Dataset Information

An α-MN collateral to γ-MNs can mitigate velocity-dependent stretch reflexes during voluntary movement: A computational study.

ABSTRACT: The primary motor cortex does not uniquely or directly produce α-MN drive to muscles during voluntary movement. Rather, α-MN drive emerges from the synthesis and competition among excitatory and inhibitory inputs from multiple descending tracts, spinal interneurons, sensory inputs, and proprioceptive afferents. One such fundamental input is velocity-dependent stretch reflexes in lengthening (antagonist) muscles, which are thought to be inhibited by the shortening (agonist) muscles. It remains an open question, however, the extent to which velocity-dependent stretch reflexes disrupt voluntary movement, and whether and how they are inhibited in limbs with numerous monoand multi-articular muscles where agonist and antagonist roles become unclear and can switch during a movement. We used a computational model of a Rhesus Macaque arm to simulate movements with feedforward α-MN commands only, and with added velocity-dependent stretch reflex feedback. We found that velocity-dependent stretch reflex caused movement-specific, typically large and variable disruptions to the arm endpoint trajectories. In contrast, these disruptions became small when the velocity-dependent stretch reflexes were simply scaled by the α-MN drive to each muscle (equivalent to an α-MN excitatory collateral to its homologous γ-MNs, but distinct from α-γ co-activation. We argue this circuitry is more neuroanatomically tenable, generalizable, and scalable than α-γ co-activation or movement-specific reciprocal inhibition. We propose that this mechanism at the homologous propriospinal level, by locally and automatically regulating the highly nonlinear neuro-musculo-skeletal mechanics of the limb, could be a critical low-level enabler of learning, adaptation, and performance via cerebellar and cortical mechanisms.

SUBMITTER: Niyo G

PROVIDER: S-EPMC10723443 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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Publications

An alpha- to gamma-motoneurone collateral can mitigate velocity-dependent stretch reflexes during voluntary movement: A computational study.

Niyo Grace G Almofeez Lama I LI Erwin Andrew A Valero-Cuevas Francisco J FJ

bioRxiv : the preprint server for biology 20240604

The primary motor cortex does not uniquely or directly produce alpha motoneurone (<i>α</i>-MN) drive to muscles during voluntary movement. Rather, <i>α</i>-MN drive emerges from the synthesis and competition among excitatory and inhibitory inputs from multiple descending tracts, spinal interneurons, sensory inputs, and proprioceptive afferents. One such fundamental input is velocity-dependent stretch reflexes in lengthening muscles, which should be inhibited to enable voluntary movement. It rema ...[more]

PMID: 38106121

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Project description:Disinhibition of reflexes is a problem amongst spastic patients, for it limits a smooth and efficient execution of motor functions during gait. Treadmill belt accelerations may potentially be used to measure reflexes during walking, i.e. by dorsal flexing the ankle and stretching the calf muscles, while decelerations show the modulation of reflexes during a reduction of sensory feedback. The aim of the current study was to examine if belt accelerations and decelerations of different intensities applied during the stance phase of treadmill walking can evoke reflexes in the gastrocnemius, soleus and tibialis anterior in healthy subjects. Muscle electromyography and joint kinematics were measured in 10 subjects. To determine whether stretch reflexes occurred, we assessed modelled musculo-tendon length and stretch velocity, the amount of muscle activity, as well as the incidence of bursts or depressions in muscle activity with their time delays, and co-contraction between agonist and antagonist muscle. Although the effect on the ankle angle was small with 2.8±1.0°, the perturbations caused clear changes in muscle length and stretch velocity relative to unperturbed walking. Stretched muscles showed an increasing incidence of bursts in muscle activity, which occurred after a reasonable electrophysiological time delay (163-191 ms). Their amplitude was related to the muscle stretch velocity and not related to co-contraction of the antagonist muscle. These effects increased with perturbation intensity. Shortened muscles showed opposite effects, with a depression in muscle activity of the calf muscles. The perturbations only slightly affected the spatio-temporal parameters, indicating that normal walking was retained. Thus, our findings showed that treadmill perturbations can evoke reflexes in the calf muscles and tibialis anterior. This comprehensive study could form the basis for clinical implementation of treadmill perturbations to functionally measure reflexes during treadmill-based clinical gait analysis.

Project description:In neurological diseases, muscles often become hyper-resistant to stretch due to hyperreflexia, an exaggerated stretch reflex response that is considered to primarily depend on the muscle's stretch velocity. However, there is still limited understanding of how different biomechanical triggers applied during clinical tests evoke these reflex responses. We examined the effect of imposing a rotation with increasing velocity vs. increasing acceleration on triceps surae muscle repsonse in children with spastic paresis (SP) and compared the responses to those measured in typically developing (TD) children. A motor-operated ankle manipulator was used to apply different bell-shaped movement profiles, with three levels of maximum velocity (70, 110, and 150°/s) and three levels of maximum acceleration (500, 750, and 1,000°/s2). For each profile and both groups, we evaluated the amount of evoked triceps surae muscle activation. In SP, we evaluated two additional characteristics: the intensity of the response (peak EMG burst) and the time from movement initiation to onset of the EMG burst. As expected, the amount of evoked muscle activation was larger in SP compared to TD (all muscles: p < 0.001) and only sensitive to biomechanical triggers in SP. Further investigation of the responses in SP showed that peak EMG bursts increased in profiles with higher peak velocity (lateral gastrocnemius: p = 0.04), which was emphasized by fair correlations with increased velocity at EMG burst onset (all muscles: r > 0.33-0.36, p ≤ 0.008), but showed no significant effect for acceleration. However, the EMG burst was evoked faster with higher peak acceleration (all muscles p < 0.001) whereas it was delayed in profiles with higher peak velocity (medial gastrocnemius and soleus: p < 0.006). We conclude that while exaggerated response intensity (peak EMG burst) seems linked to stretch velocity, higher accelerations seem to evoke faster responses (time to EMG burst onset) in triceps surae muscles in SP. Understanding and controlling for the distinct effects of different biological triggers, including velocity, acceleration but also length and force of the applied movement, will contribute to the development of more precise clinical measurement tools. This is especially important when aiming to understand the role of hyperreflexia during functional movements where the biomechanical inputs are multiple and changing.

Dataset Information

An α-MN collateral to γ-MNs can mitigate velocity-dependent stretch reflexes during voluntary movement: A computational study.

Publications

An alpha- to gamma-motoneurone collateral can mitigate velocity-dependent stretch reflexes during voluntary movement: A computational study.

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