健康成人感觉门抑制P50实验研究

目的 应用脑诱发电位新技术探讨健康成人听觉P50特点.方法 应用美国Nicolet Bravo脑电生理仪,采用条件刺激(S1)-测试刺激(S2)模式对58名健康成人作了听觉P50检测.结果 S1-P50潜伏期和波幅与S2-P50潜伏期和波幅在三个脑区无统计学差异.Cz脑区显示,健康成人S1-P50潜伏期(59.6±11.1)ms,波幅(6.1±3.3)μV;S2-P50潜伏期(68.7±24.6)ms,波幅(1.9±1.3)μV.S2-P50波幅显著低于S1-P50波幅(t=9.02,P<0.01).P50潜伏期和波幅无性别差异.结论 听觉P50电位具有抑制性特点,其变化可反映大脑正常感觉门抑制的功能状态.     

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。     

孤独症患儿感觉抑制P50试验研究

目的 了解孤独症患儿感觉门控 (SG)抑制P50的特点.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37例孤独症患儿和30名正常儿童作了听觉P50检测.结果 孤独症组P50抑制明显减弱;S2-P50波幅增加[正常对照组 (2.5±2.0)μV,孤独症组(4.9±3.1) μV,P<0.01].与正常对照组相比,孤独症组S1-P50降低 [正常对照组(5.7±3.7)μV,孤独症组(3.0±2.4)μV,P<0.01].P50抑制明显减弱,即S1-S2比值明显降低 [正常对照组(3.9±2.7) μV,孤独症组(1.5±1.1) μV,P<0.01].结论 孤独症的SG亦存在异常,表现为抑制不足.     

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.     

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.     

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。     

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。     

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。     

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.     

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.     

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。     

接触性热痛诱发电位对糖尿病小纤维神经病变的评价作用

目的 借助接触性热痛诱发电位(CHEP)为糖尿病神经病变的小纤维神经损害寻求一种新的无创客观定量方法.方法 选取糖尿病患者46例和健康人40名,应用CHEP刺激器,控制温度52℃,分别刺激所有受试者右侧前臂、手背、小腿皮肤,采用Keypoint.net肌电图仪于cz点分别记录N波潜伏期及N-P波波幅;同时行右侧上下肢感觉传导测定.结果 健康对照组各个刺激部位CHEP的引出率为100%,而糖尿病组46例中前臂7例、手背9例、小腿16例未引出肯定CHEP波形.糖尿病组较对照组N波潜伏期延长,N-P波波幅减低.糖尿病组中25例上肢感觉传导正常,其前臂刺激Cz记录的N-P波波幅较对照组减低[分别为(34.0±12.6)、(48.4 ±17.5)μV,Z=-3.151,P<0.01],N波潜伏期差异无统计学意义;手背刺激CHEP潜伏期较对照组延长[分别为(420.4±27.8)、(407.2±24.6)ms,t=2.015,P=0.048],波幅减低[分别为(28.2±10.1)、(43.0±16.6)μV,Z=-3.712,P<0.01].18例下肢感觉传导正常,其小腿刺激CHEP潜伏期延长[分别为(473.5±46.6)、(448.6±35.0)ms,t=2.219,P=0.031],波幅减低[(23.8±7.4)、(41.5±18.5)μV,Z=-3.855,P<0.01].结论 糖尿病患者在早期即有小纤维神经选择性受累,CHEP能够为其提供新的客观定量方法,具有潜在的临床应用价值.     

Auditory temporal processes in normal-hearing individuals and in patients with auditory neuropathy.

OBJECTIVE: To study objectively auditory temporal processing in a group of normal hearing subjects and in a group of hearing-impaired individuals with auditory neuropathy (AN) using electrophysiological and psychoacoustic methods. METHODS: Scalp recorded evoked potentials were measured to brief silent intervals (gaps) varying between 2 and 50ms embedded in continuous noise. Latencies and amplitudes of N100 and P200 were measured and analyzed in two conditions: (1) active, when using a button in response to gaps; (2) passive, listening, but not responding. RESULTS: In normal subjects evoked potentials (N100/P200 components) were recorded in response to gaps as short as 5ms in both active and passive conditions. Gap evoked potentials in AN subjects appeared only with prolonged gap durations (10-50ms). There was a close association between gap detection thresholds measured psychoacoustically and electrophysiologically in both normals and in AN subjects. CONCLUSIONS: Auditory cortical potentials can provide objective measures of auditory temporal processes. SIGNIFICANCE: The combination of electrophysiological and psychoacoustic methods converged to provide useful objective measures for studying auditory cortical temporal processing in normals and hearing-impaired individuals. The procedure used may also provide objective measures of temporal processing for evaluating special populations such as children who may not be able to provide subjective responses.     

芪参复康胶囊、丁螺环酮对焦虑症患者事件相关电位P300的影响

目的 评价芪参复康胶囊、丁螺环酮对焦虑症患者认知功能的影响.方法 将本院70例焦虑症患者按随机数字表法分两组,中药组(35例)给予芪参复康胶囊,西药组(35例)给予丁螺环酮.两组患者于治疗前、治疗后6周进行HAMA评定及P300检查,另选36名健康志愿者(对照组)行P300检查.分析两组患者治疗前后对认知功能的影响.结果 (1)与治疗前相比,治疗后HAMA评分中药组[(27.4±5.4)分vs.(5.2±2.2)分]和西药组[(27.2±6.2)分vs.(6.7±2.6)分]均降低(P＜0.05),且中药组HAMA减分率高于西药组[(80.7±4.5)％vs.(75.4±5.1)％,P＜0.05].(2)与治疗前相比,两组治疗后P3潜伏期均缩短[中药组:(382.1±76.8)ms vs.(292.1±70.4)ms,P＜0.05;西药组:(384.6±73.6)ms vs.(323.6±61.1)ms,P＜0.05],N2、P3波幅均升高[中药组:N2(3.6±1.7)μVvs.(5.8±2.1)μV,P3(6.2±2.3)μV vs.(9.8±2.2)μV,P＜0.05;西药组:N2(3.5±1.6)μV vs.(4.0±1.4)μV,P3(6.3±2.1)μV vs.(7.8±2.7)μV,P＜0.05].(3)与对照组相比,治疗前中药组、西药组P3潜伏期均延迟,N2、P3波幅均降低(P＜0.05);治疗后中药组P3潜伏期及N2、P3波幅差异无统计学意义(P＞0.05),西药组P3潜伏期及N2、P3波幅仍偏低(P＜0.05).结论 芪参复康胶囊、丁螺环酮治疗均可缓解焦虑症临床症状及改善其认知功能,而芪参复康胶囊提高患者信息加工的感知觉识别与编码的疗效优于丁螺环酮.     

Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment.

OBJECTIVE: Mild cognitive impairment (MCI) is a selective episodic memory deficit in the elderly with a high risk of Alzheimer's disease. The amplitudes of a long-latency auditory evoked potential (P50) are larger in MCI compared to age-matched controls. We tested whether increased P50 amplitudes in MCI were accompanied by changes of middle-latency potentials occurring around 50 ms and/or auditory brain-stem potentials. METHODS: Auditory evoked potentials were recorded from age-matched controls (n = 16) and MCI (n = 17) in a passive listening paradigm at two stimulus presentation rates (2/s, 1/1.5 s). A subset of subjects also received stimuli at a rate of 1/3 s. RESULTS: Relative to controls, MCI subjects had larger long-latency P50 amplitudes at all stimulus rates. Significant group differences in N100 amplitude were dependent on stimulus rate. Amplitudes of the middle-latency components (Pa, Nb, P1 peaking at approximately 30, 40, and 50 ms, respectively) did not differ between groups, but a slow wave between 30 and 49 ms on which the middle-latency components arose was significantly increased in MCI. ABR Wave V latency and amplitude did not differ significantly between groups. CONCLUSIONS: The increase of long-latency P50 amplitudes in MCI reflects changes of a middle-latency slow wave, but not of transient middle-latency components. There was no evidence of group difference at the brain-stem level. SIGNIFICANCE: Increased slow wave occurring as early as 50 ms may reflect neurophysiological consequences of neuropathology in MCI.     

Contribution of different EEG frequencies to auditory evoked potential abnormalities in schizophrenia.

OBJECTIVE: We have shown previously [Clin Neurophysiol 2003;114:79] that phase reorganization of the ongoing electroencephalogram (EEG) plays an important role in the generation of auditory evoked potential (EP) components with a latency between 50 and 200 ms. In the present study, we investigate whether schizophrenia patients suffer from phase synchronization deficits as compared to normal subjects. METHODS: The auditory EPs from 20 normal subjects and 19 schizophrenia patients were analyzed. EPs were obtained using a double stimulus paradigm, in which two identical tone bursts (S1 and S2) were delivered with an average inter-stimulus interval of 500 ms and an inter-pair interval of 8 s. The Piecewise Prony Method (PPM) was used to decompose single trial auditory evoked potentials into different frequency bands. Pre- and post-stimulus phase histograms were compared for each frequency band to determine the degree of phase synchronization produced by auditory stimulation in the two populations. RESULTS: The S1 stimulus produced significantly less (P < 0.05) phase synchronization in schizophrenia patients than in normal subjects in the 2-12 Hz frequency range. Far fewer and smaller inter-population phase synchronization differences were seen for the S2 stimulus. Both populations showed more phase synchronization for S1 than S2. A significant correlation (P < 0.01) between N100 amplitude and phase synchronization 100 ms post S1 was observed for the normal population but not for the schizophrenia group. The correlation between P200 amplitude and phase synchronization 200 ms post S1 was significant for the normal group (P < 0.01) and the schizophrenia group (P < 0.03). CONCLUSIONS: Schizophrenia patients have a phase synchronization deficiency, as compared to a normal control group, especially for the first stimulus, in the 2-12 Hz frequency range. This deficiency explains the lower EP amplitudes and may be a significant factor contributing to reduced sensory gating reported in schizophrenic subjects. SIGNIFICANCE: The research presented here contributes to the understanding of the mechanism underlying sensory gating in health and gating deficiencies in schizophrenia.     

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。     

Bitemporal lesions dissociate auditory evoked potentials and perception

We studied auditory evoked potentials (AEPs) in an 82-year-old female patient who became suddenly deaf following the second of two strokes. The patient showed markedly elevated pure tone thresholds, was unable to discriminate sounds and could not understand speech. Brain-stem auditory evoked potentials (BAEPs) were normal. CT scans revealed bilateral lesions of the superior temporal plane which included auditory cortex. Two experiments were performed. In the first, tones, complex sounds and speech stimuli were presented at intensities above and below the patient's perceptual threshold. P1, N1 and P2 components were elicited by each of the stimuli--whether or not they were perceived. In particular, stimuli presented below threshold evoked large amplitude, short latency responses comparable to those produced in a control subject. In a second experiment, the refractory properties of the N1-P2 were examined using trains of tones. They were also found to be similar to those of normal subjects. Shifts in the pitch of the tones near the end of the train (when refractory effects were maximal) evoked N1-P2s with enhanced amplitudes, although the change in pitch was not perceived by the patient. In both experiments AEP scalp topographies were normal. The results suggest that bitemporal lesions of auditory cortex can dissociate auditory perception and long-latency auditory evoked potentials. A review of evoked potential studies of cortical deafness suggests that the neural circuits responsible for N1-P2 generation lie in close proximity to those necessary for auditory perception.     

Effects of age on event-related potentials in chronic alcoholics: a multimodal study.

To test different versions of the premature aging hypothesis in alcoholics, brainstem auditory evoked potentials (BAEPs), long-latency auditory evoked potentials (LAEPs), P3 and visual evoked potentials (VEPs) were recorded in 32 alcoholic subjects. The phenomena in patients' event-related potentials (ERPs) differ from those observed in normal aging subjects and become more pronounced with age. ANOVA showed a significant effect by group (alcoholic patients/controls) on certain parameters of BAEPs (III, III-V, I-V), VEPs (P100 latency) and LAEPs (N1-P2 amplitude and N2 latency) unaffected by age, while age had a significant effect on some parameters of LAEPs (N2-P3 amplitude, P3 latency) unaffected, or less affected by chronic alcohol consumption. At a clinical level, abnormalities in BAEPs and VEPs seem good early trouble indices in alcoholic patients, while alterations in latencies and amplitudes of LAEPs appear in older patients. These data seem to be in favor of a critical age or critical abuse in the action of alcohol, in place of the classical hypothesis of premature aging.     

Hemispheric asymmetry of late auditory evoked response induced by pitch changes in infants: influence of sleep stages

Late auditory evoked potentials (LAEPs) have been recorded in response to a 1000 Hz standard (occurrence 80%) or a 2000 Hz deviant (occurrence 20%) tone on the left (T3) and right (T4) temporal scalp in 6-week-old full-term newborns during pure quiet or active sleep states. Sleep states were permanently controlled by polygraphic recording including EEG, EOG, EMG, EKG and respiratory movements. During quiet sleep LAEPs consisted of a clear polygraphic response: N1-P2-N2. Mean latencies ranges in T3 and T4 were: N1 = 28–70 ms; P2 = 343–407 ms;N2 = 966–1178 ms; and P3 = 1461–1492 ms. During active sleep LAEPs consisted of a N1-P2-N2 response. Mean latency ranges on T3 and T4 were: N1 = 36–79 ms; P2 =278–304 ms; N2 = 555–620 ms. N2 latency was significantly shorter in AS than in QS. Amplitude of the N1-P2-N2 complex was significantly lower during active sleep. In response to standard stimuli, mean amplitudes and latencies of the LAEP were similar on T3 and T4 during active or quiet sleep states. In response to deviant stimuli mean amplitude of the N1-P2-N2 complex was significantly higher and mean latencies of N1 and N2 were significantly shorter on T3 during quiet sleep. No significant difference was observed during active sleep. These results confirm that sleep stages have a considerable influence on cortical auditory pathways. The auditory message is amplified during quiet sleep and inhibited during active sleep. Therefore sleep states need to be controlled to analyze LAEPs in young children. Furthermore our results show that unexpected auditory stimuli are differentiated in the temporal area of the left hemisphere of 6-week-old infants. This represents a functional correlate of the known hemispherical asymmetry in the speech region of the temporal cortex.