Search

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.

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.

INTRODUCTION: The distinction between the schizophrenia spectrum and other types of disorders may be clinically relevant in terms of its predictive validity as suggested by studies showing schizophrenia spectrum patients have more unfavourable outcomes compared to other psychotic disorders. The present study aimed to investigate whether basic self-disturbances and neurocognitive processes that have been linked to psychosis risk have discriminative power for schizophrenia spectrum disorders in patients presenting with first episode psychosis (FEP) and at ultra-high risk for psychosis (UHR). METHODS: 38 FEP patients, 48 UHR patients, and 33 healthy controls were assessed for basic self-disturbances (using the Examination of Anomalous Self-Experience, EASE, interview), source monitoring and aberrant salience (behavioural tasks to measure neurocognitive constructs). Clinical groups were divided into patients with schizophrenia spectrum disorders and those with other non-spectrum disorders and were further compared on measures controlling for symptom severity and age. RESULTS: Basic self-disturbances distinguished schizophrenia spectrum from non-spectrum disorders in the 'FEP only' sample, F = 19.76, p

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.

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.

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.

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.

Emerging research suggests that hoarding individuals display atypical activation in their anterior cingulate cortex (ACC). Hemodynamic studies have found a biphasic pattern of ACC activity in hoarding individuals that appears sensitive to possession-related decision-making. Electrophysiological studies suggest that hoarding individuals display a blunted error-related negativity (ERN); an event-related potential originating from the ACC that indexes error-detection. These neural abnormalities may reflect an error sensitivity in hoarding individuals as they acquire and discard, however it may also reflect the hyper-emotionality often reported by individuals who hoard. The present study aimed to examine the emotional sensitivity of the error-related negativity in hoarding individuals outside a possession-related context. Seventeen hoarding individuals and 16 healthy controls underwent continuous electroencephalography (EEG) as they completed Go/No-Go (GNGT) tasks design to elicit the ERN. Identical GNGT tasks were completed both before and after watching a negative mood induction video, and self-reported distress was measured throughout. Neither group displayed any neural effect of the negative mood induction, however the hoarding group displayed a pattern of blunted ERN consistent with previous research. This study provides additional evidence that hoarding individuals display blunted indices of error-detection outside possession-related decision-making. Future research could explore if this reflects a pathophysiology shared with other psychiatric disorders that feature a blunted ERN, and if error-detection is also abnormal as hoarding individuals acquire and discard their possessions.

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.

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.

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.

BackgroundSelf-monitoring biases and overconfidence in incorrect judgments have been suggested as playing a role in schizophrenia spectrum disorders. Little is known about whether self-monitoring biases may contribute to early risk factors for psychosis. In this study, action self-monitoring (i.e., discrimination between imagined and performed actions) was investigated, along with confidence in judgments among ultra-high risk (UHR) for psychosis individuals and first-episode psychosis (FEP) patients.MethodsThirty-six UHR for psychosis individuals, 25 FEP patients and 33 healthy controls (CON) participated in the study. Participants were assessed with the Action memory task. Simple actions were presented to participants verbally or non-verbally. Some actions were required to be physically performed and others were imagined. Participants were asked whether the action was presented verbally or non-verbally (action presentation type discrimination), and whether the action was performed or imagined (self-monitoring). Confidence self-ratings related to self-monitoring responses were obtained.ResultsThe analysis of self-monitoring revealed that both UHR and FEP groups misattributed imagined actions as being performed (i.e., self-monitoring errors) significantly more often than the CON group. There were no differences regarding performed actions as being imagined. UHR and FEP groups made their false responses with higher confidence in their judgments than the CON group. There were no group differences regarding discrimination between the types of actions presented (verbal vs non-verbal).ConclusionsA specific type of self-monitoring bias (i.e., misattributing imagined actions with performed actions), accompanied by high confidence in this judgment, may be a risk factor for the subsequent development of a psychotic disorder.

Sensory attenuation refers to reduced brain responses to self-initiated sensations relative to those produced by the external world, a distinction that is vital for dynamic motor control and our sense of agency. Typically, willed vocalizations elicit larger N1 reduction of the auditory evoked potential compared to indirectly evoked sounds, such as tones generated by button-presses, which is attributed to the prediction and cancellation of incoming signals enabled by speech motor commands. However, physical confounds exist, including different stimuli and the increased motor artefact associated with mouth vs. finger movements. The present study investigated N1 attenuation to physically identical sounds evoked by hand, eye, and mouth-initiated movements. Twenty-eight healthy participants had their electroencephalogram (EEG) recorded as they blew into a microphone, pressed a button, or moved their eye to generate a pure tone. We found that N1 and P2 response was most reduced in the blow initiation condition, and that both blow and button-press but not saccade initiated tones elicited significantly reduced N1 and P2 amplitude compared to external initiation. This indicates that the eliciting motor action markedly influences ERP response to auditory stimuli. Given that saccades are never associated with sounds, finger movements sometimes are, and mouth movements often are, the pattern of results suggests that N1 attenuation to self-initiated sounds may depend on existing associations between the initiating action and resultant sensation.

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.

Recent research has shown that perceptual processing of stimuli previously associated with high-value rewards is automatically prioritized even when rewards are no longer available. It has been hypothesized that such reward-related modulation of stimulus salience is conceptually similar to an “attentional habit.” Recording event-related potentials in humans during a reinforcement learning task, we show strong evidence in favor of this hypothesis. Resistance to outcome devaluation (the defining feature of a habit) was shown by the stimulus-locked P1 component, reflecting activity in the extrastriate visual cortex. Analysis at longer latencies revealed a positive component (corresponding to the P3b, from 550–700 ms) sensitive to outcome devaluation. Therefore, distinct spatiotemporal patterns of brain activity were observed corresponding to habitual and goal-directed processes. These results demonstrate that reinforcement learning engages both attentional habits and goal-directed processes in parallel. Consequences for brain and computational models of reinforcement learning are discussed.SIGNIFICANCE STATEMENTThe human attentional network adapts to detect stimuli that predict important rewards. A recent hypothesis suggests that the visual cortex automatically prioritizes reward-related stimuli, driven by cached representations of reward value; that is, stimulus–response habits. Alternatively, the neural system may track the current value of the predicted outcome. Our results demonstrate for the first time that visual cortex activity is increased for reward-related stimuli even when the rewarding event is temporarily devalued. In contrast, longer-latency brain activity was specifically sensitive to transient changes in reward value. Therefore, we show that both habit-like attention and goal-directed processes occur in the same learning episode at different latencies. This result has important consequences for computational models of reinforcement learning.

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 (

BACKGROUND: Auditory verbal hallucinations (AVH) are one of the hallmarks of psychosis, but they also appear in 5–10 % of healthy individuals. Structural and functional imaging studies implicate the superior temporal gyrus and inferior frontal language areas in generation of AVH. Here, we examined white matter in tracts interconnecting these regions with advanced diffusion imaging methods. We aimed to reveal pathophysiologic substrates for AVH across several datasets, consisting of first episode and chronic schizophrenia patients as well as healthy individuals with and without AVH. METHODS: Diffusion MRI data were analyzed using diffusion tractography to extract fiber connections forming language networks: arcuate fasciculus (AF), inferior occipito-frontal fasciculus (IFOF), and the genu and isthmus of the corpus callosum (CC). Several measures of white matter microstructure were averaged over these white matter structures, including extracellular free water (FW) and tissue-specific fractional anisotropy (FAt), axial and radial diffusivity (ADt, RDt). Measures were compared between patients with and without hallucinations, and healthy, non-hallucinating controls across multiple datasets (total of 650 healthy controls and 550 patients at various stages of schizophrenia). RESULTS: We identified significant microstructural abnormalities in language connections across patients with established schizophrenia and healthy individuals with AVH, albeit to lesser degree. These changes were characterized by increased extracellular FW and RDt, as well as decreased FAt. Notably, microstructural variability was associated with positive symptoms and AVH, independent of diagnostic status and illness stage (first episode and chronic schizophrenia). CONCLUSIONS: Our data point to shared neural substrates for auditory verbal hallucinations across heterogeneous schizophrenia populations and healthy individuals; compatible with dimensional models of psychosis.

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.

Individuals who hoard report poor tolerance for uncertainty. They also exhibit error-monitoring abnormalities and increased activation of the anterior cingulate during possession-relevant decision-making, potentially reflecting a context-dependent error sensitivity. Together, these underlying vulnerabilities may lead individuals who hoard to avoid uncertain acquiring and discarding decisions. The current study explored electrophysiological indices of error-monitoring (error-related negativity; ERN) in possession-related and possession-unrelated contexts, and how this related to self-reported intolerance of uncertainty (IU). Undergraduate students (N = 29) completed self-report measures of hoarding symptoms and intolerance of uncertainty, and then engaged in a Go/NoGo task and a novel Discard/NoDiscard task with concurrent EEG measurement. Regression analyses revealed that hoarding symptoms predicted ERN amplitude for possession-related errors but not possession-unrelated errors, and that this relationship was influenced by IU in possession-related contexts. These findings have theoretical implications for understanding vulnerability in hoarding.

Reduction of auditory event-related potentials (ERPs) to self-initiated sounds has been considered evidence for a predictive model in which copies of motor commands suppress sensory representations of incoming stimuli. However, in studies which involve arbitrary auditory stimuli evoked by sensory-unspecific motor actions, learned associations may underlie ERP differences. Here, in a new paradigm, eye motor output generated auditory sensory input, a naïve action-sensation contingency. We measured the electroencephalogram (EEG) of 40 participants exposed to pure tones, which they produced with either a button-press or volitional saccade. We found that button-press-initiated stimuli evoked reduced amplitude compared to externally initiated stimuli for both the N1 and P2 ERP components, whereas saccade-initiated stimuli evoked intermediate attenuation at N1 and no reduction at P2. These results indicate that the motor-to-sensory mapping involved in speech production may be partly generalized to other contingencies, and that learned associations also contribute to the N1 attenuation effect.

Recent research has shown that reward learning can modulate oculomotor and attentional capture by physically salient and task-irrelevant distractor stimuli, even when directing gaze to those stimuli is directly counterproductive to receiving reward. This value-modulated oculomotor capture effect may reflect biased competition in the oculomotor system, such that the relationship between a stimulus feature and reward enhances that feature's representation on an internal priority map. However, it is also possible that this effect is a result of reward reducing the threshold for a saccade to be made to salient items. Here, we demonstrate value-modulated oculomotor capture when two reward-associated distractor stimuli are presented simultaneously in the same search display. The influence of reward on oculomotor capture is found to be most prominent at the shortest saccade latencies. We conclude that the value-modulated oculomotor capture effect is a consequence of biased competition on the saccade priority map and cannot be explained by a general reduction in saccadic threshold.

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.

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.

Background Debate exists over the extent to which dysfunctions arising from mild traumatic brain injury (mTBI) are distinct from posttraumatic stress disorder (PTSD). Methods This study investigated 1) the white matter integrity of participants with either mTBI or PTSD, and 2) the relationship between white matter integrity and postconcussive syndrome. The sample comprised 110 civilians (mTBI group = 40; PTSD group = 32; age- and sex-matched trauma-exposed control subjects = 38) recruited from community advertising. Indicators of white matter abnormalities were fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity. PTSD symptoms were indexed by the Clinician-Administered PTSD Scale, and postconcussive symptoms were assessed using the Somatic and Psychological Health Report measure. Results Fractional anisotropy was reduced in mTBI participants in the corpus callosum, tracts of the brainstem, projection fibers, association fibers, and limbic fibers compared with both PTSD and trauma-exposed control subjects. This decrease in fractional anisotropy was observed in the context of concurrent changes in radial diffusivity, axial diffusivity, and mean diffusivity. Postconcussive symptoms were largely explained by PTSD severity rather than by changes in brain white matter. mTBI appears to be characterized by distinct reductions in white matter integrity, and this cannot be attributed to PTSD. Conclusions PTSD symptoms appear to be more strongly associated with postconcussive syndrome than with white matter compromise. These findings extend epidemiological evidence of the relative associations of PTSD and mTBI with postconcussive syndrome.

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.

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.

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.

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.

Brain white matter abnormalities are evident in individuals with schizophrenia, and also their first-degree relatives, suggesting that some alterations may relate to underlying genetic risk. The ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2 (ST8SIA2) gene, which encodes the alpha-2,8-sialyltransferase 8B enzyme that aids neuronal migration and synaptic plasticity, was previously implicated as a schizophrenia susceptibility gene. This study examined the extent to which specific haplotypes in ST8SIA2 influence white matter microstructure using diffusion-weighted imaging of individuals with schizophrenia (n = 281) and healthy controls (n = 172), recruited across five Australian sites. Interactions between diagnostic status and the number of haplotype copies (0 or ≥1) were tested across all white matter voxels with cluster-based statistics. Fractional anisotropy (FA) in the right parietal lobe was found to show a significant interaction between diagnosis and ST8SIA2 protective haplotype (p ST8SIA2 risk haplotype copy number did not show any differential effects on white matter. This study provides a link between a common disease-associated haplotype and specific changes in white matter microstructure, which may relate to resilience or risk for mental illness, providing further compelling evidence for involvement of ST8SIA2 in the pathophysiology of schizophrenia.

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.

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.

© Medicinska naklada, Zagreb, Croatia. Objective: Right frontal function, as indicated by the N200 component of the event-related potential during target detection, has previously been associated with excitement (excitement, impulsivity, hostility, uncooperativeness) in men with a long-term diagnosis of schizophrenia. The current study investigated excitement in relation to N200 in men who had recently experienced their first episode of psychosis. Subjects and methods: Twenty men who had recently suffered their first psychotic episode underwent a clinical interview and auditory oddball task. Results: Multiple linear regression analysis showed that 58% of the variance in the excitement symptom cluster was explained by a positive association with frontal midline N200 amplitude and an inverse association with right frontal N200 amplitude. The latter was not apparent in the initial correlation, suggesting suppression by the midline activity. These associations were not explained by drug use, medication or negative symptoms. However, the correlation between excitement and midline N200 was stronger in drug users, and that between right frontal N200 and excitement was stronger in nonusers. Conclusion: Findings support the independent contributions to excitement of mechanisms reflected in midline and right frontal N200 amplitude respectively during the early stages of psychosis. BIAL foundation