Biology subjects

Charalambous, C. C.

Publications and source records attributed to Charalambous, C. C..

4 recordsLinked to original sources

bioRxiv2023

Intermuscular coherences of plantarflexors during walking suggest distinct neural origin and function for alpha and beta/low-gamma bands after stroke

Plantarflexors provide propulsion during walking (late stance) and receive input from both corticospinal tract (CST) and corticoreticulospinal tract (CReST). Both descending motor tracts exhibit some frequency-specificity, which allows potential differentiation of neural drive from each tract using intermuscular coherence (IMC). Stroke may differentially affect each tract, thus impair the function of plantarflexors. However, the evidence concerning this frequency-specificity and its relation to plantarflexors neuromechanics post-stroke remains very limited. Here, we investigated the intermuscular coherences of alpha, beta, and low-gamma bands between the Soleus (SOL), Lateral Gastrocnemius (LG), and Medial Gastrocnemius (MG) muscles and their relationships with walking-specific measures (propulsive impulse; speed). Fourteen individuals with chronic stroke walked on a treadmill at self-selected and fast walking speed (SSWS and FWS, respectively). Inter-limb IMC comparisons revealed that beta LG-MG (SSWS) and low-gamma SOL-LG (FWS) IMCs were degraded on the paretic side. At the same time, within each limb, the IMCs, which were significantly different to a surrogate dataset denoting random coherence, were in the alpha band (both speeds). Further, alpha LG-MG IMC was positively correlated with propulsive impulse in the paretic limb (SSWS). Findings suggest differential functional role of alpha and beta/low-gamma, which may be related to the frequency-specificity of the underlying descending drives. The persistence of alpha in plantarflexors and its strong positive relationship with propulsive impulse suggests relative preservation and/or upregulation of CReST. Future research should address whether entraining motor system at alpha frequencies via neuromodulation can improve the neuromechanical function of paretic plantarflexors and subsequently promote post-stroke walking recovery. Key Points SummaryO_LICortical and subcortical motor drives may be frequency-specific, have a role in walking, and be degraded after stroke. C_LIO_LIWhether this frequency-specificity exists and how it is related to neuromechanical function of ankle plantarflexors post-stroke remains to be determined. C_LIO_LIHere, we investigated bilaterally the intermuscular coherences of alpha, beta, and low-gamma bands for the Soleus (SOL), Lateral Gastrocnemius (LG), and Medial Gastrocnemius (MG) muscles and their relationships with walking-specific measures (propulsive impulse; self-selected and fast speed) during treadmill walking in individuals post-stroke. C_LIO_LIThe beta LG-MG (self-selected speed) and low-gamma SOL-LG (fast speed) were degraded on the paretic side. C_LIO_LIAlpha coherence was significantly present across plantarflexors mainly on the non-paretic side (both speeds). C_LIO_LIParetic alpha LG-MG was positively correlated with paretic propulsive impulse (self-selected speed). C_LIO_LIGiven that paretic propulsive impulse is impaired post-stroke, entraining the motor system at alpha frequency via neuromodulation may improve propulsive impulse and subsequently promote post-stroke walking recovery. C_LI

neuroscience↗

bioRxiv2023

A novel biomechanical indicator for impaired ankle dorsiflexion function during walking in individuals with chronic stroke

Ankle dorsiflexion function during swing phase of the gait cycle contributes to foot clearance and plays an important role in walking ability post-stroke. Commonly used biomechanical measures such as foot clearance and ankle joint excursion have limited ability to accurately evaluate dorsiflexor function in stroke gait. We retrospectively evaluated ankle angular velocity and ankle angular acceleration as direct measures for swing phase dorsiflexor function in post-stroke gait of 61 chronic stroke survivors. Our linear regression models revealed that peak ankle angular velocity (AAVP), peak ankle angular acceleration (AAAP), peak dorsiflexion angle (DFAP) and peak foot clearance (FCLP) during swing had a significant relationship (p < 0.05) with impaired dorsiflexion function. AAAP and DFAP accounted for the most variance of dorsiflexion function. Additionally, AAVP, AAAP, FCLP during swing, correlated significantly with all clinical outcome measures of walking ability. DFAP during swing had a positive correlation only with FMA-LE. Post-hoc Williams t-tests, used to compare the magnitude of difference between two non-independent correlations, revealed that the correlation between all clinical measures and DFAP were significantly weaker than with AAVP and AAAP. We also found that correlation between FMA-LE and FCLP was weaker than with AAVP and AAAP. We found an excellent test-retest reliability for both AAVP (ICC = 0.968) and AAAP (ICC = 0.947). These results suggest that DFAP may only be associated with non-task specific isolated dorsiflexion movement, but not during walking. FCLP is associated with dorsiflexion function and walking ability measures but not as strongly as AAVP and AAAP possibly because FCLP is influenced by contribution from hip and knee joint movements during walking. Therefore, we believe that AAVP and AAAP both can be used as reliable measures of impaired dorsiflexion function in post-stroke gait.

bioengineering↗

bioRxiv2022

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 ([≥]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↗

bioRxiv2021

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↗