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Genetic influences modulating executive functions engaging prefrontal cortical brain systems were investigated in 141 male subjects. The effects of variations in two genes implicated in dopamine and GABA activities in the prefrontal cortex: rs4680 (Val158/Met polymorphism of the catechol-o-methyltransferase gene—COMT) and rs3749034 (C/T) substitution in the promoter region of the glutamic acid decarboxylase gene (GAD1) were studied on antisaccade (AS) performance in healthy subjects and schizophrenic patients. Genotyping revealed a trend towards a reduced proportion of COMT Val/Met heterozygotes and a significantly increased frequency of the GAD1 rs3749034 C allele in schizophrenic patients relative to controls. Patients had elevated error rates, increased AS latencies and increased latency variability (coefficient of variation) compared to controls. The influence of polymorphisms was observed only in patients but not in controls. A substantial effect of the COMT genotype was noted on the coefficient of variation in latency, and this measure was higher in Val homozygotes compared to Met allele carriers (p < 0.05) in the patient group. The outcome from rs3749034 was also disclosed on the error rate (higher in T carriers relative to C homozygotes, p < 0.01) and latency (increased in C homozygotes relative to T carriers, p < 0.01). Binary logistic regression showed that inclusion of the genotype factor (i.e., selective estimation of antisaccade measures in CC carriers) considerably increased the validity of the diagnostic model based on the AS measures. These findings may well be derived from specific genetic associations with prefrontal cortex functioning in schizophrenia.

The study tested whether the antisaccade (AS) performance and Contingent Negative Variation (CNV) measures differed between the first-episode and chronic patients to provide the evidence of PFC progressive functional deterioration. Subjects included 15 first-episode and 20 chronic schizophrenic patients (with the duration of illness more than 5 years), and 21 control subjects. The first-episode and chronic patients had significantly elevated error percent (p < .05, effect size 1.10 and p < .001, effect size 1.25), increased AS latencies (p < .01, effect size 1.18 and p < .001, effect size 1.69), and increased latencies variability (p < .01, effect size 1.52 and p < .001, effect size 1.37) compared to controls. Chronic patients had marginally significant increase of the response latency (p = .086, effect size .78) and latency variability (p < .099, effect size .63) compared to first-episode ones. Results of CNV analysis revealed that chronic patients only exhibited robustly declined frontal CNV amplitude at Fz (p < .05, effect size .70), F3 (p < .05, effect size .88), and F4 (p < .05, effect size .71) sites compared to controls. The obtained results might be related to specific changes in prefrontal cortex function over the course of schizophrenia.

Prepulse modification of the acoustic startle response (ASR) and P50 gating are potential neurophysiological endophenotypes of schizophrenia and may be used in the construction of valid clinical biomarkers. Such approach requires a large amount of data obtained in the representative samples from different gender, socio-typological and ethnic groups, replicating studies using the similar protocols and meta-analyses. This is a replication study of ASR and the first study of P50 suppression in Russian patients with schizophrenia (n = 28) and healthy controls (n = 25). ASR and P50 were estimated according to standard protocols. Patients exhibited increased baseline ASR latency (d = 0.35, p = .026) and reduced prepulse inhibition (PPI) at 60 ms interval (d = 0.39, p = .003) and 120 ms interval (d = 0.37, p = .005) relative to controls. In the P50 test patients displayed greater S2 response amplitude (d = 0.24, p = .036) and deficit of P50 suppression (d = 0.43, p = .001). No correlations of PPI and P50 suppression were found in both groups. Only in controls prepulse ASR facilitation (at 2500 ms interval) positively correlated with P50 suppression (r = –.514, p = .013). In patients PPI displayed significant correlations with Difficulty in abstract thinking (N5: r = –.49, p = .005) and Hallucination (P3: r = .40, p = .036) PANSS scales. Logistic regression showed that the combination of PPI and P50 suppression could serve as a diagnostic predictor. Obtained results demonstrated that both PPI and P50 could be regarded as potential schizophrenia biomarkers in Russian population.

Contingent negative variation (CNV) topography, hemispheric asymmetry and time-course were investigated in healthy subjects and non-medicated paranoid schizophrenic patients in two antisaccade paradigms with the short (800-1000 ms) and long (1200-1400 ms) durations of the fixation period. EEG and electrooculogram (EOG) were recorded. Saccade characteristics and mean amplitudes of slow cortical potentials time-locked to peripheral target were analyzed in 23 healthy volunteers and 19 schizophrenic patients. Compared to healthy control subjects, schizophrenic patients had significantly slower antisaccades and committed significantly more erroneous saccades in the both antisaccade tasks. The prolongation of the fixation period resulted in noticeable decrease of error percent in patients group. The analysis of CNV time-course has revealed two distinct stages in both groups. The early CNV stage was represented by a negative wave with the maximal amplitude over midline fronto-central area, and the late stage was characterized by increased CNV amplitude at the midline and left parietal electrode sites. In healthy subjects the simultaneous activation of frontal and parietal areas was observed in the paradigm with the shorter fixation interval; the increase of the fixation period produced consecutive activation of these areas. Schizophrenic patients' CNV amplitude was generally smaller than that of healthy subjects. The most pronounced between-group differences of the negative shift amplitude were revealed at frontal electrode sites during the early CNV stage in both modifications of the antisaccade task. The deficit of frontal activation revealed in patients at the early stage of antisaccade preparatory set in both antisaccadic paradigms may be related to pathogenesis of paranoid schizophrenia. Se ha investigado la topografía de la variación contingente negativa (CNV), su curso temporal, y asimetría hemisférica en sujetos normales y en pacientes esquizofrénicos paranoides no medicados durante dos paradigmas de movimientos antisacádicos con duración corta (800-1000 ms) y larga (1200-1400 ms) del periodo de fijación. Se registraron el EEG y electro-oculograma. Las características de los movimientos sacádicos y las amplitudes medias de los potenciales corticales lentos relacionados a objetivos periféricos se analizaron en 23 voluntarios sanos y 19 pacientes esquizofrénicos. Comparados con el grupo sano control, los pacientes esquizofrénicos tuvieron movimientos antisacádicos significativamente más lentos y cometieron significativamente más movimientos sacádicos erróneos en ambas tareas antisacádicas. La prolongación del periodo de fijación resultó en un decremento notable del porcentaje de errores en el grupo de pacientes. El análisis del curso temporal de la CNV ha revelado dos etapas distintas en ambos grupos. La etapa temprana de la CNV estuvo representada por una onda negativa con amplitudes máximas en regiones fronto-centrales de la línea media y la etapa tardía estuvo caracterizada por un incremento de la amplitud de la CNV en electrodos parietales izquierdos y de la línea media. En sujetos sanos se observó activación simultánea de áreas parietales y frontales durante el paradigma de intervalo de fijación corto; el incremento del periodo de fijación produjo activación consecutiva de estas áreas. La amplitud de la CNV de pacientes esquizofrénicos fue generalmente menor que la de los sujetos sanos. Las diferencias más pronunciadas entre-grupos en la amplitud de la deflección negativa fueron evidentes en electrodos frontales durante la etapa temprana de la CNV en ambas modificaciones de la tarea antisacádica. El déficit de la activación frontal demostrado en pacientes durante el estado temprano de la preparación antisacádica en ambos paradigmas puede estar relacionado con la patogénesis de la esquizofrenia paranoide.

Se ha investigado la topografía de la variación contingente negativa (CNV), su curso temporal, y asimetría hemisférica en sujetos normales y en pacientes esquizofrénicos paranoides no medicados durante dos paradigmas de movimientos antisacádicos con duración corta (800-1000 ms) y larga (1200-1400 ms) del periodo de fijación. Se registraron el EEG y electro-oculograma. Las características de los movimientos sacádicos y las amplitudes medias de los potenciales corticales lentos relacionados a objetivos periféricos se analizaron en 23 voluntarios sanos y 19 pacientes esquizofrénicos. Comparados con el grupo sano control, los pacientes esquizofrénicos tuvieron movimientos antisacádicos significativamente más lentos y cometieron significativamente más movimientos sacádicos erróneos en ambas tareas antisacádicas. La prolongación del periodo de fijación resultó en un decremento notable del porcentaje de errores en el grupo de pacientes. El análisis del curso temporal de la CNV ha revelado dos etapas distintas en ambos grupos. La etapa temprana de la CNV estuvo representada por una onda negativa con amplitudes máximas en regiones fronto-centrales de la línea media y la etapa tardía estuvo caracterizada por un incremento de la amplitud de la CNV en electrodos parietales izquierdos y de la línea media. En sujetos sanos se observó activación simultánea de áreas parietales y frontales durante el paradigma de intervalo de fijación corto; el incremento del periodo de fijación produjo activación consecutiva de estas áreas. La amplitud de la CNV de pacientes esquizofrénicos fue generalmente menor que la de los sujetos sanos. Las diferencias más pronunciadas entre-grupos en la amplitud de la deflección negativa fueron evidentes en electrodos frontales durante la etapa temprana de la CNV en ambas modificaciones de la tarea antisacádica. El déficit de la activación frontal demostrado en pacientes durante el estado temprano de la preparación antisacádica en ambos paradigmas puede estar relacionado con la patogénesis de la esquizofrenia paranoide.