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Up to two-thirds of stroke survivors experience persistent sensorimotor impairments. Recovery relies on the integrity of spared brain areas to compensate for damaged tissue. Deep grey matter structures play a critical role in the control and regulation of sensorimotor circuits. The goal of this work is to identify associations between volumes of spared subcortical nuclei and sensorimotor behaviour at different timepoints after stroke. We pooled high-resolution T1-weighted MRI brain scans and behavioural data in 828 individuals with unilateral stroke from 28 cohorts worldwide. Cross-sectional analyses using linear mixed-effects models related post-stroke sensorimotor behaviour to non-lesioned subcortical volumes (Bonferroni-corrected, P

Quadriceps dysfunction persists after anterior cruciate ligament reconstruction (ACLR), yet the etiology remains elusive. Inhibitory and facilitatory intracortical networks (ie, intracortical excitability) may be involved in quadriceps dysfunction, yet the investigation of these networks early after ACLR is sparse. The purposes of this study were to examine (a) changes in intracortical excitability in athletes after ACLR compared to uninjured athletes during the course of postoperative rehabilitation, (b) the association between intracortical excitability and quadriceps strength in athletes after ACLR. Eighteen level I/II athletes after ACLR between the ages of 18 to 30 years and eighteen healthy sex, age, and activity matched athletes were tested at three‐time points: (a) 2 weeks after surgery, (b) achievement of a "quiet knee" defined as full range of motion and minimal effusion, (c) return to running time point defined as achievement of a quadriceps index ≥80% and at least 12 weeks post‐ACLR. Short‐interval intracortical inhibition (SICI) and intracortical facilitation (ICF), measured via transcranial magnetic stimulation and isometric quadriceps strength were examined bilaterally at each time point. There was a significant group × limb interaction (P =.017) for ICF. The ACLR group demonstrated asymmetric ICF (greater in the nonsurgical limb) compared to controls and a significant relationship between SICI and quadriceps strength of the surgical limb at the quiet knee time point (P =.018). ACLR individuals demonstrate differential effects on ICF between limbs. Also, SICI is associated with isometric quadriceps strength after ACLR, suggesting increased inhibition of the motor cortex may contribute to impaired quadriceps strength following ACLR. [ABSTRACT FROM AUTHOR]

* OBJECTIVE: To investigate corticospinal and spinal reflexive excitability and quadriceps strength in healthy athletes and athletes after anterior cruciate ligament reconstruction (ACLR) over the course of rehabilitation. S DESIGN: Prospective cohort study. * METHODS: Eighteen athletes with ACLR and 18 healthy athletes, matched by sex, age, and activity, were tested at (1) 2 weeks after surgery, (2) the "quiet knee" time point, defined as full range of motion and minimal effusion, and (3) return to running, defined as achieving a quadriceps index of 80% or greater. We measured (1) corticospinal excitability, using resting motor threshold (RMT) and motor-evoked potential amplitude at a stimulator intensity of 120% of RMT (MEP120) to the vastus medialis, (2) spinal reflexive excitability, calculating the ratio of the maximal Hoffmann reflex to the maximal M-wave to the vastus medialis, and (3) isometric quadriceps strength. * RESULTS: The ACLR group had higher RMTs in the nonsurgical limb and higher MEP120 in the surgical limb at all time points. The healthy-athlete group did not have interimb differences. The RMT was positively associated with quadriceps strength 2 weeks after surgery; MEP120 was associated with quadriceps strength at all time points. * CONCLUSION: Compared to healthy athletes, athletes after ACLR had altered corticospinal excitability that did not change from 2 weeks after surgery to the time of return to running. [ABSTRACT FROM AUTHOR]

Background: Acute exercise can increase motor cortical excitability and enhance motor learning in healthy individuals, an effect known as exercise priming. Whether it has the same effects in people with stroke is unclear. Objectives: The objective of this study was to investigate whether a short, clinically-feasible high-intensity exercise protocol can increase motor cortical excitability in non-exercised muscles of chronic stroke survivors. Methods: Thirteen participants with chronic, unilateral stroke participated in two sessions, at least one week apart, in a crossover design. In each session, they underwent either high-intensity lower extremity exercise or quiet rest. Motor cortical excitability of the extensor carpi radialis muscles was measured bilaterally with transcranial magnetic stimulation before and immediately after either exercise or rest. Motor cortical excitability changes (post-exercise or rest measures normalized to pre-test measures) were compared between exercise vs. rest conditions. Results: All participants were able to reach the target high-intensity exercise level. Blood lactate levels increased significantly after exercise (p <.001, d = 2.85). Resting motor evoked potentials from the lesioned hemisphere increased after exercise (mean 1.66; 95% CI: 1.19, 2.13) compared to the rest condition (mean 1.23; 95% CI: 0.64, 1.82), p =.046, d = 2.76, but this was not the case for the non-lesioned hemisphere (p =.406, d = 0.25). Conclusions: High-intensity exercise can increase lesioned hemisphere motor cortical excitability in a non-exercised muscle post-stroke. Our short and clinically-advantageous exercise protocol shows promise as a potential priming method in stroke rehabilitation. [ABSTRACT FROM AUTHOR]

Acute high-intensity exercise coupled with motor practice improves the retention of motor learning in neurologically intact adults. However, whether exercise could improve the retention of locomotor learning after stroke is still unknown. Here, we investigated the effect of exercise intensity and timing on the retention of a novel locomotor learning task (i.e. split-belt treadmill walking) after stroke. Thirty-seven people post stroke participated in two sessions, 24 h apart, and were allocated to active control (CON), treadmill walking (TMW), or total body exercise on a cycle ergometer (TBE). In session 1, all groups exercised for a short bout (~5 min) at low (CON) or high (TMW and TBE) intensity and before (CON and TMW) or after (TBE) the locomotor learning task. In both sessions, the locomotor learning task was to walk on a split-belt treadmill in a 2:1 speed ratio (100% and 50% fast-comfortable walking speed) for 15 min. To test the effect of exercise on 24 h retention, we applied behavioural and computational analyses. Behavioural data showed that neither high-intensity group showed greater 24 h retention compared to CON, and computational data showed that 24 h retention was attributable to a slow learning process for sensorimotor adaptation. Our findings demonstrated that acute exercise coupledwith a locomotor adaptation task, regardless of its intensity and timing, does not improve retention of the novel locomotor task after stroke. We postulate that exercise effects on motor learning may be context specific (e.g. type of motor learning and/or task) and interact with the presence of genetic variant (BDNF Val66Met). [ABSTRACT FROM AUTHOR]

Background: People post-stroke can learn a novel locomotor task but require more practice to do so. Implementing an approach that can enhance locomotor learning may therefore improve post-stroke locomotor recovery. In healthy adults, an acute high-intensity exercise bout before or after a motor task may improve motor learning and has thus been suggested as a method that could be used to improve motor learning in neurorehabilitation. However, it is unclear whether an acute high-intensity exercise bout, which stroke survivors can feasibly complete in neurorehabilitation session, would generate comparable results. Objective: To determine a feasible, high-intensity exercise protocol that could be incorporated into a post-stroke neurorehabilitation session and would result in significant exercise-induced responses. Methods: Thirty-seven chronic stroke survivors participated. We allocated subjects to either a control (CON) or one of the exercise groups: treadmill walking (TMW), and total body exercise (TBE). The main exercise-induced measures were: average intensity (% max intensity) and time spent (absolute: seconds; normalized: % total time) at target exercise intensity, and magnitudes of change in serum lactate (mmol/l) and brain-derived neurotrophic factor (BDNF; ng/ml). Results: Compared to CON, both exercise groups reached and exercised longer at their target intensities and had greater responses in lactate. However, the TBE group exercised longer at target intensity and with greater lactate response than the TMW group. There were no significant BDNF responses among groups. Conclusions: An acute high-intensity exercise bout that could be incorporated into a neurorehabilitation learning-specific session and results in substantial exercise-induced responses is feasible post-stroke. [ABSTRACT FROM AUTHOR]