阿尼西坦改善慢性精神分裂症患者认知功能的临床研究

目的探讨阿尼西坦改善慢性精神分裂症患者认知功能的疗效。方法将64例慢性精神分裂症患者随机分为研究组32例和治疗组32例,分别予以奎的平(350±50)mg/d治疗8周,研究组同时合并阿尼西坦100mg/d,并于治疗前及治疗后分别进行阳性和阴性症状量表(PANSS)、简明精神状态量表(MMSE)、中国修订韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)及威斯康星卡片分类测定(WCST)等评定,并与正常人组成的对照组进行比较。结果治疗前研究组和治疗组的MMSE、WMS及WAIS-RC均低于对照组,差异有显著性(P〈0.05),提示患者的认知功能有广泛性损害。治疗后研究组MMSE、WCST、WMS、WAIS-RC分数与治疗前比较差异有显著性(P〈0.05),而治疗后治疗组的WCST、WMS、WAIS-RC分数与治疗前比较无显著性差异(P〈0.05)。结论阿尼西坦改善慢性精神分裂症患者的认知功能疗效确切。     

坦度螺酮辅助治疗精神分裂症临床研究

目的探讨坦度螺酮辅助治疗精神分裂症患者的临床疗效及认知功能改善效果。方法 64例精神分裂症患者随机分为对照组32例和研究组32例,治疗12周。治疗前及治疗后第12周末分别进行阳性和阴性症状量表(PANSS)、韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)及不良反应症状量表(TESS)测定以评定疗效及不良反应。结果治疗第12周末研究组WCST的总测验数、持续错误数、随机错误数评分显著低于对照组(P0.05),临床有效率、WAIS-RC的语言量表、操作量表、总智商量表、WMS总分评分显著高于对照组(P0.05)。2组TESS评分差异无统计学意义(P0.05)。结论坦度螺酮可明显改善精神分裂患者的精神症状及认知功能,且安全性较高。     

吡拉西坦改善慢性精神分裂症患者认知功能的临床研究

目的 探讨吡拉西坦改善慢性精神分裂症患者认知功能的效果。方法 对68例慢性精神分裂症患者随机分为试验组和治疗组。治疗前进行阳性和阴性症状量表(PANSS)、简明精神状态量表(MMSE)、中国修订韦氏成人智力量表、韦氏记忆量表(WMS)及威斯康星卡片分类测验等评定,然后经利培酮(2.7±0.8)mg/d治疗8周。研究组与利培酮治疗同步使用吡拉西坦1200mg/d治疗,治疗组仅用利培酮治疗。治疗后第8周末再次进行上述评定,将结果与正常人组成的对照组进行比较。结果 治疗前研究组和治疗组的MMSE、WMS及WAIS-RC均低于对照组,差异有非常显著性(P<0.05),提示患者组的认知功能呈广泛性损害;研究组治疗后认知功能评定MMSE、MCST、WMS、WAIS-RC分数与治疗前比较有显著性差异(P<0.05);而治疗组治疗后认知功能测定MCST、WMS、WAIS-RC分数与治疗前比较无差异性(P>0.05)。结论 吡拉西坦对神经细胞有激活、保护和修复作用,能有效改善患者的认知功能,疗效确切。     

双益平对精神分裂症患者认知功能影响的对照研究

目的观察双益平对精神分裂症患者认知功能的影响。方法将76例诊断为精神分裂症的患者随机分成2组,其中一组(n=36)给予双益平治疗；另一组(n=40)为对照组,治疗8周,在入组前、治疗8周末分别进行韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)及副反应量表(TESS)评分,比较双益平组对精神分裂症患者认知功能产生的影响。结果两组8周后,双益平组认知功能的改善与对照组比较差异有显著性。结论双益平能改善精神分裂症患者的认知功能,其中尤以对记忆的改善为突出。     

丙戊酸钠改善精神分裂症患者认知功能障碍的对照研究

目的 探讨丙戊酸钠改善精神分裂症患者认知功能障碍的疗效.方法 将80例精神分裂症患者随机分成研究组(40例)和对照组(40例),研究组患者使用新型抗精神病药合并丙戊酸钠系统治疗,对照组患者单用新型抗精神病药物系统治疗,共治疗8周.全部病例在治疗前后分别进行阳性和阴性综合征量表(PANSS)、韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)进行疗效评定,应用治疗中需处理的不良反应症状量表(TESS)评定不良反应.结果 与基线时比较,两组在治疗后第4、8周末PANSS总分及各因子分均有明显降低(P＜0.05),研究组治疗后第8周末PANSS总分及各因子分均显著低于对照组(P＜0.05).治疗后第8周末,两组WMS、WAIS-RC、WCST评分与基线时比较,除即刻记忆评分外其余各项评分差异均有统计学意义(P＜0.05),两组间比较,除即刻记忆评分外其余各项评分均有显著性差异(P ＜0.05,P＜0.01).结论 丙戊酸钠对精神分裂症患者的认知功能障碍有明显改善效果.     

重酒石酸卡巴拉汀对难治性精神分裂症立体定向手术后短期认知功能障碍的初步探讨

目的探讨胆碱酯酶抑制剂对改善立体定向手术后短期认知功能障碍临床效果。方法由2名精神科医师统一标准,采用简明精神量表(BPRS)与PANSS精神量表评估将50例患者分为以阳性症状为主和以阴性症状为主。根据不同的症状行立体定向手术治疗。采用简易智力状态量表(MMSE)、龚氏修订的韦氏成人智力测定量表(WAIS-RC)和韦氏记忆量表(WMS)于手术前2 d和术后5 d明确患者存在认知功能障碍为入选病例,随机、盲法分为药物组和对照组,3个月后回访。结果患者经立体定向手术3个月后,采用简明精神量表(BPRS)与PANSS精神量表评估,患者精神症状控制好,有统计学意义。在给予胆碱酯酶抑制剂后采用简易智力状态量表(MMSE)、韦氏成人智力量表(WAIS-RC)和韦氏记忆量表(WMS)评定后,在术后3个月内,药物组患者认知功能明显提高,有统计学意义(P<0.05),对照组认知功能有所改善,但无统计学意义(P>0.05)。结论胆碱酯酶抑制剂对于改善立体定向手术后短期认知功能障碍有效果。     

利培酮联合认知治疗对首发精神分裂症患者认知功能及社会功能的影响

目的探讨利培酮联合认知治疗对首发精神分裂症患者认知功能的影响并观察出院后的社会功能,为首发精神分裂症的治疗提供参考。方法选取2015年1月-2017年6月在佛山市第三人民医院就诊的符合《国际疾病分类(第10版)》(ICD-10)诊断标准的首发精神分裂症患者100例,采用随机数字表法分为对照组(利培酮治疗)和研究组(利培酮联合认知治疗)各50例,两组均治疗8周。在治疗前及治疗8周后,采用阳性和阴性症状量表(PANSS)、副反应量表(TESS)、韦氏成人智力量表中国修订版(WAIS-RC)及韦氏记忆量表(WMS)分别评定精神症状、不良反应和认知功能。对两组患者进行1年随访,于出院1月及1年后采用个体和社会功能量表(PSP)评定患者的社会功能并追踪出院1年后的复发情况。结果治疗8周后,两组PANSS总评分及各分量表评分均低于治疗前(P均0.01),但两组PANSS评分差异无统计学意义(P0.05);两组WAIS-RC及WMS评分均高于治疗前,且研究组WAIS-RC及WMS各项评分均高于对照组,差异均有统计学意义(P0.05或0.01)。出院1年后,研究组PSP评分高于对照组,差异有统计学意义(P0.05);研究组复发率低于对照组,差异有统计学意义(χ~2=11.415,P0.01)。结论利培酮联合认知治疗与单用利培酮对首发精神分裂症患者的精神症状改善效果无差异,但联合治疗对认知功能及社会功能的改善效果优于单用利培酮,且复发率更低。     

齐拉西酮对首发精神分裂症患者认知功能的影响

目的探讨齐拉西酮和氯丙嗪对首发精神分裂症患者认知功能的影响。方法将符合入组标准的首发精神分裂症86例随机分为齐拉西酮组与氯丙嗪组,分别进行8周的系统治疗,使用阳性与阴性症状量表(PANSS)评定疗效,治疗时出现的症状量表(TESS)评定不良反应,韦氏成人智力量表(WAISR)、韦氏记忆量表(WMS)和威斯康星卡片分类测验(WCST)评定治疗前后患者认知功能的改变。结果治疗后86例PAN-SS总分明显下降,两组之间差异无显著性(均P>0.05);齐拉西酮不良反应较氯丙嗪少,治疗前两组患者均有认知功能损害,治疗8周后,齐拉西酮组患者的认知功能有明显提高,而氯丙嗪组则无明显改善。结论齐拉西酮治疗精神分裂症疗效与氯丙嗪相当,且不良反应小,在改善认知功能方面优于氯丙嗪。     

文拉法辛治疗精神分裂症患者认知功能障碍的疗效

目的：探讨文拉法辛对精神分裂症患者认知功能障碍的治疗作用。方法：对43例达到显著进步以上的精神分裂症患者,随机分为文拉法辛组(22例)和对照组(2l例)分别给予文拉法辛和安慰剂治疗6周。采用韦氏成人智力量表(WAIS)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)及副反应量表(TESS)进行评分。结果：治疗后以文拉法辛组认知功能改善显著较好。结论：文拉法辛对改善精神分裂症患者的认知功能障碍有益。     

利培酮联合脑蛋白水解片对精神分裂症患者认知功能障碍的疗效

目的探讨临床中利培酮与脑蛋白水解片联合治疗对精神分裂症患者认知功能障碍的影响。方法将90例精神分裂症患者采用随机数字表分为研究组和对照组,各45例。两组均给予利培酮治疗,研究组加用脑蛋白水解片治疗,疗程8周。采用威斯康星卡片分类测验(WCST)、韦氏成人智力量表(WAIS)和韦氏记忆量表(WMS)评估两组治疗效果。结果治疗前,两组的WCST,WMS和WAIS各项指标和评分比较差异无统计学意义(P0.05);治疗后,两组的WCST中相关指标及WMS和WAIS的评分较治疗前有明显改善,且组间比较差异有统计学意义(P0.05)。研究组不良反应发生率为11.0%,对照组不良反应发生率为17.7%,两组比较差异无统计学意义(P0.05)。结论临床中对于精神分裂症患者实施利培酮与脑蛋白水解片联合治疗效果显著,能够有效地改善患者认知功能,提高治疗安全性。     

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.     

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.     

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.