100例2型糖尿病患者交感神经皮肤反应研究

目的探讨交感神经皮肤反应(SSR)检测在评价2型糖尿病(T2DM)自主神经损害中的价值.方法对100例T2DM患者进行SSR检测,30例健康志愿者作为对照.结果2组SSR的起始潜伏期、N波潜伏期、波幅、面积比较差异有显著性意义(P＜0.05),P波潜伏期差异无显著性意义(P＞0.05).T2DM组72例(72%)患者至少有一肢SSR异常.血糖控制满意组和血糖控制不良组比较,起始和N波潜伏期差异有统计学意义(P＜0.05),波幅和面积无显著性意义(P＞0.05).T2DM组病程＜5年与病程≥5年比较,潜伏期、波幅、面积差异均无统计学意义(P＞0.05).结论SSR可作为评价T2DM自主神经损害的客观电生理指标;T2DM患者SSR与血糖控制水平相关,与病程无关.     

2型糖尿病患者视觉诱发电位改变及其相关因素分析

目的探讨2型糖尿病患者视觉诱发电位(pattern visual evoked potential,P-VEP)改变的特点及其与各临床因素之间的关系。方法对109例2型糖尿病患者及40例健康体检者进行P-VEP的检测,病例组按病程分为病程<5年组、5年≤病程<10年组、病程≥10年组。回顾性分析各组生化指标、肌电图等临床资料与P-VEP改变的相关性。应用SPSS统计软件进行统计学处理。结果病例组P-VEP总异常率为27.52%,病程<5年组P-VEP异常8例(20.00%),5年≤病程<10年组P-VEP异常8例(25.81%),病程≥10年组P-VEP异常14例(36.84%),各组间其异常率比较差异无统计学意义(P>0.05)。P100潜伏期的改变:病程≥10年组的P100潜伏期较对照组明显延长(P<0.05),病程<5年组、5年≤病程<10年组的P100潜伏期较对照组无明显变化(P>0.05)。P100枕中波幅改变:5年≤病程<10年组,病程≥10年组的枕中波幅较对照组明显降低(P<0.05),病程<5年组的枕中波幅较对照组无明显变化(P>0.05)。周围神经病变严重组(病变神经数>4条)的枕中波幅较周围神经病变较轻组(病变神经数≤4条)明显降低(P<0.05)。非条件Logistic逐步回归分析显示病程和糖化血红蛋白是2型糖尿病患者视力损害的相关因素。结论 P-VEP是早期发现2型糖尿病患者视神经病变的无创检测手段。病程和糖化血红蛋白是2型糖尿病患者视神经病变的相关因素。     

皮肤交感反应在2型糖尿病自主神经病的应用价值

目的探讨皮肤交感反应(SSR)对2型糖尿病性自主神经病中的诊断价值。方法将199例2型糖尿病患者分为周围神经传导正常组(78例)和周围神经传导异常组(121例)进行SSR检测,比较SSR与常规电生理检测的敏感性,并分析SSR与病程、亚临床的关系。结果周围神经传导异常组的糖尿病患者SSR异常率明显高于周围神经传导正常组(P<0.05),病程越长,SSR异常率越高,异常程度越明显。病程超过10a的糖尿病患者潜伏期最长,波幅降低最明显,消失率最高(P<0.05)。结论 SSR异常程度与糖尿病周围神经损害的程度相一致,SSR可作为评价糖尿病周围神经损害及植物神经状况的客观指标。     

脑卒中偏瘫患者的神经电生理研究

目的研究脑卒中偏瘫患者周围神经的神经电生理变化。方法选择南昌大学第三附属医院脑卒中偏瘫患者180例,3～7 d、6个月进行肢体神经传导、针极肌电图、交感神经皮肤反应(SSR)测定。结果 180例患脑卒中偏瘫患者急性期1例检测出双侧腓肠神经传导速度减慢,针极肌电图正常;病程6个月时,56例出现NCV异常,运动神经总异常率为3.6%,感觉神经总异常率6.4%,SCV异常率高于MCV异常率。肌电图:①患侧:21例出现插入电位延长,18例有自发电位;②健侧:4例出现插入电位及自发电位。SSR:脑卒中偏瘫患者急性期、病程6个月时,健侧、患侧SSR潜伏期、波幅与正常值比较差异有统计学意义(P0.05),而健侧潜伏期、波幅及患侧潜伏期、波幅比较差异无统计学意义(P0.05)。6个月与急性期对比,患侧及健侧下肢、健侧上肢潜伏期差异有统计学意义(P0.01),患侧上肢潜伏期及所有肢体波幅差异无统计学意义(P0.05)。结论脑卒中偏瘫患者在病程6个月出现周围神经损害,SCV异常率高于MCV异常率,而在急性期出现SSR抑制、自主神经功能异常。     

交感皮肤反应对帕金森病自主神经损害的诊断价值

目的探讨交感皮肤反应(SSR)对帕金森病(PD)患者自主神经损害的诊断价值。方法选择62例PD患者(PD组)和26例年龄、性别、身高相匹配的健康志愿者(健康对照组)进行上下肢SSR检测。将PD组根据有无自主神经症状分为有症状组和无症状组;根据Hoehn-Yahr分级将PD组分为早期PD组(1～2期)和中晚期PD组(3～5期)。结果①与健康对照组比较,PD无论有症状组还是无症状组SSR潜伏期延长和波幅下降(均P0.05);有症状组较无症状组潜伏期延长和波幅下降(均P0.05);②与健康对照组比较,不论中晚期PD组还是早期PD组SSR潜伏期延长和波幅下降(均P0.05),中晚期PD组较早期PD组潜伏期显著延长和波幅下降(均P0.05);③SSR上下肢潜伏期与Hoehn-YaHr分级呈显著性正相关(P0.01),SSR上下肢波幅与Hoehn-YaHr分级呈显著性负相关(P0.01)。结论①SSR是检测PD患者自主神经功能障碍的客观敏感手段,可发现亚临床自主神经损害,有助于早期诊断;②PD患者运动系统障碍越重,出现自主神经病变的程度越重。     

2型糖尿病患者皮肤交感反应异常情况及其相关因素

目的探讨2型糖尿病患者皮肤交感反应(SSR)异常情况及其相关因素。方法对354例2型糖尿病患者及65名健康体检者进行SSR检测。根据SSR参考值将2型糖尿病患者分为SSR正常组和SSR异常组,比较两组的临床资料。采用Logistic回归分析2型糖尿病患者SSR异常的相关因素。结果 SSR正常组为238例(67.23%),SSR异常组为116例(32.77%)。SSR异常组中上肢异常率(16.95%)显著低于下肢异常率(27.68%)(P=0.001)。与SSR正常组比较,SSR异常组病程显著延长,神经传导速度(NCV)异常及糖尿病视网膜病变比率显著增高(均P0.01),其余各指标差异均无统计学意义。Logistic回归分析显示,视网膜病变(OR=1.588,95%CI:0.991~2.545,P=0.045)及NCV异常(OR=3.052,95%CI:1.847~5.042,P=0.000)是2型糖尿病患者SSR异常的独立相关因素。结论糖尿病患者SSR的异常率为32.77%;下肢异常率明显高于上肢。糖尿病病程越长,越容易发生SSR异常。糖尿病视网膜病变和NCV异常是2型糖尿病患者SSR异常相关的独立相关因素。     

交感皮肤反应对糖尿病自主神经病变的诊断价值

目的探讨交感皮肤反应（sympathetic skin response,SSR）在糖尿病自主神经病变诊断中的价值。方法对186例糖尿病周围神经病（Diabetic peripheral neuropathy,DPN）患者和203例糖尿病非DPN患者进行SSR检测,同时对102例健康人进行SSR检测。结果SSR起始潜伏期异常率高于波幅异常率,下肢的异常率高于上肢异常率。DPN患者中,174例（93.5%）SSR异常,其中32例未引出SSR,142例起始潜伏期延长,109例波幅下降。203例DM非DPN患者中,46例（22.7%）SSR起始潜伏期延长和/或波幅下降,其中19例有出汗异常,4例在检查后数月出现出汗异常。结论SSR是早期诊断糖尿病自主神经病变的敏感手段,可发现亚临床神经病,并与病情进展相吻合。     

酒依赖患者自主神经及感觉功能的电生理研究

目的探讨酒依赖(AD)患者自主神经及感觉功能的电生理特征。方法对56例AD患者和30例健康对照者进行交感神经皮肤反应(SSR)体感诱发电位(SEP)及感觉神经传导速度(SCV)测定,分析SSR反应波及SEP上肢N20、下肢P40电位波幅、潜伏期和正中神经、胫神经感觉传导速度。于酒精戒断2个月时随访AD组患者的SSR。结果与正常对照组比较,AD组SSR异常率及反应波缺失率均显著升高(χ~2=7.860,P=0.005;χ~2=64.655,P=0.000)。与正常对照组比较,AD组入组时及酒精戒断后SSR波幅均显著降低,潜伏期显著延长(均P0.01)。与入组时比较,AD组酒精戒断后波幅、潜伏期差异无统计学意义(均P0.05)。AD组与正常对照组SEP上肢N20电位和下肢P40电位波幅、潜伏期及上肢正中神经、下肢胫神经SCV差异均无统计学意义(均P0.05)。AD患者酒依赖持续时间和日饮酒量分别与SSR潜伏期呈正相关(r=0.335,P=0.017;r=0.369,P=0.008),与SSR波幅呈负相关(r=-0.294,P=0.038;r=-0.310,P=0.028)。结论 AD患者存在周围神经损害,以C类交感神经节后纤维和传导痛温觉Aδ纤维功能障碍等小纤维损害为主,深感觉传导路尚无明显影响,SSR可为AD提供周围神经早期损害的客观指标。     

2型糖尿病患者交感神经皮肤反应及F波的研究

目的:探讨交感神经皮肤反应(SSR)及F波在2型糖尿病周围神经病中的诊断价值。对64例2型糖尿病患者进行交感神经皮肤反应(SSR)及F波检测,并与40例正常人进行对比分析。结果:患者组上下肢SSR的潜伏期及波幅,F波的平均潜伏期,F波时限及F波出现率均较对照组有显著性差异,SSR异常率为42.2％,F波的异常率为37.5％,SSR及F波导常与患者的病程相关,而与血糖水平无关。结论:SSR及F波可作为评价2型糖尿患者自主神经及周围运动纤维近端损害的客观指标。     

不同年龄脑卒中和非卒中者事件相关电位P300研究

目的检测不同年龄脑卒中患者和非卒中查体者事件相关电位P300的变化,观察认知功能的改变.方法脑卒中(卒中组)36例,非卒中者(对照组)56例,分三个年龄段(36～50岁、51～60岁、61～70岁),其中卒中者又按病程分为急性发病后＜2周,2周～6月,＞6月等观察.P300检查采用NDI-500神经电检测仪.计算机显示结果后打印记录.结果(1)卒中组与对照组比较P300潜伏期明显延长(p＜0.001),波幅显著变小(p＜0.001);(2)不同年龄段二组相比P300潜伏期明显延长,波幅显著减少.且对照组中年龄61～70岁组其P300潜伏期比36～50岁组明显延长;(3)卒中病程＞6月组P300潜伏期与＜2周组相比明显延长(p＜0.05),波幅明显减少(p＜0.05);(4)小病灶者P300潜伏期与大病灶者相比无明显差别(p＞0.05).结论年龄是影响学习记忆的一个重要因素,随年龄增高,认知功能下降.脑卒中病人存在明显认知障碍.卒中病程越长患者认知功能越差.     

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.