低频重复经颅磁刺激对酒依赖患者急性戒断后焦虑、抑郁和复饮的效果

目的探讨低频重复经颅磁刺激(rTMS)对酒依赖急性戒断后焦虑、抑郁和复饮的疗效,为改善酒依赖患者预后提供参考。方法选取在绵阳市第三人民医院住院的、符合《国际疾病分类(第10版)》(ICD-10)酒精依赖诊断标准的急性戒断后的102例患者为研究对象。采用随机数字表法分为研究组(n=50)和对照组(n=52)。两组患者均接受常规治疗,研究组加用rTMS,对照组应用伪刺激,治疗共8周。于治疗前和治疗第2、4、8周末进行汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表17项版(HAMD-17)评定,在患者出院后3、6月末评定其复饮情况。结果治疗第2、4、8周末,研究组HAMA和HAMD-17评分均低于治疗前(P均0. 01),且研究组均低于对照组,差异均有统计学意义(P均0. 01);在患者出院后3、6月末,研究组复饮率均低于对照组(P均0. 05)。结论低频rTMS可能有助于改善酒依赖患者急性戒断后的焦虑、抑郁情绪和复饮情况。     

奥沙西泮与劳拉西泮对伴肝功能异常酒精戒断综合征患者的疗效及安全性比较

目的:比较奥沙西泮与劳拉西泮对伴有肝功能异常的酒依赖患者替代治疗的临床疗效及安全性。方法:将酒依赖患者随机分成奥沙西泮组(48例)和劳拉西泮组(47例),两组在常规对症治疗的基础上,分别口服奥沙西泮或劳拉西泮7 d。采用临床机构酒精依赖戒断评估表(CIWA-Ar)评定疗效,及治疗中出现的症状量表(TESS)评定治疗安全性;同时观察肝功能谷丙转氨酶(ALT)和谷草转氨酶(AST)指标。结果:治疗1 d和2 d,奥沙西泮组CIWA-Ar评分低于劳拉西泮组(t=3. 351,P=0. 001; t=4. 096,P=0. 000);治疗3 d,奥沙西泮组TESS评分低于劳拉西泮组(t=-2. 074,P=0. 041);治疗结束,奥沙西泮组ALT和AST水平低于劳拉西泮组(t=2. 207,P 0. 05; t=4. 472,P 0. 01)。结论:与劳拉西泮相比,奥沙西泮对伴有肝功能异常的酒精戒断综合征患者疗效更好、安全性更高。     

重复经颅磁刺激改善失眠患者主观睡眠质量的Meta分析

目的系统评价重复经颅磁刺激(rTMS)对失眠患者主观睡眠质量的疗效,为rTMS治疗失眠提供循证依据。方法系统检索PubMed、Embase、Cochrane Library、万方数据库、维普中文期刊数据库、中国生物医学文献数据库和中国期刊全文数据库,纳入关于rTMS治疗失眠或睡眠障碍的随机对照研究。由两名研究者独立筛选文献、提取数据,并对纳入文献的方法学质量进行评价。采用RevMan 5.2进行Meta分析,采用Stata 13.0分析发表偏倚。结果最终纳入13篇文献,共889例患者。Meta分析结果显示:rTMS治疗组睡眠质量改善的效果优于对照组(SMD=-1.11,95%CI:-1.46～-0.76,Z=6.22,P0.01)。亚组分析结果显示,针对原发性和继发性失眠患者,rTMS治疗组睡眠质量改善的效果均优于对照组(原发性:SMD=-1.22,95%CI:-1.72～-0.72,Z=4.77,P0.01;继发性:SMD=-1.04,95%CI:-1.55～-0.54,Z=4.04,P0.01)。高频和低频rTMS对患者睡眠质量评分的改善效果均优于对照组(高频:SMD=-0.44,95%CI:-0.76～-0.13,Z=2.73,P0.01;低频:SMD=-1.24,95%CI:-1.61～-0.86,Z=6.45,P0.01)。结论高频或低频rTMS联合常规治疗对失眠患者主观睡眠质量的改善效果更佳,对原发性和继发性失眠均有效。     

重复经颅磁刺激治疗抑郁症负性认知及情绪的疗效观察

目的探讨药物治疗基础上联合重复经颅磁刺激(repetitive transcranial magnetic stimulation,rTMS)对抑郁症患者负性认知及情绪的影响。方法将抑郁症患者60例随机分为研究组(n=30,在氟西汀治疗的基础上联合rTMS)及对照组(n=30,单用氟西汀治疗),在治疗前、治疗2周、4周、6周末,采用汉密尔顿抑郁量表24项版本(Hamilton rating scale for depression,HAMD-24)评估患者抑郁程度,采用自动思维量表(automatic thoughts questionnaire,ATQ)评估患者负性认知情况。结果重复测量方差分析显示,HAMD-24评分的组别×时间交互作用无统计学意义(F=0.455,P=0.586),组别主效应(F=11.754,P=0.001)与时间主效应(F=787.600,P0.001)均有统计学意义,随时间推移,两组HAMD评分降低均有统计学意义(P0.001)。治疗6周末研究组的HAMD减分率高于对照组(77.1%±6.8%vs.72.4%±9.7%,t=2.152,P=0.036)。ATQ评分的组别×时间交互作用有统计学意义(F=6.512,P=0.004),治疗后两组ATQ评分降低均有统计学意义(P0.001),且研究组在治疗2周末、4周末、6周末的评分均低于对照组(P0.05)。结论药物联合rTMS不仅有助于改善抑郁症患者的抑郁情绪,也有利于改善其负性认知。     

高频rTMS联合度洛西汀对青年首发广泛性焦虑障碍的疗效及认知功能的影响

目的探讨高频重复经颅磁刺激(rTMS)联合度洛西汀对青年首发广泛性焦虑障碍(GAD)的临床疗效、安全性及对认知功能的影响。方法将符合《国际疾病分类(第10版)》(ICD-10)广泛性焦虑障碍诊断标准的90例首发青年患者分为研究组和对照组,研究组接受高频rTMS(10 Hz)联合度洛西汀治疗,对照组接受伪经颅磁刺激联合度洛西汀治疗,观察期4周。于治疗前采用汉密尔顿抑郁量表17项版(HAMD-17)评定抑郁状况,治疗前和治疗第1、2、4周末采用汉密尔顿焦虑量表(HAMA)评定疗效,治疗前和治疗第4周末使用MATRICS共识认知成套测验(MCCB)评定认知功能,治疗第4周末采用副反应量表(TESS)评定不良反应。结果治疗后各时点,两组HAMA评分均较同组治疗前低(P均0.01)。治疗4周末,研究组治疗总有效率高于对照组(88.89%vs.73.81%,χ~2=2.100,P=0.040),研究组推理及问题解决、社会认知领域评分均高于对照组(P均0.05)。治疗后,两组TESS评分比较差异无统计学意义[(2.48±0.86)分vs.(2.14±0.78)分,χ~2=0.640,P=0.420]。结论高频rTMS联合度洛西汀对GAD的疗效更好,且有助于改善推理及问题解决、社会认知等认知功能。     

右佐匹克隆联合米氮平对慢性失眠障碍的疗效分析

目的探讨右佐匹克隆联合米氮平对慢性失眠障碍患者的临床疗效。方法按随机数字法将82例慢性失眠患者分成研究组42例,对照组40例,对照组给予口服右佐匹克隆(1.5～3mg/d),研究组在对照组的基础上联合口服米氮平(15～30mg/d)治疗,在治疗前,治疗后1、2、4周分别对两组研究对象进行匹兹堡睡眠指数(PSQI)、不良反应量表(TESS)的评定;并以PSQI量表减分率进行有效率评定。同时在治疗前、治疗后4周对两组研究对象进行整夜睡眠呼吸监测(PSG),通过PSG睡眠指标观察对比两组治疗前后的变化。结果治疗后两组PSQI总分较治疗前均逐步下降,治疗4周后研究组有效率92.9%,对照组80%,差异具有统计学意义(χ2=11.296,P=0.010);研究组PSQI总分明显低于对照组,差异有统计学意义(P0. 05)。经治疗两组均出现TST延长,ATA、AT明显减少,SL明显缩短,SE明显提高,REM潜伏期缩短,REM、N2时间延长,与治疗前差异均有统计学意义(P0. 05);其中研究组对比治疗前还有N3时间及比例的明显增加,差异有统计学意义(P0. 05);治疗后研究组在TST、N2、N3时间及N3比例的增加,SL、ATA、AT的减少,SE的提高方面均较对照组明显,差异具有统计学意义(P0. 05)。结论右佐匹克隆联合米氮平对慢性失眠的治疗较单一使用右佐匹克隆疗效要好;安全性高,能加深睡眠,减少觉醒。     

重复经颅磁刺激对躯体形式障碍患者的临床疗效研究

目的:探讨重复经颅磁刺激(rTMS)联合度洛西汀治疗躯体形式障碍的疗效及安全性。方法:将45例躯体形式障碍患者按就诊顺序分为研究组(22例)和对照组(23例);给予两组患者口服度洛西汀(40～60 mg/d),疗程4周;在此基础上研究组联合rTMS每日1次、每周5次、共3周。治疗前及治疗后1、2、3、4周应用汉密尔顿抑郁量表(HAMD-17)减分率评定疗效,应用治疗中出现的症状量表(TESS)评定不良反应。结果:治疗后两组HAMD-17评分随时间进展明显下降,第3、4周末研究组HAMD-17评分明显低于对照组(P均0.05);研究组显效率(80.95%)明显高于对照组(56.52%)(P0.05);研究组不良反应发生率(27.3%)与对照组(43.5%)比较差异无统计学意义。结论:与单用度洛西汀治疗相比,rTMS结合度洛西汀治疗躯体形式障碍起效快、疗效优、不良反应相似。     

右侧低频rTMS联合艾司西酞普兰治疗综合医院首发抑郁症患者的随机对照研究

目的探讨右侧低频rTMS联合艾司西酞普兰治疗综合医院首发抑郁症患者临床疗效。方法选择符合ICD-10抑郁症诊断标准的首发患者。分为研究组和对照组,两组均服艾司西酞普兰(10mg/天)。研究组联用2周rTMS治疗,对照组联用伪刺激。采用HAMD-17、HAMA、TESS于治疗前、第2、4周末评价疗效和副反应。结果 1.治疗第4周,研究组有效率为94.7%,对照组为42.5%;2.研究组在治疗第2周末显示出明显疗效,与对照组比较有显著差异;3.治疗2周后研究组的HAMA低于对照组差异有显著性;4.仅有局部疼痛的反应。结论右侧低频经颅磁刺激联合艾司西酞普兰治疗综合医院首发抑郁症患者的疗效优予单一药物治疗,并能缩短治疗起效的时间。     

阿戈美拉汀联合rTMS对首发抑郁症认知功能的影响

目的探讨阿戈美拉汀联合rTMS治疗首发抑郁症的疗效及认知功能的影响。方法将90例首发抑郁症患者用EpiCalc 2000随机分为两组,各45例,在阿戈美拉汀治疗基础上,研究组给予rTMS治疗,对照组给予伪刺激治疗。分别于治疗第0、1、2、4周末采用汉密尔顿抑郁量表(HAMD-17)评定疗效、用韦氏智力测验(WAIS)中数字符号、数字广度、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)、连线测验(TMT)、词语流畅性测验(VFT)评定认知功能。结果在治疗后第1、2、4周末研究组HAMD评分明显低于对照组;4周末研究组有效率高于对照组;4周末研究组WCST非持续错误数、VFT重复数较治疗前减少,对照组TMT-A提笔次数较治疗前减少。与对照组比较,研究组治疗后第4周末WCST持续错误数、TMT连线时间较少,VFT总数较高,以上均有统计学差异(P0.05)。结论 rTMS联合阿戈美拉汀治疗首发抑郁症安全、快速、有效,并改善认知功能。     

重复经颅磁刺激联合艾司西酞普兰治疗抑郁障碍的疗效观察

目的:探讨重复经颅磁刺激(rTMS)对艾司西酞普兰治疗抑郁障碍(MDD)的增效作用。方法:采用前瞻性随机-对照方法,将80例MDD患者分为研究组(rTMS+艾司西酞普兰,n=40)和对照组(单用艾司西酞普兰,n=40),疗程12周。以治疗前后汉密尔顿抑郁17项量表(HAMD-17)和自动思维问卷(ATQ)评分为疗效评估指标,治疗中出现的症状量表(TESS)记录不良反应。结果:①共完成74例,研究组(38例)和对照组(36例)间性别、年龄、婚姻、受教育年限和病程等一般情况比较差异无统计学意义;②治疗第2、4周末研究组有效率显著高于对照组(P均0.05);第4、8周末研究组治愈率显著高于对照组(P均0.05)。③治疗后两组ATQ总分较基线时显著下降(P均0.01),两组间比较差异无统计学意义;治疗过程中两组不良反应发生率比较差异无统计学意义。结论:rTMS联合艾司西酞普兰治疗MDD的疗效优于单用艾司西酞普兰,且缩短了起效时间,是较好的增效方法。     

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.     

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.     

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.     

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.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

Une phénoménologie de la dépendance à l'alcool. Une expérience primordiale de la « nostrité »

The phenomenological approach to alcoholism interestingly focuses on specific dynamics of interpersonal relationships displaying the founding of the Self from a primary “us” and its original basis in the human feast. Priorities for treatment intervention recommend to involve social setting and relationships of the patients, reaching their active participation to a motivational and long term group treatment, underlying the specific therapeutic effect of world exchanges. Biopsychosocial determination of alcoholism could be primarily based on components of interpersonal relationships. Regarding social background, drinking is one of the most famous supports for the achievement of the feast, a founding marker of present time. Taking an existential point of view, the feast appears as the heart of mankind because it presents a primary “us”, a plural state which indicates the beginning and founding of the Self from the others. During the feast, we regularly have to reach our Self from the “us” while avoiding two main dangers, drunkenness, an increase in the dizziness of upright verticality, and addiction, an opposite vertical surrender to alcohol and falling into in the alcoholic relapse, both situations imply a spatial domination and the disappearance of others. Treatment programs of alcohol addicts need to integrate the necessity of reaching the existential basic trust from the support of a group to the appropriation of the community which can be defined as an original “usness”.