According to the predictive coding theory, the brain predicts future sensory inputs based on previous experiences. When there is a mismatch between the expected and the actual stimulus, a mismatch response is transmitted from low to high cortical levels to adapt the predictive model. An important cortical area for somatosensory mismatch responses is the secondary somatosensory (S2) cortex, which has reciprocal connections with the cerebellum. This study aims to characterize the role of the cortico-cerebellar interactions in the modulation of S2 cortex responses according to the predictability of afferent tactile and proprioceptive somatosensory inputs. We enrolled 20 right-handed healthy adults who underwent three functional magnetic resonance imaging (fMRI) runs (6 min each, block-design) consisting of twelve 30-s alternating blocks (10 brain volumes/block, 120 brain volumes/session) of tactile oddball paradigms. The fMRI signals within the contralateral S1 (cS1), ipsilateral S2 (iS2), and contralateral S2 (cS2) cortices; within the cortical areas involved in multimodal sensory mismatch detection (i.e., the right anterior insula (AIns), temporoparietal junction (TPJ), middle frontal gyrus (MFG), and supplementary motor are/anterior cingular cortex (SMA/ACC)); and within the ipsilateral cerebellar lobule 8 (iCL8) and 6 (iCL6) were extracted using region-of-interest (ROI) analyses and compared using ANOVA. The modulation of cortico-cerebellar functional connectivity by afferent stimuli predictability was studied using psychophysiological interaction (PPI) analyses. Predictable tactile stimuli were associated with significantly lower fMRI signals within cS1 and bilateral S2 cortices, and the right AIns, TPJ, and MFG compared to random tactile stimuli. PPI analyses showed that predictable tactile stimuli were associated with a significant increase in the functional connectivity (negative correlation) between cS2 cortex and iCL8 BOLD levels, with no significant correlation during random tactile stimulation. This effect, identified by the PPI analyses, occurred solely between the cerebellum and cS2 cortex and not with the other cortical mismatch areas. This study provides evidence for a cerebello-cortical interplay between iCL8 and the cS2 cortex in tactile somatosensory mismatch responses. The lower BOLD response in the S2 cortex observed for predictable tactile stimuli is likely mediated by an inhibitory influence of the cerebellum on the somatosensory cortex when tactile inputs are predictable.

The excitability of the sensorimotor (SM1) cortices is reflected in the bilateral ~20 Hz beta oscillations. The extent to which these oscillations subtend the interhemispheric inhibition (IHI) captured by the Transcranial Magnetic Stimulation (TMS) ipsilateral Silent Period (iSP) protocol remains unclear. Therefore, we investigated the relationship between movement-related beta suppression and the iSP, along with their role for manual dexterity. Forty adults underwent an Electroencephalography assessment of beta suppression during volitional left-hand movement and a TMS assessment of iSP recorded from the right hand. In both cases, left SM1 beta oscillations (contralateral to the activated right SM1) were monitored through a proxy signal—the Electromyography of the contracted right hand. Bimanual dexterity was assessed with the Purdue Pegboard. Volitional movement caused significant bilateral SM1 beta suppression in nearly all participants (≥85%). ISPs were observed in every participant. In the proxy signal for the left SM1, the iSP coincided with TMS-evoked high-amplitude beta bursts. These bursts showed significant phase alignment across participants 10–70 ms after the TMS pulse. There was no significant association between the left-/right-hemisphere beta suppression, iSP, and bimanual dexterity. Our results highlight the distinct nature of beta oscillation changes during volitional movement compared with TMS-iSP and show that TMS induces IHI via transcallosal generation of phase-aligned beta bursts. Furthermore, our data suggest that only the initial phase of a beta burst carries an inhibitory effect. It also highlights the possibility of evoking a beta burst with the iSP protocol, opening perspectives for future neuroimaging and modeling studies.