scholarly journals Theta phase synchrony is sensitive to corollary discharge abnormalities in early illness schizophrenia but not in the clinical high-risk syndrome

2019 ◽  
Author(s):  
Judith M. Ford ◽  
Brian J. Roach ◽  
Rachel L. Loewy ◽  
Barbara K. Stuart ◽  
Judith M. Ford ◽  
...  

ABSTRACTBackgroundAcross the animal kingdom, responses in auditory cortex are dampened during vocalizing compared to passive listening, reflecting the action of the corollary discharge mechanism. In humans, it is seen as suppression of the EEG-based N1 event-related potential, with less N1-suppression seen in people with schizophrenia and those at clinical high risk (CHR) for psychosis. Because N1 is an admixture of theta (4-7Hz) power and phase synchrony, we asked which is responsible for N1 effects and if they outperform the sensitivity of N1 to corollary discharge and schizophrenia.MethodsTheta phase and power values were extracted from EEG data acquired from CHR youth (n=71), early illness schizophrenia patients (ESZ; n=84), and healthy controls (HC; n=103) as they said /ah/ (Talk) and then listened to the sounds played back (Listen). A principal components analysis extracted theta inter-trial coherence (ITC; phase consistency) and event related spectral power, peaking in the N1 latency range.ResultsTheta ITC-suppression (Cohen d=1.46) was greater than N1-suppression in HC (Cohen d=.63). Both were both reduced in ESZ, but only N1-suppression was reduced in CHR. When deprived of the variance shared with theta-ITC suppression, N1-suppression was no longer sensitive to HC vs. ESZ or HC vs. CHR group differences. Deficits in theta ITC-suppression were correlated with delusions (p=.007) in ESZ. Suppression of theta power was not affected by Group.ConclusionsTheta ITC-suppression may provide a simpler assay of the corollary discharge mechanism than N1-suppression. Deficits in circuits that generate low frequency oscillations may be an important component of schizophrenia.

Author(s):  
Brian J Roach ◽  
Judith M Ford ◽  
Rachel L Loewy ◽  
Barbara K Stuart ◽  
Daniel H Mathalon

Abstract Background Prior studies have shown that the auditory N1 event-related potential component elicited by self-generated vocalizations is reduced relative to played back vocalizations, putatively reflecting a corollary discharge mechanism. Schizophrenia patients and psychosis risk syndrome (PRS) youth show deficient N1 suppression during vocalization, consistent with corollary discharge dysfunction. Because N1 is an admixture of theta (4–7 Hz) power and phase synchrony, we examined their contributions to N1 suppression during vocalization, as well as their sensitivity, relative to N1, to corollary discharge dysfunction in schizophrenia and PRS individuals. Methods Theta phase and power values were extracted from electroencephalography data acquired from PRS youth (n = 71), early illness schizophrenia patients (ESZ; n = 84), and healthy controls (HCs; n = 103) as they said “ah” (Talk) and then listened to the playback of their vocalizations (Listen). A principal component analysis extracted theta intertrial coherence (ITC; phase consistency) and event-related spectral power, peaking in the N1 latency range. Talk–Listen suppression scores were analyzed. Results Talk–Listen suppression was greater for theta ITC (Cohen’s d = 1.46) than for N1 in HC (d = 0.63). Both were deficient in ESZ, but only N1 suppression was deficient in PRS. When deprived of variance shared with theta ITC suppression, N1 suppression no longer differentiated ESZ and PRS individuals from HC. Deficits in theta ITC suppression were correlated with delusions (P = .007) in ESZ. Theta power suppression did not differentiate groups. Conclusions Theta ITC-suppression during vocalization is a more sensitive index of corollary discharge-mediated auditory cortical suppression than N1 suppression and is more sensitive to corollary discharge dysfunction in ESZ than in PRS individuals.


2020 ◽  
Vol 74 (10) ◽  
pp. 527-534 ◽  
Author(s):  
Naoya Oribe ◽  
Yoji Hirano ◽  
Elisabetta Re ◽  
Raquelle I. Mesholam‐Gately ◽  
Kristen A. Woodberry ◽  
...  

2019 ◽  
Vol 85 (10) ◽  
pp. S34
Author(s):  
Judith Ford ◽  
Brian Roach ◽  
Rachel Loewy ◽  
Barbara Stuart ◽  
Daniel Mathalon

2021 ◽  
Vol 12 ◽  
Author(s):  
Jennifer H. Foss-Feig ◽  
Sylvia B. Guillory ◽  
Brian J. Roach ◽  
Eva Velthorst ◽  
Holly Hamilton ◽  
...  

Psychosis rates in autism spectrum disorder (ASD) are 5–35% higher than in the general population. The overlap in sensory and attentional processing abnormalities highlights the possibility of related neurobiological substrates. Previous research has shown that several electroencephalography (EEG)-derived event-related potential (ERP) components that are abnormal in schizophrenia, including P300, are also abnormal in individuals at Clinical High Risk (CHR) for psychosis and predict conversion to psychosis. Yet, it is unclear whether P300 is similarly sensitive to psychosis risk in help-seeking CHR individuals with ASD history. In this exploratory study, we leveraged data from the North American Prodrome Longitudinal Study (NAPLS2) to probe for the first time EEG markers of longitudinal psychosis profiles in ASD. Specifically, we investigated the P300 ERP component and its sensitivity to psychosis conversion across CHR groups with (ASD+) and without (ASD–) comorbid ASD. Baseline EEG data were analyzed from 304 CHR patients (14 ASD+; 290 ASD–) from the NAPLS2 cohort who were followed longitudinally over two years. We examined P300 amplitude to infrequent Target (10%; P3b) and Novel distractor (10%; P3a) stimuli from visual and auditory oddball tasks. Whereas P300 amplitude attenuation is typically characteristic of CHR and predictive of conversion to psychosis in non-ASD sample, in our sample, history of ASD moderated this relationship such that, in CHR/ASD+ individuals, enhanced – rather than attenuated - visual P300 (regardless of stimulus type) was associated with psychosis conversion. This pattern was also seen for auditory P3b amplitude to Target stimuli. Though drawn from a small sample of CHR individuals with ASD, these preliminary results point to a paradoxical effect, wherein those with both CHR and ASD history who go on to develop psychosis have a unique pattern of enhanced neural response during attention orienting to both visual and target stimuli. Such a pattern stands out from the usual finding of P300 amplitude reductions predicting psychosis in non-ASD CHR populations and warrants follow up in larger scale, targeted, longitudinal studies of those with ASD at clinical high risk for psychosis.


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