Gait is one of the fundamental behaviors we use to interact with the world. The functionality of the locomotor system is thus related to enriching interactions with our environment. The posterior parietal cortex (PPC) has been found to contribute to motor adaptation during both visuomotor and postural adaptation tasks. Additionally, structural or functional deficits of the PPC lead to impairments in gaits such as shortened steps and increased step width. Based on the aforementioned roles of the PPC, and the importance of gait adaptability, the current investigation sought to identify the role of the PPC in gait adaptation. To achieve this, we performed transcranial direct current stimulation (tDCS) over the bilateral PPC before performing a split-belt treadmill gait adaptation paradigm. We used three stimulation conditions in a within-subject design. tDCS was administered in a randomized and double-blinded order. Following each stimulation session, subjects first performed baseline walking with both belts running at the same speed. Then, subjects walked for 15 min on an uncoupled treadmill, with the belts being driven at a 3:1 speed ratio. Last, they returned to normal (i.e., tied-belt) walking for 5 min. Results from 15 young and healthy subjects identified that subjects required more steps to adapt to split-belt walking following the suppression of the left hemisphere PPC, contralateral to the fast belt. Furthermore, while suppression of the left hemisphere PPC did not increase the number of steps required to re-adapt to tied-belt walking, this condition did lead to increased magnitude of after-effects. Together, these findings indicate that the PPC is involved in locomotor adaptation. These results support previous literature regarding the upper body or postural adaptation and extend these findings to the realm of gait. Results highlight the PPC as a potential target for neurorehabilitation designed to improve gait adaptability.
Conditional learning is an important component of our everyday activities (e.g., handling a phone or sorting work files) and requires identification of the arbitrary stimulus, accurate selection of the motor response, monitoring of the response, and storing in memory of the stimulus-response association for future recall. Learning this type of conditional visuomotor task appears to engage the premotor dorsal region (PMd). However, the extent to which PMd might be involved in specific or all processes of conditional learning is not well understood. Using transcranial magnetic stimulation (TMS), we demonstrate the role of human PMd in specific stages of learning of a novel conditional visuomotor task that required subjects to identify object center of mass using a color cue and to apply appropriate torque on the object at lift onset to minimize tilt. TMS over PMd, but not vertex, increased error in torque exerted on the object during the learning trials. Analyses of digit position and forces further revealed that the slowing in conditional visuomotor learning resulted from impaired monitoring of the object orientation during lift, rather than stimulus identification, thus compromising the ability to accurately reduce performance error across trials. Importantly, TMS over PMd did not alter production of torque based on the recall of learned color-torque associations. We conclude that the role of PMd for conditional learning is highly sensitive to the stage of learning visuomotor associations. NEW & NOTEWORTHY Conditional learning involves stimulus identification, motor response selection, response monitoring, memory encoding, and recall of the learned association. Premotor dorsal (PMd) has been implicated for conditional learning. However, the extent to which PMd might be involved in specific or all stages of conditional learning is not well understood. The novel finding of our study is that PMd appears to be involved with monitoring motor responses, a sensorimotor integration stage essential for conditional learning.
Neuronal firing rate variability prior to movement onset contributes to trial-to-trial variability in primate behavior. However, in humans, whether similar mechanisms contribute to trial-to-trial behavioral variability remains unknown. We investigated the time-course of trial-to-trial variability in corticospinal excitability (CSE) using transcranial magnetic stimulation (TMS) during a self-paced reach-to-grasp task. We hypothesized that CSE variability will be modulated prior to the initiation of reach and that such a modulation would explain trial-to-trial behavioral variability. Able-bodied individuals were visually cued to plan their grip force before exertion of either 30% or 5% of their maximum pinch force capacity on an object. TMS was delivered at six time points (0.5, 0.75, 1, 1.1, 1.2, and 1.3 s) following a visual cue that instructed the force level. We first modeled the relation between CSE magnitude and its variability at rest (n = 12) to study the component of CSE variability pertaining to the task but not related to changes in CSE magnitude (n = 12). We found an increase in CSE variability from 1.2 to 1.3 s following the visual cue at 30% but not at 5% of force. This effect was temporally dissociated from the decrease in CSE magnitude that was observed from 0.5 to 0.75 s following the cue. Importantly, the increase in CSE variability explained at least ∼40% of inter-individual differences in trial-to-trial variability in time to peak force rate. These results were found to be repeatable across studies and robust to different analysis methods. Our findings suggest that the neural mechanisms underlying modulation in CSE variability and CSE magnitude are distinct. Notably, the extent of modulation in variability in corticospinal system prior to grasp within individuals may explain their trial-to-trial behavioral variability.