心理干预对抑郁症患者焦虑的影响

目的探讨心理干预对抑郁症患者焦虑情绪的影响。方法将60例符合CCMD-3诊断标准且伴有焦虑症状(HAMA≥14分)的抑郁症患者随机分为观察组(30例)和对照组(30例)。对照组进行常规治疗护理,观察组在此基础上给予心理干预,并对患者及家属进行健康指导,分别用汉米尔顿焦虑量表(HAMA)进行评分。结果观察组HAMA减分率自入院后第一周未即显著高于对照组(P＜0．01)。结论实施心理干预可降低患者焦虑的程度。     

百乐眠联合氟哌噻吨美利曲辛治疗冠心病合并焦虑症状患者的疗效

目的：探讨百乐眠联合氟哌噻吨美利曲辛（商品名：黛力新）对冠心病合并焦虑症状患者的疗效。方法将冠心病合并焦虑症状患者随机分为两组,对照组只给予常规冠心病治疗药物＋黛力新治疗,试验组给予常规冠心病治疗药物＋百乐眠＋黛力新治疗,治疗时间为4周。观察比较两组患者的有效率和汉密尔顿焦虑量表（HAMA）评分。结果治疗2周和4周时,两组患者与治疗前比较, HAMA评分均明显降低,且试验组评分更低,差异均有统计学意义（P＜0．01）。治疗4周后,试验组总有效率为92.9％,明显高于对照组的80．5％,差异有统计学意义（χ2＝18．28,P ＜0．01）。结论百乐眠联合黛力新能够有效改善冠心病患者的焦虑症状。     

低频rTMS治疗以疼痛症状为主的焦虑患者疗效观察

目的：探讨低频重复经颅磁刺激（低频rTMS）对以疼痛症状为主焦虑患者的治疗作用。方法68例以疼痛症状为主焦虑患者随机分为2组,对照组33例,口服常规抗焦虑药物;治疗组35例,在口服抗焦虑药物的同时,加用低频重复经颅磁刺激治疗,疗程4周,以汉密尔顿焦虑量表（HAMA）、疼痛视觉模拟评分（VAS）对患者的焦虑程度、疼痛程度及改善状况进行评定,并将2组疗效作对比。结果2组治疗前后 HAMA评分和VAS评分对比,差异均有统计学意义（P＜0.05）,组间比较差异有统计学意义（ P＜0.05）;总有效率治疗组94.29％,对照组81.82％,差异有统计学意义（ P＜0.05）。结论低频重复经颅磁刺激（低频rTMS）治疗以疼痛症状为主的焦虑患者安全有效。     

药物联合心理干预治疗卒中后抑郁/焦虑的临床研究

目的探讨帕罗西汀联合早期心理干预对卒中后抑郁／焦虑患者日常生活能力和神经功能康复的影响。方法采用抑郁自评量表（SDS）、焦虑自评量表（SAS）对272例脑卒中患者进行抑郁／焦虑状态评定，其中患有卒中后抑郁合并焦虑的81名患者分别接受单用帕罗西汀治疗、帕罗西汀联合心理干预治疗以及不干预。采用斯堪的那维亚脑卒中量表（SSS）、Barthel指数（BI）、汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）评测治疗前后的疗效。结果急性脑卒中病人卒中后抑郁并焦虑患病率为29．78％，抑郁与焦虑共病率为65．85％；治疗组Ⅰ和治疗组ⅡHAMD、HAMA、SSS评分减少和BI评分增加与对照组比较均有显著性差异（P〈0．01），治疗组ⅡHAMD、HAMA、SSS评分减少和BI评分增加较治疗组Ⅰ有显著差异（P均〈0．05）。结论卒中后抑郁／焦虑病人单用药物帕罗西汀或给予帕罗西汀合并心理干预治疗均能提高患者神经功能康复程度和生活能力恢复，而且帕罗西汀合并心理干预治疗疗效更满意。     

良性阵发性位置性眩晕与前庭性偏头痛患者焦虑抑郁状态比较研究

目的 比较良性阵发性位置性眩晕（benign paroxysmal positional vertigo,BPPV）患者和前庭性偏头痛 （vestibular migraine,VM）患者焦虑、抑郁的发生率和特点。 方法 收集2016年9月-2017年9月诊断为BPPV和VM患者各50例。对两组患者进行眩晕残障量表 （dizziness handicap inventory,DHI）和医院焦虑抑郁量表（hospital anxiety and depression scale,HADS）评 定,比较两组基线资料和DHI 、HADS评分的差异。 结果 治疗前BPPV组存在明显眩晕残障者32例（64%）,存在焦虑抑郁者15例（30%）,治疗后分 别为3例（6%）和2例（4%）,差异有统计学意义（P＜0.001和P =0.001）;治疗前VM组存在明显眩晕 残障者38例（76%）,存在焦虑抑郁者为28例（56%）,治疗后分别为12例（24%）和8例（16%）,差异 均有统计学意义（均P＜0.001）。治疗前VM组DHI[55.00（44.00～70.00）vs 31.00（20.00～45.00）,P ＜0.001]和HADS评分[13.50（6.00～20.00）vs 6.00（3.75～10.00）,P =0.001]高于BPPV组,其中DHI评 分中情感、躯体和功能3个分项的评分也均高于BPPV组,差异均有统计学意义。治疗后VM组DHI[22.00 （12.00～34.00）vs 0（0～4.00）,P＜0.001]和HADS评分[7.50（2.00～10.50）vs 0（0～3.00）,P＜0.001] 仍高于BPPV组,其中DHI评分中情感、躯体和功能3个分项的评分也均高于BPPV组,差异均有统计学 意义。 结论 VM患者焦虑抑郁严重程度高于BPPV患者,两组经治疗后焦虑抑郁的发生率均有显著下降。     

曲唑酮与地西泮治疗焦虑性神经症的临床对照研究

目的 评价曲唑酮治疗焦虑性神经症的临床症疗效副反应。方法 对56例焦虑性神经症患者,应用曲唑酮（28例）,地西泮（28例）进行对照治疗,疗程4周。采用副反应量表（TESS）和焦虑自评量表（SAS）、Hamilton焦虑量表（HAMA）评定疗效和副反应。结果 曲唑酮与地西泮的疗效相似（P＞0．05）。治疗第4周末SAS,HAMA以及HAMA因子的减分率两组均有非常显著性（P＜0．01）。副反应两药相似,曲唑酮的主要副反应为困倦和嗜睡。结论 曲唑酮治疗焦虑性神经症有效,副反应轻微。     

心理剧治疗对强迫症患者焦虑、抑郁及生活质量的影响

目的探讨心理剧治疗对强迫症患者焦虑、抑郁及生活质量的影响。方法将100例强迫症患者随机均分为研究组和对照组，在两组均给予足量足疗程的药物治疗及接受一般健康教育的基础上，仅对研究组辅以心理剧治疗，4周为一个疗程。生活质量测评工具SF-36量表、Yale—Brown强迫症量表（Y—BOCS）、17项汉密顿抑郁量表（HAMD17）、汉密顿焦虑量表（HAMA）对两组患者进行治疗前后效果评定。结果干预后研究组患者的Y—BOCS总分和HAMD17HAMA总分值均显著低于对照组（P〈0．01），而疗效显著高于对照组（P〈0．01），研究组患者的显效率显著高于对照组（P〈0．01），研究组患者的SF-36量表各维度分值显著高于对照组（P〈0．01）。结论心理剧治疗可巩固患者的疗效，并改善其焦虑、抑郁情绪，能显著提高患者的心理健康水平及生活质量，可作为一种有效的心理治疗手段应用于临床。     

综合护理对抑郁症伴焦虑患者的临床疗效

目的探讨综合护理对抑郁症伴焦虑患者的临床疗效。方法收集2012年3月至2014年3月于我科治疗的抑郁症伴焦虑患者共80例,随机分为观察组与对照组,每组各40例。对照组在常规药物治疗的基础上,采用常规护理,观察组在常规药物治疗的基础上采用综合护理干预,6周后对比两组患者治疗前后的汉密尔顿抑郁量表评分(HAMD)、焦虑量表评分(HAMA)、临床疗效总评量表之疾病严重程度评分(CGI-SI)。结果两组患者干预前HAMA,HAMD和CGI-SI评分,组间比较无明显差异(P0.05)。干预6周后,两组患者的HAMA,HAMD和CGI-SI评分较干预前均降低,且观察组上述量表评分均显著低于对照组,上述差异均有统计学意义(P0.01)。结论在常规治疗和护理的基础上,采用综合护理方法干预,能更显著改善抑郁症伴焦虑患者的抑郁焦虑情绪,更快地改善患者的病情严重程度,具有肯定的临床疗效。     

伴不同程度焦虑症状的抑郁症患者文拉法辛的疗效比较

目的:比较伴不同程度焦虑症状的抑郁症患者文拉法辛的疗效。方法:224例抑郁症患者根据汉密尔顿焦虑量表(HAMA)评分分为明显焦虑组(HAMA≥14分,158例)及可能焦虑组(HAMA 14分,66例),均给予文拉法辛单药治疗52周。治疗前进行汉密尔顿抑郁量表-17 (HAMD-17)、HAMA和自杀意念自评量表(SIOSS)测评;以治疗后HAMD减分率≥50%为有效;治疗后第2周末HAMD减分率≥25%为早期起效;比较两组治疗后第2、4、8、12、52周时的疗效。结果:明显焦虑组146例(91. 78%)、可能焦虑组61例(91. 80%)完成随访;明显焦虑组的自杀风险率(60. 1%)显著高于可能焦虑组(25. 8%)(P 0. 01);治疗前后各时间点HAMD评分显著高于可能焦虑组(P 0. 05或P 0. 01);治疗后早期起效率(治疗后2周)、持续有效率(治疗后4周)、临床痊愈率(治疗后8周)、持续临床痊愈率(治疗后12周)显著低于可能焦虑组(P均0. 05);复发率(29. 1%)显著高于可能焦虑组(15. 2%)(P 0. 05)。结论:文拉法辛对无或伴轻度焦虑症状的抑郁症患者疗效明显好于伴有明显焦虑症状的患者。     

度洛西汀治疗广泛性焦虑障碍的疗效和安全性

目的调查度洛西汀治疗广泛性焦虑障碍（GAD）的疗效及安全性。方法将符合DSM—IV广泛性焦虑障碍诊断标准的住院患者随机分为度洛西汀组38例和文拉法辛组37例,进行为期8周的治疗观察;于基线时、治疗2,4,8周末评定汉密尔顿焦虑量表（HAMA）判断临床疗效;基线时及治疗8周末评定席汉残疾量表（SDS）评定社会功能恢复状况;药物不良反应量表（TESS）评价安全性。结果两组治疗2,4,8周末在有效率、HAMA评分方面与基线时比较差异有统计学意义（P〈0．01）,两组间比较差异无统计学意义（P〉0．05）;治疗8周末两组sDs评分均较基线时有明显改善,差异有统计学意义（P〈0．01）,两组间比较有统计学意义（P〈0．05）;两组均未见严重药物不良反应。结论度洛西汀治疗广泛性焦虑障碍起效快、疗效好、安全性高,同时对社会功能恢复起到积极作用。     

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 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.     

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.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.