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Resumen Antecedentes: la esquizofrenia es una enfermedad crónica que genera gran discapacidad, para la cual se han reportado biomarcadores potenciales, pero sin suficiente validez clínica. El mismatch negativity (MMN) y el P3a son potenciales relacionados con eventos que han demostrado ser indicadores neurofisiológicos del procesamiento auditivo pre-atencional y potenciales biomarcadores. Objetivo: evaluar el MMN y P3a en pacientes con diagnóstico de esquizofrenia y su relación con variables sociodemográficas y clínicas. Método: estudio cuantitativo transversal de 23 sujetos con esquizofrenia (ESQ) y 22 controles sanos (SN). Las amplitudes promedio y latencias del MMN/P3a para la condición infrecuente en duración y frecuencia fueron obtenidas mediante un paradigma oddball auditivo en un EEG de 32 canales. Resultados: se encontraron diferencias para la condición frecuencia en la amplitud del MMN (p=0.046; CI 95% 0.009; 0.87) y la amplitud del P3a (p=0.042; CI 95% 0.025; 1.24) entre los grupos; la amplitud del MMN fue menor en el grupo ESQ (-0.36 DE 0.51 µV) en comparación con los participantes del grupo de SN (-0.81 DE 0.89 µV), mientras que la amplitud del P3a fue menor en el grupo SN (0.18 DE 0.97 µV) versus el grupo ESQ (0.82 DE 1.05 µV). En relación con las variables sociodemográficas y clínicas, las asociaciones con el P3a fueron moderadas y con el MMN débiles. Conclusiones: la reducción de la amplitud del MMN a la condición frecuencia exhibe mayor utilidad que el P3a como medida de alta estabilidad en pacientes con esquizofrenia, lo que reitera su posible uso como biomarcador.
Abstract Background: schizophrenia is a chronic disease that generates great disability, which currently has potential biomarkers but without sufficient clinical validity. Mismatch negativity (MMN) and P3a are event-related potentials that have been shown to be neurophysiological indicators of pre-attentional auditory processing and potential biomarkers. Objective: to evaluate MMN and P3a in patients with a diagnosis of schizophrenia and their relationship with sociodemographic and clinical variables. Method: a quantitative cross-sectional study of 23 subjects with schizophrenia and 22 healthy controls was performed. The average amplitudes and latencies of the MMN/P3a for the condition infrequent in duration and infrequent in frequency were obtained using an auditory oddball paradigm on a 32-channel EEG. Results: differences were found for the frequency condition in the amplitude of the MMN (p=0.046; 95% CI 0.009; 0.87) and the amplitude of the P3a (p=0.042; 95% CI 0.025; 1.24) between the groups; MMN amplitude was lower in schizophrenia (-0.36 SD 0.51 µV) compared to healthy controls (-0.81 SD 0.89 µV), while P3a amplitude was lower in healthy controls (0.18 SD 0.97 µV) versus the group with schizophrenia (0.82 SD 1.05 µV). In regard to sociodemographic and clinical variables, the associations with P3a were moderate, and showed weak MMN. Conclusions: MMN amplitude reduction to the frequency condition exhibits greater utility than P3a as a measure of high stability in schizophrenia, restating its potential use as a biomarker.
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Objective:To investigate the relationship between cognitive function and brain event-related potential in patients with lacunar cerebral infarction.Methods:A total of 464 patients with lacunar cerebral infarction admitted to the Department of Neurology, Kailuan General Hospital from 2014 to 2019 were prospectively selected as observation subjects (case group). According to mini-mental state examination (MMSE) score, the patients in the case group were divided into 352 cases of lacunar cerebral infarction with normal cognition and 112 cases of mild cognitive impairment. At the same time, 100 healthy volunteers were selected as the control group. All subjects were assessed by simple intelligent mental state, Zung self-rating anxiety scale, Zung self-rating depression scale and brain event-related potential P3a and P3b. The measurement data of normal distribution adopts one-way ANOVA, the measurement data of non normal distribution adopts Kruskal Wallis H test, and the counting data adopts χ2. Multivariate statistical analysis was performed by unconditional Logistics (stepwise method). Results:The proportions of smokers in control group, lacunar cerebral infarction cognitive normal group and lacunar cerebral infarction mild cognitive impairment group were 20.00% (20/100), 38.07% (134/352) and 46.42% (52/112), respectively. The proportions of drinkers were 18.00% (18/100), 33.24% (117/352), 33.93% (38/112), respectively. The proportions of hypertension were 38.00% (38/100), 58.24% (205/352), 59.82% (67/112), respectively. The proportions of hyperhomocysteinemia were 19.00% (19/100), 34.00% (120/352) and 68.75% (77/112), respectively, and the differences among the three groups were statistically significant ( χ2 values were 15.66, 7.91, 11.86 and 54.57, respectively; P<0.001, 0.019, 0.003, <0.001). The peak latency CZ leads of visual P3b wave group N2 were (271.48±40.65), (285.67±44.08) and (290.57±68.41) ms, respectively. PZ leads were (276.70±50.92), (287.86±43.28) and (312.16±62.75) ms. P3b peak latency FZ leads were (392.67±42.50), (405.82±52.43) and (410.34±64.27) ms. CZ leads were (395.04±42.44), (412.51±55.86) and (433.28±66.32) ms. PZ leads were (398.24±40.93), (411.17±49.48) and (435.78±67.69) ms. N2 amplitude CZ leads were (-3.99±2.81), (-3.60±3.00) and (-2.70±2.37) μV, PZ leads were (-3.18±2.69), (-2.91±2.62) and (-1.87±2.89) μV, respectively. Leads P3b amplitude of FZ were 5.27 (3.27, 7.40), 4.21 (2.31, 6.49) and 3.12 (1.61, 5.08) μV. CZ leads were 4.81 (2.78, 6.71), 4.15 (2.76, 6.16) and 3.51 (1.75, 5.15) μV. PZ leads were 5.17 (3.03, 6.97), 4.40 (2.89, 6.12) and 3.43 (1.52, 5.34) μV. There were statistically significant differences among the 3 groups ( F=3.29, 14.49, 3.95, 11.73, 14.06, 5.66 and 3.57, H=18.23, 10.33,18.25; P=0.027, <0.001, 0.025, <0.001, <0.001, 0.004, 0.042, <0.001, 0.006, <0.001). The peak latency FZ leads of visual P3a wave group N2 were 265.00 (256.00, 286.00), 277.00(260.00,300.00), 282.00(270.00,304.00) ms, respectively. CZ leads weres 274.00(255.00,305.00), 285.00(262.00,329.00), 293.50(270.00,346.00) ms. P3a peak latency FZ leads were (413.83±49.58), (429.83±55.38) and (449.04±54.79) ms, CZ leads were (441.53±61.78), (457.12±69.29) and (460.23±72.24) ms. PZ leads were (430.14±54.53), (462.31±69.2) and (470.02±74.92) ms. N2 amplitude FZ leads were (-6.34±3.13), (-5.72±2.96) and (-4.92±2.05) μV, respectively. Leads P3a amplitude of FZ were 4.00 (2.28, 5.55), 3.15 (2.14, 4.91) and 2.80 (2.19, 4.19) μV. CZ lead were 3.37 (1.98, 4.66), 2.73 (1.70, 3.97) and 2.41 (1.64, 3.45) μV. There were statistically significant differences among the three groups ( H=13.92, 8.65, 9.17, 10.02, F=8.18, 6.33, 10.73, 4.62, P =0.001,0.013,0.010,0.007, <0.001,0.002, <0.001,0.010). Logistic regression analysis showed that alcohol consumption, P3b peak latency and wave amplitude PZ lead, N1 wave amplitude of visual P3a group FZ lead were the influencing factors of MMSE ( OR=0.04, 1.01, 0.76, 1.51, 95% Cl were 0.00-0.30, 1.00-1.03, 0.59-0.97, 1.08-2.10, P=0.002,0.007,0.029,0.016). Conclusion:The peak latency and amplitude of endogenous psychological cognitive potentials N2, P3b and P3a of event-related potentials P3b and P3a in patients with lacunar cerebral infarction were prolonged and decreased. At the same time, with the occurrence of clinical cognitive impairment, the peak latency and amplitude of these cognitive potentials were further prolonged and decreased more significantly. Alcohol consumption, P3b peak latency and PZ lead of visual P3b wave group, and FZ lead of N1 wave of visual P3a wave group were the influencing factors of simple intelligent mental state.
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Objective To explore the changes of attention cognitive function by studying Oddball task behavior and event-related potentials(ERPs) in children with first-episode tic disorder(TD). Methods Oddball task was tested in 30 children with TD and 30 normal children,and their behavioral data and P3a/P3b components of ERPs were analyzed. Results Children with TD had a lower hitting number (49(48, 50)) than control group (50(49,50),P<0. 05). The main effect of group ( F=6. 047,P=0. 015) and the interaction effect between group and condition (F=4. 619,P=0. 034) on the amplitude of P3a were signifi-cant(P<0. 05). The amplitude of P3a component ((5. 91±4. 51)μV ) in TD group were smaller than that in the control group((9. 57±5. 80)μV)(P<0. 05). However,there was no significant interaction effect be-tween group and condition on P3a latency,P3b amplitude and latency (P>0. 05). Conclusion Attentional orienting is impaired in children with TD.
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BACKGROUND AND PURPOSE: Neuropsychological and neuroimaging studies both suggest that frontal lobe dysfunction is present in migraineurs. Since P3a abnormalities manifest in other diseases associated with attention problems, such as attention deficit hyperactivity disorder, we hypothesized that migraine patients have P3a abnormalities, particularly in the frontal region. METHODS: Event-related potentials were measured using a passive auditory oddball paradigm in 16 female migraineurs (aged 22.9+/-2.0 years, mean+/-SD) during the interictal period and in 16 age-matched healthy females (22.6+/-2.0 years). The amplitudes and latencies were analyzed independently using repeated-measures analysis of variance. Nonparametric statistical testing using a cluster-level randomization method was performed to localize the abnormalities. RESULTS: The mean P3a amplitude at frontal areas during the third trials was significantly lower in migraineurs (1.06 microV) than in controls (1.69 microV, p=0.026). P3a amplitudes were negatively correlated with the duration of the migraine history (r=-0.618, p=0.014). Cluster-based nonparametric statistical analysis showed that the amplitudes over left frontal areas were significantly lower in migraine patients than in controls. CONCLUSIONS: A reduced P3a amplitude of migraineurs reflects attentional deficits and frontal dysfunction. The negative correlation between P3a amplitude and the duration of the migraine history suggests that attentional deficits and frontal dysfunction are either the cause or the result of headache.
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Female , Humans , Attention Deficit Disorder with Hyperactivity , Evoked Potentials , Frontal Lobe , Headache , Migraine Disorders , Neuroimaging , Oxalates , Random AllocationABSTRACT
Objective To investigate effects of driving fatigue on auditory involuntary attention.Method Between-groups design was used.The control group included 13 taxi drivers after adequate rest while the fatigue group included 13 taxi drivers who had been driving for 10 h.Auditory oddball pattern was adopted.The standard stimulus was 800 Hz,probability 80%;target stimulus was 1 000 Hz,probability 10%;novel stimulus was sound generated by computer or other sound,probability 10%.Subjects were asked to press the mouse upon hearing the target sound.Result The distribution of P3a was mainly around the frontal-central area of the subjects in control group;the amplitude of P3a was evidently lowered in subjects after driving fatigue.Conclusion The ability of auditory involuntary attention declines after driving fatigue.
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OBJECTIVES: Using 3-stimulus auditory "oddball" paradigm reflecting fronto/central and temporo/parietal functions simultaneously, we examined patients with schizophrenia. METHODS: Fifteen patients with schizophrenia from outpatient clinic and fifteen normal controls from hospital staffs were recruited for the study. To elicit P3a and P3b, 3-stimulus auditory oddball paradigm was employed. The 3-stimulus auditory oddball paradigm was composed of standard tone (1,000 Hz, 75 dB, 80%), target tone (2,000 Hz, 75 dB, 10%) and distracter (White noise, 95 dB, 10%). RESULTS: P3a and P3b were prominent in fronto/central and temporo/parietal areas, respectively, in both schizophrenics and normal controls. The P300 amplitude in patients with schizophrenia was reduced across P3a and P3b (p<0.01). The P300 latency in patients with schizophrenia was delayed across P3a and P3b (p<0.01). CONCLUSION: These results were consistent with frontal and temporo-parietal lobe dysfunctions in schizophrenics. The 3-stimulus auditory paradigm could be applied for patients with schizophrenia and useful for further exploration the disorder.
Subject(s)
Humans , Ambulatory Care Facilities , Evoked Potentials , Noise , SchizophreniaABSTRACT
OBJECTIVES: Using 3-stimulus auditory "oddball" paradigm reflecting fronto/central and temporo/parietal functions simultaneously, we examined patients with schizophrenia. METHODS: Fifteen patients with schizophrenia from outpatient clinic and fifteen normal controls from hospital staffs were recruited for the study. To elicit P3a and P3b, 3-stimulus auditory oddball paradigm was employed. The 3-stimulus auditory oddball paradigm was composed of standard tone (1,000 Hz, 75 dB, 80%), target tone (2,000 Hz, 75 dB, 10%) and distracter (White noise, 95 dB, 10%). RESULTS: P3a and P3b were prominent in fronto/central and temporo/parietal areas, respectively, in both schizophrenics and normal controls. The P300 amplitude in patients with schizophrenia was reduced across P3a and P3b (p<0.01). The P300 latency in patients with schizophrenia was delayed across P3a and P3b (p<0.01). CONCLUSION: These results were consistent with frontal and temporo-parietal lobe dysfunctions in schizophrenics. The 3-stimulus auditory paradigm could be applied for patients with schizophrenia and useful for further exploration the disorder.
Subject(s)
Humans , Ambulatory Care Facilities , Evoked Potentials , Noise , SchizophreniaABSTRACT
Objective To investigate the generative and regulatory effects of AchMR on P 3a and its mechanism in different subregions of rabbit cingulate gyrus. Methods Event related potentials(ERPs) P 3a potentials in Normal, AcgI, AcgⅡand Pcg regions were recorded after microinfusion of 0.5 mmol/L scopolamine at three different time points(instantly, at the 15th minute and at the 30th minute), 2 mmol/L acetylcholine and 1 mmol/L scopolamine. Results The P 3a amplitude decreased and/or P 3a latency increased with scopolamine in time and dose dependent pattern in AcgⅠ, AcgⅡ and Pcg, and P 3a might disappear only in AcgⅠ and the P 3a again be recorded after microinfusion of acetylcholine in AcgⅠ. Conclusion The action of AchMR in AcgⅠ area markedly affects the generation and/or regulation of P 3a and confirms the AcgⅠ is the source of rabbit P 3a potential. The action of neurons in AcgⅠ might facilitate the P 3a potential.