The present study examined how increasing the rate of steady-state stimulation affects schizophrenia-normal differences on the N1 auditory-evoked potential, an index of auditory integration. Dense-array EEG was recorded while schizophrenia and normal subjects heard 1 kHz tones amplitude modulated at 10, 20, 40, or 80 Hz. Spectral power across frequency and time was calculated. The typically lower N1 amplitude in schizophrenia, observed at the 10 Hz burst rate, increased to nearly equal that of normal individuals at 20 Hz. Unlike normal subjects, schizophrenia subjects' power at N1 failed to increase at the 40 and 80 Hz burst rates. These results suggest steady-state stimuli, up to a point, provide the extra information needed for schizophrenia patients to more efficiently integrate auditory information.
"Auditory sensory processing abnormalities in schizophrenia (SZ) have been quantified with transient evoked responses (e.g., N/M100) to abrupt stimulus onsets (Rosburg et al., 2008) and auditory steady-state responses (aSSR) to repeating auditory stimulation (e.g., a 40 Hz steady-state stimulus is a repetition every 25 ms). Low N100 amplitude in SZ is one of the most replicated effects in this literature (Shelley et al., 1999; Blumenfeld and Clementz, 2001; Ford et al., 2001; Gilmore et al., 2004; Hamm et al., in press). Theoretically, deficiencies of excitatory drive on (Goff and Coyle, 2001) and/or coordination between (Benes and Berretta, 2001) neuronal ensembles supporting auditory stimulus processing cause these abnormalities in SZ. "
[Show abstract][Hide abstract] ABSTRACT: Individuals with schizophrenia (SZ) have deviations in auditory perception perhaps attributable to altered neural oscillatory response properties in thalamo-cortical and/or local cortico-cortical circuits. Previous EEG studies of auditory steady-state responses (aSSRs; a measure of sustained neuronal entrainment to repetitive stimulation) in SZ have indicated attenuated gamma range (≈40 Hz) neural entrainment. Stimuli in most such studies have been relatively brief (500-1000 ms) trains of 1 ms clicks or amplitude modulated pure tones (1000 Hz) with short, fixed interstimulus intervals (200-1000 ms). The current study used extended (1500 ms), more aurally dense broadband stimuli (500-4000 Hz noise; previously demonstrated to elicit larger aSSRs) with longer, variable interstimulus intervals (2700-3300 ms). Dense array EEG (256 sensor) was collected while 17 SZ and 16 healthy subjects passively listed to stimuli modulated at 15 different frequencies spanning beta and gamma ranges (16-44 Hz in 2 Hz steps). Results indicate that SZ have augmented aSSRs that were most extreme in the gamma range. Results also constructively replicate previous findings of attenuated low frequency auditory evoked responses (2-8 Hz) in SZ. These findings (i) highlight differential characteristics of low versus high frequency and induced versus entrained oscillatory auditory responses in both SZ and healthy stimulus processing, (ii) provide support for an NMDA-receptor hypofunction-based pharmacological model of SZ, and (iii) report a novel pattern of aSSR abnormalities suggesting that gamma band neural entrainment deviations among SZ may be more complex than previously supposed, including possibly being substantially influenced by physical stimulus properties.
Schizophrenia Research 04/2012; 138(1):1-7. DOI:10.1016/j.schres.2012.04.003 · 3.92 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Schizophrenia patients have difficulty distinguishing relevant from irrelevant auditory information. Auditory oddball paradigms are commonly used to investigate the processing of stimulus relevance. The present study used dense-array EEG and distributed source reconstructions to examine schizophrenia-normal differences in the processing of targets and standards as a function of the temporal sequence of stimuli. Brain responses were evaluated separately for early and late standards (standards 1-3 and 4-6 following a target, respectively) and early and late targets (those following 2-3 standards and 4-6 standards, respectively). The latencies of peaks (N1, P2, P3) in the event-related potential (ERP) waveforms did not differ between schizophrenia and normal subjects. However, schizophrenia-normal differences in neural activity, derived from minimum norm estimation, occurred at specific times during stimulus processing as a function of stimulus sequence. Schizophrenia patients displayed smaller activity than normals in early ERPs (left hemispheric N1, right frontal P2) to late targets, and they produced P3-like responses to late standards. Furthermore, during the P2/N2 time interval, opposite patterns of brain activity were elicited in schizophrenia and normal subjects in response to standards, indicating different neural responses to the same stimulus events. These results suggest attention allocation to task-irrelevant stimuli in schizophrenia, consequent upon insufficient representation of stimulus significance and context. Thus, schizophrenia compromises the ability to properly use context to solve even simple cognitive problems.
Cognitive Brain Research 08/2005; 24(2):215-27. DOI:10.1016/j.cogbrainres.2005.01.020 · 3.77 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The electroencephalogram (EEG) recorded from the human scalp is widely used to study cognitive and brain functions in schizophrenia. Current research efforts are primarily devoted to the assessment of event-related potentials (ERPs) and event-related oscillations (EROs), extracted from the ongoing EEG, in patients with schizophrenia and in clinically unaffected individuals who, due to their family history and current mental status, are at high risk for developing schizophrenia. In this article, we discuss the potential usefulness of ERPs and EROs as genetic vulnerability markers, as pathophysiological markers, and as markers of possible ongoing progressive cognitive and cortical deterioration in schizophrenia. Our main purpose is to illustrate that these neurophysiological measures can offer valuable quantitative biological markers of basic pathophysiological mechanisms and cognitive dysfunctions in schizophrenia, yet they may not be specific to current psychiatry's diagnosis and classification. These biological markers can provide unique information on the nature and extent of cognitive and brain dysfunction in schizophrenia. Moreover, they can be utilized to gain deeper theoretical insights into illness etiology and pathophysiology and may lead to improvements in early detection and more effective and targeted treatment of schizophrenia. We conclude by addressing several key methodological, conceptual, and interpretative issues involved in this research field and by suggesting future research directions.
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