艾司西酞普兰合并奥氮平治疗难治性抑郁症疗效观察

目的 探讨艾司西酞普兰合并奥氮平对难治性抑郁症的临床疗效.方法 将55例难治性抑郁症患者随机分为研究组(艾司西酞普兰合并奥氮平)和对照组(单用艾司西酞普兰),疗程为12周,采用汉密尔顿抑郁量表(HAMD)评定临床疗效,副反应量表(TESS)评定不良反应.结果 治疗结束后,两组HAMD评分较治疗前均有显著性降低(P＜0.05).治疗后第8、12周末,研究组的HAMD评分显著低于对照组,且差异有显著性意义(P＜0.05).两组副作用均较小,研究组仅在体重增加、嗜睡方面较对照组高,差异有显著性意义(P＜0.05).结论 艾司西酞普兰合并奥氮平治疗难治性抑郁症能明显提高疗效,安全可靠.     

草酸艾司西酞普兰联合氨磺必利治疗抑郁症的效果和安全性研究

目的探讨氨磺必利联合草酸艾司西酞普兰治疗抑郁症的有效性和安全性。方法采用随机数字表法将符合《国际疾病分类(第10版)》(ICD-10)抑郁症诊断标准的78例抑郁症患者分为草酸艾司西酞普兰组(对照组,n=40)和草酸艾司西酞普兰联合氨磺必利组(研究组,n=38),疗程8周。于治疗前和治疗后第2、4、6、8周末采用汉密尔顿抑郁量表17项版(HAMD-17)评定疗效,采用副反应量表(TESS)评定安全性和不良反应。结果治疗2周后,两组HAMD-17总评分比较差异有统计学意义(P0.01)。治疗4周后,研究组HAMD-17焦虑躯体化因子评分、体重因子评分、阻滞因子评分及总评分均较对照组低(P0.05或0.01)。两组总有效率差异有统计学意义(χ2=2.734,P0.01)。研究组与对照组口干、恶心、呕吐及便秘的发生率差异有统计学意义(P0.01)。结论在抑郁症的临床治疗过程中,相对于单用草酸艾司西酞普兰,联合用药可能会更有效地改善躯体症状,减轻早期消化道不良反应,加快起效时间。     

小剂量氨磺必利联合草酸艾司西酞普兰对抑郁症 患者疲乏症状的疗效

目的 探讨小剂量磺必利联合草酸艾司西酞普兰对抑郁伴有疲乏症状患者的总体疗效及 耐受性。方法 选择2017 年9 月至2018 年6 月在荆门市口腔医院心理科门诊或住院治疗的抑郁症患者 100 例为研究对象,按照随机数字表法分为研究组和对照组各50 例,对照组口服草酸艾司西酞普兰,研 究组在此基础上合用小剂量的氨磺必利,治疗前后采用汉密尔顿抑郁量表（HAMD-17）和疲乏严重程度 量表（FSS）对患者治疗效果进行评分,评价两组患者总体疗效。结果 （1）两组患者一般资料比较差异 无统计学意义（P＞ 0.05）;（2）两组患者治疗前HAMD 量表评分差异无统计学意义,治疗1 周、2 周及4 周 后,两组患者的HAMD 评分均明显减低,但研究组减分值明显高于对照组,两组比较差异有统计学意义 （P＜ 0.01）;（3）两组患者治疗前FSS 评分差异无统计学意义,治疗2 周末FSS 评分均降低,研究组差异有 统计学意义（P＜0.05）,而对照组差异无统计学意义（P＞0.05）;两组患者治疗4周末时FSS评分继续降低, 研究组减分值高于对照组,两组的组内比较及组间比较差异均有统计学意义（均P＜ 0.05）;（4）研究组不 良反应发生率［16%（8/50）］和对照组［14%（7/50）］比较差异无统计学意义。结论 小剂量氨磺必利联 合草酸艾司西酞普兰对于抑郁症患者抑郁情绪及疲乏症状疗效更佳,不良反应相当。     

艾司西酞普兰联合奎硫平治疗难治性抑郁症患者的对照研究

目的:比较艾司西酞普兰联合奎硫平治疗难治性抑郁症的疗效和安全性方法:74例门诊和住院的难治性抑郁症患者,随机分为研究组38例(艾司西酞普兰联合奎硫平治疗)和对照组36例(单用艾司西酞普兰治疗),治疗8周.采用17项汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HA-MA)评价症状严重程度,治疗中出现的症状量表(TESS)评定不良反应. 结果:两组治疗后HAMD和HAMA评分较治疗前均有显著性降低(P均＜0.01);第8周研究组与对照组有效率分别为57.9％、33.3％,两组疗效差异有统计学意义(P＜0.05).研究组和对照组与药物不良反应差异无统计学意义(P＞0.05). 结论:艾司西酞普兰合并奎硫平治疗难治性抑郁症与单用艾司西酞普兰相比,起效较快,疗效较好,同样安全.     

阿立哌唑对难治性抑郁症的增效作用

目的：探讨艾司西酞普兰联合阿立哌唑治疗难治性抑郁症的疗效及安全性。方法：62例难治性抑郁症患者随即分为合用组（艾司西酞普兰联合阿立哌唑）32例,单用组（单用艾司西酞普兰）30例,疗程8周。于治疗前和治疗2、4、8周分别用汉密尔顿抑郁量表（HAMD）及治疗中出现的症状量表（TESS）评定疗效与不良反应。结果：两组HAMD评分较治疗前均显著下降（P〈0.01）;两组不良反应差异无统计学意义（P均〉0.05）。结论：艾司西酞普兰联合阿立哌唑治疗难治性抑郁症疗效明显优于单用艾司西酞普兰,安全性较高。     

艾斯西酞普兰合并认知疗法治疗酒依赖伴抑郁的临床对照研究

目的 评价艾司西酞普兰合并认知治疗对酒依赖伴抑郁障碍的临床疗效及安全性.方法 采用随机数字法将62例伴抑郁障碍的酒依赖患者分成艾司西酞普兰合并认知治疗组(研究组)和单用艾司西酞普兰治疗组(对照组)各31例,治疗8周,于治疗前及治疗后第1、2、4、8周末采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、临床总体印象量表(CGI)及治疗中出现的症状量表(TESS)评定临床疗效及不良反应.结果 治疗后第2、4、8周末两组HAMD、HAMA及CGI评分与治疗前比较差异均有统计学意义(P＜0.01);两组间HAMD、HAMA及CGI评分在治疗后第1、2、4、8周末比较差异均有统计学意义(P＜0.05或0.01);两组有效率分别为93.55％和74.20％,差异有统计学意义(P＜0.05);两组不良反应发生率差异无统计学意义(P＞0.05).结论 艾司西酞普兰合并认知治疗对酒依赖伴抑郁障碍的疗效优于单用艾司西酞普兰,且起效更快,不良反应相当.     

艾司西酞普兰与西酞普兰改善癫痫发作患者抑郁症状的对照研究

目的 探讨艾司西酞普兰与西酞普兰改善癫痫发作患者抑郁症状的效果.方法 将158例伴发抑郁症状的癫痫发作患者随机分为研究组(80例)和对照组(78例),研究组给予艾司西酞普兰系统治疗,对照组给予西酞普兰系统治疗,疗程均为4周.入组患者应用汉密尔顿抑郁量表(HAMD)与不良反应量表(TESS)在基线及治疗后第1、2、4周末分别评定疗效与不良反应.结果 与基线相比,研究组HAMD评分在第1周末即有显著性降低(P＜0.05),而对照组HAMD评分在第2周末才有显著性降低(P＜0.05).在治疗后的第1、2、4周末,研究组HAMD评分均低于对照组(P＜0.05).在治疗后的第4周末,研究组临床整体疗效优于对照组(P＜0.05).两组均未出现严重不良反应.结论 艾司西酞普兰和西酞普兰均可有效、安全地改善癫痫发作患者的抑郁症状,而艾司西酞普兰起效更快,疗效更好.     

认知疗法合并艾司西酞普兰治疗女性抑郁症患者的疗效

目的:比较艾司西酞普兰合并认知治疗与单用艾司西酞普兰对女性抑郁症患者的疗效。方法:60例女性抑郁症患者随机分为研究组(艾司西酞普兰合并认知治疗组)30例,对照组(单用艾司西酞普兰组)30例,治疗8周。治疗前及治疗1、2、4和8周分别采用汉密尔顿抑郁量表(HAMD)评定疗效。结果:治疗2周开始,两组HAMD评分均显著下降。研究组治疗1周HAMD明显下降。研究组较对照组HAMD下降更显著。两组不良反应差异无显著性。结论:艾司西酞普兰合并认知治疗对女性抑郁症患者疗效明显,安全性高。     

盐酸文拉法辛和草酸艾司西酞普兰治疗抑郁症的对照研究

目的 比较盐酸文拉法辛和草酸艾司西酞普兰治疗抑郁症患者的疗效和安全性.方法 69例抑郁症患者随机分为盐酸文拉法辛组和草酸艾司西酞普兰组.盐酸文拉法辛治疗剂量150～225 mg/d,草酸艾司西酞普兰治疗剂量10～20 mg/d,采用汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)以及副反应评定量表(TESS)评定疗效和不良反应,观察时间为期8周.结果 两组药物在治疗终末期疗效以及不良反应差异没有统计学意义(P＞0.05).在治疗第6周末草酸艾司西酞普兰组HAMD/HAMA总评分低于盐酸文拉法辛组(P＜0.05).结论 盐酸文拉法辛与草酸艾司西酞普兰对抑郁症患者均有较好的疗效,安全性一致,但是后者起效更快.     

艾司西酞普兰合并喹硫平改善难治性抑郁症患者症状及社会功能的对照研究

目的 探讨艾司西酞普兰合并喹硫平改善难治性抑郁症患者症状及社会功能的效果.方法 将81例难治性抑郁症患者随机分为研究组(艾司西酞普兰合并喹硫平系统治疗)和对照组(艾司西酞普兰系统治疗),共治疗4周.在基线及治疗后第1、2、4周末采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、社会功能缺陷量表(SDSS)及副反应量表(TESS)评定疗效及不良反应.结果 在治疗后第1周末,研究组HAMD及HAMA评分较基线即有显著性降低(P＜0.05),而对照组HAMD及HAMA评分在第4周末才有显著性降低(P＜0.05).治疗第1周末、第2周末及第4周末,研究组的HAMD及HAMA评分均显著低于对照组,差异均有显著性(P＜0.05).在治疗后第2周末,研究组SDSS总分较基线即有显著性降低(P＜0.05),而对照组SDSS总分在第4周末才有显著性降低(P＜0.05).治疗第2周末及第4周末,研究组的SDSS总分均显著低于对照组,差异均有显著性(P＜0.05).两组均未出现严重不良反应.结论 艾司西酞普兰合并喹硫平可有效、快速的改善难治性抑郁症患者的抑郁焦虑症状及社会功能.     

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.     

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.     

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.     

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.     

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.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.