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。     

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。     

老年期抑郁症抗抑郁药物治疗前后感觉门控P50改变

目的 探讨老年期抑郁症的感觉门控(Sensory Gating,SG)P50特征及其在抗抑郁治疗后的变化.方法 采用条件刺激(S1)-测试刺激(S2)模式对38例老年期(发病年龄＞60岁)抑郁症患者和正常对照组的42名健康老人进行P50检测,前者在给予帕罗西汀20mg/d治疗16个月末再次检测.使用17项汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD17)评估患者治疗前后的抑郁症状.结果 与正常对照组比较,患者组S2-P50波幅增高[(2.89±1.02)μV vs (1.30±1.07) μV,P<0.01)],潜伏期延迟[ (64.14±14.69) ms vs (55.92±17.73) ms,P<0.05) ],提示P50抑制明显减弱;与治疗前相比,患者组在治疗16个月末的所有P50指标均无明显改变(P>0.05).治疗前后感觉门控P50指标S2/S1、S1-S2和100(1-S2/S1)与HAMD17分值无相关(P>0.05).结论 老年期抑郁症患者感觉门控抑制存在明显缺损,具有跨状态稳定性,可能为素质性.     

惊跳反射弱刺激抑制及P50在精神分裂症中的应用

目的 探讨精神分裂症患者的惊跳反射弱刺激抑制(PPI)的特点.方法 应用美国Nicolet Bravo脑电生理仪,采用听觉感觉刺激模式对30例精神分裂症患者和28名正常人做听觉PPI及P50检测.结果 病例组PPI低于正常对照组;病例组的S1-P50降低、S2-P50增高、P50抑制明显减弱、S1-S2和100 (1-S2/S1)均下降.结论 精神分裂症患者存在感觉运动门控缺陷,PPI可作为一项实验室指标用于临床.     

感觉门控P50对精神分裂症诊断价值的初步探讨

目的探讨听觉感觉门控电位P50对精神分裂症的诊断价值。方法共入组56例患者（患者组）和22名正常对照（对照组）。患者符合美国精神障碍诊断与统计手册第4版（DSM-IV）的精神分裂症诊断标准。采用听觉条件（S1）-测试刺激（S2）范式检测P50电位,计算S2与S1波幅的比值即P50比值。使用阳性与阴性综合征量表（PANSS）评定患者的精神症状。结果患者组P50比值（89.7±57.1）高于对照组（47.2±26.4）,差异有统计学意义（t=2.97,P〈0.01）。患者组P50比值与PANSS总分和病程之间无相关性（r值分别为0.123、0.119）。P50比值的ROC曲线下面积（AUC）=0.743。以34为临界值,灵敏度和特异度分别为96.4%和45.5%;以50为临界值,灵敏度和特异度分别为80.4%和50.0%。结论精神分裂症患者存在感觉门控障碍,P50比值与其病情和病程无关,P50比值在精神分裂症有中等诊断价值。     

精神分裂症首次发病患者治疗前后感觉门控功能的动态观察

目的探讨精神分裂症首次发病(以下简称首发)患者治疗前后的听觉诱发电位P50变异的意义。方法应用美国Bravo脑电生理仪,采用条件刺激(S1)-测试刺激(S2)模式,分别于治疗前(66例)、治疗第5周(42例)和第12周(32例)对首发精神分裂症患者(患者组)进行P50检测,同时用阳性和阴性症状量表(PANSS)评定患者的临床症状;并以正常人(对照组,92名)的P50做比较。结果(1)治疗前,患者组的S1-P50波幅[(3±2)μV]低于对照组[(6±3)μV],S2-P50波幅[(4±2)μV]高于对照组[(2±1)μV],均P<0.01;患者组S2/S1比值[(81±40)%]高于对照组[(42±21)%],S1-S2波幅[(2±1)μV]低于对照组[(3±2)μV],100(1-S2/S1)值(19±17)低于对照组(58±21),差异均有统计学意义(P<0.05~0.01)。(2)患者组的S2/S1、S1-S2和100(1-S2/S1)与PANSS评分无相关性(P>0.05)。(3)与治疗前比较,患者组在治疗第5周末及第12周末P50的各项指标均无明显改变(均P>0.05)。结论P50变异可能是精神分裂症患者的早期改变,具有一定的属性标志特性,值得进一步随访研究。     

激励模式对社区精神分裂症患者社会功能的影响

目的 探讨激励模式对社区精神分裂症患者社会功能的影响.方法 400例精神分裂症患者随机分为研究组（200例）和对照组（200例）,研究组患者在药物干预的基础上以激励模式干预2年,对照组患者仅给予药物干预.入组时和入组后每3个月使用阳性和阴性综合征量表（PANSS）评定疾病严重程度,以个人和社会功能量表（PSP）评定社会功能.结果 研究结束时研究组PANSS总分及各分量表评分比入组时显著降低（P＜0.05）,研究组PANSS总分及各分量表评分显著低于对照组（P＜0.05）.与入组时比较,研究结束时研究组PSP总分显著升高,各分量表评分均显著降低（P＜0.05）.研究结束时研究组PSP总分显著高于对照组,各分量表评分显著低于对照组（P＜0.05）.结论 激励模式能够改善社区精神分裂症患者的病情与社会功能.     

首发和慢性精神分裂症急性期患者的感觉门控P50

目的探讨病程对精神分裂症感觉门控抑制缺陷的影响。方法对58名健康志愿者、38例首发精神分裂症急性期患者和36例慢性精神分裂症急性期患者进行感觉门控研究。应用听觉P50抑制评估感觉门控,实验模式为条件刺激（S1）-测试刺激（S2）模式。结果首发患者、慢性患者及对照组的S1波幅分别为（3.7±2.5）μV、（4.5±2.0）μV和（5.8±3.8）μV（F=5.P〈053,.01）,首发患者的S1波幅低于对照组（P〈0.01）;S2波幅分别为（2.8±1.1）μV、（3.5±1.5）μV和（2.1±1.4）μV（F=11.47,P〈0.01）,首发和慢性患者的S2波幅均高于对照组（P分别为0.02,小于0.01）,并且慢性患者的S2波幅高于首发患者（P=0.02）。P50抑制指标在三组之间差异均有统计学意义（P均小于0.01）,首发和慢性患者的S2/S1波幅比均大于对照组（P均小于0.01）,而S1-S2波幅差值和100（1-S2/S1）均低于对照组（P均小于0.01）,但首发患者和慢性患者之间P50抑制指标差异无统计学意义（P均大于0.05）。结论首发精神分裂症和慢性精神分裂症均存在明显的感觉门控P50抑制缺陷,病程对精神分裂症的感觉门控P50抑制缺陷无明显影响。     

首发强迫症感觉门控变异及与临床症状的相关性

目的:了解首发强迫症(OCD)患者的听觉P50变异特点,探讨感觉门控抑制与强迫症状的关系。方法:应用美国Nicolet Bravo脑诱发电位仪,采用听觉条件刺激(S1)-测试刺激(S2)模式对42例OCD患者和46名正常志愿者进行听觉P50检测;应用Yale-Brown强迫量表进行临床症状评定。结果:与正常组相比,强迫症组S2-P50波幅升高(P<0.05),S1-S2和100(1-S2/S1)均降低,差异有统计学意义(P均<0.01)。经Pearson相关分析,Yale-Brown强迫量表评分强迫思维因子分与S2-P50波幅呈正相关(P<0.05),与100(1-S2/S1)呈负相关(P<0.05)。结论:首发强迫症患者的感觉门控变异特点为抑制不足,强迫思维与感觉门控抑制程度有一定的相关性。     

易肇事精神分裂症患者应用程式化技能训练的疗效研究

目的 探讨程式化技能训练对易肇事精神分裂症患者的疗效.方法 将102例易肇事精神分裂症患者随机分为训练组(51例)和对照组(51例).两组患者接受常规药物及康复治疗的同时,仅对训练组进行8周的程式化技能训练.训练结束后对两组均进行半年的随访,并采用阳性和阴性症状量表(PANSS)在入组时、训练结束时、随访第3,6个月时进行评估.结果 与入组时相比,训练组患者训练结束时的PANSS总分、阳性量表分、阴性量表分均显著降低(P＜0.05).训练结束后及随访期,训练组患者的PANSS部分项目评分显著低于对照组患者(P＜0.05).结论 程式化技能训练对易肇事精神分裂症患者的精神症状具有康复作用.     

利培酮单药治疗对精神分裂症患者前脉冲抑制和P50的影响

目的:探讨非典型抗精神病药利培酮单药治疗对首发和慢性精神分裂症患者前脉冲抑制(PPI)和P50的影响.方法:采用事件相关电位检测急性期精神分裂症首发患者(首发组,n=81)和慢性精神分裂症患者(慢性组,n=92)利培酮治疗前及治疗6～8周后PPI和P50各项指标,结果与59名健康对照者(正常对照组)比较.结果:与正常对...     

P50 gating at acute and post-acute phases of first-episode schizophrenia

Deficit in P50 sensory gating has repeatedly been shown in schizophrenia. In order to determine the contribution of trait and/or state features to P50 gating deficit in schizophrenia we evaluated the P50 gating in patients with first-episode schizophrenia (FES) at acute and post-acute phases. Subject groups comprised 16 patients with FES and 24 healthy controls. Patients were tested at the acute phase of the illness and retested at the post-acute phase when their positive symptoms improved. During the testing at the acute phase five patients were neuroleptic-naive and the others were taking atypical antipsychotics which were started recently in order to control the acute excitation. Patients were receiving risperidone, olanzapine or quetiapine treatment at the post-acute phase. P50 gating was impaired in patients at the acute phase compared to controls. However, at the post-acute phase P50 gating was increased compared to the acute phase, reaching to the gating values of controls. P50 gating improvement might be emerged from atypical antipsychotic medication, although this can only be definitively determined by randomized studies including different antipsychotics.     

首发精神分裂症患者及其一级亲属感觉门控P50研究

目的探讨首发精神分裂症患者及其未患病的一级亲属感觉门控电位P50的特征。方法采用条件-测试听觉刺激模式对50例首发精神分裂症患者(患者组)、40名未患病的一级亲属(亲属组)和50名正常人(正常对照组)进行P50检测,比较3组P50各成分之间的差异。结果患者组、亲属组和正常对照组3组之间P50潜伏期比较,差异无统计学意义(P>0.05);患者组和亲属组测试刺激所诱发的P50(S2-P50)波幅(中位数1.69uV和1.39uV)高于正常对照组(0.92uV),而2组条件与测试刺激P50波幅的差值(中位数0.16uV和0.44uV)与P50抑制率(中位数10.23%和19.10%)低于正常对照组(1.32uV与62.29%),差异均有统计学意义(P<0.01);正常对照组内男女性别组间P50各项指标比较差异无统计学意义(P>0.05)。结论精神分裂症患者及其未患病的一级亲属均存在P50感觉门控功能异常,提示P50可能是精神分裂症的遗传素质指标。     

Association of cognitive and P50 suppression deficits in chronic patients with schizophrenia

ObjectiveCognitive deficits are core symptoms of schizophrenia; however, their pathophysiological mechanisms are still unclear. A sensory gating deficit, as reflected by P50 suppression, has been repeatedly shown in schizophrenia patients, which may be associated with cognitive deficits in this disorder. The present study was to examine the relationship between the P50 suppression and cognitive deficits in patients with schizophrenia, which is still under-investigated.MethodWe recruited 38 chronic schizophrenia patients and 32 matched healthy controls, and assessed their cognition with the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and P50 suppression with the electroencephalography system.ResultsThe total and its 4 index scores (all p < 0.05) except for the visuospatial/ constructional index of RBANS were significantly lower in patients compared with healthy controls. However, only the language and attention passed Bonferroni corrections. Patients displayed a significantly higher P50 ratio, higher S2 amplitude, and lower S1 amplitude (all p < 0.05) than healthy controls. Interestingly, only in the patients, the S1 amplitude was associated with both language and attention, and the S2 amplitude with both visuospatial/ constructional and language (all p < 0.05), although all of these significances did not pass the Bonferroni corrections. The P50 ratio was not associated with any of the RBANS scores (all p > 0.05).ConclusionsOur results suggest the P50 suppression deficits in Chinese patients with schizophrenia, which may be associated with cognitive impairments of this illness. Moreover, the amplitude of S1 and the amplitude of S2 may be involved in the different cognitive domain deficits in schizophrenia patients.SignificanceThis study suggests that the P50 components may possibly be effective biomarkers for cognitive deficits in patients with schizophrenia.     

Prepulse inhibition and P50 suppression are both deficient but not correlated in schizophrenia patients.

BACKGROUND: Inhibitory measures such as prepulse inhibition of the acoustic startle reflex (PPI) and event related potential P50 suppression have been widely reported to show deficits in schizophrenia patients. The relationship between PPI and P50 suppression in schizophrenia patients has remained unclear. METHODS: One hundred fifty-six schizophrenia patients and 104 normal comparison subjects (NCS) were tested on PPI and P50 suppression. RESULTS: Eighty-one patients and 70 NCS had valid and scorable data on both PPI and P50 suppression paradigms. As in the larger groups, these cohorts had deficits on both PPI (p < .05) and P50 suppression (p < .05). Analyses revealed a weak, but significant correlation between PPI and P50 suppression in the NCS group (r = .33, p < .05) but not in the patient group (r = .03, ns). CONCLUSIONS: Although PPI and P50 suppression were both reduced in the patients, they were not correlated. This divergence suggests that these gating functions are complementary or redundant levels of "protection" against processes that may lead to cognitive fragmentation.     

Association study of polymorphisms in the alpha 7 nicotinic acetylcholine receptor subunit and catechol-o-methyl transferase genes with sensory gating in first-episode schizophrenia

The purpose of the current study was to explore the association of auditory P50 sensory gating (P50) and prepulse inhibition (PPI) of schizophrenia with polymorphisms in the CHRNA7 and COMT genes. One hundred and fourty patients with schizophrenia participated in this study. They were administered the tests P50 and PPI. Moreover, three single nucleotide polymorphisms (SNPs) (rs2337980, rs1909884 and rs883473) in CHRNA7 and three SNPs (rs4680, rs737865 and rs165599) in COMT were selected to be genotyped by polyacrylamide gel microarray techniques. P50 index showed significant reduction in S2 amplitude between wild-type and mutation groups in the COMT rs4680. S1 amplitude of mutation group in the COMT rs737865 was also lower compared to wild-type group. PPI index revealed a shorter pulse latency of mutation group in the rs4680. The suppression ratio of mutation group was lower in COMT rs165599. Negative findings were shown between comparisons in all the CHRNA7 SNPs. We find that P50 and PPI may be influenced by COMT rs4680 polymorphisms in schizophrenia; more excitingly, we find that P50 might be influenced by COMT rs737865 polymorphisms and PPI may be influenced by COMT rs165599 polymorphisms in schizophrenia, and their mutations are associated with the reduction of the risk of P50 or PPI defects in schizophrenia. Futher studies with a larger number of subjects are needed to verify the present findings.     

Meta-analysis of the P300 and P50 waveforms in schizophrenia

Objective: To determine whether patients with schizophrenia have abnormalities in the P300 and P50 waves and to quantify the magnitude of any differences from controls. Method: We conducted a systematic search for articles published between January 1994 and August 2003 that reported P50 or P300 measures in schizophrenic patients and controls. Metaregression analyses were performed using a random effects model. The pooled standardised effect size (PSES) was calculated as the difference between the means of the two groups divided by the common standard deviation. Results: We identified 46 studies suitable for analysis of P300 measures, including 1443 patients and 1251 controls. There were 20 P50 studies including 421 patients and 401 controls. The PSES for the P300 amplitude was 0.85 (95% CI: 0.65 to 1.05; p<0.001), and for the P300 latency was −0.57 (95% CI: −0.75 to −0.38; p<0.001). The PSES of the P50 ratio was −1.56 (95% CI: −2.05 to −1.06; p<0.001). There were no significant differences between patients and controls in P50 latency. Across-study variations in filters, task difficulty, antipsychotic medication and duration of illness did not influence the PSES significantly. Conclusions: This meta-analysis confirms the existence of ERP deficits in schizophrenia. The magnitude of these deficits is similar to the most robust findings reported in neuroimaging and neuropsychology in schizophrenia.