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。     

卒中后抑郁患者感觉门控P50的变化探讨

目的探讨卒中后抑郁患者的听觉诱发电位P50的变化。方法应用脑电生理仪,采用条件刺激(S1)-试验刺激(S2)双声刺激模式记录听觉P50诱发电位,比较卒中后抑郁患者和正常人听觉P50诱发电位的差异。结果实验组S2-P50波幅显著高于正常组S2-P50波幅(2.09±1.05)(P<0.05);实验组P50抑制减弱,S2/S1比值(0.81±0.35)与正常组(0.37±0.23)比较显著增高(P<0.05);实验组S2-S1波幅的差(1.59±0.71)与正常组(4.85±2.24)比较显著减小(P<0.01)。结论卒中后抑郁患者存在感觉门控P50的异常,感觉门控P50可能成为对于卒中后抑郁评价的一种方法。     

抑郁首次发作患者感觉门控P50的研究

目的研究抑郁首次发作(以下简称首发)患者的感觉门控P50特点。方法对39例符合国际疾病分类第10版抑郁发作诊断标准的首次抑郁发作患者(患者组)采用17项汉密尔顿抑郁量表(HAMD17)评定病情严重程度,并进行感觉门控P50检测,与40名健康志愿者(对照组)进行比较。结果(1)患者组P50测试刺激波(S2-P50)的波幅[(2.30±1.04)μV]低于条件刺激波(S1-P50)波幅[(3.48±1.66)μV],但高于对照组S2-P50波幅[(1.54±1.26)μV;P<0.01];患者组的S2/S1波幅比值[(70±23)%]高于对照组[(42±26)%;P<0.01],而S1-S2波幅绝对差值[(1.19±1.48)μV]却低于对照组[(2.17±2.16)μV;P<0.05];患者组P50抑制度[(29±23)%]也低于对照组[(57±26)%;P<0.01]。(2)经Pearson相关分析,患者组HAMD17量表评分与P50各指标无相关(P>0.05)。结论抑郁症首发患者感觉门控抑制存在明显缺损,不能有效滤过无关信息。     

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。     

30名健康儿童的感觉门控P50研究

目的 应用诱发电位新技术探讨健康儿童感觉门控 (SG) P50特点.方法 应用美国Nicolet脑电生理仪,采用条件刺激(S1)-测试刺激(S2)模式对30名健康儿童进行听觉P50检测.结果 健康儿童Cz脑区S1-P50潜伏期(60.7±11.9)ms,波幅(5.7±3.3)μV;S2-P50潜伏期(65.4±22.0)ms,波幅(2.4±1.3)μV.S2-P50波幅显著低于S1-P50(P<0.01).S2/S1比值为(42.8±21.0)%;S1-S2波幅和100(1-S2/S1)波幅分别为(3.3±2.6)μV和(57.9±21.0)μV.结论 听觉P50电位具有抑制性特征,其变化可反映大脑健康儿童SG的功能状态.     

伴有凶杀行为精神分裂症患者听觉感觉门控P50的随访研究

目的 随访分析伴有凶杀行为的精神分裂症患者听觉感觉门控电位P50的变化.方法 采用条件-测试刺激模式,对25例伴有凶杀行为的精神分裂症患者(患者组)和27名正常对照者(对照组)进行P50检测和比较,经过抗精神病药物治疗3个月后,有11例患者完成了P50随访,同时应用阳性和阴性症状量表(PANSS)评定患者的精神症状.结果 ①与对照组相比,患者组在入组未用药时和随访3个月时的S2-P50波幅均较高(P<0.01),S2/S1比值均较大(P<0.01),S1-S2差值(P<0.05)和100(1-S2/S1)值均较小(P<0.01).患者组P50波幅、潜伏期和P50抑制指标在入组时和3个月时的差异均无统计学意义(P>0.05).②与入组时相比,3个月时患者组PANSS总分、阳性量表分、一般精神病理量表分以及反应缺乏、思维障碍、激活性、偏执、抑郁、攻击等6个症状群得分降低(P<0.05).③患者组在入组时和3个月时S2/S1比值、S1-S2差值和100(1-S2/S1)等P50抑制指标与病程、PANSS各指标均无相关(P>0.05).结论 伴有凶杀行为的精神分裂症患者感觉门控存在异常,且P50抑制指标可能是该人群的素质指标.     

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.     

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。     

焦虑症患者感觉门控的研究

目的 了解焦虑症的听觉诱发电位P50特点.方法 应用美国Nicolet Bravo脑电生理仪,采用听觉条件刺激(S1)-测试刺激(S2)模式对36例焦虑症患者和45名正常人作了听觉P50检测.结果 (1)焦虑症P50抑制明显减弱;S2-P50波幅正常人(2.2±0.9)μV,患者组(2.8±1.8)μV,P<0.05.(2)与正常对照组相比,焦虑症组S1-P50降低(S1-P50正常组(5.2±3.1) μV,患者组(3.9±1.2)μV,P<0.05).(3)P50抑制明显减弱,即S1-S2比值明显降低(正常组3.0±1.9,患者组1.1±2.4,P<0.01).结论 焦虑症的感觉门同样也存在异常,表现为抑制不足,能通过听觉P50进行定量检测.     

典型与非典型抗精神病药对首发精神分裂症P50感觉门控的作用

目的 比较典型与非典型抗精神病药对P50感觉门控的作用.方法 运用条件-测试刺激模式和刺激序列模式两种方法检测61例首发精神分裂症患者(治疗前后)和36名正常对照的P50听觉诱发电位.患者组依治疗情况分为典型抗精神病药(奋乃静,舒必利)治疗组(简称典型组)和非典型抗精神病药(氯氮平、奥氮平、利培酮和喹硫平)治疗组(简称非典型组),比较两组治疗前后P50感觉门控的差异.结果 治疗前,典型组和非典型组条件-测试刺激模式S2-P50波幅、P50抑制和刺激序列模式高频刺激P50波幅、P50抑制指标均差于对照组,差异均有统计学意义(P<0.05).治疗后,典型组条件-测试刺激模式S2-P50波幅、P50抑制指标虽有改善但与治疗前的差异无统计学意义(P>0.05),但刺激序列模式P50波幅、P50抑制明显改善,与治疗前的差异有统计学意义(P<0.05);非典型组两种模式下P50波幅、P50抑制指标均明显改善,与治疗前的差异均有统计学意义(P<0.05).结论 典型抗精神病药能够改善刺激序列模式P50感觉门控功能,但不能改善条件-测试刺激模式P50感觉门控功能;非典型抗精神病药物能同时改善条件-测试刺激模式和刺激序列模式P50感觉门控功能.     

抑郁症的强迫症状及强迫与抑郁关系的研究

自从Ｎｅｉｍａｎ(1980)提出强迫与抑郁为常见的共存症状以来,许多的临床研究表明:强迫症最常见的并发症是焦虑、抑郁,而抑郁症中也常伴有强迫症状[1～3]。目前临床公认的Ｈａｍｉｌｔｏｎ抑郁量表(ＨＡＭＤ)[4]中,强迫症状被列入评定抑郁症状的一项常规内容,可见两者的密切联系。本研究调查了伴强迫症状抑郁症患者的症状学特征,并与不伴强迫症状的抑郁症及强迫症患者进行病例对照分析。现报道如下。1　资料和方法11　病例选择与分组111　伴强迫症状的抑郁症组(以下简称抑郁伴强迫组):收集我院1996年8月至1997年12月入院150例符合中国精神疾…     

强迫症、抑郁症及焦虑症患者事件相关电位的比较研究

目的　探讨强迫症 (OCD)、抑郁症 (CD)及焦虑症 (CA)患者三种事件相关电位 (ERP)的变异。方法　应用美国NicoletSpirit脑诱发电位仪 ,采用光和声成对刺激、反应时间以及听觉靶 非靶刺激序列技术 ,检测 31例OCD、2 0例CD和 17例CA及 2 8名正常人 (NC)的关联性负变 (CNV)、P3 0 0 及失匹性负波 (MMN)。结果　 (1)CNV :M1波幅CD组 [(5± 4 ) μV]和CA组 [(7± 4 ) μV]低于NC组 [(14±6 ) μV]和OCD组 [(16± 6 ) μV ;P <0 0 5和P <0 0 1]。指令信号后负变化的出现率CD组 (6 0 % )、OCD组 (45 % )和CA组 (35 % )均高于NC组 (4% ;P <0 0 1)。 (2 )P3 0 0 :在靶刺激中 ,N2 潜伏期在四组间的差异有非常显著性 (P <0 0 1) ,其中OCD组 [(2 78 9± 2 2 7)ms]和CD组 [(2 77 3± 2 1 8)ms]的潜伏期均长于NC组 [(2 5 9 0± 14 0 )ms],CA组短于CD组和OCD组 (P <0 0 1) ;P3 波幅在四组间的差异亦有非常显著性 (P <0 0 1) ,其中OCD组 [(3 4± 1 5 ) μV]、CD组 [(2 9± 1 3) μV]和CA组 [(3 3± 1 3) μV]均低于NC组 [(5 9± 2 1) μV]。在非靶刺激中 ,CA组P2 波幅低于OCD组和NC组 (P <0 0 5 )。 (3)MMN :OCD组、CD组及NC组之间潜伏期和波幅的差异有显著性和非常显著性 (P <0 0 5和P <0 0 1)。其中OCD     

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。     

伴攻击行为男性青少年的感觉门控功能及情绪特征

目的 分析伴有攻击行为的男性青少年的愤怒情绪特征及听感觉门控电位P50的变化及意义.方法 42例伴攻击行为的男性青少年（研究组）和46例健康对照（对照组）进行听觉诱发电位P50的检测以评估感觉门控功能,应用状态特质愤怒表达问卷-儿童青少年版（STAXI-CA）及Barratt冲动量表第11版（BIS-11）评估男性青少年的愤怒情绪及冲动特征.结果 （1）研究组STAXI-CA中特质愤怒评分明显高于对照组（P＜0.01）.研究组的躯体语言愤怒、易怒性情、愤怒反应、外显愤怒表达因子评分高于对照组（P＜0.05）,而内隐愤怒表达因子评分低于对照组（P＜0.01）.（2）研究组BIS-11中的运动因子、认知复杂性因子、缺少计划因子评分和冲动总分高于对照组（P＜0.05,P＜0.01）.（3）与对照组比较,研究组的S1-P50波幅下降、S2-P50波幅增高、S2-P50潜伏期延长、S2/S1增加、S1-S2下降、P50抑制率下降,差异均具有统计学意义（P ＜0.05,P＜0.01）.结论 伴攻击行为的男性青少年存在愤怒及冲动情绪调节缺陷、感觉门控功能缺陷.     

强迫症患者的事件相关脑电位实验研究

背景 强迫症在辅助诊断上目前还缺乏客观的实验室依据。近年来国内外对强迫症的事件相关脑电位进行了研究,结果并不一致。分析其主要原因与所使用仪器、技术性能有关。为此本研究使用国际标准化的美国Nicolet脑电生理仪,并以较成熟的关联性负变、P300及失匹性负波3种事件相关脑电位为手段,并设临床上较多见的抑郁症和广泛性焦虑症为疾病对照,进一步探讨强迫症的脑电生理机制,为临床诊断及治疗提供参考依据。 方法 应用美国Nicolet Spirit 脑诱发电位仪,采用光和声成对刺激以及“听觉靶-非靶刺激序列”技术,对38例强迫症、20例抑郁症和18例广泛性焦虑症及28名正常人的关联性负变(CNV)、P300及失匹性负波(MMN)作了检测。3组疾病组病例均选自2002年5月至2005年12月上海市精神卫生中心,经2名以上的高年资医师确诊并符合中国精神障碍分类方案第三版（CCMD-3）中的强迫症和抑郁症及广泛性焦虑症诊断标准;听力均正常,并无躯体疾病或其他精神疾病,均为右利手。3组对象均未使用过精神科药物。结果 ①CNV：M1波幅抑郁症组[(5±4)μV]和广泛性焦虑症组[(7±4)μV]低于正常组[(14±6)μV]和强迫症组(16±6)μV,指令信号后负变化的出现率抑郁症组(60%)、强迫症组(45%)和广泛性焦虑症组(35%)均高于正常组(4%),上述组间差异均有统计学意义（P<0.05或P<0.01）。②P300：在靶刺激中,N2潜伏期在4组间的差异有统计学差异(P<0.01),其中强迫症组[(276±22)ms]和抑郁症组[(277±22)ms]的潜伏期均长于正常组[(259±14)ms],广泛性焦虑症组短于抑郁症组和强迫症组(P<0.01);P3波幅在4组间的差异亦有统计学差异(P<0.01),其中强迫症组[(3.4士1.6)μV]、抑郁症组[(2.9±1.3)μV]和广泛性焦虑症组[(3.3士1.3)μV]均低于正常组[(5.9土2.1)μV]。在非靶刺激中,广泛性焦虑症组P2波幅低于强迫症组和正常组(P<0.05)。③MMN：强迫症组、抑郁症组及正常组之间潜伏期和波幅的差异有统计学差异(P<0.05或P<0.01)。其中强迫症组和抑郁症组的潜伏期长于正常组(P<0.05);强迫症组的波幅高于正常组(P<0.05),抑郁症组的波幅低于正常组(P<0.05)和强迫症组(P<0.01)。结论 ERPs波幅一高一低变异特点可能对鉴别强迫症和抑郁症有参考意义。     

Psychopharmacological treatment differences in autogenous and reactive obsessions: A retrospective chart review

Background: Identification of homogeneous subgroups of obsessive compulsive disorder (OCD) patients may have important implications for improving effective treatment options. It has been proposed that obsessive thoughts can be classified into two subtypes, i.e. autogenous and reactive obsessions. Although it has been shown that patients with autogenous obsessions may display a worse response to treatment, no studies have yet addressed whether there is a different need for the psychopharmacological treatment options in the subtypes of OCD patients. Aim: To investigate the clinical characteristics and treatment differences between autogenous (A-OCD) and reactive (R-OCD) subtypes of OCD patients. Methods: Both OCD subgroups (n = 50 for A-OCD, n = 130 for R-OCD) were compared with each other in terms of their demographic and clinical parameters. Odds ratio values for gender, treatment options, co-morbidity, severity of OCD, and response to treatment were computed. Multivariate hierarchical regression analyses were performed to identify any predictors for treatment options, severity of OCD, and response to treatment. Results: Our results indicated that the A-OCD and R-OCD groups differed from each other on some demographic and clinical variables in addition to their psychopharmacological treatment needs. Patients in the A-OCD group were found to be prescribed an atypical antipsychotic 2.3 times more likely than the R-OCD group. The odds for a combination treatment, or the improvement of OCD symptoms from baseline levels did not differ between the two subtypes of obsession groups. Conclusions: Autogenous and reactive subtypes of obsessions may need to be offered different psychopharmacological treatment options.     

Personality and Alexithymic Disparity in Obsessive-Compulsive Disorder Based on Washing and Checking

The aim of this study was to investigate pathway relationship of personality characteristics and alexithymic traits in OCD symptoms of obsession, and compulsive behavior of washing and checking. Two-hundred and seventy patients diagnosed with OCD were consecutively recruited from the psychiatric outpatient department of a teaching hospital. Structural equation modeling showed those more neurotic, less extraverted and with higher levels of alexithymia difficulty identifying feelings (DIF), difficulty describing feelings (DDF) and externally oriented thinking (EOT) were more likely to develop obsessive thoughts. Those less extraverted was more prone to develop washing compulsions, and those more neurotic were more likely to develop checking compulsions. EOT was the only alexithymic trait to have no gender difference within this group of patients with OCDs. The different personality and alexithymic trait pathways found between OCD obsession, washing and checking symptoms provide support that they may be different subtypes within the OCD diagnosis. Obsession was associated with washing, but not checking. Furthermore, no gender difference was found between the obsession and compulsive symptoms. Extraversion and neuroticism can be used to differentiate washing and checking, and alexithymia to differentiate washing and obsessions. This should be taken into consideration for intervention targeting patients with different OCD symptoms.     

Prevalence and clinical correlates of obsessive–compulsive disorder in schizophrenia

Obsessive compulsive symptoms frequently occur in a substantial proportion of patients with schizophrenia. The term schizoobsessive has been proposed to delineate this subgroup of schizophrenia patients who present with obsessive–compulsive symptoms/disorder. However, whether this co-occurrence is more than just co-morbidity and represents a distinct subgroup remains controversial. A striking variation is noted across studies examining prevalence of obsessive–compulsive symptoms/disorder in schizophrenia patients and their impact on clinical profile of schizophrenia. Hence, in this study, we examined the prevalence of obsessive–compulsive symptoms/disorder in a large sample of consecutively hospitalized schizophrenia patients and compared the clinical and functional characteristics of schizophrenia patients with and without obsessive–compulsive symptoms/disorder. We evaluated 200 consecutive subjects with the DSM-IV diagnosis of schizophrenia using the Structured Clinical Interview for DSM-IV Axis I disorders, Positive and Negative Syndrome Scale, Yale–Brown Obsessive–Compulsive Scale, Brown Assessment of Beliefs Scale, Clinical Global Impression-Severity scale, Global Assessment of Functioning Scale, Family Interview for Genetic Studies and World Health Organization Quality of Life scale. The prevalence of obsessive–compulsive symptoms in patients with schizophrenia was 24% (n = 48); 37 of them had obsessive–compulsive disorder (OCD) and 11 had obsessive–compulsive symptoms not amounting to a clinical diagnosis of OCD (OCS). Schizophrenia patients with OCS/OCD had an earlier age at onset of schizophrenia symptoms, lower positive symptoms score, higher co-morbidity with Axis II disorders, higher occurrence of OCD in family and better quality of life. Findings of the study indicate a higher prevalence of OCS/OCD in schizophrenia. Schizophrenia patients with and without OCS/OCD have comparable clinical profile with few exceptions. High rates of OCD in first degree relatives suggest possible genetic contributions and differences in neurobiology. Finally, evidence to consider schizoobsessive as a distinct diagnostic entity is inconclusive and warrants further studies.     

Differential sensory gating functions between smokers and non-smokers among drug-naive first episode schizophrenic patients

Although an acute effect of cigarette smoking and nicotine on sensory gating of schizophrenias has been investigated in published papers, the chronic effect of cigarette smoking on this phenomenon has not yet been reported. We report the effects of chronic cigarette smoking, without new acute exposure before testing, on sensory gating using the P50 auditory evoked potential in a group of drug-naive first episode schizophrenic smokers and healthy smokers. Sensory gating was evaluated using auditory P50 suppression elicited using the conditioning (S1)-testing (S2) paradigm. Fifty six male drug-naive first episode schizophrenic patients were compared to 41 healthy male controls. Patients were classified into subgroups of current smokers (n = 18) and non-smokers (n = 38) to explore the effects of smoking on sensory gating. All subjects did not smoke a cigarette for at least 1 h prior to testing. Schizophrenic patients showed an increased S2 amplitude and a poorer sensory gating as measured by both S2/S1 ratio and S1-S2 difference of P50 amplitude, as compared to healthy controls. However, smokers showed an increased S1 amplitude and better sensory gating than did non-smokers both in schizophrenia patients and healthy controls. Our findings support a sensory gating deficit among first episode schizophrenic patients. However, it was less pronounced among schizophrenic patients who were current cigarette smokers, suggesting a positive effect of chronic cigarette smoking on ameliorating this sensory gating deficit in schizophrenia. Our findings of the present study present new evidence supporting the self-medication hypothesis of self-medication by cigarette smoking in schizophrenia to possibly ameliorate pre-existing functional deficits.