Self-suppression refers to the phenomenon that sensations initiated by our own movements are typically less salient, and elicit an attenuated neural response, compared to sensations resulting from changes in the external world. Evidence for self-suppression is provided by previous ERP studies in the auditory modality, which have found that healthy participants typically exhibit a reduced auditory N1 component when auditory stimuli are self-initiated as opposed to externally initiated. However, the literature investigating self-suppression in the visual modality is sparse, with mixed findings and experimental protocols. An EEG study was conducted to expand our understanding of self-suppression across different sensory modalities. Healthy participants experienced either an auditory (tone) or visual (pattern-reversal) stimulus following a willed button press (self-initiated), a random interval (externally initiated, unpredictable onset), or a visual countdown (externally initiated, predictable onset-to match the intrinsic predictability of self-initiated stimuli), while EEG was continuously recorded. Reduced N1 amplitudes for self- versus externally initiated tones indicated that self-suppression occurred in the auditory domain. In contrast, the visual N145 component was amplified for self- versus externally initiated pattern reversals. Externally initiated conditions did not differ as a function of their predictability. These findings highlight a difference in sensory processing of self-initiated stimuli across modalities, and may have implications for clinical disorders that are ostensibly associated with abnormal self-suppression.
Schizophrenia patients have been shown to exhibit subnormal levels of electrophysiological suppression to self-initiated, button press elicited sounds. These self-suppression deficits have been shown to improve following the imposition of a subsecond delay between the button press and the evoked sound. The current study aimed to investigate whether nonclinical individuals who scored highly on the personality dimension of schizotypy would exhibit similar patterns of self-suppression abnormalities to those exhibited in schizophrenia. Thirty-nine nonclinical individuals scoring above the median (High Schizotypy) and 41 individuals scoring below the median (Low Schizotypy) on the Schizotypal Personality Questionnaire (SPQ) underwent electroencephalographic recording. The amplitude of the N1-component was calculated while participants (1) listened to tones initiated by a willed button press and played back with varying delay periods between the button press and the tone (Active conditions) and (2) passively listened to a series of tones (Listen condition). N1-suppression was calculated by subtracting the amplitude of the N1-component of the auditory evoked potential in the Active condition from that of the Listen condition, while controlling for the activity evoked by the button press per se. The Low Schizotypy group exhibited significantly higher levels of N1-suppression to undelayed tones compared to the High Schizotypy group. Furthermore, while N1-suppression was found to decrease linearly with increasing delays between the button press and the tone in the Low Schizotypy group, this was not the case in the High Schizotypy group. The findings of this study suggest that nonclinical, highly schizotypal individuals exhibit subnormal levels of N1-suppression to undelayed self-initiated tones and an abnormal pattern of N1-suppression to delayed selfinitiated tones. To the extent that these results are similar to those previously reported in patients with schizophrenia, these findings provide support for the existence of a neurophysiological "continuum of psychosis".
Background A ‘continuum of psychosis’ refers to the concept that psychotic-like experiences occur to certain extents in the healthy population and to more severe extents in individuals with psychotic disorders. If this concept is valid, neurophysiological abnormalities exhibited by patients with schizophrenia should also be present, to an attenuated degree, in non-clinical individuals who score highly on the personality dimension of schizotypy. Patients with schizophrenia have consistently been shown to exhibit electrophysiological suppression abnormalities to self-generated speech. The present study aimed to investigate whether these electrophysiological suppression abnormalities were also present in non-clinical individuals who scored highly on schizotypy. Methods Thirty-seven non-clinical individuals scoring High (above median) and 37 individuals scoring Low (below median) on the Schizotypal Personality Questionnaire (SPQ; a commonly used schizotypy scale) underwent electroencephalographic (EEG) recording. The amplitude of the N1 component of the auditory-evoked potential was measured while participants (a) vocalized simple syllables (Talk condition), (b) passively listened to a recording of these vocalizations (Listen condition) and (c) listened to a recording of the vocalizations whilst simultaneously watching a video depicting the sound-wave of the forthcoming vocalizations, allowing them to be temporally predicted (Cued Listen condition). Results The Low Schizotypy group exhibited significantly reduced N1-amplitude in the Talk condition relative to both the Listen and Cued Listen conditions; that is, they exhibited significant N1-suppression. The High Schizotypy group exhibited significantly lower levels of N1-suppression compared to the Low Schizotypy group. Furthermore, whilst the Cued Listen condition induced significantly lower N1-amplitudes compared to the Listen condition in the Low Schizotypy group, this was not the case for the High Schizotypy group. Conclusions The results suggest that non-clinical, highly schizotypal individuals exhibit subnormal levels of N1-suppression to self-generated speech, similar to the N1-suppression abnormalities which have previously been reported in patients with schizophrenia. This finding provides empirical support for the existence of a neurophysiological ‘continuum of psychosis’.
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.
Background Certain migrant groups are at an increased risk of psychotic disorders compared to the native-born population; however, research to date has mainly been conducted in Europe. Less is known about whether migrants to other countries, with different histories and patterns of migration, such as Australia, are at an increased risk for developing a psychotic disorder. We tested this for first-generation migrants in Melbourne, Victoria. Methods This study included all young people aged 15–24 years, residing in a geographically-defined catchment area of north western Melbourne who presented with a first episode of psychosis (FEP) to the Early Psychosis Prevention and Intervention Centre (EPPIC) between 1 January 2011 and 31 December 2016. Data pertaining to the at-risk population were obtained from the Australian 2011 Census and incidence rate ratios were calculated and adjusted for age, sex and social deprivation. Results In total, 1220 young people presented with an FEP during the 6-year study period, of whom 24.5% were first-generation migrants. We found an increased risk for developing psychotic disorder in migrants from the following regions: Central and West Africa (adjusted incidence rate ratio [aIRR] = 3.53, 95% CI 1.58–7.92), Southern and Eastern Africa (aIRR = 3.06, 95% CI 1.99–4.70) and North Africa (aIRR = 5.03, 95% CI 3.26–7.76). Migrants from maritime South East Asia (aIRR = 0.39, 95% CI 0.23–0.65), China (aIRR = 0.25, 95% CI 0.13–0.48) and Southern Asia (aIRR = 0.44, 95% CI 0.26–0.76) had a decreased risk for developing a psychotic disorder. Conclusion This clear health inequality needs to be addressed by sufficient funding and accessible mental health services for more vulnerable groups. Further research is needed to determine why migrants have an increased risk for developing psychotic disorders.
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