Illusion of control affects ERP amplitude reductions for auditory outcomes of self-generated actions.

AbstractThe reduction of neural responses to self‐generated stimuli compared to external stimuli is thought to result from the matching of motor‐based sensory predictions and sensory reafferences and to serve the identification of changes in the environment as caused by oneself. The amplitude of the auditory event‐related potential (ERP) component N1 seems to closely reflect this matching process, while the later positive component (P2/ P3a) has been associated with judgments of agency, which are also sensitive to contextual top‐down information. In this study, we examined the effect of perceived control over sound production on the processing of self‐generated and external stimuli, as reflected in these components. We used a new version of a classic two‐button choice task to induce different degrees of the illusion of control (IoC) and recorded ERPs for the processing of self‐generated and external sounds in a subsequent task. N1 amplitudes were reduced for self‐generated compared to external sounds, but not significantly affected by IoC. P2/3a amplitudes were affected by IoC: We found reduced P2/3a amplitudes after a high compared to a low IoC induction training, but only for self‐generated, not for external sounds. These findings suggest that prior contextual belief information induced by an IoC affects later processing as reflected in the P2/P3a, possibly for the formation of agency judgments, while early processing reflecting motor‐based predictions is not affected

When temporal prediction errs:ERP responses to delayed action-feedback onset

Sensory suppression effects observed in electroencephalography (EEG) index successful predictions of the type and timing of self-generated sensory feedback. However, it is unclear how precise the timing prediction of sensory feedback is, and how temporal delays between an action and its sensory feedback affect perception. The current study investigated how prediction errors induced by delaying tone onset times affect the processing of sensory feedback in audition. Participants listened to self-generated (via button press) or externally generated tones. Self-generated tones were presented either without or with various delays (50, 100, or 250 ms; in 30% of trials). Comparing listening to externally generated and self-generated tones resulted in action-related P50 amplitude suppression to tones presented immediately or 100 ms after the button press. Subsequent ERP responses became more sensitive to the type of delay. Whereas the comparison of actual and predicted sensory feedback (N1) tolerated temporal uncertainty up to 100 ms, P2 suppression was modulated by delay in a graded manner: suppression decreased with an increase in sensory feedback delay. Self-generated tones occurring 250 ms after the button press additionally elicited an enhanced N2 response. These findings suggest functionally dissociable processes within the forward model that are affected by the timing of sensory feedback to self-action: relative tolerance of temporal delay in the P50 and N1, confirming previous results, but increased sensitivity in the P2. Further, they indicate that temporal prediction errors are treated differently by the auditory system: only delays that occurred after a temporal integration window (∼100 ms) impact the conscious detection of altered sensory feedback

Movement-Related Potentials Associated with Motor Timing Errors as Determined by Internally Cued Movement Onset

Objective: Accurate motor timing is critical for efficient motor control of behaviors; however, the effect of motor timing abilities on movement-related neural activities has rarely been investigated. The current study aimed to examine the electrophysiological correlates of motor timing errors. Methods: Twenty-two healthy volunteers performed motor timing tasks while their electroencephalographic and electromyographic (EMG) activities were simultaneously recorded. The average of intervals between consecutive EMG onsets was calculated separately for each subject. Motor timing error was calculated as an absolute discrepancy value between the subjects' produced and given time interval. A movement-related potential (MRP) analysis was conducted using readings from Cz electrode. Results: Motor timing errors and MRPs were significantly correlated. Our principal finding was that only Bereitschaftpotential (BP) and motor potential (MP), not movement monitoring potential, were significantly attenuated in individuals with motor timing errors. Motor timing error had a significant effect on the amplitude of the late BP and MP. Conclusion: The findings provide electrophysiological evidence that motor timing errors correlate with the neural processes involved in the generation of self-initiated voluntary movement. Alterations in MRPs reflect central motor control processes and may be indicative of motor timing deficits.ope

An electrophysiological investigation into the role of agency and contingency on sensory attenuation

Stimuli generated by a person’s own willed actions generally elicit a suppressed neurophysiological response than physically identical stimuli that have been externally generated. This phenomenon, known as sensory attenuation, has primarily been studied by comparing the N1, Tb and P2 components of the event-related potentials (ERPs) evoked by self-initiated vs. externally generated sounds. Sensory attenuation has been implicated in some psychotic disorders such as schizophrenia, where symptoms such as auditory hallucinations and delusions of control have been conceptualised as reflecting a difficulty in distinguishing between internally and externally generated stimuli. This thesis employed a novel paradigm across five experiments to investigate the role of agency and contingency in sensory attenuation. The role of agency was investigated in in Chapter 2. 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 one second 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., pressing the button prior to 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 agency and motor actions per se have differential effects on sensory attenuation to sounds and are indexed with different ERP components. In Chapter 3, we investigated the role of contingency in sensory attenuation while using a similar ticker-tape design in Chapter 2. In the Full Contingency (FC) condition, participants again 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 (one second later) 100% of the time (Experiment 3). If the button was pressed prior to the mark, the sound was not played. In the Half Contingency (HC) condition, participants observed the same tickertape; however, if participants did not press the button by the mark, a sound would occur 50% of the time (HC-Inaction) while if the participant did press the button, a sound would also play 50% of the time (HC-Action). In Experiment 4, the design was identical, except that a button-press triggered the sound in the FC condition. The results were consistent across both Experiments in Chapter 3: while there were no differences in N1 amplitude across the FC and HC conditions, the amplitude of the Tb component was smaller in the FC condition when compared to the HC-Inaction condition. The amplitude of the P2 component was also smaller in the FC condition compared to both the HC-Action and HC-Inaction conditions. The results suggest that the effect of contingency on neurophysiological indices of sensory attenuation may be indexed by the Tb and P2 components, as opposed to the more heavily studied N1 component. Chapter 4 also investigated contingency but instead used a more ‘traditional’ self-stimulation paradigm, in which sounds immediately followed the button-press. In Chapter 4, participants observed a fixation cross while pressing a button to generate a sound. The probability of the sound occurring after the button-press was either 100% (active 100) or 50% (active 50). In the two passive conditions (passive 100 and passive 50), sounds generated in the corresponding active conditions were recorded and played back to participants while they passively listened. In contrast with the results of Chapter 3, the results of Chapter 4 showed both the classical N1 suppression effect, and also an effect of contingency of the N1, where sounds with a 50% probability generated higher N1 amplitudes compared to sounds with 100% probability. In contrast, Tb amplitude was modulated by contingency but did not show any differences between the active and passive conditions. The results of this study suggest that both sense of agency and sensory contingency can influence sensory attenuation, and thus should be considered in future studies investigating this theoretically and clinically important phenomenon

Who is talking inside my head? Establishing the neurophysiological basis of inner speech and its relation to auditory verbal hallucinations

Sensory suppression refers to the phenomenon that sensations resulting from self-generated actions feel less salient, and evoke a smaller neurophysiological response, than physically identical sensations from external sources. It is believed to be a result of an internal forward model which utilizes predictions derived from the motor command to cancel out predicted action effects. Recent research has demonstrated that this mechanism is also implicated in inner speech – the silent production of words in one’s mind. While inner speech has been conceptualized as 'a kind of action' similar to overt speech, the extent to which the two could be considered functionally equivalent remains unclear. Using a novel paradigm, this thesis presents the findings of five electrophysiological (EEG) experiments that investigated factors influencing sensory processing of inner speech, the premotor activity of inner speech production, and inner speech deficits in people with schizophrenia spectrum disorders. These topics are explored with a focus on the auditory N1 component and the contingent negative variation (CNV) of event-related potentials (ERPs). In Chapter 2, the effect of prior expectations on the sensory processing of inner speech was examined. The production of an inner phoneme resulted in a more negative N1-amplitude when its content matched with a simultaneously-presented audible phoneme, compared to a mismatch, with no difference in N1 between expected and unexpected stimuli irrespective of content. These results suggest that motor-based predictions may interact with stimulus probability in the environment to shape perceptual inference. In Chapter 3, the existence of a motoric late CNV to inner speech was established, indicating that the production of inner speech involves motor preparatory activity. This finding was confirmed by an identical experiment performed in overt speech. The premotor activity preceding inner speech was further shown to encode the expected sensory consequences of inner speech. In Chapter 4, evidence for sensory suppression deficits to inner speech in people with schizophrenia spectrum disorders was found in a two-site experiment. Differential results in hallucinators, non-hallucinators, and healthy controls suggest specificity of suppression deficits to inner speech may be associated with auditory verbal hallucinations. Together, the findings of this thesis provide insights into the neural mechanisms underlying the production and sensory processing of inner speech in health and disease, and hold important implications for the potential prevention and treatment of psychotic symptoms

Attention, prediction and sensory attenuation: A neurophysiological investigation of the internal forward model

The term ‘sensory attenuation’ describes a reduction in the subjective intensity of self-generated stimuli, and accompanying neurophysiological response, compared to those produced externally. Mechanisms underlying this phenomenon are believed to facilitate the distinction between self- and externally-generated events. Accordingly, dysfunction in sensory attenuation has been associated with symptoms involving the misattribution of perceptual experience in people with schizophrenia. Internal forward models of sensory attenuation propose that self-generated stimuli are suppressed based on predictions derived from the motor commands through which they are produced. However, much of the research into sensory attenuation has been subject to methodological confounds that limit conclusions with respect to its underlying mechanisms. Other factors, such as the role of attention, have not been thoroughly explored. This thesis presents the results of four electrophysiological studies that examined factors influencing sensory attenuation, while assessing and controlling for confounding effects. Sensory attenuation was explored through examination of the auditory N1 component of event-related potentials (ERPs), which is believed to reflect the primary cortical response to sound stimuli. Related effects were assessed based on ERP components representing motor preparation, sensory gating, attention, and error monitoring. Our results suggest that temporal predictability reduces N1 amplitudes in a manner that may often account for documented effects, while temporal control amplifies these such that the phenomenon of sensory attenuation is counteracted for stimuli that result from volitional (i.e., self-paced) movement (Chapter 2). Subsequent analyses revealed an interaction between inter-stimulus intervals and this ‘volitional enhancement’, such that shorter intervals increase its effects (Chapter 5). The results of our investigation indicate that action-effect contingency does not influence the amplitude of auditory N1 components (Chapters 3 and 4). Instead, our findings support the notion that sensory attenuation may involve effects relating to attentional suppression (Chapter 3) and control (Chapter 4). These findings provide important insights into the mechanisms underlying sensory attenuation, and implications for future research into the causes and potential treatment of schizophrenia