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BACKGROUND: Schizophrenia may be understood as a disorder of neural synchrony. There is also increasing evidence that emotional and social cognitive impairments are central to this disorder. In patients with first-episode schizophrenia, we examined whether emotion perception is associated with disruptions to high-frequency (40 Hz) gamma synchrony and whether these disruptions predict self-regulatory adaptive compensations reflected in social cognitive behaviours. METHODS: We obtained electroencephalography recordings from 28 patients with first-episode schizophrenia and matched healthy controls during perception of facial emotion under both conscious and nonconscious conditions. We extracted gamma-band synchrony from the electroencephalogram. We also used behavioural measures of emotion identification, emotional intelligence, negativity bias and social function, along with ratings of first-episode schizophrenia symptoms. We analyzed group differences and predicted social cognition to assess the potential contribution of medication. RESULTS: Within 200 ms poststimulus, patients with first-episode schizophrenia showed alterations in gamma synchrony during both conscious and nonconscious emotion perception. Stimulus-locked synchrony was reduced in patients, particularly over the temporal cortex, whereas complementary enhancements in absolute gamma synchrony (independent of stimuli) were more distributed over temporal and left parieto-occipital regions. This pattern of altered synchrony predicted poor performance on each measure of social cognition among these patients. Medication dosage did not correlate significantly with either gamma synchrony or behavioural measures in this group. LIMITATIONS: Limitations to our study include the lack of comparison between medicated and unmedicated patients or between types of medication. CONCLUSION: These findings suggest that disruptions in integrative processing of motivationally important stimuli show promise as a potential biological marker of social cognitive impairments, present from the first episode of schizophrenia, and their outcomes. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To index the extent to which treatment response in posttraumatic stress disorder (PTSD) is predicted by rostral anterior cingulate cortex (rACC) volume. METHOD: We used structural magnetic resonance imaging in a 1.5 T scanner to examine subjects with PTSD (n = 13), traumatized control subjects (n = 13) and nontraumatized control subjects (n = 13). Subjects with PTSD then participated in 8 sessions of cognitive-behavioural therapy, after which we reassessed them for PTSD. RESULTS: According to voxel-based morphometry, treatment responders had larger rACC volume than nonresponders. Further, symptom reduction was associated with larger rACC volume. CONCLUSION: Consistent with evidence for the neural bases of extinction learning, PTSD patients with larger rACC volume may be better able to regulate fear during cognitive-behavioural therapy and thus achieve greater treatment gains. [ABSTRACT FROM AUTHOR]

Self-generated overt actions are preceded by a slow negativity as measured by electroencephalogram, which has been associated with motor preparation. Recent studies have shown that this neural activity is modulated by the predictability of action outcomes. It is unclear whether inner speech is also preceded by a motor-related negativity and influenced by the same factor. In three experiments, we compared the contingent negative variation elicited in a cue paradigm in an active vs. passive condition. In Experiment 1, participants produced an inner phoneme, at which an audible phoneme whose identity was unpredictable was concurrently presented. We found that while passive listening elicited a late contingent negative variation, inner speech production generated a more negative late contingent negative variation. In Experiment 2, the same pattern of results was found when participants were instead asked to overtly vocalize the phoneme. In Experiment 3, the identity of the audible phoneme was made predictable by establishing probabilistic expectations. We observed a smaller late contingent negative variation in the inner speech condition when the identity of the audible phoneme was predictable, but not in the passive condition. These findings suggest that inner speech is associated with motor preparatory activity that may also represent the predicted action-effects of covert actions., (© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permission@oup.com.)

Action-effect predictions are believed to facilitate movement based on its association with sensory objectives and suppress the neurophysiological response to self- versus externally generated stimuli (i.e. sensory attenuation). However, research is needed to explore theorized differences in the use of action-effect prediction based on whether movement is uncued (i.e. volitional) or in response to external cues (i.e. stimulus-driven). While much of the sensory attenuation literature has examined effects involving the auditory N1, evidence is also conflicted regarding this component's sensitivity to action-effect prediction. In this study (n = 64), we explored the influence of action-effect contingency on event-related potentials associated with visually cued and uncued movement, as well as resultant stimuli. Our findings replicate recent evidence demonstrating reduced N1 amplitude for tones produced by stimulus-driven movement. Despite influencing motor preparation, action-effect contingency was not found to affect N1 amplitudes. Instead, we explore electrophysiological markers suggesting that attentional mechanisms may suppress the neurophysiological response to sound produced by stimulus-driven movement. Our findings demonstrate lateralized parieto-occipital activity that coincides with the auditory N1, corresponds to a reduction in its amplitude, and is topographically consistent with documented effects of attentional suppression. These results provide new insights into sensorimotor coordination and potential mechanisms underlying sensory attenuation., (© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permission@oup.com.)

The phenomenon of sensory self-suppression - also known as sensory attenuation - occurs when a person generates a perceptible stimulus (such as a sound) by performing an action (such as speaking). The sensorimotor control system is thought to actively predict and then suppress the vocal sound in the course of speaking, resulting in lowered cortical responsiveness when speaking than when passively listening to an identical sound. It has been hypothesized that auditory hallucinations in schizophrenia result from a reduction in self-suppression due to a disruption of predictive mechanisms required to anticipate and suppress a specific, self-generated sound. It has further been hypothesized that this suppression is evident primarily in theta band activity. Fifty-one people, half of whom had a diagnosis of schizophrenia, were asked to repeatedly utter a single syllable, which was played back to them concurrently over headphones while EEG was continuously recorded. In other conditions, recordings of the same spoken syllables were played back to participants while they passively listened, or were played back with their onsets preceded by a visual cue. All participants experienced these conditions with their voice artificially shifted in pitch and also with their unaltered voice. Suppression was measured using event-related potentials (N1 component), theta phase coherence and power. We found that suppression was generally reduced on all metrics in the patient sample, and when voice alteration was applied. We additionally observed reduced theta coherence and power in the patient sample across all conditions. Visual cueing affected theta coherence only. In aggregate, the results suggest that sensory self-suppression of theta power and coherence is disrupted in schizophrenia., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Recent evidence shows that genetic and environmental risk factors for psychotic disorders are associated with higher levels of schizotypy (or psychosis proneness) in the general population. However, little is known about how these risk factors interact. We specifically examined whether genetic loading for schizophrenia moderates the association between childhood trauma severity and schizotypy. Schizotypy was measured using the Schizotypal Personality Questionnaire (SPQ), and childhood trauma severity was measured with the Childhood Trauma Questionnaire (CTQ) among a total of 168 participants (comprising 51 healthy individuals, 56 diagnosed with schizophrenia, and 61 with bipolar disorder). Polygenic risk scores (PRS) for schizophrenia were calculated for all participants and examined as a potential moderator of associations between total scores on the CTQ and schizotypy total scores and dimensions (i.e., cognitive-perceptual, interpersonal, disorganised). Multiple linear regression models revealed associations between childhood trauma and all dimensions of schizotypy, but no associations between PRS and schizotypy. A significant interaction between PRS and childhood trauma was evident for the interpersonal and disorganised dimensions of schizotypy, as well as the total score, reflecting positive associations between childhood trauma severity and these two schizotypal dimensions, only for individuals with low or average PRS for schizophrenia. This suggests that trauma may be able to increase risk for psychosis independently of any genetic vulnerability. The present findings are consistent with the idea of several risk pathways for the development of psychotic disorders., Competing Interests: Declaration of Competing Interest Authors have no conflict-of-interest to disclose., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Stimuli that have been generated by a person's own willed motor actions generally elicit a suppressed electrophysiological, as well as phenomenological, response compared with identical stimuli that have been externally generated. This well-studied phenomenon, known as sensory attenuation, has mostly been studied by comparing ERPs evoked by self-initiated and externally generated sounds. However, most studies have assumed a uniform action-effect contingency, in which a motor action leads to a resulting sensation 100% of the time. In this study, we investigated the effect of manipulating the probability of action-effect contingencies on the sensory attenuation effect. In Experiment 1, participants watched a moving, marked tickertape while EEG was recorded. In the full-contingency (FC) condition, participants chose whether to press a button by a certain mark on the tickertape. If a button press had not occurred by the mark, a sound would be played a second later 100% of the time. If the button was pressed before the mark, the sound was not played. In the no-contingency (NC) condition, participants observed the same tickertape; in contrast, however, if participants did not press the button by the mark, a sound would occur only 50% of the time (NC-inaction). Furthermore, in the NC condition, if a participant pressed the button before the mark, a sound would also play 50% of the time (NC-action). In Experiment 2, the design was identical, except that a willed action (as opposed to a willed inaction) triggered the sound in the FC condition. The results were consistent across the two experiments: Although there were no differences in N1 amplitude between conditions, the amplitude of the Tb and P2 components were smaller in the FC condition compared with the NC-inaction condition, and the amplitude of the P2 component was also smaller in the FC condition compared with the NC-action condition. The results suggest that the effect of contingency on electrophysiological indices of sensory attenuation may be indexed primarily by the Tb and P2 components, rather than the N1 component which is most commonly studied., (© 2022 Massachusetts Institute of Technology. Published under a Creative Commons Attribution 4.0 International (CC BY 4.0) license.)

Previous cross-sectional studies have reported that adolescent patients with anorexia nervosa (AN) showed global gray matter volume (GMV) reductions at the acute phase which were restored at the weight-recovered phase, compared with healthy controls (HC). However, few studies have investigated white matter volume (WMV) or cortical thickness in the context of AN, and results have been inconsistent. Voxel-based morphometry analyses for GM and WM, and cortical thickness analyses for GM were conducted in 31 adolescent patients with AN (vs. 18 HC) in the acute phase, and 16 patients with AN (vs. 13 HC) in the follow-up weight-recovered phase, over an approximately 1-year follow-up interval. At the acute phase, the AN patients showed significant reductions of GMVs and cortical thickness in widespread brain regions, compared with HC. Significant WMV reductions were identified in the bilateral superior longitudinal fascicle, superior thalamic radiation, corona radiata, and fornix, pons, and medulla in the patients. At the weight-recovered phase, the AN patients showed a significant GMV reduction in the left hippocampus, and a WMV reduction in the pons, compared with the HC. There was no difference in cortical thickness between two groups at the weight-recovered phase. In conclusion, the widespread volumetric reductions in GM and WM, and reduced cortical thickness observed in AN patients in the acute phase were not evident in the follow-up weight-recovered phase. The volume reductions observed in the hippocampus and pons in the weight-recovered phase could potentially reflect delayed neurogenesis or recovery from starvation in the AN patients., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Objectives: Risk for psychosis in the general population is characterized by a set of multidimensional traits that are referred to as schizotypy. Higher levels of schizotypy are associated with socioeconomic disadvantage and childhood trauma, just as these risk factors are associated with schizophrenia and bipolar disorder. Here, we set out to investigate whether cumulative sociodemographic disadvantage mediates associations between childhood trauma and schizotypy in adulthood., Methods: A sociodemographic cumulative risk (SDCR) score was derived from six risk indices spanning employment, education, income, socioeconomic status, marital, and living circumstances for 197 participants that included both healthy (n = 57) and clinical samples with schizophrenia or schizoaffective disorder (n = 65) or bipolar disorder (n = 75). A series of multiple linear regressions was used to examine the direct and indirect associations among childhood trauma (measured with the Childhood Trauma Questionnaire), the SDCR index, and levels of schizotypy (measured with the Schizotypal Personality Questionnaire)., Results: Schizotypy was independently associated with trauma and the SDCR index. In addition, the SDCR index partially mediated associations between trauma and schizotypy., Conclusions: These findings in a mixed sample of healthy and clinical participants represent the full spectrum of schizotypy across health and illness and suggest that effects of childhood trauma on schizotypal personality organization may operate via cumulative socioeconomic disadvantage in adulthood., Practitioner Points: The strong associations between trauma and schizotypy suggest that systematic health screening of children exposed to early life trauma may assist to identify those at risk of developing psychosis. Clinicians should pay attention to various indicators of sociodemographic disadvantage in patients prone to psychosis, in addition to any exposure to trauma during childhood., (© 2021 The British Psychological Society.)

Sensory suppression refers to the phenomenon that sensory input generated by our own actions, such as moving a finger to press a button to hear a tone, elicits smaller neural responses than sensory input generated by external agents. This observation is usually explained via the internal forward model in which an efference copy of the motor command is used to compute a corollary discharge, which acts to suppress sensory input. However, because moving a finger to press a button is accompanied by neural processes involved in preparing and performing the action, it is unclear whether sensory suppression is the result of movement planning, movement execution, or both. To investigate this, in two experiments, we compared ERPs to self-generated tones that were produced by voluntary, semivoluntary, or involuntary button-presses, with externally generated tones that were produced by a computer. In Experiment 1, the semivoluntary and involuntary button-presses were initiated by the participant or experimenter, respectively, by electrically stimulating the median nerve in the participant's forearm, and in Experiment 2, by applying manual force to the participant's finger. We found that tones produced by voluntary button-presses elicited a smaller N1 component of the ERP than externally generated tones. This is known as N1-suppression. However, tones produced by semivoluntary and involuntary button-presses did not yield significant N1-suppression. We also found that the magnitude of N1-suppression linearly decreased across the voluntary, semivoluntary, and involuntary conditions. These results suggest that movement planning is a necessary condition for producing sensory suppression. We conclude that the most parsimonious account of sensory suppression is the internal forward model., (© 2021 Massachusetts Institute of Technology.)

Self-generated stimuli have been found to elicit a reduced sensory response compared with externally-generated stimuli. However, much of the literature has not adequately controlled for differences in the temporal predictability and temporal control of stimuli. In two experiments, we compared the N1 (and P2) components of the auditory-evoked potential to self- and externally-generated tones that differed with respect to these two factors. In Experiment 1 (n = 42), we found that increasing temporal predictability reduced N1 amplitude in a manner that may often account for the observed reduction in sensory response to self-generated sounds. We also observed that reducing temporal control over the tones resulted in a reduction in N1 amplitude. The contrasting effects of temporal predictability and temporal control on N1 amplitude meant that sensory attenuation prevailed when controlling for each. Experiment 2 (n = 38) explored the potential effect of selective attention on the results of Experiment 1 by modifying task requirements such that similar levels of attention were allocated to the visual stimuli across conditions. The results of Experiment 2 replicated those of Experiment 1, and suggested that the observed effects of temporal control and sensory attenuation were not driven by differences in attention. Given that self- and externally-generated sensations commonly differ with respect to both temporal predictability and temporal control, findings of the present study may necessitate a re-evaluation of the experimental paradigms used to study sensory attenuation., (Copyright © 2021. Published by Elsevier Inc.)

Sensory attenuation is the phenomenon that stimuli generated by willed motor actions elicit a smaller neurophysiological response than those generated by external sources. It has mostly been investigated in the auditory domain, by comparing ERPs evoked by self-initiated (active condition) and externally-generated (passive condition) sounds. The mechanistic basis of sensory attenuation has been argued to involve a duplicate of the motor command being used to predict sensory consequences of self-generated movements. An alternative possibility is that the effect is driven by between-condition differences in participants' sense of agency over the sound. In this paper, we disambiguated the effects of motor-action and sense of agency on sensory attenuation with a novel experimental paradigm. In Experiment 1, participants watched a moving, marked tickertape while EEG was recorded. In the active condition, participants chose whether to press a button by a certain mark on the tickertape. If a button-press had not occurred by the mark, then a tone would be played 1 s later. If the button was pressed prior to the mark, the tone was not played. In the passive condition, participants passively watched the animation, and were informed about whether a tone would be played on each trial. The design for Experiment 2 was identical, except that the contingencies were reversed (i.e., a button-press by the mark led to a tone). The results were consistent across the two experiments: while there were no differences in N1 amplitude between the active and passive conditions, the amplitude of the Tb component was suppressed in the active condition. The amplitude of the P2 component was enhanced in the active condition in both Experiments 1 and 2. These results suggest that motor-actions and sense of agency have differential effects on sensory attenuation to sounds and are indexed with different ERP components., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Schizotypy refers to a multidimensional construct that spans a range of cognitive, behavioral, and personality features, representing liability to psychosis on a continuum between health and illness. Schizotypy has been associated with functional and structural brain alterations as potential intermediate phenotypes on the developmental path to psychosis. We scanned the literature between February 2019 and August 1, 2020 using PubMed, Medline, APA PsycINFO, and ProQuest. We identified eligible articles conducted on participants assessed with psychometric schizotypy across the health-illness spectrum and reporting a direct statistic between schizotypy and a structural, task-related, or functional magnetic resonance imaging brain measure. Articles not peer-reviewed and not written in English were excluded. We systematically reviewed 84 studies that determined the changes in gray matter, brain activation, and connectivity associated with schizotypy in both healthy and clinical cohorts. Morphological and functional changes in the default and the frontoparietal networks, specifically frontal and temporal cortices, were most frequently associated with schizotypy. Yet, we were unable to identify consistent patterns of morphological or functional brain aberration associated with schizotypy, due to methodological differences between studies in the conceptualization and measurement of schizotypy. Efforts toward greater methodological concordance in future neuroimaging research of schizotypy are needed to improve the identification of brain-based endophenotypes for schizophrenia. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Background: Although the pathogenesis of panic attacks has been well studied in patients with panic disorder (PD), the neurobiological basis of the long-term fear memories and avoidance behavior that are often observed in PD have not been well investigated. Recent animal studies have suggested that nucleus accumbens (NAcc) plays an important role in neurobiological basis of long-term fear memories and avoidance behavior., Methods: Thirty-eight patients with PD and 38 matched healthy control subjects (HC) participated in this study. Differences in relative volumes and shape deformations of NAcc were evaluated between groups. Correlation analyses were conducted to quantify the association between structural abnormalities in the NAcc and trait, state anxiety measured by the State-Trait Anxiety Inventory (STAI)., Results: Significant volume reductions were observed in the bilateral NAcc in the patients with PD, relative to the HC. In terms of shape differences, the PD patients demonstrated significant inward deformation of the NAcc bilaterally, compared to the HC. Degree of shape deformation in the right NAcc was associated with higher scores of the STAI-Trait, and STAI-State measures in the PD patients., Limitations: All the patients received medication such as Psychotropic drug., Conclusion: Patients with PD showed reduced volumes in the NAcc, especially in lateral regions, compared with HC. Furthermore, shape deformation in the right NAcc was associated with trait anxiety and state anxiety, which has been associated with avoidance behavior., Competing Interests: Declaration of Competing Interest All authors have no conflict of interest to disclose, and agree to transfer copyright to the Elsevier., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background and Aims: The notion of basic self-disturbance has been proposed as a core feature of schizophrenia-spectrum disorders and as an indicator of future transition to psychosis in high-risk populations. However, the relation of this notion to many clinical characteristics has not been explored. The aim of this study was: (a) to investigate the distribution of self-disturbance and other symptoms dimensions in ultra-high risk (UHR), first-episode psychosis (FEP) and healthy control groups; and (b) to explore the association of self-disturbance with a history of self-harm, suicidal attempt, eating disorder symptomatology, school bullying victimization and sexual or physical abuse., Methods: Patients with UHR status (n = 38) or FEP (n = 26) and healthy controls (n = 33) were assessed with the Examination of Anomalous Self-Experience (EASE) and the Comprehensive Assessment of at Risk Mental States (CAARMS). The clinical-historical variables were assessed through medical records., Results: The FEP group scored significantly higher on the EASE than the UHR group, which scored significantly higher than the healthy control group, which had a very low score. Multivariate logistic regression analyses revealed that higher EASE score was significantly associated with a history of self-harm, disordered eating and bullying victimization (but not with suicide attempts or sexual/physical abuse) after controlling for positive, negative and depressive symptoms., Conclusion: These novel findings suggest that self-disturbance may be related to a history of school bullying victimization, self-harm and eating disorder symptomatology in patients with or at-risk of psychosis. If further confirmed, these findings are potentially relevant to clinical risk assessment and therapy., (© 2019 John Wiley & Sons Australia, Ltd.)

An auditory event is often accompanied by characteristic visual information. For example, the sound level produced by a vigorous handclap may be related to the speed of hands as they move toward collision. Here, we tested the hypothesis that visual information about the intensity of auditory signals are capable of altering the subsequent neurophysiological response to auditory stimulation. To do this, we used EEG to measure the response of the human brain ( n = 28) to the audiovisual delivery of handclaps. Depictions of a weak handclap were accompanied by auditory handclaps at low (65 dB) and intermediate (72.5 dB) sound levels, whereas depictions of a vigorous handclap were accompanied by auditory handclaps at intermediate (72.5 dB) and high (80 dB) sound levels. The dependent variable was the amplitude of the initial negative component (N1) of the auditory evoked potential. We find that identical clap sounds (intermediate level; 72.5 dB) elicited significantly lower N1 amplitudes when paired with a video of a weak clap, compared with when paired with a video of a vigorous clap. These results demonstrate that intensity predictions can affect the neural responses to auditory stimulation at very early stages (<100 msec) in sensory processing. Furthermore, the established sound-level dependence of auditory N1 amplitude suggests that such effects may serve the functional role of altering auditory responses in accordance with visual inferences. Thus, this study provides evidence that the neurally evoked response to an auditory event results from a combination of a person's beliefs with incoming auditory input.

Background: The integration of various domains or levels of analysis (clinical, neurobiological, genetic, etc.) has been a challenge in schizophrenia research. A promising approach is to use the core phenomenological features of the disorder as an organising principle for other levels of analysis. Minimal self-disturbance (fragility in implicit first-person perspective, presence and agency) is emerging as a strong candidate to play this role. This approach was adopted in a previously described theoretical neurophenomenological model that proposed that source monitoring deficits and aberrant salience may be neurocognitive/neurobiological processes that correlate with minimal self-disturbance on the phenomenological level, together playing an aetiological role in the onset of schizophrenia spectrum disorders. The current paper presents full cross-sectional data from the first empirical test of this model., Methods: Fifty ultra-high risk for psychosis patients, 39 first episode psychosis patients and 34 healthy controls were assessed with a variety of clinical measures, including the Examination of Anomalous Self-Experience (EASE), and neurocognitive and neurophysiological (EEG) measures of source monitoring deficits and aberrant salience., Results: Linear regression indicated that source monitoring (composite score across neurocognitive and neurophysiological measures), with study group as an interaction term, explained 39.8% of the variance in EASE scores (R 2  = 0.41, F(3,85) = 14.78, p < 0.001), whereas aberrant salience (composite score) explained only 6% of the variance in EASE scores (R 2  = 0.06, F(3,85) = 1.44, p = 0.93). Aberrant salience measures were more strongly related to general psychopathology measures, particularly to positive psychotic symptoms, than to EASE scores., Discussion: A neurophenomenological model of minimal self-disturbance in schizophrenia spectrum disorders may need to be expanded from source monitoring deficits to encompass other relevant constructs such as temporal processing, intermodal/multisensory integration, and hierarchical predictive processing. The cross-sectional data reported here will be expanded with longitudinal analysis in subsequent reports. These data and other related recent research show an emerging picture of neuro-features of core phenomenological aspects of schizophrenia spectrum disorders beyond surface-level psychotic symptoms., (Copyright © 2019 Elsevier Inc. All rights reserved.)

When we move our articulator organs to produce overt speech, the brain generates a corollary discharge that acts to suppress the neural and perceptual responses to our speech sounds. Recent research suggests that inner speech - the silent production of words in one's mind - is also accompanied by a corollary discharge. Here, we show that this corollary discharge contains information about the temporal and physical properties of inner speech. In two experiments, participants produced an inner phoneme at a precisely-defined moment in time. An audible phoneme was presented 300 ms before, concurrently with, or 300 ms after participants produced the inner phoneme. We found that producing the inner phoneme attenuated the N1 component of the event-related potential - an index of auditory cortex processing - but only when the inner and audible phonemes occurred concurrently and matched on content. If the audible phoneme was presented before or after the production of the inner phoneme, or if the inner phoneme did not match the content of the audible phoneme, there was no attenuation of the N1. These results suggest that inner speech is accompanied by a temporally-precise and content-specific corollary discharge. We conclude that these results support the notion of a functional equivalence between the neural processes that underlie the production of inner and overt speech, and may provide a platform for identifying inner speech abnormalities in disorders in which they have been putatively associated, such as schizophrenia., (Copyright © 2019. Published by Elsevier Inc.)

Speaking-induced suppression (SIS) is the phenomenon that the sounds one generates by overt speech elicit a smaller neurophysiological response in the auditory cortex than comparable sounds that are externally generated. SIS is a specific example of the more general phenomenon of self-suppression. SIS has been well established in nonhuman animals and is believed to involve the action of corollary discharges. This review summarizes, first, the evidence for SIS in heathy human participants, where it has been most commonly assessed with electroencephalography and/or magnetoencephalography using an experimental paradigm known as "Talk-Listen"; and second, the growing number of Talk-Listen studies that have reported subnormal levels of SIS in patients with schizophrenia. This result is theoretically significant, as it provides a plausible explanation for some of the most distinctive and characteristic symptoms of schizophrenia, namely the first-rank symptoms. In particular, while the failure to suppress the neural consequences of self-generated movements (such as those associated with overt speech) provides a prima facie explanation for delusions of control, the failure to suppress the neural consequences of self-generated inner speech provides a plausible explanation for certain classes of auditory-verbal hallucinations, such as audible thoughts. While the empirical evidence for a relationship between SIS and the first-rank symptoms is currently limited, I predict that future studies with more sensitive experimental designs will confirm its existence. Establishing the existence of a causal, mechanistic relationship would represent a major step forward in our understanding of schizophrenia, which is a necessary precursor to the development of novel treatments., (Copyright © 2019 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Aim: The Inventory of Psychotic-Like Anomalous Self-Experiences (IPASE) is a self-report measure of minimal self-disturbance. The aim of the current report was to assess the construct validity of the scale by examining its convergent validity with the gold-standard measure of minimal self-disturbance, the Examination of Anomalous Self-Experience (EASE), and its discriminant validity., Method: The sample consisted of 46 participants (21 ultra-high risk for psychosis patients, 14 first episode psychosis patients, 11 healthy controls). Correlations between the clinical instruments were examined., Results: The IPASE correlated strongly with general psychopathology and positive psychotic symptoms, moderately with negative symptoms, and weakly with manic symptoms. The strongest correlation (r = 0.92) was apparent between IPASE and EASE total scores., Conclusion: These preliminary data indicate construct validity of the IPASE, demonstrating both convergent and discriminant validity. The IPASE may be suitable as a screener measure for minimal self-disturbance, but should not be used as a replacement to measure the construct of minimal self-disturbance, which requires considerable psychopathological sophistication., (© 2018 John Wiley & Sons Australia, Ltd.)

Background: Typically, we try to protect our own bodies and this is supported by internal representations that specify one's body identity, spatial parameters, and bodily sensations, but in self-harm the body becomes the target. First acts of self-harm are typically reported in adolescence. At this age, the body also becomes more salient to one's self-concept. It may be possible that disturbances in representations of one's own body and its sensations contribute to self-harm., Methods: To investigate these links, we conducted a systematic review critically examining the potential role of body representation and sensation disturbances in self-harm (non-suicidal or suicidal) in adolescents and young adults (12-25 years)., Results: The search strategy identified 64 studies (275,183 participants) and overall, young people engaging in self-harm reported greater levels of body dissatisfaction, body disownership, and deficits in the experience and evaluation of bodily sensations compared to non-injuring control groups; however, there was subscale variability and gender differences., Conclusion: Our results emphasise the strong link between body representations and self-protection, as well as a need for investigating self-harm interventions that take body image and awareness into account., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Decreased brain activity in the frontal region, as indicated by increased slow wave EEG power measured by electrodes place on the skull over this area, in association with negative symptoms has previously been shown to distinguish ultra-high risk (UHR) individuals who later transitioned to psychosis (UHR-P) from those who did not transition (UHR-NP). The aims of the current study were to: 1) replicate these results and 2) investigate whether similar association between increased frontal slow wave activity and functioning shows any value in the prediction of transition to psychosis in UHR individuals. The brain activity, recorded using EEG, of 44 UHR individuals and 38 healthy controls was included in the analyses. Symptom severity was assessed in UHR participants and functioning was measured in both groups. The power in the theta frequency band in the frontal region of UHR individuals was higher than in controls. However, there was no difference between the UHR-P and the UHR-NP groups, and no change in slow frequency power following transition to psychosis. The correlation between delta frequency power and negative symptoms previously observed was not present in our UHR cohort, and there was no association between frontal delta or theta and functioning in either group. Increased delta power was rather correlated with depressive symptoms in the UHR group. Future research will be needed to better understand when, in the course of the illness, does the slow wave activity in the frontal area becomes impaired., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The human brain is an efficient, adaptive, and predictive machine, constructing a generative model of the environment that we then perceive and become conscious of. Here, we show that different types of prediction-errors - the discrepancies between top-down expectations and bottom-up sensory input - are integrated across processing levels and sensory modalities of the cortical hierarchy. We designed a novel, hybrid protocol in which five prediction-establishing sounds were played in rapid succession (e.g., "meow", "meow", "meow", etc.), followed by either a standard (e.g., "meow") or a deviant (e.g., "woof") prime sound, then a visual target word that was either congruent or incongruent (e.g., "cat" or "dog") with the prime sound. We found that the deviants elicited a more negative voltage than the standards at about 150 ms - the mismatch negativity (MMN), an event-related potential (ERP) sensitive to low-level perceptual violations - and that the incongruent words elicited a more negative voltage than the congruent words at about 350 ms - the N400, an ERP sensitive to high-level semantic violations. We also found that the N400 was context-dependent: the N400 was larger when the target words were preceded by a standard than a deviant. Our results suggest that perceptual prediction-errors modulate subsequent semantic prediction-errors. We conclude that our results are consistent with one of the most important assumptions of predictive coding theories: hierarchical prediction-error processing., (Copyright © 2018. Published by Elsevier B.V.)

The thalamus is believed to play crucial role in processing viscero-sensory information, and regulating the activity of amygdala in patients with panic disorder (PD). Previous functional neuroimaging studies have detected abnormal activation in the thalamus in patients with PD compared with healthy control subjects (HC). Very few studies, however, have investigated for volumetric abnormalities in the thalamus in patients with PD. Furthermore, to the best of our knowledge, no previous study has investigated for shape abnormalities in the thalamus in patients with PD. Twenty-five patients with PD and 25 HC participants (all female) were recruited for the study. A voxel-wise volume comparison analysis and a vertex-wise shape analysis were conducted to evaluate structural abnormalities in the PD patients compared to HC. The patients with PD demonstrated significant gray matter volume reductions in the thalamus bilaterally, relative to the HC. The shape analysis detected significant inward deformation in some thalamic regions in the PD patients, including the anterior nucleus, mediodorsal nucleus, and pulvinar nucleus. PD patients showed shape deformations in key thalamic regions that are believed to play a role in regulating emotional and cognitive functions., Competing Interests: The authors have declared that no competing interests exist.

Individuals with elevated hoarding symptoms report elevated symptoms of ADHD and these symptoms are related to impaired daily functioning. Neuropsychological studies have found specific deficits in attention, and a recent review of attentional data from numerous hoarding studies concluded that inattention likely represents an etiological factor in hoarding, rather than a comorbidity. Our study aimed to examine which symptoms of ADHD, inattention or hyperactivity, are related to hoarding symptom severity, and whether individuals with hoarding symptoms display a neurophysiological marker of poor attention (Theta/Beta Ratio; THBR) that might explain these associations. The THBR indexes theta power relative to beta power in the frontal cortex and is often atypical in individuals with ADHD. We hypothesised that individuals would report more severe problems with inattention and would exhibit an elevated theta/beta ratio relative to a healthy control group. We also predicted that any relationship between hoarding and inattention would be independent of anxiety and depression symptoms. 17 hoarding-symptomatic participants and 16 healthy control participants completed self-report measures relating to ADHD, hoarding and general psychopathology, and then underwent resting measures of electroencephalography (EEG). Individuals with hoarding symptoms reported greater difficulties with inattention and hyperactivity, however they did not exhibit an elevated theta/beta ratio. When taking into account recent anxiety and depression, only inattention predicted hoarding symptom severity. Further investigations may help clarify this association and help inform attention-based treatments for hoarding., (Copyright © 2018. Published by Elsevier B.V.)

The amygdala plays an important functional role in fear and anxiety. Abnormalities in the amygdala are believed to be involved in the neurobiological basis of panic disorder (PD). Previous structural neuroimaging studies have found global volumetric and morphological abnormalities in the amygdala in patients with PD. Very few studies, however, have explored for structural abnormalities in various amygdala sub-regions, which consist of various sub-nuclei, each with different functions. This study aimed to evaluate for volumetric abnormalities in the amygdala sub-nuclei, in order to provide a better understanding neurobiological basis of PD. Thirty-eight patients with PD and 38 matched healthy control (HC) participants underwent structural MRI scanning. The volume of the whole amygdala, as well as its consistent sub-nuclei, were calculated using FreeSurfer software. Relative volumes of these amygdala sub-regions were compared between the two groups. Results showed significantly smaller volumes in the right lateral and basal nuclei in the patients with PD compared with the HC. Lateral and basal nuclei are thought to play crucial role for processing sensory information related with anxiety and fear. Our results suggest that these particular amygdala sub-regions play a role in the development of PD symptoms., Competing Interests: The authors have declared that no competing interests exist.

Background: Panic disorder (PD), an anxiety disorder characterized by the recurrence of panic attacks, has been reported to be associated with volumetric changes in several brain regions. There are, however, very few studies investigating abnormalities in cortical thickness, and little is known about the relationship between cortical thickness and social dysfunction in PD., Methods: Thirty-eight patients with PD and 38 healthy control participants (HC) were recruited for this study. A whole-brain analysis was performed to evaluate groupwise differences in cortical thickness using the FreeSurfer software. Symptom severity and social functioning were evaluated with the Panic Disorder Severity Scale (PDSS) and the Global Assessment of Functioning (GAF) scale., Results: The patients with PD demonstrated a significant reduction in cortical thickness in the left rostral middle frontal cortex (MFC), compared with the HC. Correlational analyses revealed that cortical thickness in the left rostral MFC showed a significant negative relationship with PDSS score and a significant positive relationship with GAF scores in the PD patients., Limitations: All the patients received medication., Conclusion: PD patients showed reduced cortical thickness in the left rostral MFC compared with HC. Furthermore, cortical thickness in this region was associated with patients' symptom severity and degree of social dysfunction., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Self-generated speech produces a smaller N1 amplitude in the auditory-evoked potential than externally generated speech; this phenomenon is known as N1-suppression. Schizophrenia patients show less N1-suppression than healthy controls. This failure to self-suppress may underlie patients' characteristic tendency to misattribute self-generated thoughts and actions to external sources. While the cause of N1-suppression deficits to speech in schizophrenia remains unclear, structural damage to the arcuate fasciculus is a candidate, due to its ostensible role in transmitting the efference copy of the motor plan to speak. Fifty-one patients with early illness schizophrenia (ESZ), 40 individuals at clinical high-risk for psychosis (CHR), and 59 healthy control (HC) participants underwent an electroencephalogram while they spoke and then listened to a recording of their speech. N1-suppression to the spoken sounds was calculated. Participants also underwent a diffusion-tensor imaging (DTI) scan, from which the arcuate fasciculus and pyramidal tract were extracted with deterministic tractography. ESZ patients exhibited significantly less N1-suppression to self-generated speech than HC participants, with CHR participants exhibiting intermediate levels. ESZ patients also exhibited structural abnormalities in the arcuate fasciculus-specifically, reduced fractional anisotropy and increased radial diffusivity-relative to both HC and CHR. There were no between-group differences in the structural integrity of the pyramidal tract. Finally, level of N1-suppression was linearly related to the structural integrity of the arcuate fasciculus, but not the pyramidal tract, across groups. These results suggest that the self-suppression deficits to willed speech consistently observed in schizophrenia patients may be caused, at least in part, by structural damage to the arcuate fasciculus.

Sensory attenuation refers to reduced brain responses to self-initiated sensations relative to those produced by the external world. It is a low-level process that may be linked to higher-level cognitive tasks such as reality monitoring. The phenomenon is often explained by prediction error mechanisms of universal applicability to sensory modality; however, it is most widely reported for auditory stimuli resulting from self-initiated hand movements. The present series of event-related potential (ERP) experiments explored the generalizability of sensory attenuation to the visual domain by exposing participants to flashes initiated by either their own button press or volitional saccade and comparing these conditions to identical, computer-initiated stimuli. The key results showed that the largest reduction of anterior visual N1 amplitude occurred for saccade-initiated flashes, while button press-initiated flashes evoked an intermediary response between the saccade-initiated and externally initiated conditions. This indicates that sensory attenuation occurs for visual stimuli and suggests that the degree of electrophysiological attenuation may relate to the causal likelihood of pairings between the type of motor action and the modality of its sensory response., (Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved.)

Mechanisms of motor-sensory prediction are dependent on expectations regarding when self-generated feedback will occur. Existing behavioral and electrophysiological research suggests that we have a default expectation for immediate sensory feedback after executing an action. However, studies investigating the adaptability of this temporal expectation have been limited in their ability to differentiate modified expectations per se from effects of stimulus repetition. Here, we use a novel, within-participant procedure that allowed us to disentangle the effect of repetition from expectation and allowed us to determine whether the default assumption for immediate feedback is fixed and resistant to modification or is amenable to change with experience. While EEG was recorded, 45 participants completed a task in which they repeatedly pressed a button to produce a tone that occurred immediately after the button press (immediate training) or after a 100-msec delay (delayed training). The results revealed significant differences in the patterns of cortical change across the two training conditions. Specifically, there was a significant reduction in the cortical response to tones across delayed training blocks but no significant change across immediate training blocks. Furthermore, experience with delayed training did not result in increased cortical activity in response to immediate feedback. These findings suggest that experience with action-sensation delays broadens the window of temporal expectations, allowing for the simultaneous anticipation of both delayed and immediate motor-sensory feedback. This research provides insights into the mechanisms underlying motor-sensory prediction and may represent a novel therapeutic avenue for psychotic symptoms, which are ostensibly associated with sensory prediction abnormalities.

Predictive coding postulates that the brain continually predicts forthcoming sensory events based on past experiences in order to process sensory information and respond to unexpected events in a fast and efficient manner. Predictive coding models in the context of overt speech are believed to operate along auditory white matter pathways such as the arcuate fasciculus and the frontal aslant. The aim of this study was to investigate whether brain regions that are structurally connected via these white matter pathways are also effectively engaged when listening to externally-generated, temporally-predicable speech sounds. Using Electroencephalography (EEG) and Dynamic Causal Modeling (DCM) we investigated network models that are structurally connected via the arcuate fasciculus from primary auditory cortex to Wernicke's and via Geschwind's territory to Broca's area. Connections between Broca's and supplementary motor area, which are structurally connected by the frontal aslant, were also included. The results revealed that bilateral areas interconnected by indirect and direct pathways of the arcuate fasciculus, in addition to regions interconnected by the frontal aslant best explain the EEG responses to speech that is externally-generated but temporally predictable. These findings indicate that structurally connected brain regions involved in the production and processing of auditory stimuli are also effectively connected.

The regional distribution of white matter (WM) abnormalities in schizophrenia remains poorly understood, and reported disease effects on the brain vary widely between studies. In an effort to identify commonalities across studies, we perform what we believe is the first ever large-scale coordinated study of WM microstructural differences in schizophrenia. Our analysis consisted of 2359 healthy controls and 1963 schizophrenia patients from 29 independent international studies; we harmonized the processing and statistical analyses of diffusion tensor imaging (DTI) data across sites and meta-analyzed effects across studies. Significant reductions in fractional anisotropy (FA) in schizophrenia patients were widespread, and detected in 20 of 25 regions of interest within a WM skeleton representing all major WM fasciculi. Effect sizes varied by region, peaking at (d=0.42) for the entire WM skeleton, driven more by peripheral areas as opposed to the core WM where regions of interest were defined. The anterior corona radiata (d=0.40) and corpus callosum (d=0.39), specifically its body (d=0.39) and genu (d=0.37), showed greatest effects. Significant decreases, to lesser degrees, were observed in almost all regions analyzed. Larger effect sizes were observed for FA than diffusivity measures; significantly higher mean and radial diffusivity was observed for schizophrenia patients compared with controls. No significant effects of age at onset of schizophrenia or medication dosage were detected. As the largest coordinated analysis of WM differences in a psychiatric disorder to date, the present study provides a robust profile of widespread WM abnormalities in schizophrenia patients worldwide. Interactive three-dimensional visualization of the results is available at www.enigma-viewer.org.

Diffusion tensor imaging studies report childhood adversity (CA) is associated with reduced fractional anisotropy (FA) in multiple white matter tracts in adults. Reduced FA may result from changes in tissue, suggesting myelin/axonal damage, and/or from increased levels of extracellular free-water, suggesting atrophy or neuroinflammation. Free-water imaging can separately identify FA in tissue (FA T ) and the fractional volume of free-water (FW). We tested whether CA was associated with altered FA, FA T , and FW in seven white matter regions of interest (ROI), in which FA changes had been previously linked to CA (corona radiata, corpus callosum, fornix, cingulum bundle: hippocampal projection, inferior fronto-occipital fasciculus, superior longitudinal fasciculus, uncinate fasciculus). Tract-based spatial statistics were performed in 147 psychiatrically healthy adults who had completed a self-report questionnaire on CA primarily stemming from parental maltreatment. ROI were extracted according to the protocol provided by the ENIGMA-DTI working group. Analyses were performed both treating CA as a continuous and a categorical variable. CA was associated with reduced FA in all ROI (although categorical analyses failed to find an association in the fornix). In contrast, CA was only associated with reduced FA T in the corona radiata, corpus callosum, and uncinate fasciculus (with the continuous measure of CA finding evidence of a negative relation between CA and FA T in the fornix). There was no association between CA on FW in any ROI. These results provide preliminary evidence that childhood adversity is associated with changes to the microstructure of white matter itself in adulthood. However, these results should be treated with caution until they can be replicated by future studies which address the limitations of the present study.