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Dewald, J. P. A.

Publications and source records attributed to Dewald, J. P. A..

9 recordsLinked to original sources

Quantifying the Effect of Trunk Postural Control on Reaching with Progressive Shoulder Abduction Loading in Hemiparetic Stroke

Background: Adults post hemiparetic stroke exhibit motor deficits in both the trunk and arm that impact function. In the paretic arm, involuntary coupling of torques in the fingers, wrist, and elbow during shoulder abduction, known as the flexion synergy, reduces reaching function. While there have been deficits shown to exist at the trunk such as weakness and altered coordination, it remains unclear if active trunk control compounds reaching deficits. This study examined if active trunk control with progressive shoulder abduction loading impacts reaching function in stroke and control participants. Methods: Thirteen adults, 9 post hemiparetic stroke (64.11 {+/-} 6.57 years) and 4 age matched controls (66.25 {+/-} 0.96 years), completed seated reaching tasks with the trunk restrained and unrestrained while reaching with their arm coupled to the ACT-3D robotic device on a frictionless table, lifting against 25% MVT, and 50% MVT. A linear mixed effects model was used with limb as a random factor, and group, trunk restraint, and shoulder abduction load as fixed factors for quantifying changes in reaching distance expressed percent limb length (% LL). Findings: Across limbs (paretic, non-paretic, control), when the trunk was un-restrained, reaching distance was reduced (p<.05). Further reduction in reaching distance was observed in the paretic compared to the non-paretic and control (p< .05) limbs. Reaching velocity was fastest for controls (3.26 {+/-} 1.52 m/s) compared to non-paretic (3.24 {+/-} 1.19 m/s) and paretic (1.59 {+/-} 1.32 m/s) limbs in stroke. Shoulder abduction loading had an effect on reaching distance in the paretic limb (p<.05) Table: .83 {+/-} .13 % LL, 25% MVT: .77 {+/-} .14 % LL, 50% MVT: .76 {+/-} .15 %LL). Greater shoulder excursion occurred during non-paretic limb reaching compared to the paretic limb with an increase of 14.80 mm (p<.05). Conclusion: Active trunk control impacted reaching function and further reduced reaching distance in chronic hemiparetic stroke participants. However, the primary driver of reduced reaching distance was the flexion synergy. While reaching speed increased the demand at the trunk, excursions were comparable during paretic and non-paretic limb reaching, suggesting that overall trunk function was intact during this paradigm.

bioengineering↗

Intrinsic properties of spinal motoneurons degrade ankle torque control in humans

Motoneurons are the final common pathway for all motor commands and possess intrinsic electrical properties that must be tuned to control muscle across the full range of motor behaviors. Neuromodulatory input from the brainstem is likely essential for adapting motoneuron properties to match this diversity of motor tasks. A primary mechanism of this adaptation, control of dendritic persistent inward currents (PICs) in motoneurons by brainstem monoaminergic systems, generates both amplification and prolongation of synaptic inputs. While essential, there is an inherent tension between this amplification and prolongation. Although amplification by PICs allows for quick recruitment and acceleration of motoneuron discharge during discrete motor tasks, PICs must be deactivated to de-recruit motoneurons upon movement cessation. In contrast, during stabilizing or postural tasks, PIC-induced prolongation of synaptic inputs is likely critical for sustained motoneuron discharge. Here, we designed two motor tasks that show PIC amplification and prolongation may conflict and generate errors that degrade the precision of motor output in humans. This included a paradigm comprised of a discrete motor task superimposed atop a stabilizing task and a paradigm with muscle length-induced changes to the balance of excitatory and inhibitory inputs available for controlling PICs. We show that prolongation from PICs introduces deficits in ankle torque control and that these deficits are further degraded at shorter muscle lengths when PIC prolongation is greatest. These results highlight the necessity for inhibitory control of PICs and showcase issues that are introduced when inhibitory control is perturbed or constrained. Our findings suggest that, like sensory systems, errors are inherent in motor systems. These errors are not due to problems in the perception of movement-related sensory input but are embedded in the final stage of motor output.

physiology↗

A geometric approach to quantifying the neuromodulatory effects of persistent inward currents on single motor unit discharge patterns

ObjectiveAll motor commands flow through motoneurons, which entrain control of their innervated muscle fibers, forming a motor unit (MU). Owing to the high fidelity of action potentials within MUs, their discharge profiles detail the organization of ionotropic excitatory/inhibitory as well as metabotropic neuromodulatory commands to motoneurons. Neuromodulatory inputs (e.g., norepinephrine, serotonin) enhance motoneuron excitability and facilitate persistent inward currents (PICs). PICs introduce quantifiable properties in MU discharge profiles by augmenting depolarizing currents upon activation (i.e., PIC amplification) and facilitating discharge at lower levels of excitatory input than required for recruitment (i.e., PIC prolongation). Approach: Here, we introduce a novel geometric approach to estimate neuromodulatory and inhibitory contributions to MU discharge through exploiting discharge non-linearities introduced by PIC amplification during time-varying linear tasks. In specific, we quantify the deviation from linear discharge ("brace height") and the rate of change in discharge (i.e., acceleration slope, attenuation slope, angle). We further characterize these metrics on a simulated motoneuron pool with known excitatory, inhibitory, and neuromodulatory inputs and on human MUs (Tibialis Anterior: 1448, Medial Gastrocnemius: 2100, Soleus: 1062, First Dorsal Interosseus: 2296). Main ResultIn the simulated motor pool, we found brace height and attenuation slope to consistently indicate changes in neuromodulation and the pattern of inhibition (excitation-inhibition coupling), respectively, whereas the paired MU analysis ({Delta}F) was dependent on both neuromodulation and inhibition pattern. Furthermore, we provide estimates of these metrics in human MUs and show comparable variability in {Delta}F and brace height measures in MUs matched across multiple trials. SignificanceSpanning both datasets, we found brace height quantification to provide an intuitive method for achieving graded estimates of neuromodulatory and inhibitory drive to MUs on a single unit level. This complements common techniques and provides an avenue for decoupling changes in the level of neuromodulatory and pattern of inhibitory motor commands.

bioengineering↗

Feasibility of Using Wearable EMG Armbands combined with Unsupervised Transfer Learning for Seamless Myoelectric Control

Myoelectric control uses electromyography (EMG) signals as human-originated input to enable intuitive interfaces with machines. As such, recent rehabilitation robotics employs myoelectric control to autonomously classify user intent or operation mode using machine learning. However, performance in such applications inherently suffers from the non-stationarity of EMG signals across measurement conditions. Current laboratory-based solutions rely on careful, time-consuming control of the recordings or periodic recalibration, impeding real-world deployment. We propose that robust yet seamless myoelectric control can be achieved using a low-end, easy-to-"don" and "doff" wearable EMG sensor combined with unsupervised transfer learning. Here, we test the feasibility of one such application using a consumer-grade sensor (Myo armband, 8 EMG channels @ 200 Hz) for gesture classification across measurement conditions using an existing dataset: 5 users x 10 days x 3 sensor locations. Specifically, we first train a deep neural network using Temporal-Spatial Descriptors (TSD) with labeled source data from any particular user, day, or location. We then apply the Self-Calibrating Asynchronous Domain Adversarial Neural Network (SCADANN), which automatically adjusts the trained TSD to improve classification performance for unlabeled target data from a different user, day, or sensor location. Compared to the original TSD, SCADANN improves accuracy by 12{+/-}5.2% (avg{+/-}sd), 9.6{+/-}5.0%, and 8.6{+/-}3.3% across all possible user-to-user, day-to-day, and location-to-location cases, respectively. In one best-case scenario, accuracy improves by 26% (from 67% to 93%), whereas sometimes the gain is modest (e.g., from 76% to 78%). We also show that the performance of transfer learning can be improved by using a "better" model trained with "good" (e.g., incremental) source data. We postulate that the proposed approach is feasible and promising and can be further tailored for seamless myoelectric control of powered prosthetics or exoskeletons.

bioengineering↗

Variability of in vivo sarcomere length measures in the upper limb obtained with second harmonic generation microendoscopy

The lengths of a muscles sarcomeres are a primary determinant of its ability to contract and produce force. In addition, sarcomere length is a critical parameter that is required to make meaningful comparisons of both the force-generating and excursion capacities of different muscles. Until recently, in vivo sarcomere length data have been limited to invasive or intraoperative measurement techniques. With the advent of second harmonic generation microendosopy, minimally invasive measures of sarcomere length can be made for the first time. This imaging technique expands our ability to study muscle adaptation due to changes in stimulus, use, or disease. However, due to the inability to measure sarcomeres outside of surgery or biopsy, little is known about the natural, anatomical variability in sarcomere length in living human subjects. To develop robust experimental protocols that ensure data provide accurate representations of a muscles sarcomere lengths, we sought to quantify experimental uncertainty associated with in vivo measures of sarcomere lengths. Specifically, we assessed the variability in sarcomere length measured 1) within a single image, along a muscle fiber, 2) across images captured within a single trial, across trials, and across days, as well as 3) across locations in the muscle using second harmonic generation in two upper limb muscles with different muscle architectures, functions, and sizes. Across all of our measures of variability we estimate that the magnitude of the uncertainty in in vivo sarcomere length are on the order of ~0.25m. In the two upper limb muscles studied we found larger variability in sarcomere length within a single insertion than across locations. We also developed custom code to make measures of sarcomere length variability across a single fiber and determined that this codes accuracy is an order of magnitude smaller than our measurement uncertainty due to sarcomere variability. Together, our findings provide guidance for the development of robust experimental design and analysis of in vivo sarcomere lengths in the upper limb.

bioengineering↗

Serial sarcomere number is substantially decreased within the paretic biceps brachii in chronic hemiparetic stroke

A muscles structure, or architecture, is indicative of its function and is plastic; changes in input to or use of the muscle alter its architecture. Stroke-induced neural deficits substantially alter both input to and usage of individual muscles. Here, we combined novel in vivo imaging methods (second harmonic generation microendoscopy, extended field-of-view ultrasound, and fat-supression MRI) to quantify functionally meaningful muscle architecture parameters in the biceps brachii of both limbs of individuals with chronic hemiparetic stroke and in age-matched, unimpaired controls. Specifically, serial sarcomere number and physiological cross-sectional area were calculated from data collected at three anatomical scales: sarcomere length, fascicle length, and muscle volume. Our data indicate that the paretic biceps brachii had ~8,500 fewer serial sarcomeres compared to the contralateral limb (p=0.0044). In the single joint posture tested, the decreased serial sarcomere number was manifested by significantly shorter fascicles (10.7cm vs 13.6cm; p<0.0001) without significant differences in sarcomere lengths (3.58m vs. 3.54m; p=0.6787) in the paretic compared to the contralateral biceps. No interlimb differences were observed in unimpaired controls, suggesting we observed muscle adaptations associated with stroke rather than natural interlimb variability. This study provides the first direct evidence of the loss of serial sarcomeres in human muscle, observed in a population with neural impairments that lead to disuse and chronically place the affected muscle at a shortened position. This adaptation is consistent with functional consequences (increased passive resistance to elbow extension) that would amplify already problematic, neurally driven motor impairments. SIGNIFICANCE STATEMENTSerial sarcomere number determines a muscles length during maximum force production and its available length range for active force generation. Skeletal muscle length adapts to functional demands; for example, animal studies demonstrate that chronically shortened muscles decrease length by losing serial sarcomeres. This phenomenon has never been demonstrated in humans. Integrating multi-scale imaging techniques, including two photon microendoscopy, an innovative advance from traditional, invasive measurement methods at the sarcomere scale, we establish that chronic impairments that place a muscle in a shortened position are associated with the loss of serial sarcomeres in humans. Understanding how muscle adapts following impairment is critical to the design of more effective clinical interventions to mitigate such adaptations and to improve function following motor impairments.

bioengineering↗

Volume and intramuscular fat content of upper extremity muscles in individuals with chronic hemiparetic stroke

Stroke survivors often experience upper extremity deficits that make activities of daily living (ADLs) like dressing, cooking and bathing difficult or impossible. Survivors experience paresis, the inability to efficiently and fully activate muscles, which combined with decreased use of the upper extremity, will lead to muscle atrophy and potentially an increase in intramuscular fat. Muscle atrophy has been linked to weakness post stroke and is an important contributor to upper extremity deficits. However, the extent of upper extremity atrophy post hemiparetic stroke is unknown and a better understanding of these changes is needed to inform the direction of intervention-based research. In this study, the volume of contractile tissue and intramuscular fat in the elbow and wrist flexors and extensors were quantified in the paretic and non-paretic upper limb using MRI and the Dixon technique for the first time. Total muscle volume (p[&le;]0.0005) and contractile element volume (p[&le;]0.0005) were significantly smaller in the paretic upper extremity, for all muscle groups studied. The average percent difference between limbs and across participants was 21.3% for muscle volume and 22.9% for contractile element volume. We also found that while the percent intramuscular fat was greater in the paretic limb compared to the non-paretic (p[&le;]0.0005), however, the volume of intramuscular fat was not significantly different between upper limbs (p=0.231). The average volumes of intramuscular fat for the elbow flexors/extensors and wrist flexors/extensors were 28.1, 28.8 and 19.9, 8.8 cm3 in the paretic limb and 29.6, 27.7 and 19.7, 8.8 cm3 in the non-paretic limb. In short, these findings indicate a decrease in muscle volume and not an increase in intramuscular fat, which will contribute to the reduction in strength in the paretic upper limb.

bioengineering↗

Reduction in voluntary activation of elbow and wrist muscles in individuals with chronic hemiparetic stroke

After a stroke, descending drive is impaired due to the loss of corticospinal and corticobulbar projections which causes a reduction in voluntary activation or an inability of the nervous system to activate muscles to their full capacity, which in turn contributes to weakness of the upper extremity. Voluntary activation has not been quantified at specific joints in the upper extremity, in part because directly assessing changes descending drive is difficult. In this study, voluntary activation of elbow and wrist flexors and extensors was assessed in participants with chronic hemiparetic stroke using twitch interpolation. Twitch interpolation uses electrical stimulation to estimate voluntary activation and relies on the principle that there is an inverse relationship between the amplitude of a twitch evoked by a stimulus and the voluntary force output during stimulation (Taylor, 2009). We measured voluntary activation using twitch interpolation as well as maximum voluntary torque (MVT) of the elbow and wrist flexors and extensors in the paretic and non-paretic limb of ten participants post stroke and the dominant and non-dominant limb of 2 control participants. Results show, MVT interlimb differences were significantly greater for stroke participants compared to control, across muscle groups (p[&le;]0.005). For stroke participants, MVT interlimb differences were significantly greater at the wrist compared to the elbow (P=0.003). Voluntary activation was significantly less in the paretic limb compared to the non-paretic, dominant and non-dominant limbs, across participants and muscle groups (p<0.005 for all four muscle groups). For the stroke participants, the voluntary activation interlimb difference was significantly greater for the wrist muscles compared to the elbow muscles (p<0.005). There was a significant positive correlation (r = 0.39, P = .022) between each participants impairment level, as measured by a hand specific subscore of the Fugl-Meyer Assessment, and the wrist extensor voluntary activation in the paretic limb but the relationship was not significant for the other muscle groups.

bioengineering↗

Intervention-Induced Changes in Cortical Connectivity and Activity in Severe Chronic Hemiparetic Stroke

ObjectiveEffective interventions have demonstrated the ability to improve motor function by reengaging ipsilesional resources, which has been shown to be critical and feasible for hand function recovery even in individuals with severe chronic stroke. However, the question remains how these focal activity changes (i.e., changes in activity within motor regions) relate to altered cortico-cortico interactions within/across multiple regions. MethodsEight individuals with severe chronic stroke participated in a device-assisted intervention. Pre- and post-intervention, we collected EEG while performing hand opening with/without lifting the paretic arm. We quantified changes in focal cortical activity at movement execution and connectivity during movement preparation. ResultsPost-intervention, individuals displayed a reduction in coupling from ipsilesional M1 to contralesional M1 within gamma frequencies during movement preparation for hand opening. This was followed by a reduction in activity in contralesional primary sensorimotor cortex during movement execution. Meanwhile, during lifting and opening, a more inhibitory coupling within ipsilesional M1 from gamma to beta frequencies was accompanied by an increase in ipsilesional primary sensorimotor cortex activity. ConclusionsChanges in coupling within or between motor regions during movement preparation complement topographical activity changes at movement execution. SignificanceOur results suggest that changes in cortico-cortico interactions may lead to corresponding changes in focal cortical activity.

neuroscience↗