95%CI:-0.220~0.440;P=0.500)差异均无统计学意义。结论丘脑底核脑深部电刺激术不影响帕金森病患者的心率变异性。     

丘脑底核脑深部电刺激对帕金森病抑郁障碍的影响

目的探讨丘脑底核脑深部电刺激对帕金森病病人抑郁障碍的疗效及其机制。方法回顾性分析21例帕金森病合并抑郁障碍病人的临床资料,均行丘脑底核脑深部电刺激术,术前及术后3、6个月分别应用汉密尔顿抑郁量表(HAMD)评分和统一帕金森病评定量表(UPDRS)运动评分对抑郁障碍和运动功能进行临床评价并分析其相关性。结果术后UPDRS运动评分和HAMD评分均显著下降(均P0.05),但是抑郁症状的改善与运动功能的改善并没有明显的相关性(P0.05)。结论丘脑底核脑深部电刺激能够明显改善帕金森病病人的抑郁症状,其机制可能与丘脑底核受到刺激影响脑内神经递质的变化有关,术后运动功能的改善不是抑郁症状改善的主要原因。     

脑深部电刺激术联合药物治疗原发性帕金森病疗效观察

目的探讨脑深部电刺激术(DBS)联合药物治疗原发性帕金森病的有效性和安全性。方法共60例原发性帕金森病患者分别予常规药物治疗(30例)和脑深部电刺激术联合药物治疗(30例),采用统一帕金森病评价量表(UPDRS)和帕金森病生活质量量表(PDQUALIF)评价病情严重程度和生活质量。结果 DBS组患者UPDRS量表之精神、行为和情绪(P=0.023)、日常生活活动能力(P=0.005)、运动功能(P=0.025)和运动并发症(P=0.008)以及PDQUALIF评分(P=0.016)均低于对照组,治疗后UPDRS量表之精神、行为和情绪(P=0.003)、日常生活活动能力(P=0.016)、运动功能(P=0.001)和运动并发症(P=0.016)以及PDQUALIF评分(P=0.000)亦低于治疗前。DBS组总有效率[96.67%(29/30)]高于对照组[76.67%(23/30);χ~2=5.109,P=0.000]。结论脑深部电刺激术联合药物治疗原发性帕金森病可以有效改善临床症状,提高生活质量。     

脑深部电刺激治疗帕金森病的程控

目的探讨丘脑底核脑深部电刺激术治疗帕金森病(PD)的手术方法和脉冲发生器程控调节。方法自2000年1月～2004年2月用脑深部电刺激丘脑底核(STN)治疗帕金森病61例,其中单侧30例,双侧31例。采用磁共振扫描结合微电极记录技术进行靶点定位。术后用帕金森病评定量表(UPDRS)运动评分评价刺激效果。结果61例PD患者术后随访6～36个月,平均11．3个月。脉冲发生器开启时,在“关”状态下,UPDRS运动评分改善率45．2％;在“开”状态下,UPDRS运动评分改善率20．7％,未发现任何并发症。结论脑深部刺激(DBS)能有效控制帕金森病患者的症状,手术并发症少,术后可根据患者的症状调节参数,丘脑底核(STN)已成为治疗帕金森病的最佳靶点。     

帕金森病脑深部电极植入术后程控参数与疗效相关性研究

目的分析丘脑底核-脑深部电刺激术(STN-DBS)治疗帕金森病的术后程控参数及效果,为帕金森病STN-DBS术后程控及术后管理提供参考。方法纳入2012~2018年就诊于新疆医科大学第一附属医院87例患者,应用UPDRS-Ⅲ评分UPDRS-II日常生活活动评分UPDRS-I精神行为情绪评分量表MMSE简易精神量表PDQ-39生活质量评分量表分析手术前后帕金森病患者运动及非运动症状改善情况,评估程控参数的设置对帕金森病人症状改善及生活质量改善作用。结果帕金森病患者与术前相比,患者术后UPDRSⅠ评分UPDRSⅠⅡ评分UPDRSⅢ评分UPDRSⅣ评分改善明显,手术后随访至今,患者症状改善稳定,生活质量明显提高。结论 STN-DBS是一种安全,有效治疗帕金森病的方法,并减少药物的剂量及药物所致副作用,术后程控是脑深部电极植入器治疗的重要一环。     

脑深部电刺激术联合药物治疗帕金森病有效性和安全性的meta分析

目的评价脑深部电刺激术联合药物治疗帕金森病的有效性及安全性。方法检索在2018年9月之前于Pub Med、EMBASE、Cochrane Library、CNKI文献数据库中DBS治疗帕金森病的临床研究。按纳入标准和排除标准进行资料筛选和提取,利用Rev Man 5. 3软件进行数据分析。结果纳入11个研究共274名帕金森患者。Meta分析显示:5年单纯DBS治疗与术后5年基线差异有统计学意义(P 0. 01),运动症状较术后基线改善,UPDRS-III(SMD=-21. 31,95%CI:-25. 18～-17. 44);术后5年单纯DBS治疗与药物联合DBS治疗差异有统计学意义(P 0. 01),运动症状UPDRSIII (SMD=-7. 26,95%CI:-9. 02～-5. 02)、生活质量UPDRS-II (SMD=-4. 2,95%CI:-6. 02～-2. 82)较单纯手术治疗有改善;术前术后LEDD (SMD=453. 76,95%CI:394. 31～513. 21)差异有统计学意义(P 0. 01)。DBS副作用发生率较低,脑出血发生率4. 4%,感染6例(2. 2%);癫痫3例(1. 1%)。结论脑深部电刺激术在术后5年无论是单纯手术治疗或手术联合药物治疗均能改善患者的运动症状及生活质量,较术前明显降低了左旋多巴类药物的用量,且副作用少,安全性高。     

脑深部电刺激双侧丘脑底核对帕金森病"冻结足"的治疗作用

目的 探讨脑深部电刺激(DBS)双侧丘脑底核(STN)治疗帕金森病(PD)的冻结足(FOG)的临床效果.方法 对13例合并有冻结足的PD患者行双侧丘脑底核脑深部电刺激术,至少随访12个月.采用UPDRS运动评分(UPDRSⅢ)、UPDRS日常生活能力评分(UPDRSⅡ)及UPDRSⅡ中的第14项"Freezing"项目的评分(FOG),分别对患者进行术前1周、术后6个月、12个月在药物治疗"开、关"期的基础评分及随访期间刺激器开启时的评分,尤其是"Freezing"项目得分多少及变化.进行统计学分析.结果 术后13例PD患者运动功能症状改善良好,UPDRSⅢ、UPDRSⅡ评分下降显著(P＜0.01).在手术后的6、12个月,刺激器开启时患者"关"期的冻结足评分明显下降(P＜0.01),而"开"期的冻结足没有改善(P＞0.05).结论 STN-DBS能显著改善PD患者"关"期的冻结足,而对"开"期的冻结足没有显著影响.     

脑深部刺激电极埋置术治疗帕金森病疗效研究

目的 探讨脑深部刺激电极埋置术治疗帕金森病的疗效及其作用机制。方法 对32例帕金森病患者应用微电极导向立体定向技术,于丘脑底核埋置体外可控性脑深部刺激电极,对其疗效和预后进行随访。结果患者术后僵硬、震颤和运动迟缓等症状明显缓解,术前、术后统一帕金森病评分量表(unified Parkinson's disease ratingscale,UPDRS)运动评分和日常生活能力(activities of daily living,ADL)评分有显著性差异(P<0.01),部分患者由药物引起的开-关现象也有明显缓解;协同服用的多巴胺类药物的用量也有不同程度的减少。所有患者术中及术后均无严重的并发症,术后随访疗效肯定。结论 丘脑底核放置深部脑刺激电极,能明显改善帕金森病患者的临床症状,提高手术的安全性,并发症少。     

丘脑底核电刺激治疗帕金森病的临床应用

目的探讨脑深部电刺激术治疗帕金森病的手术方法和脉冲发生器程控调节。方法自2000年1月至2005年10月用脑深部电刺激丘脑底核治疗帕金森病126例,其中单侧46例,双侧80例。采用磁共振扫描结合微电极记录技术进行靶点定位。术后用UPDRS运动评分评价刺激效果。结果82例帕金森病患者术后随访6～60个月,平均11.8个月。脉冲发生器开启时,在“关”状态下,UPDRS运动评分改善率45.2%;在“开”状态下,UPDRS运动评分改善率25.7%,未发现任何并发症。结论脑深部电刺激丘脑底核能有效控制帕金森病患者的症状,手术并发症少,术后可根据患者的症状调节参数。     

立体定向脑深部电刺激术治疗帕金森病

目的探讨立体定向脑深部电刺激术治疗帕金森病的手术方法和效果。方法对20例具有双侧症状的中晚期帕金森患者行双侧丘脑底核脑深部电刺激治疗。术中采用立体定向技术结合1.5T磁共振扫描及微电极记录技术进行靶点精准定位植入电极,术后采用统一帕金森病评分量表(UPDRS)运动评分评价刺激效果。结果术后随访6个月5年,平均3年,神经刺激器工作时,患者运动评分明显改善。肢体异动2例,脑出血1例。无明显的永久并发症和副作用。结论立体定向脑深部电刺激术的安全性较高,可明显改善帕金森病患者的运动功能。     

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.     

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 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.     

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.     

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.     

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.