The sudden cancellation of a motor action, known as response inhibition (RI), is fundamental to human motor behavior. The behavioral selectivity of RI can be studied by cueing cancellation of only a subset of a planned response, which markedly delays the remaining executed components. The present study examined neurophysiological mechanisms that may contribute to these delays. In two experiments, human participants received single- and paired-pulse transcranial magnetic stimulation while performing a bimanual anticipatory response task. Participants performed most trials bimanually (Go trials) and were sometimes cued to cancel the response with one hand while responding with the other (Partial trials). Motor evoked potentials were recorded from left first dorsal interosseous (FDI) as a measure of corticomotor excitability (CME) during Go and Partial trials. CME was temporally modulated during Partial trials in a manner that reflected anticipation, suppression, and subsequent initiation of a reprogrammed response. There was an initial increase in CME, followed by suppression 175 ms after the stop signal, even though the left hand was not cued to stop. A second increase in excitability occurred prior to the (delayed) response. We propose an activation threshold model to account for nonselective RI. To investigate the inhibitory component of our model, we investigated short-latency intracortical inhibition (sICI), but results indicated that sICI cannot fully explain the observed temporal modulation of CME. These neurophysiological and behavioural results indicate that the default mode for reactive partial cancellation is suppression of a unitary response, followed by response reinitiation with an inevitable time delay.

Two weeks of iTBS-primed therapy improves upper limb function at the chronic stage of stroke, for at least 1 month postintervention, whereas therapy alone may not be sufficient to alter function. This indicates a potential role for iTBS as an adjuvant to therapy delivered at the chronic stage.

The ability to prevent unwanted movement is fundamental to human behavior. When healthy adults must prevent a subset of prepared actions, execution of the remaining response is markedly delayed. We hypothesized that the delay may be sensitive to the degree of similarity between the prevented and continued actions. Fifteen healthy participants performed an anticipatory response inhibition task that required bilateral index finger extension or thumb abduction with homogeneous digit pairings, or a heterogeneous pairing of a combination of the two movements. We expected that the uncoupling of responses required for selective movement prevention would be more difficult with homogeneous (same digit, homologous muscles) than heterogeneous pairings (different digits, nonhomologous muscles). Measures of response times (and asynchrony between digits) during action execution, stopping performance, and electromyography from EIP (index finger extension) and APB (thumb abduction) were analyzed. As expected, selective trials produced a delay in the remaining movement compared with execution trials. Successful performance in the selective condition occurred via suppression of the entire prepared response and subsequent selective reinitiation of the remaining component. Importantly, the delayed reinitiation of motor output was sensitive to the degree of similarity between responses, occurring later but at a faster rate with homogeneous digits. There were persistent aftereffects from the selective condition on the motor system, which indicated greater levels of inhibition and a higher gain were necessary to successfully perform selective trials with homogeneous pairings. Overall, the results support a model of inhibition of a unitary response and selective reinitiation, rather than selective inhibition.

Cowie MJ, MacDonald HJ, Cirillo J, Byblow WD. Proactive modulation of long-interval intracortical inhibition during response inhibition.

Reactive response inhibition (RI) is the cancellation of a prepared response when it is no longer appropriate. Selectivity of RI can be examined by cueing the cancellation of one component of a prepared multi-component response. This substantially delays execution of other components. There is debate regarding whether this response delay is due to a selective neural mechanism. Here we propose a computational activation threshold model (ATM) and test it against a classical “horse-race” model using behavioural and neurophysiological data from partial RI experiments. The models comprise both facilitatory and inhibitory processes that compete upstream of motor output regions. Summary statistics (means and standard deviations) of predicted muscular and neurophysiological data were fit in both models to equivalent experimental measures by minimizing a Pearson Chi-square statistic. The ATM best captured behavioural and neurophysiological dynamics of partial RI. The ATM demonstrated that the observed modulation of corticomotor excitability during partial RI can be explained by nonselective inhibition of the prepared response. The inhibition raised the activation threshold to a level that could not be reached by the original response. This was necessarily followed by an additional phase of facilitation representing a secondary activation process in order to reach the new inhibition threshold and initiate the executed component of the response. The ATM offers a mechanistic description of the neural events underlying RI, in which partial movement cancellation results from a nonselective inhibitory event followed by subsequent initiation of a new response. The ATM provides a framework for considering and exploring the neuroanatomical constraints that underlie RI.