An observed reduction in the neurophysiological response to self- versus externally-generated stimuli (i.e., sensory attenuation) is often attributed to prediction-based internal forward models. However, despite common use of the auditory N1 in studies of sensory attenuation, there is limited evidence regarding its sensitivity to action-effect contingency (i.e., the probability of action eliciting a stimulus). Theorised differences regarding the role of prediction in sensorimotor processes influencing stimulus-driven and volitional action have also not been thoroughly examined. 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 resulting stimuli. The results demonstrate that, despite an apparent role in motor preparation (i.e., indicated in readiness potential amplitude), action-effect contingency does not influence primary cortical response to sound (i.e., N1 amplitude). We highlight evidence supporting the attribution of sensory attenuation to attentional mechanisms rather than action-effect predictions.

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.