精神分裂症精神残疾影响因素的研究进展

精神残疾指各类精神障碍持续一年以上未痊愈,存在认知、情感和行为障碍,影响日常生活和社会参与的状态［1］。精神分裂症是引发精神残疾的主要原因,83％的精神分裂症患者最终会出现精神残疾［2］。有研究证实,精神分裂症患者在前驱期已经表现出明显的社会功能缺陷,缺陷程度随着病程进展不断加重,最终出现严重的精神残疾［3］。患者不同程度的精神残疾和治疗费用给家庭和社会带来沉重的心理和经济负担。因此,积极探索精神分裂症患者的精神残疾的影响因素已成为研究热点。现就目前国内外精神分裂症精神残疾影响因素的研究进行归纳总结,将影响因素加以提炼,分为保护性和危险性因素,以期为强化保护性因素、降低危险性因素,改善患者的社会功能,延缓精神残疾提供新的视角。     

认知行为疗法治疗精神分裂症的研究进展北大核心CSCD

精神分裂症是一种慢性迁延性疾病,治疗周期长,患者的认知功能受损严重,社会功能逐步退化[1].尽管药物治疗是治疗精神分裂症并预防复发的主要方法,但仍有25％～40％的有效服药患者饱受残留精神症状的困扰[2].精神分裂症的认知行为疗法（cognitive behavior therapy,CBT）是指在药物治疗的基础上联合使用CBT来改善患者精神症状,从而达到治疗效果[3].近十年来,随着CBT越来越多的应用于治疗精神分裂症中,其相关研究也从简单的个案研究发展到随机对照研究,并取得了一些成果.我们就CBT治疗精神分裂症的基本方法及效果等方面进行综述.     

综合干预对非慢性精神分裂症患者预后的影响

单一的抗精神病药物治疗可良好改善精神分裂症患者的阳性症状,但对于影响精神分裂症患者预后和结局的阴性症状和社会功能疗效并不一定理想[1].因此,近年来探索抗精神病药物治疗结合社会技能训练、职业康复等综合干预,是人们正在积极探索对精神分裂症治疗更为有效的一种方法.本研究比较了综合干预与单一抗精神病药物治疗对130例非慢性精神分裂症患者为期2年的效果.     

家庭心理干预对首发精神分裂症患者的影响

目的:探讨家庭心理干预对首发精神分裂症患者社会功能及复发率的影响。方法:采用随机抽样方法将84例首发精神分裂症住院患者随机分为干预组和药物组。干预组在药物治疗的基础上,从患者精神症状基本缓解开始实施家庭心理干预。药物组仅接受药物治疗。入组时和治疗9个月、1年后分别进行简明精神病评定量表(BPRS)和社会功能缺陷筛选量表(SDSS)评定。结果:经9个月的家庭心理干预后,干预组BPRS总分及自知力因子分与药物组相比明显降低。1年后两组患者的治愈率、复发率和病残率均以干预组显著较好。结论:家庭心理干预对提高精神分裂症患者疗效,改善其社会功能,防止复发有重要作用。     

残疾精神分裂症患者综合医疗干预效果研究

目的：了解青岛市残疾精神分裂症患者综合医疗干预的效果。方法：对500例残疾精神分裂症患者在综合医疗干预前后进行精神卫生调查表、社会功能缺陷筛选量表（SDSS），治疗中出现的症状量表（TESS），阳性与阴性症状量表（PANSS）进行评定。结果：残疾精神分裂症患者在综合医疗干预后，其疗效、药物不良反应、服药依从性、社会功能均有改善，用药种类非典型抗精神病药使用增多，典型抗精神病药的使用减少。结论：对残疾精神分裂症患者的综合医疗干预有利于患者的全面康复。     

全程干预对首发精神分裂症患者的影响

目的:探讨全程综合性干预对首发精神分裂症患者社会功能及生活质量的影响。方法:将116例首发精神分裂症患者随机分为干预组和药物组各58例,其中脱落7例。两组均接受抗精神病药治疗,干预组同时接受全程综合干预措施1年。采用简明精神病评定量表(BPRS)、住院病人护士观察量表(NOSIE-30)、社会功能缺陷量表(SDSS)和生活质量综合评定问卷(GQOLI)分别于入组时及干预结束时进行评估。结果:入组时,两组所有量表评分差异均无显著性;干预结束时,干预组的BPRS、NOSIE-30中的总消极因素及SDSS评分均明显低于药物组;而NOSIE-30总分、总积极因素及GQOLI评分均明显高于药物组。结论:全程综合性干预措施有助于改善首发精神分裂症患者的精神症状,促进其社会功能的恢复,提高其生活质量。     

应用职业康复疗法治疗慢性精神分裂症的疗效分析

鉴于在医院内应用职业康复疗法对部分精神病患者的症状和社会功能的康复有效[1] 。为此 ,我们对 6 0例慢性精神分裂症患者 ,在原来治疗方案不变的情况下 ,增加职业康复项目 ,以观察其临床效果 ,现报告于后。1　对象与方法1 1　对象　为 6 0例慢性精神分裂症住院患者 ,均符合ＣＣＭＤ - 2 -Ｒ中精神分裂症诊断标准。病程在 5年以上。急性症状已消失 ,病情趋于平稳。采用社会功能评定量表 (ＳＳＳＩ)评定其精神残疾 ,(残疾等级大于 3级 )。在评定过程中原有药物治疗不变。本文均为男性。随机分为试验组 (30例 )为参与职业康复治疗者 ,对照组 (…     

病程小于5年的精神分裂症患者认知功能的影响因素

关于首发与慢性精神分裂症患者的认知功能研究,提示认知功能损害可能是精神分裂症的一个独立症状维度,其影响因素包括精神症状、性别、年龄、病程、遗传素质、自知力、预后与转归、药物等,其中病程的影响有不一致报道[1-2].本研究对病程5年以内的精神分裂症患者的认知功能相关因素进行了探讨.     

抗精神病药单用与结合心理社会干预对非慢性精神分裂症患者一年结局的影响

目的 比较抗精神病药单用与结合心理社会干预对非慢性精神分裂症患者1年结局的影响.方法 多中心随机对照研究,将1239例病程≤5年、稳定期的精神分裂症患者随机分为单纯药物治疗组(以下简称药物组,635例)和药物结合心理社会干预组(以下简称干预组,604例)治疗随访1年.心理社会干预包括健康教育、家庭干预、技能训练及认知行为治疗.主要结局指标为各种原因造成的治疗中断率、疾病复发率和再入院率;次要结局指标为自知力与治疗态度问卷(ITAQ)、健康状况问卷(SF-36)、大体评定量表(GAS)和社会功能缺陷筛选量表(SDSS)评分的变化.结果 (1)干预组和药物组总的治疗中断率分别为32.8%和46.8%[相对危险度(RR)=1.61],复发率分别为13.8%和21.3%(RR=1.76),再入院率分别为6.5%和11.2%(RR=1.99),差异均有统计学意义(P均<0.01～0.05).(2)干预组ITAQ总分变化值[(4.7±0.1)分]、6项SF-36因子分改善值、GAS总分变化值[(6.9±0.2)分]、SDSS总分变化值[(1.5±0.1)分]均明显高于药物组[分别为(1.5±0.1)分、(3.7±0.2)分、(1.0±0.1)分;P均<0.01～0.05].结论 抗精神病药结合心理社会干预治疗非慢性精神分裂症患者,中断率、复发率和再入院率均低于单用抗精神病药患者,自知力、治疗依从性、生活质量、社会功能的改善优于单用抗精神病药患者.     

精神分裂症患者社会功能的影响因素

随着治疗技术的不断进展,促进精神分裂症患者社会功能的康复、回归社会,已经成为现代精神分裂症治疗的最终目标.但影响社会功能的因素较为复杂[1].我们选用多项检测注意、执行功能、心理运算能力的神经心理测量工具,以及临床精神症状及社会功能的评估量表,探讨影响精神分裂症社会功能的因素,从而为更有效地提高患者社会功能提供参考.     

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.