精神分裂症首次发病患者和健康成年人听觉感觉门控电位P50的研究

目的探讨精神分裂症首次发病(以下简称首发)患者和健康成年人听觉感觉门控电位P50的特点。方法采用听觉条件(S1)测-试刺激(S2)范式对58例首发精神分裂症患者(患者组)和108名健康成年人(正常对照组)进行P50检测,评定阳性和阴性症状量表(PANSS)。结果(1)在Cz、Fz和Pz脑区,正常对照组S1所诱发的P50波(S1-P50)潜伏期与S2所诱发的P50波(S2-P50)潜伏期的差异无统计学意义(P>0.05);S2-P50波幅[分别为(2.2±1.4)μV,(2.3±1.5)μV,(2.1±1.4)μV]低于S1-P50波幅[分别为(5.6±3.3)μV,(5.6±3.9)μV,(4.9±2.8)μV;P<0.01];S2/S1比值、S1-S2差值和100(1-S2/S1)的差异无统计学意义(P>0.05)。(2)与正常对照组比较,患者组在Cz、Fz和Pz脑区的S1-P50波幅低(Pz:Z=-2.030,P=0.042,余P<0.01),S2-P50波幅高;S2/S1比值高,S1-S2差值小,100(1-S2/S1)值低(P均<0.01)。(3)患者组的S2/S1比值、S1-S2差值和100(1-S2/S1)值与PANSS总分[(138.49±15.30)分]无相关性(P>0.05)。结论首发精神分裂症患者的感觉门控功能有异常,能通过感觉门控电位P50定量表达。     

抑郁首次发作患者感觉门控P50的研究

目的研究抑郁首次发作(以下简称首发)患者的感觉门控P50特点。方法对39例符合国际疾病分类第10版抑郁发作诊断标准的首次抑郁发作患者(患者组)采用17项汉密尔顿抑郁量表(HAMD17)评定病情严重程度,并进行感觉门控P50检测,与40名健康志愿者(对照组)进行比较。结果(1)患者组P50测试刺激波(S2-P50)的波幅[(2.30±1.04)μV]低于条件刺激波(S1-P50)波幅[(3.48±1.66)μV],但高于对照组S2-P50波幅[(1.54±1.26)μV;P<0.01];患者组的S2/S1波幅比值[(70±23)%]高于对照组[(42±26)%;P<0.01],而S1-S2波幅绝对差值[(1.19±1.48)μV]却低于对照组[(2.17±2.16)μV;P<0.05];患者组P50抑制度[(29±23)%]也低于对照组[(57±26)%;P<0.01]。(2)经Pearson相关分析,患者组HAMD17量表评分与P50各指标无相关(P>0.05)。结论抑郁症首发患者感觉门控抑制存在明显缺损,不能有效滤过无关信息。     

首次发病的精神分裂症患者感觉门控P50特征及其相关因素

目的:探讨首次发病的精神分裂症患者感觉门控P50特征及其相关临床因素。方法:给予87例首发未服药的精神分裂症住院患者(患者组)单一利培酮(4~6 mg/d)治疗,疗程10周;治疗前后分别进行阳性和阴性综合征量表(PANSS)评定及P50检测;以PANSS减分率50%分割点将患者分为有效组和无效组;P50检测结果与86名健康志愿者(对照组)比较;分析患者组P50指标与临床因素的关系。结果:患者组治疗前P50听觉条件(S1)、测试刺激(S2)潜伏期显著长于对照组,S1波幅及S1-S2波幅差值显著低于对照组,S2/S1显著高于对照组(P均0.01);治疗后S1、S2波幅较治疗前显著下降(P均0.01);有效组与无效组间P50各项指标差异无统计学意义;治疗前S2波幅与PANSS阳性症状分呈正相关;S1-S2波幅差值与病程、PANSS中一般精神病理分呈负相关;S2波幅/S1波幅与病程、PANSS总分及一般精神病理分正相关(P均0.05)。结论:首发精神分裂症患者P50抑制缺陷;其与患者的病程、精神病理症状相关;利培酮治疗对P50 S1、S2波幅有影响,但可能未改善其抑制缺陷。     

首发精神分裂症感觉门控P50研究

目的研究首发精神分裂症患者和健康成年人两种诱发模式P50感觉门控的特点,以及两种诱发模式P50抑制率的一致性。方法运用条件-测试刺激模式和刺激序列模式检测41例首发精神分裂症患者(患者组)和30名正常对照(对照组)的听觉诱发电位P50,计算P50抑制率。结果患者组和对照组比较:①两种模式P50潜伏期差异无统计学意义(P>0.05);②条件-测试刺激模式:测试刺激P50波幅[(1.72±1.26)μVvs(0.87±0.66)μV]和P50抑制率[(0.27±0.30)vs(0.63±0.31)]差异有统计学意义(P<0.01),条件刺激P50波幅差异无统计学意义(P>0.05);③刺激序列模式:5.1Hz、9.9Hz高频刺激P50波幅[(1.38±0.61)μVvs(0.84±0.77)μV、(1.18±0.68)μVvs(0.71±0.63)μV,P均小于0.05]和P50抑制率[(0.24±0.23)vs(0.52±0.26)、(0.35±0.26)vs(0.57±0.17),P均小于0.01]差异有统计学意义,0.9Hz低频刺激P50波幅差异无统计学意义(P>0.05);④Spearman相关分析未发现患者组两种诱发模式P50抑制率显著相关(P>0.05)。结论精神分裂症患者表现出两种P50感觉门控功能缺陷,同一患者两种不同诱发模式的P50抑制率不一致,提示其可能具有不同的中枢神经机制。     

精神分裂症与抑郁症患者视觉P300电位的随访比较

目的　探讨精神分裂症和抑郁症患者事件相关电位 (ERPs)P3 0 0 的P3 波异常的意义。方法　对 2 1例精神分裂症、15例抑郁症患者在未服药和停药半年后的发病期及 2年缓解期后采用视觉图像辨认作业引出中央点P3 0 0 ,并与 2 4名正常对照者进行比较。结果　两病例组在发病期P3 潜伏期 [精神分裂症组 (431± 42 )ms,抑郁症组 (40 5± 32 )ms]延长、波幅 [精神分裂症组 (4 7± 2 0 ) μV ,抑郁症组 (5 3± 2 7) μV]下降 ,与对照组 [(36 7± 13)ms、(9 3± 3 1) μV]间的差异有显著性 ;缓解期复查仅精神分裂症组P3 潜伏期 [(410± 30 )ms]及波幅 [(7 1± 3 3) μV]异常较明显 ,抑郁症组潜伏期[(374± 9)ms,波幅为 (8 1± 4 1) μV]与对照组间的差异无显著性。结论　精神分裂症P3 波异常具一定跨状态稳定性 ,其中潜伏期的延长更为稳定 ;而在抑郁症则与临床状态有关。     

30名健康儿童的感觉门控P50研究

目的 应用诱发电位新技术探讨健康儿童感觉门控 (SG) P50特点.方法 应用美国Nicolet脑电生理仪,采用条件刺激(S1)-测试刺激(S2)模式对30名健康儿童进行听觉P50检测.结果 健康儿童Cz脑区S1-P50潜伏期(60.7±11.9)ms,波幅(5.7±3.3)μV;S2-P50潜伏期(65.4±22.0)ms,波幅(2.4±1.3)μV.S2-P50波幅显著低于S1-P50(P<0.01).S2/S1比值为(42.8±21.0)%;S1-S2波幅和100(1-S2/S1)波幅分别为(3.3±2.6)μV和(57.9±21.0)μV.结论 听觉P50电位具有抑制性特征,其变化可反映大脑健康儿童SG的功能状态.     

利培酮对精神分裂症患者血浆高香草酸的影响

目的　探讨利培酮对精神分裂症患者中枢多巴胺代谢产物血浆高香草酸 (pHVA)的影响。方法　 30例精神分裂症住院患者 (患者组 )纳入研究 ,利培酮治疗平均剂量为 (3 2± 1 1)mg/d ,共观察 6周。以阳性和阴性症状量表 (PANSS)评定疗效 ,以高效液相库仑阵列电化学检测法测定患者治疗前后的 pHVA含量。 30例健康志愿者作为对照组 ,检测pHVA水平。 结果　 (1)患者组治疗前 pHVA含量 [(7 9± 4 0 ) μg /L]与对照组含量 [(8 8± 4 1) μg /L]的差异无显著性 (P >0 0 5 ) ,而患者组治疗后 pHVA含量 [(5 3± 2 7) μg/L]明显低于治疗前 (P <0 0 1) ;(2 )治疗前患者组 pHVA与PANSS阳性症状评分 [(2 0 7± 4 1)分 ]存在正相关 (r =0 39,P <0 0 0 1) ,与基线PANSS阴性症状评分 [(19 7± 5 1)分 ]存在负相关 (r =- 0 35 ,P <0 0 1) ;(3)基础pHVA含量及其治疗前后差值[(2 6± 1 3) μg/L]与PANSS阳性症状评分减分值 [(10 8± 4 1)分 ]均分别呈正相关 (r =0 4 8,P <0 0 1;r=0 6 0 ,P <0 0 0 1)。结论　患者组治疗前pHVA可部分反映精神分裂症症状 (尤其是阳性症状 )的严重程度 ,基础 pHVA含量及治疗前后pHVA水平的变化与利培酮治疗阳性症状的疗效相关。     

强迫症患者治疗前后脑诱发电位的比较研究

目的 探讨强迫症(OCD)诱发脑电指标变异的意义。方法 应用美国Nicolet Spirit脑诱发电位仪,记录35例OCD患者(OCD组)和28名健康人(NC组)的事件相关电位P300、脑干听觉反应(ABR)和视觉诱发电位(VEP)。对其中23例OCD患者于治疗5个月后再次检测P300、ABR和VEP。结果 (1)治疗前,OCD组P300-P3靶波幅[(3.51±1.60)μV]低于NC组[(5.90±2.10)μV,P<0.01];ABR-波V绝对潜伏期[(6.40±0.41)ms]长于NC组[(5.50±0.33)ms,P<0.01],波V波幅[(0.35±0.10)μV]高于NC组[(0.16±0.09)μV,P<0.01];VEP-P2潜伏期[(199±39)ms]长于NC组[(183±28)ms,P<0.05]。(2)治疗后,OCD组随强迫思维和行为改善,脑电诱发电位中仅P300-P3靶波幅升高[治疗前后分别为(4.50±1.30)μV和(6.01±1.50)μV;P<0.01],VEP-P2潜伏期缩短[分别为(199±30)ms和(183±28)ms;P<0.05],余各项差异均无显著性。结论 OCD患者P300和VEP变化与临床状态有关,ABR的变异则有待继续跟踪。     

伴暴力攻击行为的精神分裂症患者感觉门控电位P50研究

目的探讨伴暴力攻击行为的精神分裂症患者感觉门控电位P50的特异性,为预测患者暴力攻击行为提供客观生物学标志。方法纳入符合《国际疾病分类(第10版)》(ICD-10)诊断标准的精神分裂症患者135例,根据修订版外显攻击行为量表(MOAS)评分,将患者分为攻击组(n=70)和非攻击组(n=65)。按年龄、性别等匹配原则招募健康对照组(n=60)。采用日本光电公司生产的MEB-9200诱发电位仪对所有受试者行感觉门控电位P50测试。结果攻击组波幅S2高于非攻击组和健康组,差异均有统计学意义[(9.86±6.04)μV vs.(7.06±3.88)μV,P=0.004;(9.86±6.04)μV vs.(7.82±3.87)μV,P=0.031]。攻击组、非攻击组及健康组中,波幅S2/S1≥0.5者占比分别为72.88%、43.86%和30.00%,攻击组高于非攻击组和健康组,差异均有统计学意义(P均0.01)。攻击组波幅差(S1-S2)低于非攻击组和健康组,差异均有统计学意义[(4.35±9.39)μV vs.(9.89±8.48)μV,P=0.001;(4.35±9.39)μV vs.(13.42±9.81)μV,P0.01]。结论精神分裂症患者暴力攻击行为的发生可能与其特异性的感觉门控功能缺失有关。     

情感性精神障碍感觉性诱发电位变异与自杀行为史的关联性研究

目的　探讨情感性精神障碍患者感觉性诱发电位 (SEP)变异与自杀行为史的关系及其临床意义。方法　应用美国尼高力公司Spirit脑诱发电位仪 ,检测 39例抑郁症 (抑郁症组 )患者、2 2例躁狂症 (躁狂症组 )患者和 33名正常对照者 (对照组 )的视觉诱发电位 (VEP)、听觉诱发电位 (AEP)和体感诱发电位 (SSEP) ,并对两患者组中有无自杀史者的测定结果进行比较。结果　 (1 )抑郁症组在VEP中的P2 潜伏期 [有自杀史者为 (2 1 1± 2 1 )ms,无自杀史者为 (2 0 9± 1 7)ms]长于正常对照组 [(1 94±1 9)ms;P <0 0 1和P <0 0 5]。 (2 )抑郁症组和躁狂症组SEP主成分的波幅均低于对照组。 (3)在VEP中 ,抑郁症组中有自杀史者的P3波幅 [(2 7± 1 8) μV]低于无自杀史者 [(5 5± 2 3) μV] ;躁狂症组中有自杀史者的P2 波幅 [(2 9± 1 8) μV]低于无自杀史者 [(5 5± 2 3) μV] ;在AEP中 ,躁狂症组中有自杀史者的P2 波幅 [(3 7± 1 9) μV]低于无自杀史者 [(5 1± 2 3) μV] ,差异有显著性和非常显著性 (P <0 0 5和P <0 0 1 )。结论　感觉性诱发电位是辅助评价自杀倾向的客观方法之一     

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.     

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.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

Un nouveau cadre conceptuel de travail pour une psychiatrie revisitée ? Introduction à deux articles de E. Kandel

In two articles which appeared in the American Journal of Psychiatry and that were subsequently translated for Évolution Psychiatrique, E. Kandel examines the bases for a reinterpreted psychiatry that is prepared to confront the major challenge of the 3rd millenium: that of insight into the mind and brain. This requires a major reorganization of the discipline, which involves a reinvestment of the scientific approach and a critical  assessment of the data provided by psychoanalytical psychiatry and cognitive neurosciences. Seven concepts have therefore been proposed for interactive re-examination: consciousness, the unconscious, memory, emotion, development, desire, impulse. The dynamic relations existing between genetics and the environment allow one to see how evolutions are possible from actions at different levels, both psychotherapeutic and pharmacological. Imaging and other techniques provide additional objective information to the process of human interaction which remains the basis of psychiatry. A common framework for psychiatry and the neurosciences, a reconsideration and renewal of the psychoanalytical approach are both possible and necessary.     

Opioids and the developing organism: A comprehensive bibliography, 1984–1988

A comprehensive bibliography of the literature concerned with opioids and the developing organism for 1984-1988 is presented. Utilized with companion papers (Neurosci. Biobehav. Rev. 6:439-479; 1982; 8:387-403; 1984), these articles cover the clinical and laboratory references beginning in 1875. For the years 1984, 1985, 1986, 1987, and 1988, a total of 877 citations were recorded. A series of indexes accompanies the citations in order to make the literature more accessible. These indexes are divided into clinical and laboratory topics, and subdivided into such topics as the type of opioid explored and the general area of biological interest (e.g., physiology).     

La biologie et le futur de la psychanalyse : un nouveau cadre conceptuel de travail pour une psychiatrie revisitée

The American Journal of Psychiatry has received a number of letters in response to my earlier “Framework” article (1). Some of these are reprinted elsewhere in this issue, and I have answered them briefly there. However, one issue raised by some letters deserves a more detailed answer, and that relates to whether biology is at all relevant to psychoanalysis. To my mind, this issue is so central to the future of psychoanalysis that it cannot be addressed with a brief comment. I therefore have written this article in an attempt to outline the importance of biology for the future of psychoanalysis.     

Facteurs de risque environnementaux à la schizophrénie

Schizophrenia is currently a major concern, its prevalence being estimated at around 1% and its social consequences being severe. The elucidation of the pathophysiology of the disease is difficult due to the great variability of clinical expressions, the instability of the clinical symptoms during the evolution and the absence of reliable biological markers. The existence of a familial aggregation in schizophrenia is well known, the risk of presenting the disease for first-degree relatives of patients being 5 to 10 times higher than the risk observed in the general population. The genetic component was further confirmed by twin and adoption studies. Although the concordance for the disease is higher (40 to 70%) among monozygotic twins as compared with dizygotic twins (15%) it does not reach 100%, which implies that environmental factors modulate the effects of the genotype. However, the role of these factors and especially their interaction with genetic factors remain unclear but the implications of some specific environmental factors are well documented by recent research data. The current literature on sex differences in schizophrenia is consistent. Several studies have suggested that male and female patients may differ in age at the onset and expression of clinical symptoms. Complications during pregnancy or birth-giving may increase the risk of developing schizophrenia later in life. The major complications are oxygen deprivation during pregnancy, bleeding, maternal malnutrition or infection (exposure to influenza, for example). A low birth weight is associated with an increased risk of schizophrenia. Psychoses are more common among people living in an urban environment and among those born during winter months. Schizophrenia is probably more prevalent in people who are living promiscuously, are subject to toxic abuse, poor nutrition and stress but here more precise data are needed. Moreover, immigrants have a higher risk of developing psychotic disorders. In addition, head traumas are associated with an increased risk of schizophrenia. Though they are contentious, some studies suggest that substance abuse (cannabis use in European countries) is related to the development of schizophrenia, especially in people with genetic vulnerability. Moreover, substance misuse may worsen the symptoms. If the environment is sufficiently stressful, people with a high genetic vulnerability will develop some degree of mental illness, including schizophrenia. Conversely, a less stressful or a protective environment may decrease the risk of its onset in persons with a predisposition to schizophrenia.     

Introduction: Goals

Summary: Epilepsy is characterized by recurrent seizures. Many epilepsies with focal seizures as well as convulsive generalized seizures respond satisfactorily to antiepileptic drugs (AEDs) that reduce repetitive firing (e.g., phenytoin, carbamazepine, and valproate) or that augment GABA_A-mediated inhibition (e.g., phenobarbital and benzodiazepines). A number of drugs presently under development, such as NMDA receptor antagonists, loreclezole, losigamone, meth-ysticine, and dextromethorphan, are promising in acute animal models of otherwise drug-resistant convulsant activity. As a result of recent studies in both experimental models and surgically resected human epileptic brain, the prospects for development of AEDs have significantly improved. Several new AEDs recently have reached the commercial market or are in experimental or clinical trials. A comparative presentation of the standing of the new AEDs with respect to their efficacy and side effects is necessary, but still very difficult. Because initial experience with new AEDs is restricted to populations with severe drug-resistant epilepsy, the crucial question whether potential new AEDs can alter prognosis is not yet definitively answered. There is a clear need to compare the effects of standard AEDs and new AEDs in naive patients and over longer follow-up periods. Moreover, because of the strong desire to develop antiepileptic therapy that directly treats the primary etiology of a given epileptic syndrome , or modifies the neurobiological processes that cause recurrent seizures, better experimental epilepsy models for chronic epilepsy and further clinical studies are necessary to increase the knowledge on the pathophysiology of distinct epileptic syndromes. In this respect, studies on the differences between responders and nonresponders to a given AED treatment are extremely valuable.