Objectives The primary purpose of this study was to determine if acceleration metrics derived from monitoring outside of treatment are responsive to change in upper extremity (UE) function. The secondary purposes were two-fold: The first was to compare metric values during task-specific training and while in the free-living environment. The second was to establish metric associations with an in-clinic measure of movement capabilities. Design Before-After Observational Study Setting Inpatient Hospital (primary purpose); Outpatient Hospital (secondary purpose) Participants Individuals (n=8) with UE hemiparesis < 30 days post stroke (primary purpose); Individuals (n=27) with UE hemiparesis ≥ 6 months post stroke (secondary purpose). Methods The inpatient sample was evaluated for UE movement capabilities and monitored with wrist-worn accelerometers for 22 hours outside of treatment before and after multiple sessions of task-specific training. The outpatient sample was evaluated for UE movement capabilities and monitored during a single session of task-specific training and the subsequent 22 hours outside of clinical settings. Main Outcome Measures Action Research Arm Test and acceleration metrics quantified from accelerometer recordings. Results Five metrics improved in the inpatient sample, along with UE function as measured on the ARAT: use ratio, magnitude ratio, variation ratio, median paretic UE acceleration magnitude, and paretic UE acceleration variability. Metric values were greater during task-specific training than in the free-living environment, and each metric was strongly associated with ARAT score. Conclusions Multiple metrics that characterize different aspects of UE movement are responsive to change in function. Metric values are different during training than in the free-living environment, providing further evidence that what the paretic UE does in the clinic may not generalize to what it does in everyday life.

Acute intermittent hypoxia (AIH) enhances voluntary motor output in humans with central nervous system damage. The neural mechanisms contributing to these beneficial effects are unknown. We examined corticospinal function by evaluating motor evoked potentials (MEPs) elicited by cortical and subcortical stimulation of corticospinal axons and the activity in intracortical circuits in a finger muscle before and after 30 min of AIH or sham AIH. We found that the amplitude of cortically and subcortically elicited MEPs increased for 75 min after AIH but not sham AIH while intracortical activity remained unchanged. To examine further these subcortical effects, we assessed spike-timing dependent plasticity (STDP) targeting spinal synapses and the excitability of spinal motoneurons. Notably, AIH increased STDP outcomes while spinal motoneuron excitability remained unchanged. Our results provide the first evidence that AIH changes corticospinal function in humans, likely by altering corticospinal-motoneuronal synaptic transmission. AIH may represent a novel noninvasive approach for inducing spinal plasticity in humans.

Although increased time within specific phases correlates with decreases in the magnitude of upper extremity kinetics linked to overuse injuries, it also correlates with decreased ball speed. Based on these findings, it may appear that minimizing the risk of injury (ie, decreased kinetics) and maximizing performance quality (ie, increased ball speed) are incompatible with one another. However, there may be an optimal balance in timing that is effective for satisfying both outcomes.

Recovery of lower-limb function after spinal cord injury (SCI) likely depends on transmission in the corticospinal pathway. Here, we examined whether paired corticospinal-motoneuronal stimulation (PCMS) changes transmission at spinal synapses of lower-limb motoneurons in humans with chronic incomplete SCI and aged-matched controls. We used 200 pairs of stimuli where corticospinal volleys evoked by transcranial magnetic stimulation (TMS) over the leg representation of the motor cortex were timed to arrive at corticospinal-motoneuronal synapses of the tibialis anterior (TA) muscle 2 ms before antidromic potentials evoked in motoneurons by electrical stimulation of the common peroneal nerve (PCMS+) or when antidromic potentials arrived 15 or 28 ms before corticospinal volleys (PCMS-) on separate days. Motor evoked potentials (MEPs) elicited by TMS and electrical stimulation were measured in the TA muscle before and after each stimulation protocol. After PCMS+, the size of MEPs elicited by TMS and electrical stimulation increased for up to 30 min in control and SCI participants. Notably, this was accompanied by increases in TA electromyographic activity and ankle dorsiflexion force in both groups, suggesting that this plasticity has functional implications. After PCMS-, MEPs elicited by TMS and electrical stimulation were suppressed if afferent input from the common peroneal nerve reduced TA MEP size during paired stimulation in both groups. In conclusion, PCMS elicits spike-timing-dependent changes at spinal synapses of lower-limb motoneurons in humans and has potential to improve lower-limb motor output following SCI. Approaches that aim to enhance corticospinal transmission to lower-limb muscles following spinal cord injury (SCI) are needed. We demonstrate that paired corticomotoneuronal stimulation (PCMS) can enhance plasticity at spinal synapses of lower-limb motoneurons in humans with and without SCI. We propose that PCMS has potential for improving motor output in leg muscles in individuals with damage to the corticospinal tract.