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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Used to study filtering abnormalities in schizophrenia, the paired-click paradigm suffers from poor test-retest reliability of the gating ratio, calculated from the P50 component of the ERP recorded at Cz approximately 50 ms following each of two stimuli. This study sought to improve reliability by assessing 50-ms gating at primary auditory cortices (PAC), the main generators of the P50 Cz component. MEG source modeling was used, taking advantage of the tangentially oriented PAC sources. Ten healthy subjects underwent three sessions, during which Cz-based and PAC-derived gating was measured. Unlike Cz P50, gating ratios at bilateral PACs achieved an intraclass coefficient of .8 or greater. Variability of gating within the same subject was also significantly smaller for bilateral PACs than for Cz P50. Paired-click gating ratio reliability can be improved by examining the individual PACs rather than composite scalp-recorded activity.
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PMID:Improved test-retest reliability of 50-ms paired-click auditory gating using magnetoencephalography source modeling. 1724 Nov 43

Pervasive deficits of attention and set switching have been reported in schizophrenia, prompting efforts to identify the information processing mechanisms associated with these deficits. Recent evidence suggests that set switching may be intact in schizophrenia when the task switch requires only a change in the relevance of perceptual dimensions (e.g., attentional set switches) but decision-to-response mappings (intentional set) are maintained across trials in a cued task switching procedure. The goal of the present research was to replicate this finding and to test its direct corollary, which is the unconventional prediction that individuals with schizophrenia will evidence an intact, switch-sensitive P3(b) brain response to cued switches of attentional set. This prediction was tested in a group of 20 individuals with schizophrenia and 20 healthy comparison participants using event-related brain potential methodology and a cued task-switching task. Attentional set switching costs were equivalent between the two groups despite a set maintenance deficit in schizophrenia. Moreover, a posterior-parietal P3(b) component of the ERP was found to be equally sensitive to attentional set switching in schizophrenia and comparison groups, indicating a "healthy" brain response to switches of attentional set in schizophrenia. These results suggest that the dynamic control of attentional set may be preserved in schizophrenia and that previously reported executive deficits may be specific to the control of intentional task set and to deficits of task set maintenance.
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PMID:Event related brain potential evidence for preserved attentional set switching in schizophrenia. 1746 90

During talking, a corollary discharge prepares cortex for self-generated sounds, minimizing responsiveness and providing a way to recognize sounds as self-generated. When we talk, we are the agent producing the sound and know what sound to expect. The auditory ERP N1 is normally suppressed during talking, but less so in schizophrenia, perhaps due to deficits in agency and expectancy inherent to talking. N1 was assessed in 27 patients (23 schizophrenia, 4 schizoaffective) and 26 controls. During talking, subjects said "ah" every 1-2 s. During agency, subjects pressed a button to deliver "ah" every 1-2 s. During expectancy, "ah" followed a visual warning. Talking yielded greatest N1 suppression in controls and greatest suppression failure in patients. Agency and expectancy had modest suppression effects on N1 and only in controls. Group differences in expectancy and agency could not account for failed corollary discharge during talking in patients.
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PMID:Dissecting corollary discharge dysfunction in schizophrenia. 1756 58

Disturbances of auditory information processing have repeatedly been shown in schizophrenia. To contribute to a better understanding of the neurophysiological underpinnings of habituation in auditory processing and its disturbance in schizophrenia we used three different approaches to analyze auditory evoked responses, namely phase-locking (PL) analyses, single trial amplitudes, and averaged event-related potentials (P50 and N100). Given that brain oscillations reflect the neuronal correlates of information processing we hypothesized that PL and amplitudes reflect even more essential parts of auditory processing than the averaged ERP responses. In 32 schizophrenia patients and 32 matched controls EEG was continuously recorded using an auditory paired click paradigm. PL of the lower frequency bands (alpha and theta) was significantly reduced in patients whereas no significant differences were present in higher frequencies (gamma and beta). Alpha and theta PL and amplitudes showed a marked increase after the first click and to a minor degree after the second one. This habituation was more prominent in controls whereas in schizophrenia patients the response to both clicks differed only slightly. N100 suppression was significantly reduced in schizophrenia patients whereas no group differences were present with respect to the P50. This corresponded to the finding that gamma mostly contributed to the prediction of the P50 response and theta mostly to the N100 response. Our data showed that analyzing phase and amplitude in single trials provides more information on auditory information processing and reflects differences between schizophrenia patients and controls better than analyzing the averaged ERP responses.
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PMID:Sensory gating revisited: relation between brain oscillations and auditory evoked potentials in schizophrenia. 1816 Feb 61

Language abnormalities in schizophrenia are regarded as a hallmark of the disease. Clinical investigations provided accurate descriptions of the different manifestations of abnormal language use, and behavioral studies suggested several mechanisms that might contribute to these abnormalities. This review focuses on semantic memory dysfunction and, primarily, on functional methodologies such as ERP and fMRI that provide more direct measures of abnormal neural mechanisms related to language use in schizophrenia. In addition, the review points to future directions of study of the areas that received little attention thus far and whose investigation might contribute to a more detailed understanding of semantic memory dysfunction in schizophrenia.
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PMID:Future directions for examining semantic memory in schizophrenia spectrum disorders. 1845 Jan 77

Amplitude reduction of the oddball P3 wave is a well-replicated but non-specific finding of schizophrenia. The time-frequency analysis of single-trial ERP data allows to specify in a reliable manner whether the P3 reduction in schizophrenia is due to the decreased P3 response in single trials or due to the inter-trial variability in the timing of the response. Since the delta response most strongly contributes to the P3 amplitude, we focused to the low frequency range of the time-frequency transformed data. EEG was recorded from chronic schizophrenia patients and matched healthy controls during a simple visual oddball task. The wavelet transforms of the averaged ERP and the single trials were computed to investigate the amplitudes of the evoked (phase-locked) and total (phase-locked+non-phase-locked) delta (1-3 Hz) responses, respectively. Evoked delta activity and P3 amplitude to target stimuli were both reduced significantly in patients with schizophrenia, whereas no such difference was obtained for the total delta activity. The significant reduction of the evoked delta response and the absence of such a difference in the total delta response of schizophrenia patients reveals that the delta band response is weakly phase-locked to stimulus in schizophrenia. This result suggests that the reduced P3 amplitudes in the averaged ERPs of schizophrenia patients result from a temporal jitter in the activation of neural circuits engaged in P3 generation.
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PMID:P3 and delta band responses in visual oddball paradigm in schizophrenia. 1857 23

Abnormal language in schizophrenia has been regarded as a hallmark of this disorder. Language abnormalities include loose and unusual associations, tangentiality, and inability to maintain a topic. Recent theories of language dysfunction have invoked working memory abnormalities, as well as abnormal processes within semantic memory in schizophrenia. Two views, often construed as opposing, have been offered to account for language peculiarities in schizophrenia: one holds that initial processes of activation are abnormal while the other holds that late processes of context utilization might be disturbed. We suggest that these views may be complementary rather than mutually exclusive. Given the relative paucity of data on the early processes within semantic networks, we present new evidence using ERP short SOA paradigm that these processes are abnormal in schizophrenia. Furthermore, reduced N400 in the unrelated condition found in this study suggests that the abnormality was related to inefficient early inhibitory processes.
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PMID:Abnormal inhibitory processes in semantic networks in schizophrenia. 1984 Aug 22

Decreased P300 amplitude has been reported in schizophrenics during their first episode. The brain sources that contribute to this abnormality have not yet been well documented, and were investigated in the present study using high density EEG recordings. Nineteen drug-naive first episode schizophrenics were compared to 25 normal controls. Auditory P300 was elicited using an oddball paradigm. The brain sources of P300 ERP were reconstructed by performing low resolution of electromagnetic tomography (LORETA) analysis. No group difference in P300 latency was found. P300 amplitude was smaller for schizophrenics than for controls. Topographical analysis revealed that P300 amplitude reduction in schizophrenics was significant over left and medial regions of interest (ROIs). LORETA analysis of the P300 peak revealed that, the brain sources of P300 were symmetrically distributed over left and right hemispheres among the normal controls, but were asymmetrically distributed among the patients, with a reduction predominantly over the left temporal area. Statistical non-Parametric Mapping analysis identified 29 voxels of a significant group difference, which focused on left insula, left superior temporal gyrus (STG) and left postcentral gyrus (PCG). In addition, the mean P300 current source density over left insula, left STG and left PCG correlated inversely with the patients' Positive and Negative Syndrome Scale scores. The neural substrates that contributed to the decreased P300 amplitude in drug-naive first episode schizophrenia relatively focused on left STG and its nearby areas. These areas are probably involved in the pathogenesis of schizophrenia, and possible mechanisms for pathology need to be further clarified.
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PMID:Decreased P300 current source density in drug-naive first episode schizophrenics revealed by high density recording. 2000 91

Electroencephalography (EEG) and related methodologies offer the promise of predicting the likelihood that novel therapies and compounds will exhibit clinical efficacy early in preclinical development. These analyses, including quantitative EEG (e.g. brain mapping) and evoked/event-related potentials (EP/ERP), can provide a physiological endpoint that may be used to facilitate drug discovery, optimize lead or candidate compound selection, as well as afford patient stratification and Go/No-Go decisions in clinical trials. Currently, the degree to which these different methodologies hold promise for translatability between preclinical models and the clinic have not been well summarized. To address this need, we review well-established and emerging EEG analytic approaches that are currently being integrated into drug discovery programs throughout preclinical development and clinical research. Furthermore, we present the use of EEG in the drug development process in the context of a number of major central nervous system disorders including Alzheimer's disease, schizophrenia, depression, attention deficit hyperactivity disorder, and pain. Lastly, we discuss the requirements necessary to consider EEG technologies as a biomarker. Many of these analyses show considerable translatability between species and are used to predict clinical efficacy from preclinical data. Nonetheless, the next challenge faced is the selection and validation of EEG endpoints that provide a set of robust and translatable biomarkers bridging preclinical and clinical programs.
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PMID:Aligning strategies for using EEG as a surrogate biomarker: a review of preclinical and clinical research. 2093 62

INTRODUCTION: Schizophrenia is currently diagnosed on the basis of patient reports and clinical observations. A diagnosis based on aetiology is inherently more reliable due to being closer to the disease process than the overt clinical manifestations. Accordingly, recent research in schizophrenia has focused on the development of biomarkers in a bit to improve the reliability and neurobiological relevance of the diagnosis. Visual information processing is one of these promising fields of recent biomarker research. AREAS COVERED: This article provides an overview of the available literature regarding deficits in schizophrenia detectable through psychophysical (contrast and motion sensitivity, visual backward-masking), ERP (P1 and N1 visual evoked potentials) and oscillatory (signal power and phase-locking factor of evoked oscilations) measures and their validity as trait or state biomarkers of the disease. The methodology included a search on articles related to visual information processing in schizophrenia on the PubMed database. EXPERT OPINION: Biomarker research in schizophrenia is a rapidly expanding area. Evidence exists to suggest that both psychotic and manic symptoms are associated with visual processing abnormalities. A specific impairment confined to the magnocellular component of the visual system might be a trait biomarker of schizophrenia.
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PMID:New visual information processing abnormality biomarker for the diagnosis of Schizophrenia. 2200 64


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