Search bioRxiv⌕ Search

Biology subjects

Borich, M. R.

Publications and source records attributed to Borich, M. R..

14 recordsLinked to original sources

Anticipatory Gaze Reveals Individual Differences in Implicit Sequence Learning Before Motor Performance

Implicit sequence learning is commonly inferred from changes in motor performance, although anticipatory gaze behavior may provide complementary information about emerging perceptual sequence knowledge. We tracked anticipatory gaze and response time on every trial of a reach-grasp-and-move sequence-learning task to examine when individual differences became detectable in each measure. Between-participant differences became detectable earlier in anticipatory gaze than in response time, with this ordering preserved in 95.5% of participant-level bootstrap resamples. Across the repeated sequence, anticipatory gaze became increasingly frequent, and most participants showed faster responses on anticipatory-gaze trials. Exploratory analyses further indicated that participants differed in the trial-to-trial persistence of anticipatory gaze, but these gaze characteristics were not reliably associated with sequence-specific motor learning expressed at the end of the session. Together, these findings show that anticipatory gaze and motor performance provide related but non-redundant information about implicit sequence learning where individual differences in perceptual knowledge may be detectable before corresponding differences are apparent in behavioral performance.

neuroscience↗

Higher cortical beta oscillatory power before balance perturbations is associated with worse balance in older adults with Parkinson's Disease, but not in age-matched older adults

Elevated beta activity is hypothesized to reflect reduced flexibility in updating motor and sensory states, which may impair the rapid integration of sensory information required for balance. Therefore, we predicted that higher cortical beta power immediately before balance perturbations would be associated with poorer clinical balance performance, particularly in individuals with Parkinson's Disease (PD). Seventeen individuals with PD (median Hoehn & Yahr = 2) and eighteen neurotypical older adults stood on a translating platform while 32-channel electroencephalography was recorded. For each participant, the cortical component contributing most strongly to the perturbation-evoked N1 response, a balance-related cortical response localized to the supplementary motor area, was identified. Oscillatory beta power (13-30 Hz) during the one-second period immediately preceding perturbation onset was extracted from this N1-related cortical source and parameterized using Fitting Oscillations and One-Over-F (FOOOF). Balance ability was assessed using the Mini-Balance Evaluation Systems Test (Mini-BESTest). Beta power derived from this N1-related source did not differ between groups; however, within individuals with PD, higher pre-perturbation beta power was associated with lower Mini-BESTest scores, a relationship not observed in neurotypical older adults. A subset of older adults exhibited an additional, higher-frequency beta peak absent in PD, suggesting heterogeneity in cortical beta dynamics with aging. These findings suggest that elevated cortical beta oscillations immediately preceding balance perturbations are linked to clinically meaningful balance impairment in PD, supporting beta activity as a potential cortical biomarker of balance dysfunction in this population.

neuroscience↗

A Primary Central Source Determines Perturbation-Evoked N1 Amplitudes but not Latencies in Younger Adults

The balance perturbation-evoked N1 potential is a reliable cortical response during reactive balance control that is correlated to a variety of cognitive and motor functions. Although the supplementary motor area (SMA) has been identified as the primary source of the N1, it is less understood whether other brain regions contribute to N1 recorded at the scalp. We used source localization on electroencephalography (EEG) data from 25 younger adults recorded during backward whole-body perturbations during stance. We identified the sources that contribute to channel-based N1 recordings and quantified their impact on N1 amplitude and latency. In younger adults, N1 amplitudes can be explained by one single source in a central midline cortical region covering the SMA. When reconstructing N1 signals using backprojections with one versus all independent components (IC) identified as brain sources there was no difference in peak amplitudes and a small but significant difference in N1 peak latencies. Parallel brain sources thus deflect the time course of the N1, but not its magnitude. Brain areas associated with ICs contributing to the shift in N1 latency varied between participants. Our results emphasize the dominant influence of central cortical areas on the N1 response, informing hypothesizes regarding the nature of the signal and its functional role. Importantly, the extent and location of other cortical structures that influence N1 timing, such as parietal cortex areas and the anterior cingulate cortex, may further elucidate cortical contributions to balance. These markers could be crucial for the early detection of balance problems in clinical populations. NEW & NOTEWORTHYWe demonstrate that channel-level amplitudes of the balance perturbation-evoked N1 in younger adults primarily reflect neural activity originating from cortical central midline regions, particularly the SMA. In contrast, contributions from parallel active brain regions evoked by balance perturbations are indicated by an influence on N1 peak latencies. Our findings imply that the perturbation-evoked N1, unlike other evoked potentials, is not a mixture of multiple neural sources in younger adults.

neuroscience↗

Cortical response to balance perturbation is more sensitive in modern dancers than nondancers during biomechanically similar balance recovery

Motor skill expertise can facilitate more automatic movement, engaging less cortical activity while producing appropriate motor output. Accordingly, cortical-evoked N1 responses to balance perturbation, assessed using electroencephalography (EEG), are smaller in young and older adults with better balance. These responses may thus reflect individual balance challenge versus functional, or objective, task difficulty. However, the effect of balance expertise on cortical responses to balance perturbation has not been studied. We hypothesized that balance ability gained though long-term training facilitates more automatic balance control. Using professional modern dancers as balance experts, we compared cortical-evoked responses and biomechanics of the balance-correcting response between modern dancers and nondancers. We predicted that modern dancers would have smaller cortical-evoked responses and better balance recovery at equivalent levels of balance challenge. Support-surface perturbations were normalized to individual challenge levels by delivering perturbations scaled to 60% and 140% of each individuals step threshold. In contrast to our prediction, dancers exhibited larger N1 responses compared to nondancers while demonstrating similar biomechanical responses. Our results suggest dancers have greater cortical sensitivity to balance perturbations than nondancers. Further, dancer N1 responses modulated across perturbation magnitudes according to differences in objective task difficulty. In contrast, nondancer N1 responses modulated as a function of individual challenge level. Our findings suggest dance training increases sensitivity of the initial, cortical N1 response to balance perturbation, supporting postural alignment to an objective reference. The N1 response may reflect differences in balance-error processing that are altered with specific long-term training and may have implications for rehabilitation. NEW & NOTEWORTHYModern dancers show larger cortical responses to balance perturbations than nondancers, suggesting a greater sensitivity to perturbations. These results contrast with evidence of larger cortical-evoked responses in young adults with poorer balance, consistent with the cortical N1 response being a balance error assessment signal. Whereas nondancers scaled cortical responses by individual differences in N1 amplitude, dancers cortical responses were scaled to objective differences in perturbation magnitude, suggesting increased postural awareness due to training.

neuroscience↗

Cortically-mediated muscle responses to balance perturbations increase with perturbation magnitude in older adults with and without Parkinson's disease

We lack a clear understanding of how cortical contributions to balance are altered in aging and Parkinsons disease (PD), which limits development of rehabilitation strategies. Processes like balance control are typically mediated through brainstem circuits, with higher-order circuits becoming engaged as needed. Using reactive balance recovery, we investigated how hierarchical neural mechanisms shape balance- correcting muscle activity across task difficulty in older adults (OAs) with and without PD. We hypothesize that feedback loops involving brainstem and cortical circuits contribute to balance control, and cortical engagement increases with challenge, aging, and PD. We decomposed perturbation-evoked agonist and antagonist muscle activity into hierarchical components based on latency using neuromechanical models consisting of two feedback loops with different delays to reflect different neural conduction and processing times. Agonist muscle activity was decomposed into two components that both increased with balance challenge in both groups. The first component occurred [~]120ms and the second occurred [~]210ms, consistent with the latencies of brainstem and transcortical circuits, respectively. Exploratory comparisons to young adults revealed larger transcortical components in OA and PD groups at lower balance challenge levels, consistent with increased cortical involvement with aging. Antagonist muscle activity included destabilizing and stabilizing components, with the destabilizing component correlating to balance ability in OAs but not in PD. These findings demonstrate that neuromechanical models can identify changes in the hierarchical control of balance without direct brain measurements. Identifying cortical contributions during balance control may complement clinical measures of balance ability to inform balance rehabilitation and assistive devices. NEW & NOTEWORTHYA neuromechanical model can decompose perturbation evoked muscle activity into components attributed to brainstem and higher-order sensorimotor feedback based on latency. In older adults with and without PD contributions from higher-order neural circuits increase with balance challenge and are related to clinical measures of balance ability. Interpreting the neural substrates of motor output for balance may reveal individual differences in the hierarchical control of balance, that could inform rehabilitation.

neuroscience↗

Test-retest reliability of perturbation-evoked cortical activity reflects stable individual differences in reactive balance control

There is a growing interest in measuring cortical activity during balance control for understanding mechanisms of impaired balance with aging and neurological dysfunction. The most well-characterized electrophysiological signal elicited by a balance disturbance is the perturbation-evoked N1 potential that peaks 100-200 msec post-perturbation and is thought to reflect error processing. We previously found associations between the N1 and individual differences in balance ability, suggesting it may be a potential biomarker of balance health. However, a potential biomarker of balance function will be limited by its reliability and clinical feasibility, which has yet to be established. Here, we characterized the reliability of the N1 elicited by standing balance perturbations within and between sessions over a one-week interval in 10 younger and 14 older adults. A subset of older adults (n=12) completed a session approximately one year prior to the main experiment. We extracted N1 amplitude and latency from the Cz electrode using an advanced, computationally-intensive approach that relies on large amounts of data (e.g., 64 channels, many trials), Test-retest reliability was assessed using the intra-class correlation coefficient (ICC). Internal consistency was quantified by split-half reliability using the Spearman correlation coefficient. N1s varied across individuals (amplitude:12-82{micro}V, latency: 142-282ms), yet within individuals, the N1 showed excellent test-retest reliability (ICC>0.9) across a one-week and one-year time span. N1 amplitude reached excellent internal reliability for each session and group (r>0.9), that generally plateaued within 6 trials, while more trials were needed to reliably measure N1 latency. Similar results were obtained when quantifying N1s using a minimal approach performed with only three electrodes and simple preprocessing. Overall, the N1 is stable within and across sessions, and is largely independent of approach suggesting it could be a clinically-feasible biomarker of balance function. Characterizing reliability in populations with neurologic dysfunction and in different environmental contexts will be necessary to enhance our understanding of the N1, optimize experimental design, and determine its predictive validity of clinical outcomes (e.g., falls risk).

neuroscience↗

Distinct cortical correlates of perception and motor function in balance control

Fluctuations in brain state alter how we perceive our body and generate movements but have not been investigated in functional whole-body behaviors. During reactive balance control, we recently showed that evoked brain activity is associated with balance ability in healthy young individuals. Further, in individuals with Parkinsons disease, impairments in whole-body motion perception in reactive balance are associated with clinical balance impairment. Here we investigated brain activity during whole-body motion perception in reactive balance in healthy young adults. We hypothesized that flexibility in brain states underlies successful perception and movement during whole-body movement. We characterized two cortical sensorimotor signals using electroencephalography localized to the supplementary motor area: 1) the "N1 response", a perturbation-evoked potential that decreases in amplitude with expectancy and is larger in individuals with lower balance function; and 2) pre-perturbation beta oscillatory activity, a rhythm that favors maintenance of the current sensorimotor state and is inversely associated with perception in seated somatosensory perceptual tasks. In a two-alternative forced choice task, participants judged whether pairs of backward support-surface perturbations during standing were in the "same" or "different" direction. As expected, lower whole-body perception was associated with lower balance ability. Within a perturbation pair, N1 attenuation was larger on correctly perceived trials and associated with better balance, but not perception. In contrast, pre-perturbation beta power was higher on incorrectly perceived trials and associated with poorer perception, but not balance. Taken together, flexibility in different cortical processes influences perceptual accuracy but have distinct associations with balance and perceptual ability.

neuroscience↗

Data-driven biomarkers outperform theory-based biomarkers in predicting stroke motor outcomes

Chronic motor impairments are a leading cause of disability after stroke. Previous studies have predicted motor outcomes based on the degree of damage to predefined structures in the motor system, such as the corticospinal tract. However, such theory-based approaches may not take full advantage of the information contained in clinical imaging data. The present study uses data-driven approaches to predict chronic motor outcomes after stroke and compares the accuracy of these predictions to previously-identified theory-based biomarkers. Using a cross-validation framework, regression models were trained using lesion masks and motor outcomes data from 789 stroke patients (293 female/496 male) from the ENIGMA Stroke Recovery Working Group (age 64.9{+/-}18.0 years; time since stroke 12.2{+/-}0.2 months; normalised motor score 0.7{+/-}0.5 (range [0,1]). The out-of-sample prediction accuracy of two theory-based biomarkers was assessed: lesion load of the corticospinal tract, and lesion load of multiple descending motor tracts. These theory-based prediction accuracies were compared to the prediction accuracy from three data-driven biomarkers: lesion load of lesion-behaviour maps, lesion load of structural networks associated with lesion-behaviour maps, and measures of regional structural disconnection. In general, data-driven biomarkers had better prediction accuracy - as measured by higher explained variance in chronic motor outcomes - than theory-based biomarkers. Data-driven models of regional structural disconnection performed the best of all models tested (R2 = 0.210, p < 0.001), performing significantly better than predictions using the theory-based biomarkers of lesion load of the corticospinal tract (R2 = 0.132, p< 0.001) and of multiple descending motor tracts (R2 = 0.180, p < 0.001). They also performed slightly, but significantly, better than other data-driven biomarkers including lesion load of lesion-behaviour maps (R2 =0.200, p < 0.001) and lesion load of structural networks associated with lesion-behaviour maps (R2 =0.167, p < 0.001). Ensemble models - combining basic demographic variables like age, sex, and time since stroke - improved prediction accuracy for theory-based and data-driven biomarkers. Finally, combining both theory-based and data-driven biomarkers with demographic variables improved predictions, and the best ensemble model achieved R2 = 0.241, p < 0.001. Overall, these results demonstrate that models that predict chronic motor outcomes using data-driven features, particularly when lesion data is represented in terms of structural disconnection, perform better than models that predict chronic motor outcomes using theory-based features from the motor system. However, combining both theory-based and data-driven models provides the best predictions.

neuroscience↗

Global brain health modulates the impact of lesion damage on post-stroke sensorimotor outcomes

Sensorimotor performance after stroke is strongly related to focal injury measures such as corticospinal tract lesion load. However, the role of global brain health is less clear. Here, we examined the impact of brain age, a measure of neurobiological aging derived from whole brain structural neuroimaging, on sensorimotor outcomes. We hypothesized that stroke lesion damage would result in older brain age, which would in turn be associated with poorer sensorimotor outcomes. We also expected that brain age would mediate the impact of lesion damage on sensorimotor outcomes and that these relationships would be driven by post-stroke secondary atrophy (e.g., strongest in the ipsilesional hemisphere in chronic stroke). We further hypothesized that structural brain resilience, which we define in the context of stroke as the brains ability to maintain its global integrity despite focal lesion damage, would differentiate people with better versus worse outcomes. We analyzed cross-sectional high-resolution brain MRI and outcomes data from 963 people with stroke from 38 cohorts worldwide using robust linear mixed-effects regressions to examine the relationship between sensorimotor behavior, lesion damage, and brain age. We used a mediation analysis to examine whether brain age mediates the impact of lesion damage on stroke outcomes and if associations are driven by ipsilesional measures in chronic ([&ge;]180 days) stroke. We assessed the impact of brain resilience on sensorimotor outcome using logistic regression with propensity score matching on lesion damage. Stroke lesion damage was associated with older brain age, which in turn was associated with poorer sensorimotor outcomes. Brain age mediated the impact of corticospinal tract lesion load on sensorimotor outcomes most strongly in the ipsilesional hemisphere in chronic stroke. Greater brain resilience, as indexed by younger brain age, explained why people have better versus worse sensorimotor outcomes when lesion damage was fixed. We present novel evidence that global brain health is associated with superior post-stroke sensorimotor outcomes and modifies the impact of focal damage. This relationship appears to be due to post-stroke secondary degeneration. Brain resilience provides insight into why some people have better outcomes after stroke, despite similar amounts of focal injury. Inclusion of imaging-based assessments of global brain health may improve prediction of post-stroke sensorimotor outcomes compared to focal injury measures alone. This investigation is important because it introduces the potential to apply novel therapeutic interventions to prevent or slow brain aging from other fields (e.g., Alzheimers disease) to stroke.

neuroscience↗

Experience-dependent learning and myelin plasticity in individuals with stroke

BackgroundInjury to brain myelin disrupts motor performance and learning, however it is not clear if myelination is modulated by skilled motor practice or by recovery after stroke. Multi-component relaxation imaging can be used to measure water trapped between myelin bilayers which is expressed as myelin water fraction. The purpose of this study was to examine the effect of experience-dependent learning on myelin plasticity using multi-component relaxation imaging in individuals with stroke. MethodsThirty-two individuals with chronic stroke (>6 months) and twenty-seven healthy controls completed 4 weeks of skilled motor practice using a complex, gamified reaching task. Multi-component relaxation imaging-derived myelin water fraction was obtained before and after training. Seven brain regions associated with motor learning and sensorimotor function were investigated. ResultsAll participants improved task-specific reaching movements after training. In individuals with stroke: 1) pre-training myelin water fraction was lower in motor brain regions but higher in the cingulum compared to controls, 2) pre-training myelin water fraction in motor and sensorimotor regions was positively associated with learning rate, and 3) myelin water fraction was increased in the ipsilesional (contralateral to the trained arm) superior longitudinal fasciculus following skilled motor practice. ConclusionsFindings indicate that after stroke, myelin water fraction is related to measures of motor learning and modulated by 4 weeks of skilled motor practice with the paretic limb. Myelin water fraction can be enhanced in the chronic stage of stroke and may be an important target for upper-limb motor recovery.

neuroscience↗

Chronic stroke sensorimotor impairment is related to smaller hippocampal volumes: An ENIGMA analysis

Persistent sensorimotor impairments after stroke can negatively impact quality of life. The hippocampus is involved in sensorimotor behavior but has not been widely studied within the context of post-stroke upper limb sensorimotor impairment. The hippocampus is vulnerable to secondary degeneration after stroke, and damage to this region could further weaken sensorimotor circuits, leading to greater chronic sensorimotor impairment. The purpose of this study was to investigate the cross-sectional association between non-lesioned hippocampal volume and upper limb sensorimotor impairment in people with chronic stroke. We hypothesized that smaller ipsilesional hippocampal volumes would be associated with worse upper-limb sensorimotor impairment. Cross-sectional T1-weighted brain MRIs were pooled from 357 participants at the chronic stage after stroke (>180 days post-stroke) compiled from 18 research cohorts worldwide in the ENIGMA Stroke Recovery Working Group (age: median = 61 years, interquartile range = 18, range = 23-93; 135 women and 222 men). Sensorimotor impairment was estimated from the Fugl-Meyer Assessment of Upper Extremity scores. Robust mixed-effects linear models were used to test associations between post-stroke sensorimotor impairment and hippocampal volumes (ipsilesional and contralesional separately; Bonferroni-corrected, p-value < 0.025), controlling for age, sex, lesion volume, and lesioned hemisphere. We also performed an exploratory analysis to test whether sex differences influence the relationship between sensorimotor impairment and hippocampal volume. Upper limb sensorimotor impairment was positively associated with ipsilesional (p = 0.005; d = 0.33) but not contralesional (p = 0.96; d = 0.01) hippocampal volume, such that impairment was worse for participants with smaller ipsilesional hippocampal volume. This association remained significant independent of lesion volume or other covariates (p = 0.001; d = 0.36). Evidence indicates an interaction between sensorimotor impairment and sex for both ipsilesional (p = 0.008; d = -0.29) and contralesional (p = 0.006; d = -0.30) hippocampal volumes, whereby women showed progressively worsening sensorimotor impairment with smaller hippocampal volumes compared to men. The present study has identified a novel association between chronic post-stroke sensorimotor impairment and ipsilesional, but not contralesional, hippocampal volume. This finding was not due to lesion size and may be stronger in women. We also provide supporting evidence that smaller hippocampal volume post-stroke is likely a consequence of ipsilesional damage, which could provide a link between vascular disease and other disorders, such as dementia.

neuroscience↗

Prefrontal-motor and somatosensory-motor cortical network interactions during reactive balance are associated with distinct aspects of balance behavior in older adults

Heightened reliance on the cerebral cortex for postural stability with aging is well-known, yet the cortical dynamics of balance control, particularly in relationship to balance function, is unclear. Here we aimed to investigate motor cortical activity in relationship to the level of balance challenge presented during reactive balance recovery, and identify circuit-specific interactions between motor cortex and prefrontal or somatosensory regions to metrics of balance function that predict fall risk. Using electroencephalography, we assessed motor cortical beta power, and beta coherence during balance reactions to perturbations in older adults. We found that individuals with greater somatosensory-motor beta coherence at baseline and lower beta power evoked over motor regions following perturbations demonstrated higher general clinical balance function. At the group-level, beta coherence between prefrontal-motor regions reduced during balance reactions. Older adults with the highest post-perturbation prefrontal-motor coherence showed greater cognitive dual-task interference and elicited stepping reactions at lower perturbation magnitudes. Our results support motor cortical beta activity as a potential biomarker for individual level of balance challenge and implicate prefrontal-and somatosensory-motor cortical networks in different aspects of balance control in older adults. Cortical network activity during balance may provide a neural target for precision-medicine efforts aimed at fall-prevention with aging.

neuroscience↗

Non-lesioned subcortical brain volumes are associated with post-stroke sensorimotor behavior across 28 cohorts worldwide: An ENIGMA Stroke Recovery study

Background and PurposeUp to two-thirds of stroke survivors experience persistent sensorimotor impairments. Recovery relies on the integrity of spared brain areas to compensate for damaged tissue. Subcortical regions play critical roles 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 behavior at different timepoints after stroke. MethodsWe pooled high-resolution T1-weighted MRI brain scans and behavioral data in 828 individuals with unilateral stroke from 28 cohorts worldwide. Cross-sectional analyses using linear mixed-effects models related post-stroke sensorimotor behavior to non-lesioned subcortical volumes (Bonferroni-corrected, p<0.004). We tested subacute ([&le;]90 days) and chronic ([&ge;]180 days) stroke subgroups separately, with exploratory analyses in early stroke ([&le;]21 days) and across all time. Sub-analyses in chronic stroke were also performed based on class of sensorimotor deficits (impairment, activity limitations) and side of lesioned hemisphere. ResultsWorse sensorimotor behavior was associated with a smaller ipsilesional thalamic volume in both early (n=179; d=0.68) and subacute (n=274, d=0.46) stroke. In chronic stroke (n=404), worse sensorimotor behavior was associated with smaller ipsilesional putamen (d=0.52) and nucleus accumbens (d=0.39) volumes, and a larger ipsilesional lateral ventricle (d=-0.42). Worse chronic sensorimotor impairment specifically (measured by the Fugl-Meyer Assessment; n=256) was associated with smaller ipsilesional putamen (d=0.72) and larger lateral ventricle (d=-0.41) volumes, while several measures of activity limitations (n=116) showed no significant relationships. In the full cohort across all time (n=828), sensorimotor behavior was associated with the volumes of the ipsilesional nucleus accumbens (d=0.23), putamen (d=0.33), thalamus (d=0.33), and lateral ventricle (d=-0.23). ConclusionsWe demonstrate significant relationships between post-stroke sensorimotor behavior and reduced volumes of subcortical gray matter structures that were spared by stroke, which differ by time and class of sensorimotor measure. These findings may provide additional targets for improving post-stroke sensorimotor outcomes.

neuroscience↗

Cortical beta oscillatory activity evoked during reactive balance recovery scales with perturbation difficulty and individual balance ability

I.Cortical beta oscillations (13-30 Hz) reflect sensorimotor cortical activity, but have not been fully investigated in balance recovery behavior. We hypothesized that more challenging balance conditions would lead to greater recruitment of cortical sensorimotor brain regions for balance recovery. We predicted that beta power would be enhanced when balance recovery is more challenging, either due to more difficult perturbations or due to lower intrinsic balance ability. In 19 young adults, we measured beta power evoked over motor cortical areas (Cz electrode) during 3 magnitudes of backward support-surface translational perturbations using electroencephalography. Peak beta power was measured during early (50-150 ms), late (150-250 ms), and overall (0-400 ms) time bins, and wavelet-based analyses quantified the time course of evoked beta power and agonist and antagonist ankle muscle activity. We further assessed the relationship between individual balance ability measured in a challenging beam walking task and perturbation-evoked beta power within each time bin. In balance perturbations, cortical beta power increased [~]50 ms after perturbation onset, demonstrating greater increases with increasing perturbation magnitude. Balance ability was negatively associated with peak beta power in only the late (150-250 ms) time bin, with higher beta power in individuals who performed worse in the beam walking task. Additionally, the time course of cortical beta power followed a similar waveform as the evoked muscle activity, suggesting these evoked responses may be initially evoked by shared underlying mechanisms. These findings support the active role of sensorimotor cortex in balance recovery behavior, with greater recruitment of cortical resources under more challenging balance conditions. Cortical beta power may therefore provide a biomarker for engagement of sensorimotor cortical resources during reactive balance recovery and reflect the individual level of balance challenge.

neuroscience↗