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Background Persistent sensorimotor impairments after stroke can negatively impact quality of life. The hippocampus is vulnerable to poststroke secondary degeneration and is involved in sensorimotor behavior but has not been widely studied within the context of poststroke upper-limb sensorimotor impairment. We investigated associations between non-lesioned hippocampal volume and upper limb sensorimotor impairment in people with chronic stroke, hypothesizing that smaller ipsilesional hippocampal volumes would be associated with greater sensorimotor impairment. Methods and Results Cross-sectional T1-weighted magnetic resonance images of the brain were pooled from 357 participants with chronic stroke from 18 research cohorts of the ENIGMA (Enhancing NeuoImaging Genetics through Meta-Analysis) Stroke Recovery Working Group. Sensorimotor impairment was estimated from the FMA-UE (Fugl-Meyer Assessment of Upper Extremity). Robust mixed-effects linear models were used to test associations between poststroke sensorimotor impairment and hippocampal volumes (ipsilesional and contralesional separately; Bonferroni-corrected, P

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

Relapsing-remitting Multiple Sclerosis is the most common demyelinating neurodegenerative disease and is characterized by periods of relapses and generation of various motor symptoms. These symptoms are associated with the corticospinal tract integrity, which is quantified by means of corticospinal plasticity which can be probed via transcranial magnetic stimulation and assessed with corticospinal excitability measures. Several factors, such as exercise and interlimb coordination, can influence corticospinal plasticity. Previous work in healthy and in chronic stroke survivors showed that the greatest improvement in corticospinal plasticity occurred during in-phase bilateral exercises of the upper limbs. During in-phase bilateral movement, both upper limbs are moving simultaneously, activating the same muscle groups and triggering the same brain region respectively. Altered corticospinal plasticity due to bilateral cortical lesions is common in MS, yet, the impact of these type of exercises in this cohort is unclear. The aim of this concurrent multiple baseline design study is to investigate the effects of in-phase bilateral exercises on corticospinal plasticity and on clinical measures using transcranial magnetic stimulation and standardized clinical assessment in five people with relapsing-remitting MS. The intervention protocol will last for 12 consecutive weeks (30–60 minutes /session x 3 sessions/week) and include in-phase bilateral movements of the upper limbs, adapted to different sports activities and to functional training. To define functional relation between the intervention and the results on corticospinal plasticity (central motor conduction time, resting motor threshold, motor evoked potential amplitude and latency) and on clinical measures (balance, gait, bilateral hand dexterity and strength, cognitive function), we will perform a visual analysis and if there is a potential sizeable effect, we will perform statistical analysis. A possible effect from our study, will introduce a proof-of-concept for this type of exercise that will be effective during disease progression. Trial registration: ClinicalTrials.gov NCT05367947. [ABSTRACT FROM AUTHOR]

Alpha and beta oscillations have been assessed thoroughly during walking due to their potential role as proxies of the corticoreticulospinal tract (CReST) and corticospinal tract (CST), respectively. Given that damage to a descending tract after stroke can cause walking deficits, detailed knowledge of how these oscillations mechanistically contribute to walking could be utilized in strategies for post-stroke locomotor recovery. In this review, the goal was to summarize, synthesize, and discuss the existing evidence on the potential differential role of these oscillations on the motor descending drive, the effect of transcranial alternate current stimulation (tACS) on neurotypical and post-stroke walking, and to discuss remaining gaps in knowledge, future directions, and methodological considerations. Electrophysiological studies of corticomuscular, intermuscular, and intramuscular coherence during walking clearly demonstrate that beta oscillations are predominantly present in the dorsiflexors during the swing phase and may be absent poststroke. The role of alpha oscillations, however, has not been pinpointed as clearly. We concluded that both animal and human studies should focus on the electrophysiological characterization of alpha oscillations and their potential role to the CReST. Another approach in elucidating the role of these oscillations is to modulate them and then quantify the impact on walking behavior. This is possible through tACS, whose beneficial effect on walking behavior (including boosting of beta oscillations in intramuscular coherence) has been recently demonstrated in both neurotypical adults and stroke patients. However, these studies still do not allow for specific roles of alpha and beta oscillations to be delineated because the tACS frequency used was much lower (i.e., individualized calculated gait frequency was used). Thus, we identify a main gap in the literature, which is tACS studies actually stimulating at alpha and beta frequencies during walking. Overall, we conclude that for beta oscillations there is a clear connection to descending drive in the corticospinal tract. The precise relationship between alpha oscillations and CReST remains elusive due to the gaps in the literature identified here. However, better understanding the role of alpha (and beta) oscillations in the motor control of walking can be used to progress and develop rehabilitation strategies for promoting locomotor recovery. [ABSTRACT FROM AUTHOR]

Key points: The corticoreticulospinal tract (CReST) is a descending motor pathway that reorganizes after corticospinal tract (CST) injury in animals.In humans, the pattern of CReST innervation to upper limb muscles has not been carefully examined in healthy individuals or individuals with CST injury.In the present study, we assessed CReST projections to an arm and hand muscle on the same side of the body in healthy and chronic stoke subjects using transcranial magnetic stimulation.We show that CReST connection strength to the muscles differs between healthy and stroke subjects, with stronger connections to the hand than arm in healthy subjects, and stronger connections to the arm than hand in stroke subjects.These results help us better understand CReST innervation patterns in the upper limb, and may point to its role in normal motor function and motor recovery in humans. The corticoreticulospinal tract (CReST) is a major descending motor pathway in many animals, but little is known about its innervation patterns in proximal and distal upper extremity muscles in humans. The contralesional CReST furthermore reorganizes after corticospinal tract (CST) injury in animals, but it is less clear whether CReST innervation changes after stroke in humans. We thus examined CReST functional connectivity, connection strength, and modulation in an arm and hand muscle of healthy (n = 15) and chronic stroke (n = 16) subjects. We delivered transcranial magnetic stimulation to the contralesional hemisphere (assigned in healthy subjects) to elicit ipsilateral motor evoked potentials (iMEPs) from the paretic biceps (BIC) and first dorsal interosseous (FDI) muscle. We operationalized CReST functional connectivity as iMEP presence/absence, CReST projection strength as iMEP size and CReST modulation as change in iMEP size by head rotation. We found comparable CReST functional connectivity to the BICs and FDIs in both subject groups. However, the pattern of CReST connection strength to the muscles diverged between groups, with stronger connections to FDIs than BICs in healthy subjects and stronger connections to BICs than FDIs in stroke subjects. Head rotation modulated only FDI iMEPs of healthy subjects. Our findings indicate that the healthy CReST does not have a proximal innervation bias, and its strong FDI connections may have functional relevance to finger individuation. The reversed CReST innervation pattern in stroke subjects confirms its reorganization after CST injury, and its strong BIC connections may indicate upregulation for particular upper extremity muscles or their functional actions. Key points: The corticoreticulospinal tract (CReST) is a descending motor pathway that reorganizes after corticospinal tract (CST) injury in animals.In humans, the pattern of CReST innervation to upper limb muscles has not been carefully examined in healthy individuals or individuals with CST injury.In the present study, we assessed CReST projections to an arm and hand muscle on the same side of the body in healthy and chronic stoke subjects using transcranial magnetic stimulation.We show that CReST connection strength to the muscles differs between healthy and stroke subjects, with stronger connections to the hand than arm in healthy subjects, and stronger connections to the arm than hand in stroke subjects.These results help us better understand CReST innervation patterns in the upper limb, and may point to its role in normal motor function and motor recovery in humans. [ABSTRACT FROM AUTHOR]

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]

Neuromuscular impairments, such as quadriceps weakness and activation deficits, persist after anterior cruciate ligament reconstruction (ACLR). Recent research demonstrating changes in the function of the primary motor cortex after ACLR posits that quadriceps impairments may be influenced by reduced corticospinal excitability. The purpose of this study was to investigate whether the integrity of the neuromotor axis of the vastus medialis is altered in subjects 2 weeks post‐ACLR compared to uninjured control subjects. Eighteen athletes 2 weeks post‐ACLR and 18 age and sex matched uninjured control subjects participated in this cross‐sectional study. We quantified corticospinal (resting motor threshold, RMT; motor evoked potential amplitudes at 120% RMT, MEP120) and intracortical (inhibition and facilitation) excitability using single and paired pulse transcranial magnetic stimulation (TMS), respectively. We assessed spinal‐reflex excitability (H‐reflex amplitude normalized to maximal M‐wave, H/M ratio) using peripheral stimulation. Subjects post‐ACLR had higher RMTs (p = 0.001), greater MEP120 amplitudes (p = 0.001), and more asymmetric facilitation (p = 0.041) than the uninjured control subjects. No significant group differences were found for intracortical inhibition (p = 0.289) and H/M ratio (p = 0.332). Our findings indicate that both intracortical and corticospinal excitability of vastus medialis are bilaterally altered in subjects 2 weeks after ACLR. Given persistent neuromuscular deficits seen after ACLR, rehabilitation strategies targeting intracortical and corticospinal deficits may potentially improve clinical outcomes. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2941–2948, 2018. [ABSTRACT FROM AUTHOR]

Distorted visual feedback (DVF) during locomotion has been suggested to result in the development of a new walking pattern in healthy individuals through implicit learning processes. Recent work in upper extremity visuomotor rotation paradigms suggest that these paradigms involve implicit and explicit learning. Additionally, in upper extremity visuomotor paradigms, the verbal cues provided appear to impact how a behavior is learned and when this learned behavior is used. Here, in two experiments in neurologically intact individuals, we tested how verbal instruction impacts learning a new locomotor pattern on a treadmill through DVF, the transfer of that pattern to overground walking, and what types of learning occur (i.e., implicit vs. explicit learning). In experiment 1, we found that the instructions provided impacted the amount learned through DVF, but not the size of the aftereffects or the amount of the pattern transferred to overground walking. Additionally, the aftereffects observed were significantly different from the baseline walking pattern, but smaller than the behavior changes observed during learning, which is uncharacteristic of implicit sensorimotor adaptation. Thus, experiment 2 aimed to determine the cause of these discrepancies. In this experiment, when VF was not provided, individuals continued using the learned walking pattern when instructed to do so and returned toward their baseline pattern when instructed to do so. Based on these results, we conclude that DVF during locomotion results in a large portion of explicit learning and a small portion of implicit learning. NEW & NOTEWORTHY The results of this study suggest that distorted visual feedback during locomotor learning involves the development of an explicit strategy with only a small component of implicit learning. This is important because previous studies using distorted visual feedback have suggested that locomotor learning relies primarily on implicit learning. This paradigm, therefore, provides a new way to examine a different form of learning in locomotion. [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]

Twenty-five samples of Byzantine glazed pottery from two archaeological sites between Limassol and Paphos region (Cyprus), dated between the 12th and 15th centuryad were studied using micro X-ray fluorescence spectroscopy, scanning electron microscopy and X-ray diffraction analysis. It was found that all the glazes contain lead, following the main manufacturing process of medieval pottery in the Mediterranean territory, while some of them contain tin, possibly for better opacity. Furthermore, it is shown that copper, iron and cobalt with nickel are responsible for the decoration colours. Finally, the application of principal component analysis revealed significant differentiation for some of the samples. [ABSTRACT FROM AUTHOR]

Abstract: In the present paper we report the use of a homemade electronic device (Multipulser), for monitoring interactions between biomolecules that may change the capacitance of an electrode. Multipulser can be used as a stand-alone, low-cost, yet effective alternative monitoring device instead of other well established commercial instruments. The operation of Multipulser is based on the integration of the electric charge used for the repetitive charging of the electrochemical cell capacitance after the application of a predetermined number of short-duration, low-amplitude voltage pulses (perturbation pulses). Multipulser was used to monitor the binding of biotinylated dextran on two different avidin modified electrode assemblies; one based on a thiol SAMs on gold and another based on Ti/TiO2 semiconductor. Measurements conducted in parallel with a commercial frequency response analyzer gave similar reaction patterns. Pulse polarity dependent behavior was revealed in the case of the Ti/TiO2-electrode assembly when bipolar potential perturbation modes were used with Multipulser. [Copyright &y& Elsevier]

Objective: To measure colonic arterial (CA) and colonic venous (CV) plasma neuropeptide concentrations during low-flow ischemia and reperfusion of the large colon in horses., Animals: 10 adult horses., Procedure: CA and CV plasma samples collected from anesthetized horses during experimentally induced low-flow colonic ischemia and reperfusion were assayed for vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), using radioimmunoassays. In 6 anesthetized horses, colonic ischemia (20% of baseline (BL]) was maintained for 3 hours, then blood flow was restored and monitored for 3 hours. Hemodynamic variables were monitored continuously and recorded at 30-minute intervals. CA resistance was calculated from colonic blood flow (Q(colon)) and mean CA pressure values at each time. Blood was obtained from CA and CV catheters at 0, 1, 2, 3, 3.25, 3.5, 4, 5, and 6 hours; plasma VIP, CGRP, and SP concentrations were quantified, using radioimmunoassays. In 4 additional horses, VIP and CGRP were measured in CA and CV blood at 0, 0.25, 0.5, 0.75, and 1 hour., Results: Heart rate was significantly increased at 5.5 and 6 hours; other alterations in systemic hemodynamic variables were not significant. Decrease in Q(colon) during ischemia was significant; Q(colon) rebounded to a value significantly greater than BL value within 5 minutes of reperfusion and was maintained above the BL value during 3 hours of reperfusion. Mean CA pressure was significantly decreased during ischemia, but returned to a value not different from the BL value by 3.25 hours. Mean CV pressure remained unchanged from the BL value during ischemia, but increased to a value significantly greater than the BL value by 3.25 hours and remained increased through 6 hours. CA resistance began to decrease during early ischemia and was significantly less than the BL value by 3.25 hours; it remained less than the BL value through 4 hours. Increase in CV VIP concentration was significant by 0.25 hour of ischemia, but decreased to a value not different from BL value by 3.25 hours. Increase in CV CGRP was significant at 3.25 hours, but this variable returned to a value not different from BL value by 3.5 hours., Conclusions: CV VIP concentration increases during low-flow colonic ischemia, and CV and CA CGRP and CA SP concentrations increase during early reperfusion.