首发与慢性精神分裂症患者的P50感觉门控特征

目的:探究首发与慢性精神分裂症患者P50感觉门控特征的差异。方法:招募门诊与住院的首发精神分裂症患者97例,慢性精神分裂症患者197例,正常对照253例。采用听觉配对刺激条件-测试范式对所有受试者进行P50指标测量。将S2波幅与S1波幅的比值作为主要结局指标。结果:首发精神分裂症组S1潜伏期、S2潜伏期均高于慢性精神分裂症组与正常对照组(均P<0.001)。首发精神分裂症组和正常对照组S1波幅与S2波幅比值低于慢性精神分裂症组[0.4(-0.4,1.7),0.4(-0.7,2.0) vs.0.6(-2.3,4.0),均P<0.05]。慢性精神分裂症组S1波幅与S2波幅差值小于首发精神分裂症组和正常对照组[1.2(-3.9,9.2)μV vs.1.7(-1.0,6.7)μV,1.9(-2.3,8.9)μV,均P<0.01]。结论:慢性精神分裂症患者P50感觉门控功能缺陷可能较首发患者严重,首发精神分裂症患者S1潜伏期、S2潜伏期延长可能为感觉门控功能的代偿表现。     

托烷司琼对慢性精神分裂症患者言语功能和听感觉门控P50作用的初步研究

选择性α7尼古丁受体激动剂DMXB-A(3-2,4-dimethoxybenzylidene anabaseine)能使听感觉门控正常化,改善认知功能[1]。感觉门控是大脑对各种感觉刺激信息的选择和过滤过程,精神分裂症患者感觉门控缺损,大脑受大量无关刺激信息超载致认知功能障碍。     

稳定期慢性精神分裂症患者听觉感觉门控诱发电位P50特点

目的:探讨慢性精神分裂症患者稳定期感觉门控指标P50的特点。方法:选取137例符合美国精神障碍诊断与统计手册第4版(DSM-IV)诊断标准的稳定期慢性精神分裂症住院患者(患者组)和153例年龄匹配的健康成年人(对照组),采用条件-测试刺激模式记录脑电信号并进行离线分析,测量P50的波幅和潜伏期进行统计分析。同时使用阳性和阴性症状量表(PANSS)评定患者的临床症状。结果:患者组S1波幅(S1V)低于对照组,S1潜伏期(S1L)比对照组延长;患者组S2-P50与S1-P50波幅的比值(S2/S1)高于对照组,患者组S1-P50与S2-P50波幅差(S1-S2)以及100(1-S2/S1)低于对照组(P<0.05)。患者组PANSS评分、病程、服用药物剂量和P50各项指标无相关性(r=-0.15~0.13,P>0.05),精神分裂症不同临床亚型(偏执型和非偏执型)之间P50各项指标差异无统计学意义(均P>0.05)。结论:慢性精神分裂症患者稳定期存在P50抑制功能减弱,与临床症状和疾病分型无明显相关。     

感觉门控P50的研究进展

感觉门控 (ｓｅｎｓｏｒｙｇａｔｉｎｇ)是大脑一种正常功能 ,指大脑能抑制无关的感觉刺激输入。广义的解释为大脑对传入感觉刺激敏感性的调节能力[1] 。此过程通过滤掉无关刺激使大脑更高级的功能不被感觉刺激所超载。感觉门控的缺损能导致无关刺激超载 ,大脑受到大量无关刺激的超载可导致与注意有关的各种精神症状[2 ] 。感觉门控是一个多时相操作活动 ,常用诱发电位范式来测量。听觉诱发电位Ｐ5 0是最常用的一种。Ｐ5 0属于一种中潜伏期诱发电位 ,是出现在听觉刺激后 30～ 90ｍｓ间的一个正相波。当给予受试者较短刺激间隔的重复刺激时 ,…     

利培酮与氯氮平治疗难治性精神分裂症对照研究

目的：观察利培酮与氯氮平对难治性精神分裂症的治疗效果及安全性。方法：分别采用口服利培酮和氯氮平治疗难治性分裂症各40例，疗程8周，以PANSS治疗前后的分值变化评定疗效，并用TESS量表观察药物的副作用。结果：利培酮对难治性精神分裂症的显效率为27．5％，总有效率为72．5％，与氯氮平治疗效果相当，但副作用较少。结论：利培酮与氯氮平对难治性精神分裂症疗效相近、副作用少，治疗依从性高，为安全、有效的一线抗精神病药物。     

利培酮合并氯氮平治疗难治性精神分裂症的对照研究

目的　探讨利培酮合并氯氮平治疗难治性精神分裂症的疗效及副作用。方法　将本院 98例难治性精神分裂症患者按病期病型配对分成氯氮平组 (A组 )和利培酮组 (B组 )及 2药联用组 (AB组 ) ,用 PANSS及 TESS评定疗效及副作用。结果　 3组 8周疗效相似 ,有效率 A组为 61 .8% ,B组为 60 % ,AB组为 62 .5 % ,(P>0 .0 5 )。治疗 4周时 AB组疗效较单用组佳。A组、AB组对阳性症状起效较快。AB组副作用比单用组少。结论　适宜剂量的利培酮与氯氮平联用治疗难治性精神分裂症安全有效 ,副作用少。利培酮与氯氮平治疗难治性精神分裂症的起效时间较以往报告的要早     

利培酮治疗精神分裂症的脑电图观察

利培酮 (Risperidome) ,商品名维思通 ,是一种新型的非经典抗精神病药物 ,属苯丙异恶唑衍生物 ,对 5—HT等受体均有较强的拮抗作用[1] 。国外自 1986年首次临床应用于治疗精神分裂症以来 ,该药以其显著的疗效、安全性、良好的耐受性而受到广泛的关注。本研究目的在于采用利培酮治疗的一组国内精神分裂症患者 ,对该药是否引起脑电图 (EEG)改变情况作一评价。1　资料与方法入组标准 :①本文精神分裂症病人均符合中国精神疾病分类方案与诊断标准 (CCMD— 2R) [2 ] ;②年龄 :14～ 70岁 ,平均年龄 31岁 ;③排除患有严重躯体性疾病、脑器质性…     

利培酮合并米氮平治疗精神分裂症阴性症状

抗精神病药联合抗抑郁药治疗精神分裂症阴性症状疗效肯定[2,4],但联合作用机制不同的抗抑郁药时,其疗效和安全性如何,国内尚未见报道。本研究对利培酮单用、合用米氮平或帕罗西汀的疗效和安全性进行了比较。1对象与方法1.1对象从2005年10月至2006年11月共收集绍兴市第七人民医院以阴性症状为主的精神分裂症住院患者120例。入组标准:符合ICD-10精神分裂症诊断标准,阳性和阴性综合征量表(PANSS)总分≥60分,阴性因子分≥30分。排除标准:抑郁症、分裂症后抑郁、分裂情感性精神障碍患者,严重躯体疾病、脑器质性疾病、癫痫、物质滥用患者,妊娠…     

奎硫平、利培酮对首发精神分裂症患者认知功能及P300的影响

目的:比较利培酮和奎硫平对首发精神分裂症患者认知功能的影响。方法:采用随机对照研究连续观察12周,利培酮组32例,剂量范围为1～7mg/d,奎硫平组35例,剂量范围25～750mg/d。进行PANSS、韦氏记忆量表(WMS)和事件相关电位P_(300)检查。结果:首发精神分裂症患者的长时记忆、短时记忆、瞬时记忆及记忆商数(MQ)受损较为明显,与对照组比较差异有显著性(P<0.05)。P_(300)电位成分中P_2、N_2及P_3潜伏期明显延长,P_2及P_3波幅明显降低,与对照组比差异均有显著性(P<0.05)。经过12周治疗,奎硫平和利培酮组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,两组相比差异无显著性(P>0.05),说明两药的疗效相当。服用奎硫平及利培酮治疗的患者WMS 的再认、联想、理解及记忆商(MQ)均明显高于治疗前,治疗后两组患者WMS 各项目之间比较差异均无显著性(P>0.05);两组在治疗前后P_(300)各指标之间差异无显著性。结论:首发精神分裂症患者存在着认知功能障碍,奎硫平与利培酮对改善首发精神分裂症认知功能的作用相当。     

利培酮合并舒必利治疗精神分裂症阴性症状疗效观察

目的探讨利培酮合并舒必利治疗精神分裂症阴性症状的临床疗效及安全性。方法用利培酮合并舒必利治疗以阴性症状为主的精神分裂症60例,采用阳性与阴性症状量表(PANSS)、阴性症状评定量表(SANS)和副反应量表(TESS)评定疗效和不良反应,疗程6周。结果治疗6周,阴性症状的有效率为81.7%。结论利培酮合并舒必利治疗以阴性症状为主的精神分裂症疗效确切,不良反应少。     

Reliability of P50 auditory event-related potential indices of sensory gating

We examined the reliability of three traditional P50 auditory event-related potential indices under paired-click conditions: (a) the conditioning response (C), (b) the testing response (T), and (c) the testing to conditioning suppression ratio (T/C). Three alternative indices, (a) the (C?T) difference, (b) the (C?T)/(C+T) adjusted difference, and (c) the (T?T) residualized difference, where T′ is the regression of T on C, were also studied. The N 100 wave was used as a generalizability check. Although C and T amplitudes were reliably were reliably measured by traditional means, the T/C suppression ratio was not. for psychometric reasons that are described, the reliability of the suppression ratio is undermined principally by the correlation between C and T. The C?T difference score is a promising alternative to the unreliable T/C suppression ratio. Theoretical consequences of changed metrics are discussed.     

Effects of risperidone on auditory information processing in neuroleptic-naive patients with schizophrenia spectrum disorders

Early effects of risperidone (2.5 +/- 1 mg/day) on auditory information processing were investigated in 9 neuroleptic naive patients with schizophrenia spectrum disorders and 9 healthy controls by using event-related potentials (ERPs). ERPs were elicited during active auditory "oddball" paradigm and were recorded before and after two weeks of treatment. Baseline P3 latencies were significantly delayed in patient group. Risperidone treatment did not change P3 amplitudes and latencies. However, P2 amplitudes were reduced in parallel with the clinical improvement measured by Positive and Negative Syndrome Scale (PANSS). Although risperidone did not change neural bases of active attention after two weeks of treatment, the reduction of P2 amplitude suggests that risperidone may affect auditory information processing in patients with schizophrenia spectrum disorders who never have been exposed to antipsychotic treatment.     

Distinct M50 and M100 auditory gating deficits in schizophrenia

The time course of the schizophrenia auditory gating deficit may provide clues to mechanisms of impaired cognition. Magnetoencephalography was recorded during a standard paired-click paradigm. Using source strength of the M50 and M100 components for each click, calculated from dipole locations identified as underlying each component for the first click, a ratio of the second divided by the first was used to measure gating. Patients showed a left-hemisphere gating deficit in M50 and a bilateral gating deficit in M100. Hypothesizing that an early deficit may affect later processing, hierarchical regression was used to examine variance shared between the components. A left-hemisphere M100 gating deficit was coupled with the left M50 gating deficit. In contrast, a right-hemisphere M100 gating deficit was unrelated to M50 gating in either hemisphere. Investigations of interhemisphere gating relations may clarify group differences in regional connectivity and their role in gating.     

52位正常人听觉P50诱发电位结果分析

目的 :探讨正常人听觉P5 0诱发电位特征。方法 :采用条件 (C) 试验 (T)刺激模式记录5 2位正常人的听觉P5 0诱发电位 ,分别对不同性别、不同年龄组之间P5 0的差异进行组间比较分析。结果 :①P5 0波峰潜伏期为 5 7 9± 7 6ms ,C P5 0与T P5 0潜伏期差为 3 1± 2 5ms。②T P5 0波幅较C P5 0波幅显著降低 ,试验 /条件 (T/C)率为 5 8 9± 12 7%。③女性组P5 0波幅较男性组显著升高 (P <0 0 5 ) ,潜伏期和T/C率均无差异 ;年龄组比较P5 0诸成分均无显著性差异。结论 :听觉P5 0诱发电位是一种具有抑制特征的电位活动。T/C率不受性别、年龄的影响 ,其变化可以反映大脑正常感觉门控的机能状态     

Effects of attentional and stressor manipulations on the P50 gating response

The decline in amplitude of the P50 component of the event-related potential to the second of paired clicks has been suggested as a measure of preattentional gating. Two experiments were conducted to assess the effects of attention and .a psychological stressor on P50. Experiment 1 included two choice reaction time tasks designed to direct attention selectively to the first or second click in each pair. Results suggest that the NIOO component was responsive to attentional manipulations, whereas P50 was not affected. Experiment 2 examined the impact of a brief psychological stressor on the P50 response Parallel mental arithmetic tasks were administered silently and orally. Self-report and measures of autonomic activity were used to assess the level of stress occurring during the performance of the mental arithmetic tasks Results indicate that P50 suppression was sensitive to the acute stressor, the oral mental arithmetic task Implications of these findings for studies ofP50 suppression in schizophrenia are discussed.     

The sleep state-dependent midlatency auditory evoked P50 potential in various disorders

The P50 potential is a midlatency auditory evoked response which is sleep state-dependent, habituates rapidly and is blocked by the muscarinic cholinergic antagonist scopolamine. It is thought to be generated, at least in part, by ascending projections of the reticular activating system. The amplitude of the P50 potential can be used as a measure of level of arousal, while the degree of habituation to repetitive stimulation can be used as a measure of sensory gating. We studied these processes in three conditions which show sleep-wake cycle dysregulation and attentional disturbance, but differ greatly in their etiology, depression, Huntington’s disease and rotation-induced motion sickness. Subjects with depression and rotation-induced motion sickness showed significant decreases in the habituation of the second of paired evoked responses, while Huntington’s disease subjects showed decreased amplitude as well as decreases in the habituation of the second P50 potential. This waveform may represent the manifestation of pre-attentional processes, and may become a useful measure for monitoring the severity, progression and/or remission of disorders which affect these processes.     

正常成人听觉诱发电位P50的年龄和性别差异

目的:研究正常人听觉诱发电位P50特征以及年龄、性别因素的影响。方法:从北京回龙观医院职工以及附近小区居民中选取153例健康被试,按年龄分为两组,年龄1组(50岁)86人(男40人,女46人),年龄2组(≥50岁)67人(男26人,女41人)。使用脑电生理记录仪,采用条件刺激(S1)-测试刺激(S2)模式进行听觉诱发电位P50检测。结果:(1)年龄2组S2波幅高于年龄1组,但仅两组女性被试间的差异具有统计学意义[(2.44±1.68)μV vs.(1.15±1.09)μV,P0.01]。(2)年龄2组S1-S2值小于年龄1组,但仅两组男性被试间的差异具有统计学意义[(1.80±0.94)μV vs.(2.73±1.93)μV,P0.05]。(3)年龄2组门控比(S2/S1)高于年龄1组,两组女性被试间差异具有统计学意义[(58.17±42.06)vs.(31.52±31.60),P0.01],两组男性被试间有类似趋势[(41.00±31.88)vs.(25.78±36.28),P=0.09]。(4)方差分析显示,年龄和性别对S2波幅均有显著效应(P0.01),且存在交互作用(P0.05),年龄对门控比(S2/S1)有显著效应(P0.01);(5)相关分析显示,女性被试年龄与门控比呈正相关(r=0.30,P0.01),男性被试年龄与门控比无统计学意义相关(P0.05)。结论:正常人听觉诱发电位P50指标存在性别和年龄差别,50岁以上可能存在听觉门控功能减弱,尤以女性为著。     

Effects of nicotine on the amplitude and gating of the auditory P50 and its influence by dopamine D2 receptor gene polymorphism

Evidence of normalized auditory P50 suppression with acute nicotine in schizophrenia has supported the contention that elevated smoking rates in this disorder may be an attempt to correct a nicotinic receptor pathophysiology that may underly impaired sensory gating in these patients. There is very little information regarding the neurochemical or genetic pathways through which nicotine regulates P50 amplitude and its suppression in human studies. In a randomized, double-blind, placebo-controlled design with 24 non-smokers, this study examined the influence of TaqIA dopamine D2 receptor gene polymorphisms on P50 and its inhibition during nicotine gum (6 mg) administration. Within a paired click (S₁-S₂) paradigm, placebo treated A1⁺ and A1⁻ allele groups differed with respect to P50 amplitude and gating. While nicotine (relative to placebo) attenuated S₁ P50 amplitude in A1⁺ allele carriers, in the A1⁻ carriers it increased S₂ P50 amplitude and increased P50 gating as indexed by an augmented gating difference wave (GDW). These findings suggest that nicotine exerts mixed gating properties in healthy nicotine naive volunteers and that dopamine functions to alter both P50 and its gating as well as their response to acute nicotine agonist treatment.     

Attentional influence on the P50 component of the auditory event-related brain potential.

To determine if attentional factors influence the suppression of the auditory P50 in a conditioning-testing paradigm, known as the 'sensory gating' effect, we tested 10 healthy young adults in four experimental conditions. The first condition was the traditional passive conditioning-testing paradigm in which a pair of identical auditory clicks is administered at an interstimulus interval fixed at 500 ms. The effect of interest is a reduction of P50 amplitude in response to the second stimulus. In the next condition, the second stimulus could be one of two possible frequencies and subjects were required to count one and to ignore the other. The third and fourth experimental conditions involved a motor response. In the third condition, subjects were required to make a unimanual button press to the occurrence of the second stimulus. In the fourth condition, subjects were required to discriminate among two possible second stimuli, and make a unimanual button press to the occurrence of the designated stimulus. Subjects also completed four matched blocks of single stimulus (i.e., unpaired) presentations to provide a baseline for assessing the effect of the warning stimulus on the evoked response. We found, in agreement with previous results, that passive exposure to the paired stimuli produced a suppression of P50 amplitude to the second stimulus. However, we also found that suppression of P50 amplitude was not evident when subjects selectively counted the designated stimuli, and was reduced in magnitude when a simple motor response was required and when a selective motor response was based on stimulus discrimination. In addition, we observed that the amplitude of the P50 was larger with unpaired single stimuli than it was either with the first or second stimulus of a pair, regardless of processing demands. Furthermore, variations in processing demands did not affect P50 amplitude when a single stimulus was presented. This pattern of results suggests that the 'sensory gating' effect is not a simple 'hard-wired' inhibitory phenomenon. Rather, it may be one manifestation of an attention regulation process that is activated by a warning stimulus and has either inhibitory or excitatory effects on neural transmission, determined by variations in processing demands. Presentation of a warning stimulus may have an additional, unselective suppressing effect, operating independently of this attention regulating process.