Optimisation of a neuromuscular electrical stimulation paradigm for targeted strengthening of an intrinsic foot muscle

The intrinsic foot muscles stabilise and stiffen the foot during posture and locomotion. Since they are placed under continued load, these muscles merit training to meet the weight-bearing demands of everyday activities. Their strengthening is however a largely neglected area and furthermore, the occurrence of common foot-related pathologies is associated with their dysfunction. Indeed, atrophy and dysfunction of the strongest intrinsic foot muscle, abductor hallucis (AbH), is symptomatic to pes planus and Hallux Valgus. AbH’s oblique mechanical action along with an inability for its voluntary activation in many individuals limits the strengthening capacity of existing training modalities. Due to the superficial location of AbH, neuromuscular electrical stimulation (NMES) offers a solution to this problem; however, its efficacy for muscle strength gains relies on high stimulation-intensity protocols, which are uncomfortable and limit participant adherence. Therefore, the purpose of this thesis was to develop an optimised NMES paradigm that is tolerable and efficacious for a targeted strengthening intervention of AbH. The studies reported in this thesis were undertaken with the overarching aim to systematically establish a tolerable and low stimulation-intensity NMES paradigm to train AbH. With this motivation in mind, four sequential experimental studies were designed to identify the optimal mode of NMES application (muscle vs nerve) and stimulation pulse duration (Chapter 3), pulse frequency and train duration (Chapter 4), training stimulus intensity (Chapter 5), and duty-cycle (Chapter 6), respectively. A major finding from the work undertaken in this thesis was the prevalent inability to voluntary activate AbH that exists in healthy participants. Since this inability also limits the measurement of voluntary force generation following an intervention, this thesis also developed a methodological approach that overcomes this limitation. Collectively, the studies in this thesis demonstrated that NMES successfully evokes contractions from AbH irrespective of ability for its voluntary activation and can therefore be used as a training modality. The optimised NMES paradigm presented in this thesis targets the motor point of AbH using 22s-trains of 1ms pulses at 20-100-20Hz with an intensity of 200% motor threshold and a 1:4 duty-cycle. This wide-pulse, high-frequency, low-intensity paradigm promotes adherence and has the potential to depolarise sensory axons due to their lower rheobase, and evoke contractions with a contribution of the central nervous system. When delivered using long trains and an alternating frequency pattern, it can take advantage of post-tetanic potentiation to produce force, which is then preserved across trains using a duty-cycle with long rest periods. This thesis intended to bind the aforementioned experimental chapters together with a final chapter investigating the effectiveness of the developed NMES paradigm instrengthening AbH following long-term exposure. However, the implementation of this study was not possible in light of the COVID-19 pandemic and is therefore not reportedin this thesis. Nevertheless, future work in this area can benefit from the extensive methodological work undertaken in this thesis and implement a longitudinal study to better understand the clinical implications for targeted AbH strengthening via NMES

The Effects of the Addition of a Single Session of While-Body Vibration to a Bout of Treadmill Walking on Gait and Lower Extremity Spasticity in Ambulatory Children with Cerebral Palsy

Single bouts of whole-body vibration (WBV) have been shown to reduce spasticity and increase active range of motion (ROM) in adults and children with cerebral palsy (CP). The effects, while transient, may provide a time window for participating in another intervention. Treadmill training is a common intervention that allows for the massed practice of walking in a controlled environment. I hypothesized that the use of WBV as a preparatory tool prior to treadmill walking may represent a more effective paradigm than using treadmill walking in isolation. This study aimed to investigate the acute effects of the addition of WBV to treadmill walking on muscle spasticity and overground walking of ambulatory children with CP. Nine children (3M/6F) with CP aged 6-17 years, Gross Motor Function Classification System (GMFCS) levels I-III participated in this study. Subjects’ lower extremity spasticity and overground walking were evaluated before and after two interventions: 10 minutes of treadmill walking alone, and 12 minutes of WBV (20Hz, 2mm) followed by 10 minutes of treadmill walking. Some subjects showed improvements after the combined intervention. However, several subjects also demonstrated improvements following the treadmill walking alone. Changes in lower extremity spasticity and overground walking parameters demonstrated high inter-subject variability. Interestingly, the inter-subject variability of response was not correlated with age, motor ability, or baseline spasticity. It was concluded that WBV may be a promising modality to reduce spasticity and improve motor function in children with CP. However, future studies are warranted to further investigate potential factors associated with the variability of response to the modality of WBV and treadmill walking more thoroughly

Modeling and Simulation of Lower Limb Spasticity in Motor-Impaired Individuals

Spasticity is a symptom that impairs the ability to freely move and control one’s limbs through increased tone and involuntary activations in the muscles. It can cause pain and discomfort and interfere with daily life and activities such as walking. Spasticity is a result of upper motor neuron lesions and is seen commonly in survivors of stroke and brain trauma, and individuals with cerebral palsy, multiple sclerosis, and spinal cord injuries. Despite its ubiquity the phenomena is not well understood. However, the most referred to definition describes spasticity as “a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflexes.” Qualitative, subjective measures are commonly used in the clinical setting to assess spasticity, most notably the Modified Ashworth score, which has been shown to have inconsistent reliability, relying heavily on the examiner’s experience, and is inaccurate for the lower limbs. Furthermore, these subjective scores do not account for the velocity-dependence of spasticity, which is a key differentiator against other symptoms such as rigidity. Consequently, there is a need for an objective measure of spasticity that can provide a more accurate and reliable alternative or supplement to the current clinical practice, in order to improve the evaluation of treatment and rehabilitation for spasticity. To address this need, a system was developed, validated and applied for modeling the spasticity in the lower-limbs of an affected individual. An experimental setup consisted of a brace-handle system with integrated force sensors for passive actuation of each leg segment, stretching spastic muscles to assess the severity of the condition. The setup included wearable sensors sEMG and IMUs – recording muscular activity and limb segment kinematics respectively during these motions. From the data, onsets of muscular activity and subsequently the trigger points of spastic reflexes were identified, which were mapped onto the calculated joint kinematics. Based on threshold-control theory, stretch reflex threshold (SRT) models of spasticity were created for each muscle by plotting the joint velocities and positions and using regression analysis to create a dynamic threshold in the kinematic space that divided the regimes of spastic and non-spastic motion. These muscle-specific models were combined by muscle groups, leading to the creation of a novel, data-based measure that characterizes the severity of spasticity of a group of muscles. The models and measures were found to agree with the expected changes from different conditions of muscle stretch, and different levels of spasticity in the included subjects, but required more data for statistical validation. The muscle-specific models were then implemented in a spasticity controller developed for use in neuromuscular simulations, in addition to further modeling of spastic reflex characteristics. The controller was applied in a scenario simulation of the same passive movement spasticity assessments used to collect the original data, which provided additional validation of the methodology and results of the modeling. The spasticity controller was also applied in a previously developed reinforcement-learning walking agent, to see the effects of spasticity on simulated gait. Following modification and training of the new agents, the spatio-temporal parameters of gait were analyzed to determine the differences in healthy and spastic gait, which agreed with expectations and further validated the spasticity modeling. This thesis presents a system to accurately and reliably model spasticity, establishing a novel, objective measure to better characterize spasticity, validating it through demonstrations of its use that may be extended in future work to accomplish better understanding of spasticity and provide invaluable improvements to the lives of affected individuals through practical applications

The Relationship of Spasticity and Impairments in Force Regulation and Neuromuscular Fatigue Post Stroke

Hyperreflexia that causes muscle spasticity may contribute to limitations in force regulation and walking ability post stroke. Additionally, neuromuscular fatigue may reduce force regulation, which is important because fatigue can assist to strengthen muscles that control walking. Hyperreflexia may be caused by cortical disinhibition that allows Ia afferents to amplify excitatory synaptic inputs to motoneuron pools. Cortical disinhibition is presumably caused by stroke-related motor cortex damage. Although, other excitatory synaptic sources to motoneurons contribute to motor control, hyperreflexia may be one contributor that affects stroke survivors. However, hyperreflexia is reported infrequently to effect force regulation post stroke. The goal was to quantify stroke related hyperreflexia with (out) a fatiguing condition and relate the findings to clinical function. To investigate how hyperreflexia affected force regulation in a non-fatiguing condition, stimulus frequency was examined in the soleus H-reflex response of stroke survivors and healthy controls. The H-reflex is an electrical analog of the stretch reflex and gives insight into the monosynaptic sensory pathway. After repetitive stimulation, stroke survivors had less H-reflex depression as compared to controls. Additionally, the slowest walking stroke survivors had less H-reflex depression. These results may indicate hyperreflexia contributes to rate depression and walking speed post stroke. Further implications on how hyperreflexia affected force regulation were investigated with patellar tendon tap (TT) responses during a fatiguing knee extensor task in stroke survivors and healthy controls. Additionally, the contributions of voluntary muscle strength, neural drive and involuntary muscle property responses were probed. Central mechanisms may primarily affect force regulation after fatigue because stroke survivors had less muscle property and maximal voluntary contraction reductions, along with greater voluntary activation reduction as compared to controls. Likewise, stroke survivors had higher post TT responses and less TT change after fatigue, which may suggest hyperreflexia with paresis may contribute to decreased force regulation. Additionally, stroke survivors with fewer baseline central impairments had less clinical dysfunctions. Hyperreflexia and impairments in the nervous system may decrease force regulation post stroke. Moreover, quantitative metrics of neuromuscular impairments may relate to clinical function measures, which may reveal central mechanisms need to be treated to improve force regulation

Muscle Stimulation via Whole Body Vibration for Postural Control Applications

Although the ability to balance might feel effortless to the most, it should not be given for granted as even the normal process of ageing can compromise it, jeopardising people physical independence. It is therefore important to implement safe training routines that ultimately improve postural control strategies. We evaluated the suitability of whole body vibration (WBV) training –which induces muscle contraction via the stimulation of muscle spindles - for postural control applications. First, we tested the efficacy of different combinations of stimulation frequency and subjects’ posture in eliciting a response from those muscles that play a key role for the implementation of postural responses. Each combination was evaluated by jointly measuring the resulting muscular activation and soft-tissue displacement. Then, we investigated how the selected WBV stimulation affected the balance of healthy subjects. We evaluated the latter by analysing centre of pressure trajectories, muscle and cortex activation and their respective interplay. We found that high frequency vibrations, delivered to participants standing on their forefeet, evoked the greatest contraction of the plantarflexors. Undisturbed balance recorded after such stimulation was characterised by an increased sensitivity of muscle spindles. In line with the latter, the communication between the periphery and the central nervous system (CNS) increased after the stimulation and different muscle recruitment patterns were employed to maintain balance. On the posturography side, stability was found to be compromised in the acute term but seemed to have recovered over a longer term. Together, these findings suggest that, if appropriately delivered, WBV has the potential to stimulate the spindles of the plantarflexors. By doing so, vibration training seems to be able to augment the communication between the proprioceptive organs and the CNS, on which the system relies to detect and react to perturbations, leading to sensorimotor recalibration