晚发精神分裂症患者局部脑血流及认知功能的研究

目的　探讨晚发精神分裂症患者局部脑血流 (rCBF)及认知功能损害的特点。方法　对2 1例首次发病年龄≥ 5 0岁的精神分裂症患者进行脑单光子发射计算机体层摄影术 (SPECT)检查 ,并采用阳性和阴性症状量表 (PANSS)、简易精神状态量表 (MMSE)、中国修订韦克斯勒成人智力量表、韦克斯勒记忆量表 (WMS)及威斯康星卡片分类测验等进行评定 ,经利培酮 [(2 7± 0 8)mg/d ,2次 /d]治疗 8周后 ,其中 11例患者 (PANSS减分率大于 2 5 % )再次完成上述测定。 2 0名正常人完成SPECT、MMSE及WMS测定。结果　 (1)治疗前患者组左额叶、左顶叶、双侧颞下、双侧基底节及右丘脑 (P <0 0 1)的放射性计数比值 (RAR)低于对照组 (P <0 0 5 ) ,且左额叶RAR (0 85± 0 11)低于右额叶(0 86± 0 10 ;P =0 0 13) ;其MMSE评分 (2 3 33± 4 10 )低于对照组 [(2 8 35± 1 6 3)分 ,P <0 0 1];WMS总分及其大部分测验项目分亦均低于对照组 (P <0 0 1或 0 0 5 )。 (2 )治疗后患者组仅MMSE分[(2 4 73± 4 4 5 )分 ]、WMS的定向因子分 [(3 82± 1 0 8)分 ]和背数因子分 [(5 0 0± 3 4 9)分 ]高于治疗前[分别为 (2 2 4 5± 3 98)分、(3 18± 1 0 8)分和 (2 6 4± 3 88)分 ;P <0 0 5 ],而各脑区rCBF及其余认知功能的变化均无显     

阿尔茨海默病和血管性痴呆患者脑脊液中乙酰胆碱和胆碱检测及其临床意义

目的　探讨阿尔茨海默病 (AD)和血管性痴呆 (VD)患者脑脊液 (CSF)中乙酰胆碱 (ACh)和胆碱 (Ch)含量的异同以及它们与认知障碍的关系。方法　采用简易精神状态量表 (MMSE)对 2 2例AD、2 2例VD和 2 0名对照进行认知功能评分 ,利用高效液相色谱 电化学检测方法 (HPLC ECD)进行CSF的ACh和Ch检测 ,而后进行比较和分析。结果　AD组患者CSF的ACh含量 [(10 .7± 5 .1)nmol/L]低于对照组 [(34 .5± 9.0 )nmol/L](P =0 .0 0 1) ,与MMSE评分呈正相关。VD组患者CSF的ACh含量 [(16 .8± 7.4)nmol/L]也低于对照组 (P =0 .0 0 1) ,与MMSE评分呈正相关。AD组的CSF中Ch含量与对照组相比 [分别为 (6 2 7.6± 145 .1)nmol/L和 (716 .0± 15 9.4)nmol/L],差异无显著意义 ,与MMSE不呈相关关系。VD组患者CSF的Ch含量 [(887.4± 187.4)nmol/L]高于对照组 (P =0 .0 0 2 )和AD组患者 (P =0 .0 0 1)。结论　 (1)ACh的降低与认知障碍呈正相关 ,提示ACh是与记忆有关的重要神经递质 ;(2 )VD的ACh降低提示有与AD类似的发病机制 ;(3)AD患者ACh显著降低和VD患者胆碱显著增高有助于两者之间的鉴别 ;(4 )应用胆碱酯酶抑制剂来提高脑内ACh水平 ,不仅适用于AD ,也适用于VD。     

阿尔茨海默病的事件相关电位P300研究

目的　探讨阿尔茨海默病 (AD)P3 0 0 的特点以及P3 0 0 与简易智力状况检查 (MMSE)评分的相关性。方法　对 32例AD患者和 30名健康老年人应用NicoletBravo脑诱发电位仪进行事件相关电位P3 0 0 检测 ;同时用MMSE进行认知功能评估。结果　 (1)AD组MMSE评分 [(16 5 2± 2 17)分 ]低于正常对照组 [(2 6 5 7± 1 4 3)分 ,P <0 0 1]。 (2 )AD组与正常对照组相比 ,靶刺激中的P2 、N2 、P3 潜伏期长 ,P2 、P3 波幅低 ;非靶刺激P2 波幅低 (P <0 0 5～ 0 0 1) ;AD组Cz、Pz、Fz各点间的P3 0 0 指标相比 ,差异均无显著性 (P >0 0 5 )。 (3)AD组P3 0 0 靶刺激中的P2 、P3 波潜伏期与MMSE分值呈负相关 (P <0 0 5～ 0 0 1)。结论　AD患者的P3 0 0 有多指标变异 ,且与其认知功能缺损的程度有关。     

阿尔茨海默病患者红细胞超氧化物歧化酶与载脂蛋白ε_4等位基因的相互关系

目的　探讨阿尔茨海默病 (AD)患者的外周血氧化应激与载脂蛋白 (apo)Eε4 等位基因的相互关系。方法　分别测定 2 5例散发性AD患者 (AD组 )、2 0例血管性痴呆 (VD)患者、2 2名正常人(正常组 )的红细胞超氧化物歧化酶 (SOD)、血浆一氧化氮 (NO)浓度及apoE等位基因频率。结果　AD组的SOD活性 [U /mg血红蛋白 ]为 10 80± 35 1,明显高于正常组 [(818± 330 )U],P <0 0 5 ;NO浓度的差异无显著性。根据apoEε4 等位基因进行分层后 ,不携带ε4 组间SOD活性差异有显著性 ,AD组高于正常组 (P <0 0 5 )。AD患者的SOD活性与临床痴呆分级量表 (CDR)呈显著性负相关 (r =- 0 480 ,P <0 0 5 ) ,与BLESSED痴呆量表分呈显著性负相关 (r =- 0 5 2 2 ,P <0 0 1) ,正常组的SOD活性与年龄呈显著性负相关 (r=- 0 430 ,P <0 0 5 )。结论　与痴呆严重程度有关的氧化应激可能参与AD患者的病理生理变化 ,并可能受ε4 等位基因的影响     

智力竞技型休闲活动对阿尔茨海默病的影响

目的　探讨智力竞技型休闲活动 (以下简称智力活动 )对阿尔茨海默病 (AD)的影响。方法　采用分层随机整群抽样方法 ,以淄博市各层人口所占总人口比例确定各层应查≥ 5 5岁人群 ,共 6 5 6 0人 ,实查 6 348人。调查采用筛查和确诊两阶段法 ,按美国精神障碍诊断与统计手册第 4版的标准诊断痴呆 ,同时进行自编智力活动问卷调查 ,并进行流行病学及卫生统计学分析。结果 (1)查出痴呆患者共 138例 ,患病率为 2 17%。其中AD为 1 6 1% ,血管性痴呆 (VD)为 0 4 1% ,其他痴呆为0 16 %。 (2 )有智力活动组的AD患病率 (0 6 7% ,11例 )低于无智力活动组 (1 94 % ,91例 ;P <0 0 1)。(3)分层分析结果显示 ,同一层中有智力活动组的AD患病率均低于无智力活动组 (P <0 0 5和P <0 0 1)。 (4)有智力活动组的AD患病年龄 [(84± 7)岁 ]较无智力活动组 [(71± 8)岁 ]晚 (P <0 0 1) ;且痴呆的程度 (中、重度为 0 2 4 % )较无智力活动组 (1 70 % )轻 (P <0 0 1)。结论　智力活动有助于降低罹患AD的风险 ,对AD可能有保护作用。     

阿尔茨海默病患者血浆基质金属蛋白酶-3水平的对照研究

目的探讨阿尔茨海默病(AD)患者血浆基质金属蛋白酶-3(MMP-3)水平的变化。方法应用双抗体夹心酶联免疫法测定30例AD患者(AD组)、27例血管性痴呆(VD,VD组)患者及26名正常对照者(正常人组)的血浆MMP-3水平。根据简易精神状况检查量表(MMSE)评分将AD患者分为重度组(MMSE≤10分,8例)、中度组(MMSE>10分~≤20分,12例)和轻度组(MMSE>20分~<24分,10例)。血浆MMP-3水平采用方差分析进行统计学比较。结果AD组血浆MMP-3水平为(5.8±1.2)×104U/L,VD组为(5.3±0.8)×104U/L,正常人组为(4.8±0.8)×104U/L。AD组高于正常人组(P<0.001)及VD组(P<0.05),VD组亦高于正常人组(P<0.05)。AD重度组血浆MMP-3水平[(6.8±1.3)×104U/L]分别高于AD轻度组[(5.5±1.0)×104U/L]及AD中度组[(5.6±1.0)×104U/L],P均<0.05。AD组MMP-3水平与MMSE评分呈显著负相关(r=-0.450,P<0.05)。结论血浆MMP-3水平与AD严重程度相关;其水平增高可能与AD发病过程有关,其差异对AD与VD的鉴别可能有辅助价值。     

城乡社区≥55岁人群、可疑痴呆和痴呆患者死亡率及生存率的研究

目的　了解社区≥ 5 5周岁人群、可疑痴呆和痴呆患者的死亡率及生存率。方法　在1997年调查成都地区城乡社区≥ 5 5周岁人群 5 35 3人中痴呆患病率的基础上 ,于 2 0 0 0年用随机整群抽样方法抽取 384 1人调查其死亡及生存情况。在 384 1人中随访到 30 5 8人 ,死亡 391人 ,外出或迁出 392人。基线调查用美国精神障碍诊断与统计手册第 3版修订本的标准诊断痴呆 ,用临床痴呆程度评定量表评定痴呆程度。结果　 (1)基线调查时被评为筛查阴性、复查正常、可疑痴呆和痴呆的患者 ,3 3年后随访时的死亡率分别为 2 9% (2 35人 )、6 2 % (85人 )、15 0 % (19例 )和 2 8 5 % (5 2例 )。其中阿尔茨海默病 (AD)、血管性痴呆 (VD)和其他类型痴呆 (OD)患者死亡率分别为 2 8 8% (40例 )、33 9% (8例 )和 19 9% (4例 )。 (2 )筛查阴性、复查正常、可疑痴呆和痴呆患者的生存率分别为90 5 %、81 8%、6 0 0 %和 37 6 % (χ2 =36 1 31,P <0 0 0 1)。从发病时起 ,AD、VD、OD的 5 0 %生存率时间分别为 7 0年、4 2年、10 3年。结论　痴呆患者死亡率高 ,可疑痴呆者次之 ,正常人最低 ;而生存率则相反。VD患者的死亡率高于AD和OD患者且存活期短。     

强迫症、抑郁症及焦虑症患者血小板5-羟色胺浓度的对照研究

目的　研究 5 羟色胺 ( 5 HT)在强迫症发病中的作用及强迫思维与强迫动作亚组、抑郁症及焦虑症患者间血小板 5 HT含量的差异。方法　采用高效液相色谱法 ,分别测定 2 9例强迫症患者 [(强迫症组 ,根据Y BOCS强迫量表因子得分将其分为强迫思维 ( 16例 )、强迫动作 ( 7例 )和混合性( 6例 ) 3组 ]、2 0例抑郁障碍患者 (抑郁症组 )、17例焦虑障碍患者 (焦虑症组 )和 2 8名正常人 (正常人组 )的血小板 5 HT含量。结果　强迫症组血小板 5 HT水平 [( 139± 172 ) μg/L]低于正常人组 [( 2 4 8±2 15 ) μg/L]及焦虑症组 [( 397± 4 0 1) μg/L],差异具有显著性 (P =0 0 39;P =0 0 2 0 ) ;与抑郁症组 [( 2 0 2± 16 2 ) μg/L]的差异无显著性 ( P >0 0 5 ) ;强迫思维 [( 85± 6 6 ) μg/L]与强迫动作组 [( 16 9± 10 0 ) μg/L]间血小板 5 HT含量的差异有显著性 (P =0 0 2 5 )。结论　强迫症患者 5 HT浓度变化与抑郁障碍患者趋同 ,与焦虑障碍患者的差异有显著性 ;单纯强迫思维者的 5 HT浓度与单纯强迫动作患者的差异有显著性     

帕金森病患者基础PRL水平与并发痴呆及抑郁关系的研究

目的探讨帕金森病(PD)患者基础血浆泌乳素(prolactin,PRL)水平及与PD伴随的痴呆及抑郁的关系。方法测定167名在我院体检的正常老人(正常对照组)及113例PD患者(PD组)基础血浆PRL水平,并采用汉密顿抑郁量表(HAMD)、简明智能状况评价量表(MMSE)把PD患者分别划为痴呆组和非痴呆组及伴发抑郁组和非抑郁组,同时筛选同期我科收治的阿尔茨海默病(AD)患者20例及心理门诊治疗的功能性抑郁症患者50例(功能性抑郁组)。分别比较各组的PRL水平。结果PD组者的基础血浆PRL平均水平为(9.44±4.07)μg/L,与正常对照组[(9.76±3.97)μg/L]比较无统计学差异;PD伴发抑郁组平均PRL水平为(8.75±4.12)μg/L,与PD非抑郁组[(10.52±3.97)μg/L]、功能性抑郁组[(9.52±5.17)μg/L]比较均无统计学差异;PD伴发痴呆组平均PRL水平为[(5.26±4.90)μg/L],明显低于PD非痴呆组[(10.19±5.19)μg/L]及AD组[(7.85±4.25)μg/L]。结论PD患者出现痴呆时其基础血浆PRL水平降低。PD患者可能有DA、Ach、5HT能神经递质平衡的紊乱。     

精神分裂症患者与其健康同胞的注意和执行功能障碍的对照研究

目的　探讨精神分裂症患者及其健康同胞的注意、工作记忆 /执行功能的特点。方法对 5 0例精神分裂症患者 (患者组 )及其健康同胞 5 0名 (同胞组 ) ,以及 4 5名正常对照者 (正常对照组 )采用威斯康星卡片分类测验 (WCST)和持续操作测验 (CPT) ,评估注意、工作记忆 /执行功能。结果　(1)在WCST中 ,患者组及其同胞组的总测验次数 (分别为 83 4± 2 3 2和 74 1± 2 4 6 )、持续错误数 (分别为 2 5 8± 11 7和 2 2 8± 10 7)、随机错误数 (33 4± 19 2和 2 5 9± 17 1)均高于正常对照组 (分别为6 0 0± 2 1 6、14 8± 8 3和 18 1± 16 0 ;P <0 0 1)。 (2 )在CPT中 ,患者组的评分 [(2 8 4± 4 0 )分 ]低于同胞组 [(30 4± 2 3)分 ]和正常对照组 [(30 9± 2 8)分 ],而同胞组与正常对照组的差异无显著性(P >0 0 5 )。(3)患者组及其同胞组发生执行功能障碍 (分别为 2 9例和 2 5例 )和注意缺陷 (分别为 2 2例和 7例 )的例数均多于正常对照组 (分别为 9例和 4例 ;P <0 0 1) ,其中有工作记忆 /执行功能缺陷的精神分裂症患者 ,其同胞出现这一缺陷的比率 (6 6 % )高于无缺陷的精神分裂症患者的同胞 (2 8% )。(4)WCST中的持续错误数与文化程度呈负相关 (r =- 0 32 ,P <0 0 1) ,CPT与性别 (r=- 0 2     

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.