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 shows that inner speech—the silent production of words in one's mind—is accompanied by a corollary discharge that contains information about the timing and content of inner speech. The aim of the present study was to determine whether this corollary discharge contains information about the volume of inner speech. To investigate this, participants watched an animation that provided them with precise knowledge about when they should produce a “loud” or “quiet” inner sound. At the same time, they heard an audible sound that was either similar or dissimilar to the volume of the inner sound. We found that producing the inner sound attenuated the N1—an ERP signature of auditory processing—and enhanced the slow negative wave—an ERP signature of anticipation and motor preparation—compared with listening, regardless of whether the volume of the inner sound was similar or dissimilar to the audible sound. We also found that the volume of the inner sound did not differentially modulate the N1 or slow negative wave. We speculate that this might be because one of the functions of corollary discharge is to protect our auditory receptors from desensitization caused by audible sounds, and this might be redundant in the context of inner speech because inner speech does not produce an audible sound. We conclude that there might be a functional difference between the neural processes that underlie the production of inner and overt speech.

While volitional movement is thought to be initiated based on its anticipated capacity to achieve sensory goals, stimulus-driven movement may be generated with less regard for its specific effects. Sensorimotor processes that make use of action-effect predictions may therefore differ between these forms of movement, including sensory attenuation and the detection of mispredicted motor effects. In this study, we explored sensory attenuation by comparing the evoked response of externally-generated tones with those produced by participants ( n = 61), both according to their own timing (i.e., volitionally) and in response to simple visual cues (i.e., stimulus-driven). The influence of stimulus identity prediction (i.e., the predictability of tone frequency) on N1 amplitudes was not found to differ between self- and externally-generated stimuli, or on the basis of volitional control. Reduced P2 amplitudes were observed in response to self-generated tones, which may suggest that these were subject to higher levels of attentional control, including processes involved in the termination of attention. To explore misprediction sensitivity, we compared the influence of stimulus identity prediction on N2b component amplitudes. A significant interaction was found to reflect heightened sensitivity to mispredicted outcomes of volitional action, compared with those of stimulus-driven movement. In light of recent evidence that attentional suppression may attenuate the primary cortical response to outcomes of stimulus-driven movement, we propose that this mechanism might also serve to diminish misprediction sensitivity. As such, these effects may represent important features of sensorimotor processing that assist in differentiating stimuli on the basis of self-generation and intentionality.

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.

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.

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.

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.