The N1 auditory ERP and its magnetic counterpart (N1[m]) are suppressed when elicited by self-induced sounds. Because the N1(m) is a correlate of auditory event detection, this N1 suppression effect is generally interpreted as a reflection of the workings of an internal forward model: The forward model captures the contingency (causal relationship) between the action and the sound, and this is used to cancel the predictable sensory reafference when the action is initiated. In this study, we demonstrated in three experiments using a novel coincidence paradigm that actual contingency between actions and sounds is not a necessary condition for N1 suppression. Participants performed time interval production tasks: They pressed a key to set the boundaries of time intervals. Concurrently, but independently of keypresses, a sequence of pure tones with random onset-to-onset intervals was presented. Tones coinciding with keypresses elicited suppressed N1(m) and P2(m), suggesting that action–stimulus contiguity (temporal proximity) is sufficient to suppress sensory processing related to the detection of auditory events.

Forward predictions are crucial in motor action (e.g., catching a ball, or being tickled) but may also apply to sensory or cognitive processes (e.g., listening to distorted speech or to a foreign accent). According to the “internal forward model,” the cerebellum generates predictions about somatosensory consequences of movements. These predictions simulate motor processes and prepare respective cortical areas for anticipated sensory input. Currently, there is very little evidence that a cerebellar forward model also applies to other sensory domains. In the current study, we address this question by examining the role of the cerebellum when auditory stimuli are anticipated as a consequence of a motor act. We applied an N100 suppression paradigm and compared the ERP in response to self-initiated with the ERP response to externally produced sounds. We hypothesized that sensory consequences of self-initiated sounds are precisely predicted and should lead to an N100 suppression compared with externally produced sounds. Moreover, if the cerebellum is involved in the generation of a motor-to-auditory forward model, patients with focal cerebellar lesions should not display an N100 suppression effect. Compared with healthy controls, patients showed a largely attenuated N100 suppression effect. The current results suggest that the cerebellum forms not only motor-to-somatosensory predictions but also motor-to-auditory predictions. This extends the cerebellar forward model to other sensory domains such as audition.