抑郁障碍的无抽搐电休克疗法前后非匹配负波研究

目的 探讨焦虑障碍听觉认知性电位P300的特点.方法 对32例焦虑障碍患者(AN组)和30名健康成年人(NC组),应用美国脑诱发电位仪进行P300检测.结果 与NC组相比,AN组Oz点P3潜伏期后移[NC组(328±16)ms,AN组(340±18)ms,t=2.801,P<0.01],P3波幅降低[NC组(6.1±2.0)μV,AN组(4.6±2.2)μV,t=2.84,P<0.05],非靶P2波幅降低[NC组(3.1±0.8)μV,AN组 (1.9±0.9)μV,t=5.61,P<0.01].结论 焦虑障碍认知性电位P300变化诸特点值得进一步随访.     

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。     

注意缺陷多动障碍患儿的P300检测

目的 探讨注意缺陷多动障碍(ADHD)患儿事件相关电位P 300指标及其治疗前后的特点.方法 应用美国Nicolet Spirit脑诱发电位仪,记录36例ADHD患儿和32名正常儿童(NC组)的P 300,对其中33例ADHD患儿于治疗6个月后再次检测P 300.结果 (1)ADHD组P 300-N2和P3靶潜伏期长于NC组,P 300-P3靶波幅低于NC组(P<0.01).(2)利太林治疗后,ADHD组随多动症状改善,脑诱发电位中P 300-N2靶潜伏期缩短[治疗前后分别为(273±20)ms和(260±17)ms,P<0.01],P3靶波幅升高[分别为(2.9±1.9)μV和(4.6±2.0)μV,P<0.01].结论 ADHD患儿P 300有变化,治疗后随着多动症状的改善,与认知功能有关的P 300指标也有相应改善.     

神经性厌食的事件相关电位P300的实验研究

目的研究神经性厌食（AN）患者的事件相关电位P300特点。方法应用Nicolet Bravo脑电生理仪,采用纯音＂Oddball＂刺激诱发模式,对43例AN患者和34名健康对照进行认知性电位P300检测。结果 AN组P300中靶P3的潜伏期[（297.8±29.3）ms]长于健康对照组[（285.6±19.7）ms],差异有统计学意义（t=2.19,P=0.03）;AN组靶P3波幅为（6.5±3.4）μV,低于健康对照组（9.8±3.2）μV,差异有统计学意义（t=4.33,P〈0.01）。2组的靶P2、靶N2及非靶P2的潜伏期、波幅均无统计学差异。结论 AN患者的P300靶P3潜伏期延长、波幅降低。     

焦虑障碍患者的多导睡眠图研究

目的探讨建立焦虑障碍(AN)的多导睡眠图(PSG)模式。方法应用日本1518K多导睡眠生理仪,采用眼电图和下颌肌电图及脑电图技术,对25例AN患者和33名正常对照者(NC)进行PSG整夜监测。结果与NC组比较,AN组PSG主要有:REM睡眠潜伏期前移[NC组(87.8±11.7)分,AN组(59.9±19.7)分,P<0.01],醒觉时间增加[NC组(17.7±6.4)分,AN组(36.9±11.9)分,P<0.01],睡眠潜伏期延迟[NC组(19.9±9.8)分,AN组(37.7±16.7)分,P<0.01],睡眠效率下降[NC组(94.6±5.1)%,AN组(90.5±5.7)%,P<0.05],第1阶段睡眠[NC组(9.1±1.9)%,AN组(19.7±10.9)%,P<0.01]增高,第2阶段睡眠[NC组(56.2±4.7)%,AN组(47.7±22.3)%,P<0.05]降低。结论焦虑障碍患者有REM睡眠潜伏期前移、慢波睡眠S2降低等多项睡眠脑电指标的异常,应与神经生化结合进一步追踪研究。     

抑郁障碍的P300及非匹配负波实验研究

目的 建立非匹配负波(MMN)并探讨抑郁障碍的特点.方法 应用美国Nicolet Bravo脑诱发电位仪,对35例抑郁障碍和32名正常成人进行了P300和MMN检测.结果 与正常对照组相比,抑郁障碍MMN潜伏期延迟(正常组:(190±21)ms,抑郁障碍(267±27)ms,t=12.94,P<0.01),同时波幅降低(正常组(8.3±1.4)μV,抑郁障碍组(5.1±2.0)μV,t=7.52, P<0.01).结论 非匹配负波新技术可反映抑抑郁障碍及其他精神障碍诱发脑电波的自动加工过程,可推广于临床应用.     

躯体形式障碍患者认知功能的事件相关电位P300研究

目的 探讨躯体形式障碍患者认知功能的事件相关电位P300特征.方法 随机将年龄在18～65岁之间符合CCMD-3躯体形式障碍诊断标准患者30例作为实验组,选择30例性别年龄相匹配的健康者作为对照组.各组分别予听觉P300检测,比较P300潜伏期及波幅的差异.结果 实验组PZ点潜伏期[(308±21)ms],均比对照组[(298±22)ms]延长,实验组FZ、CZ、PZ、OZ点[分别为(2.4±1.6)μV、(2.6±2.3)μV、(2.6±3.3)μV、(2.4±1.9)μV]波幅比对照组[分别为(3.9±2.1)μV、(3.8±1.9)μV、(4.2±3.4)μV、(3.7±2.0)μV]降低(P<0.05及0.01).结论 躯体形式障碍患者存在认知功能障碍.     

注意缺陷多动障碍患儿哌甲酯治疗前后的脑诱发电位研究

目的 探讨注意缺陷多动障碍(ADHD)患儿4种脑诱发电位指标及其治疗前后的特点.方法 应用美国Nicolet Spirit脑诱发电位仪,记录37例ADHD患儿(ADHD组)和30名正常儿童(正常对照组)的事件相关电位P300、失配性负波(MMN)、关联性负变(CNV)和脑干听觉反应(ABR),对其中31例ADHD患儿于哌甲酯(10～15 mg口服)治疗4个月后再次检测.结果 (1)与正常对照组比较,ADHD组P300-N2靶潜伏期长,P300-P3靶波幅低;ABR-波Ⅲ绝对潜伏期短,绝对波幅波V低;MMN潜伏期长,波幅高;CNV-M2波幅低,反应时间(RT)长;差异均有统计学意义(P＜0.05～0.01).(2)哌甲酯治疗4个月后,ADHD组随多动症状改善,P300-N2靶潜伏期缩短[治疗前后分别为(278±18)ms和(261±16)ms,P＜0.01],P3靶波幅升高[分别为(2.8±1.8)μV和(4.2±1.9)μV,P＜0.05];MMN潜伏期缩短[分别为(208±24)ms和(193±24)ms,P＜0.05];CNV-M1波幅升高[分别为(10.3±5.0)μV和(14.3±4.1)μV,P＜0.01];RT缩短[分别为(478±158)ms和(349±144)ms,P＜0.01],但ABR治疗前后的差异无统计学意义(P＞0.05).结论 ADHD患儿的P300,MMN,CNV和ABR 4种脑电诱发电位较正常对照组均有改变;治疗后随多动症状的改善,与认知功能有关的P300,MMN和CNV 3项指标亦有相应的改善.     

抑郁症的事件相关脑电位P300实验研究

目的探讨抑郁症听觉事件相关电位P300的变化特点。方法对35例抑郁症患者和31名健康成年人，应用美国NieoletBravo脑诱发电位仪进行P300检测。结果与正常组相比，抑郁症组Oz点P3潜伏期延迟[正常组（315±29）ms，抑郁症组（341±31）ms，t=3．50，P〈0．01]，P2潜伏期延迟[正常组（165±19）ms，抑郁症组（175±21）ms，t=2．02，P〈0．05]，P3波幅降低[正常组（9．5±6．1）μV，抑郁症组（4．5±3．1）μV，t=4．27，P〈0．01]，非靶P2波幅降低[正常组（4．2±1．2）μV，抑郁症组（2．3±1．3）μV，t=6．14，P〈0．01]。结论P300是评定抑郁症患者大脑综合功能的有效工具，在临床上值得进一步推广应用。     

事件相关电位P300在颅脑损伤患者认知功能障碍评定中的应用

目的 探讨事件相关电位P300在颅脑损伤患者认知功能障碍评定中的应用价值。方法 选取2021年1月-9月在绵阳市第三人民医院神经外科保守治疗、并符合诊断标准的颅脑损伤患者36例作为研究组,同期在医院其他患者家属和护工中招募健康对照组共36名。采用Oddball范式对受试者进行事件相关电位P300检测,采用蒙特利尔认知评估量表（MoCA）和简易精神状态评价量表（MMSE）评定受试者的认知功能。比较两组P300的潜伏期、波幅以及MoCA和MMSE评分,比较P300潜伏期、MoCA和MMSE对颅脑损伤患者认知功能障碍的检出率。结果 研究组MoCA和MMSE评分均低于对照组[（18.08±4.29）分vs.(27.36±1.20)分,（22.53±3.54）分vs.(28.11±1.09)分,t=-12.510、-9.041,P均<0.05];研究组P300潜伏期高于对照组[（406.08±26.95）ms vs.(367.08±22.50)ms,t=6.665,P<0.05],波幅低于对照组[（7.76±0.90）μV vs.(9.87±0.99)μV,t=-9.459,P<...     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.