首发精神分裂症患者的糖代谢研究

目的　探讨首发精神分裂症患者的糖代谢情况。方法　对 86例首发精神分裂症患者及 45名健康人进行糖耐量试验(OGTT) ,并检测其空腹血浆胰岛素、C肽的浓度。结果　两组间空腹血糖、餐后 3h血糖、空腹胰岛素、C肽的差异无显著性 ,病例组餐后 1h血糖值 [( 7 89± 1 77)mmol/L]、2h的血糖值 [( 6 2 4± 1 14 )mmol/L]、OGTT血糖曲线下面积 (AUC) [( 18 2 4± 2 76)mmol/(L·h) ]比对照组 [分别为 ( 6 5 4± 1 84)mmol/L ,( 5 88± 2 78)mmol/L ,( 15 86± 1 93 )mmol/L/h ,P分别小于 0 .0 1、0 .0 5、0 0 1]要大 ;组间糖耐量减退 (IGT)的发生率无显著性差异 ( χ2 =0 5 84,P >0 0 5 ) ;偏执型患者组与青春型患者组间的空腹血糖、2h血糖值无显著性差异 (t=1 476,P均大于 0 0 5 ) ;发生IGT的病例组与未发生IGT病例组组间阳性和阴性症状量表 (PANSS)总分及 4个分量表分值的差异无显著性差异 (P均大于 0 0 5 )。结论　首发精神分裂症患者存在餐后高血糖现象。     

氯丙嗪、氯氮平、利培酮对首发精神分裂症患者糖代谢、血脂和体重的影响

目的　探讨氯丙嗪、氯氮平和利培酮对首发精神分裂症患者糖代谢、血脂和体重的影响。方法　将首发精神分裂症患者随机分为 3组 ,每组各 3 0例 ,分别单用氯丙嗪、氯氮平、利培酮治疗。于治疗前、治疗第 3周末和第 6周末做糖耐量试验 ,并检测甘油三酯、胆固醇 ,计算体重指数 [BMI,体重 (kg) /身高 (m2 ) ]。结果　氯氮平组治疗后第 3周末、第 6周末餐后 2h的血糖值和第 6周末BMI值明显高于利培酮和氯丙嗪组 ,与治疗前相比也明显升高 (P <0 0 5 )。利培酮组治疗第 6周末BMI值和餐后 1h血糖值比治疗前明显升高 (P <0 0 5 )。氯丙嗪组治疗第 6周末BMI值比治疗前明显升高 (P <0 0 5 )。结论　氯氮平对精神分裂症患者糖代谢和体重影响最大 ,其次是利培酮 ,氯丙嗪影响最小     

糖化血红蛋白异常在抗精神病药诱发糖代谢疾病中的意义

目的探讨糖化血红蛋白(HBA1C)异常在抗精神病药诱发糖代谢疾病中的意义。方法对152例空腹血糖(FPG)、糖耐量试验2H血糖(2HPG)正常的精神分裂症女性患者,按HBA1C正常/异常分层后随机分HBA1C正常组(115例,以下简称正常组)及HBA1C异常组(37例,以下简称异常组),分别给予利培酮(正常组37例,异常组12例)、氯氮平(正常组40例,异常组13例)及氯丙嗪(正常组38例,异常组12例)治疗,治疗前及治疗第6周后测定各组患者的FPG及2HPG。结果(1)仅氯氮平异常组患者治疗后2HPG[(9·5±1·8)MMOL/L]较治疗前[(7·2±1·4)MMOL/L]增高,差异有统计学意义(P<0·01)。(2)各组内治疗前、后FPG的差异均无统计学意义(P均>0·05)。(3)HBA1C水平因素与药物因素对治疗后2HPG存在交互作用(P<0·01)。(4)氯氮平异常组患者治疗后2HPG高于利培酮异常组[(7·4±1·7)MMOL/L]及氯丙嗪异常组[(7·3±1·6)MMOL/L],差异有统计学意义(P<0·01)。各正常组患者治疗后2HPG的差异均无统计学意义(P均>0·05)。(5)各异常组患者治疗前、后的合计2HPG[(7·1±1·6)MMOL/L],[(8·1±1·9)MMOL/L]均高于各正常组的合计2HPG[(6·2±1·4)MMOL/L],[(6·5±1·4)MMOL/L],差异均有统计学意义(P<0·01,<0·001)。(6)异常组与正常组比较,接受抗精神病药治疗后发生糖代谢疾病的比值比(OR)经标化为9·5,差异有统计学意义(P<0·001)。结论HBA1C异常的精神分裂症患者可能是抗精神病药诱发糖代谢疾病的高危人群。     

精神分裂症患者脑脊液单胺类神经递质含量与疗效

目的:探讨精神分裂症患者脑脊液(CSF)内多巴胺(DA)、高香草酸(HVA)含量的变化及其临床意义。　方法:86例首发精神分裂症,用利培酮治疗6个月,于治疗前及治疗6个月后采用高效液相色谱电化学(HPLC -ECD)法检测CSF中的DA及HVA含量,并与32名健康人进行对照。患者组同时用阳性与阴性症状量表(PANSS)评定临床疗效。　结果:患者组在治疗前CSF中DA和HVA含量分别为(3.2 3±0 .36 ) μmol/L和(1.99±0 .4 9) μmol/L ,显著高于对照组(2 .4 4±0 .32 ) μmol/L和(1. 4 1±0 . 37)μmol/L ;患者组治疗6个月后分别为(2 .4 9±0 .35 ) μmol/L和(1.4 2±0 .2 8) μmol/L。其治疗后降低值与PANSS总分的减分差值呈显著正相关。　结论:精神分裂症患者CSF内DA和HVA含量显著增高,利培酮对精神分裂症的疗效与DA和HVA含量的变化密切相关。同时进一步验证了精神分裂症患者中枢神经系统DA功能亢进的假说。     

利培酮及氯氮平对首发精神分裂症患者认知功能及P300的影响

目的比较利培酮和氯氮平对首发精神分裂症患者认知功能的影响。方法对64例首发精神分裂症采用随机对照研究法观察12周,利培酮组33例,平均有效治疗剂量(4.5±1.2)mg/d,氯氮平组31例,平均有效治疗剂量(269.4±133.3)mg/d。于治疗前后行阴性和阳性症状量表(PANSS)、韦氏记忆量表(WMS)和事件相关电位P300检测。结果首发精神分裂症患者在长时记忆、短时记忆、瞬时记忆及记忆商数(MQ)受损较为明显,与对照组比较有显著性差异(P<0.05)。P300电位成分中P2、N2及P3潜伏期明显延长,P2及P3波幅明显降低,与对照组比较均有显著性差异(P<0.05)。经过12周治疗利培酮和氯氮平组PANSS总分、阳性症状分、阴性症状分及一般精神病理症状分均降低,2组无显著性差异(P>0.05)。利培酮组的WMS的再认、联想及记忆商(MQ)明显高于氯氮平组;2组治疗前后P300各指标均无显著性差异。结论首发精神分裂症患者存在着认知功能障碍,利培酮对首发精神分裂症认知功能的改善明显优于氯氮平。两药均不能改善患者的P300。     

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。     

氯丙嗪和利培酮对精神分裂症患者血糖调节功能影响的动态观察

目的观察抗精神病药在治疗的不同时间精神分裂症患者血糖代谢的变化特点,探讨预防血糖调节功能损害(IGR)的有效方法。方法将213例住院精神分裂症患者分为氯丙嗪组(108例,200~650mg/d)和利培酮组(105例,3~6mg/d),均单一用药,分别于入院时、治疗第1,2,3,6个月末及1年末测定多项血糖浓度并进行对照研究。结果(1)治疗后随时间延长,两组血糖浓度均不断上升。治疗第3个月末餐后2h血糖(2hPBG)和2h糖耐量(2hPG)浓度开始升高,治疗第6个月末空腹血糖(FPG)和空腹糖化血红蛋白(HbA1c)开始升高,治疗1年末所有血糖指标均升高(均P<0.05~0.01)。(2)组内治疗前后比较,氯丙嗪组治疗第3个月末2hPG[(5.77±1.28)mmol/L]和2hPBG[(5.93±1.10)mmol/L]、治疗第6个月末HbA1c[(5.49±0.76)mmol/L]、治疗1年FPG浓度[(5.29±0.71)mmol/L]均高于治疗前[分别为(mmol/L)5.31±0.58,5.48±0.60,5.22±0.50和4.96±0.49],均P<0.05~0.01;利培酮组治疗1年末2hPBG浓度[(5.70±0.89)mmol/L]高于治疗前[(5.35±0.77)mmol/L;P<0.05]。(3)两组比较,氯丙嗪组治疗第3个月末2hPBG和HbA1c[(5.41±0.63)mmol/L]、治疗1年末2hPG[(5.92±1.34)mmol/L]和FPG[(5.29±0.71)mmol/L]浓度均高于利培酮组[分别为(mmol/L)5.55±0.83,5.23±0.50,5.54±0.91,5.08±0.59],均P<0.05~0.01。1年末,两种药物日剂量与各血糖浓度之间无显著相关性(P>0.05)。(4)两组治疗后各时间点IGR的发生率均上升;治疗1年末,氯丙嗪组IGR发生率达36.1%,高于利培酮组(22.9%;P<0.05)。(5)在完成1年观察的198例患者中,51例(25.8%)至少有1次符合IGR血糖浓度标准,但两组间的差异无统计学意义(P>0.05)。结论血糖浓度随药物治疗时间的延长而上升,其中氯丙嗪比利培酮更易引起IGR。     

利培酮联合氯氮平治疗精神分裂症阴性症状的对照观察

本组试用利培酮联合氯氮平治疗 2 0例以阴性症状为主的精神分裂症并与单独利培酮和单独氯氮平治疗比较。现将结果报道于后。1　对象和方法1.1　对象　均符合ＣＣＭＤ - 2 -Ｒ中精神分裂症的诊断标准 ,且以阴性症状为主者。年龄、性别不限 ,并随机分成三个组 :①利培酮组 ,其中男 12例 ,女 8例 ;年龄 2 0～ 4 8岁 ,平均年龄 (32 .4± 8.5 )岁 ;平均病期6 .3年。②氯氮平组 ,其中男 9例 ,女 11例 ;年龄 19～ 5 6岁 ,平均年龄 (34.5± 11.4 )岁 ;平均病期 7.8年。③利培酮联合氯氮平组 (以下简称联合组 ) ,其中男 13例 ,女 7例 ;平均年龄 (36 .…     

以阳性或阴性症状为主的精神分裂症患者脑脊液催乳素水平测定

目的　探讨以阳性症状为主 (以下简称阳性 )和以阴性症状为主 (以下简称阴性 )的精神分裂症患者脑脊液催乳素 {PRL)水平及氯氮平治疗前后的变化。方法　对 2 6例阳性精神分裂症患者 (阳性组 )和 2 2例阴性精神分裂症患者 (阴性组 )用氯氮平治疗 6周 ,用简明精神病量表 (BPRS)、阳性症状量表 (SAPS)或阴性症状量表 (SANS)评定疗效。治疗前及治疗 6周末用放射免疫测定法测定患者脑脊液PRL水平。结果　治疗前阳性组PRL水平 [(1.0 8± 0 .39) μg/L]低于阴性组 [(1.34± 0 .4 1) μg/L],P <0 .0 5 ;治疗后阳性组PRL水平 [(1.16± 0 .35 ) μg/L]较治疗前升高 ,阴性组 [(1.2 4± 0 .4 6 ) μg/L]较治疗前降低 ,差异均无显著性 (P >0 .0 5 )。两组治疗后BPRS、SAPS或SANS总分较同组治疗前下降均有极显著性差异 (P <0 .0 1)。结论　阳性和阴性精神分裂症患者脑脊液PRL基础水平有差异 ,氯氮平对精神分裂症患者脑脊液PRL水平影响较小。     

利培酮和氯氮平治疗首发精神分裂症的疗效及其药费负担的比较分析

鉴于利培酮对精神分裂症的阳性、阴性症状均有较好效果 ,但由于其药价较为昂贵 ,从而限制了临床使用。为此 ,本文选择了利培酮治疗首发精神分裂症 ,并与氯氮平对照 ,旨在评价临床疗效和药物费用之间的关系 ,现报道于后。1　对象与方法1 1　对象　①均符合ＣＣＭＤ - 2 -Ｒ诊断标准[1] 中的首发精神分裂症患者进入研究 ,并排除严重躯体疾病者。②本文共 2 0 4例 ,其中研究组 10 2例 ,男 5 7例 ,女 4 5例 ,年龄 (2 1 4 4± 9 74 )岁 ,病程 (4 6± 1 2 )个月。对照组 10 2例 ,男 5 7例 ,女 4 5例 ,年龄 (2 1 82± 8 4 5 )岁 ,病程 (4 9± 3 4 )…     

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.