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Functional MRI of Verbal Self-monitoring in Schizophrenia: Performance and Illness-Specific Effects

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TLDR
It is concluded that hypoactivation of a neural network comprised of the thalamus and frontotemporal regions underlies impaired speech monitoring in schizophrenia.
Abstract
Previous small-sample studies have shown altered frontotemporal activity in schizophrenia patients with auditory hallucinations and impaired monitoring of self-generated speech. We examined a large cohort of patients with schizophrenia (n = 63) and a representative group of healthy controls (n = 20) to disentangle performance, illness, and symptom-related effects in functional magnetic resonance imaging-detected brain abnormalities during monitoring of self- and externally generated speech in schizophrenia. Our results revealed activation of the thalamus (medial geniculate nucleus, MGN) and frontotemporal regions with accurate monitoring across all participants. Less activation of the thalamus (MGN, pulvinar) and superior-middle temporal and inferior frontal gyri occurred in poorly performing patients (1 standard deviation below controls' mean; n = 36), relative to the combined group of controls and well-performing patients. In patients, (1) greater deactivation of the ventral striatum and hypothalamus to own voice, combined with nonsignificant activation of the same regions to others' voice, associated positively with negative symptoms (blunted affect, emotional withdrawal, poor rapport, passive social avoidance) regardless of performance and (2) exaggerated activation of the right superior-middle temporal gyrus during undistorted, relative to distorted, feedback associated with both positive symptoms (hallucinations, persecution) and poor performance. A further thalamic abnormality characterized schizophrenia patients regardless of performance and symptoms. We conclude that hypoactivation of a neural network comprised of the thalamus and frontotemporal regions underlies impaired speech monitoring in schizophrenia. Positive symptoms and poor monitoring share a common activation abnormality in the right superior temporal gyrus during processing of degraded speech. Altered striatal and hypothalamic modulation to own and others' voice characterizes emotionally withdrawn and socially avoidant patients.

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Journal ArticleDOI

Cortical Activations During Auditory Verbal Hallucinations in Schizophrenia: A Coordinate-Based Meta-Analysis

TL;DR: This meta-analysis demonstrated that experiencing AVHs is associated with increased activity in fronto-temporal areas involved in speech generation and speech perception, but also within the medial temporal lobe, a structure notably involved in verbal memory.
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Nature experience reduces rumination and subgenual prefrontal cortex activation

TL;DR: A pathway by which nature experience may improve mental well-being is revealed and it is suggested that accessible natural areas within urban contexts may be a critical resource for mental health in the authors' rapidly urbanizing world.
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How can the brain's resting state activity generate hallucinations? A ‘resting state hypothesis’ of auditory verbal hallucinations

TL;DR: The 'resting state hypotheses' of AVH suggest that AVH may be traced back to abnormally elevated resting state activity in auditory cortex itself, abnormal modulation of the auditory cortex by anterior cortical midline regions as part of the default-mode network, and neural confusion between auditory cortical resting state changes and stimulus-induced activity.
Journal ArticleDOI

The neural mechanisms of hallucinations: A quantitative meta-analysis of neuroimaging studies.

TL;DR: The need for unified theoretical frameworks that account for the full range of hallucinatory experiences is discussed, with greater activity in auditory cortex during AVHs and in visual cortex during VHs supports models proposing over-stimulation of sensory cortices in the generation of these perceptual anomalies.
Journal ArticleDOI

Investigation of Anatomical Thalamo-Cortical Connectivity and fMRI Activation in Schizophrenia

TL;DR: Thalamocortical connectivity to the LPFC is altered in schizophrenia with functional consequences on working memory processing in LPFC, and the correlation with BOLD activation was accentuated in patients as compared with controls in the ventral LPFC.
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Journal ArticleDOI

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