The Muscle Activation Differences in Post-Stroke Upper Limb Flexion Synergy Based on Spinal Cord Segments: A Preliminary Proof-of-Concept Study

Objective: This study examined the activation difference of muscles innervated by cervical cord 5-6 (C5-C6) and cervical cord 8- thoracic cord 1 (C8-T1) in upper limb flexion synergy after stroke.Methods: Surface electromyography (sEMG) signals were collected during elbow flexion in stroke patients and healthy controls. The study compared normalized activation of two pairs of muscles that could cause similar joint movement but which dominated different spinal cord segments (clavicular part of the pectoralis major, PC vs. Sternocostal part of the pectoralis major, PS; Flexor carpi radialis, FCR vs. Flexor carpi ulnaris, FCU). In each muscle pair, one muscle was innervated by the same spinal cord segment (C5-C6), dominating the elbow flexion and the other was not. The comparison of the activation of the same muscle between patients and healthy controls was undertaken after standardization based on the activation of the biceps brachii in elbow flexion.Results: There was no difference between the PC and PS's normalized activation in healthy controls while the PC's normalized activation was higher than PS in stroke patients during elbow flexion. Similarly, there was no significant difference in normalized activation between FCR and FCU in healthy controls, and the same is true for stroke patients. However, the standardized activation of both FCR and FCU in stroke patients was significantly lower than that in healthy controls.Conclusion: After stroke, the activation of the distal muscles of the upper limb decreased significantly regardless of the difference of spinal cord segments; while the activation of the proximal muscles innervated by the same spinal cord segment (C5-C6) dominating the elbow flexion showed higher activation during flexion synergy. The difference in muscle activation based on spinal cord segments may be the reason for the stereotyped joint movement of upper limb flexion synergy.

Assessing the usage of indirect motor pathways following a hemiparetic stroke

A hallmark impairment in a hemiparetic stroke is a loss of independent joint control resulting in abnormal co-activation of shoulder abductor and elbow flexor muscles in their paretic arm, clinically known as the flexion synergy. The flexion synergy appears while generating shoulder abduction (SABD) torques as lifting the paretic arm. This likely be caused by an increased reliance on contralesional indirect motor pathways following damage to direct corticospinal projections. The assessment of functional connectivity between brain and muscle signals, i.e., brain-muscle connectivity (BMC), may provide insight into such changes to the usage of motor pathways. Our previous model simulation shows that multi-synaptic connections along the indirect motor pathway can generate nonlinear connectivity. We hypothesize that increased usage of indirect motor pathways (as increasing SABD load) will lead to an increase of nonlinear BMC. To test this hypothesis, we measured brain activity, muscle activity from shoulder abductors when stroke participants generate 20% and 40% of maximum SABD torque with their paretic arm. We computed both linear and nonlinear BMC between EEG and EMG. We found dominant nonlinear BMC at contralesional/ipsilateral hemisphere for stroke, whose magnitude increased with the SABD load. These results supported our hypothesis and indicated that nonlinear BMC could provide a quantitative indicator for determining the usage of indirect motor pathways following a hemiparetic stroke.

Abstract TP147: Quantitative Measures of Strength and Synergy Differentiate Individuals With Chronic Stroke With and Without Clinically Detectable Elbow Contracture

Many individuals with chronic stroke demonstrate contracture of the elbow flexors. The development of contracture may be attributable to underlying impairments such as weakness, flexion synergy, and hyperactive reflexes. This study explored differences in motor impairment and function between 17 individuals with clinically detectable elbow flexor contracture and 17 individuals with full passive range of motion. The groups did not differ in age (61.61 ± 7.99, 55.06 ± 12.48, p = 0.078), years post-stroke (12.92 ± 9.34, 10.60 ± 7.16, p = 0.423), or Fugl-Meyer Motor Assessment score (FMA, 26.35 ± 5.86, 26.47 ± 8.70, p = 0.963). The passive range limitation in the contracture group was 3 to 36° (11.65 ± 8.30°). Kinetics, kinematics, and EMG were used to quantify four motor impairments and reaching function. Shoulder abduction and elbow extension strength were measured isometrically and normalized to the unaffected side. Flexion synergy was quantified as a force-based measure assessing independent joint control. Flexor spasticity was quantified while reaching at 50% of maximum shoulder abduction as the change in biceps EMG from reach onset to peak angular velocity, normalized by maximal EMG activity. Reaching function was defined as maximum reaching distance against gravity and normalized by target distance (-10° of full extension). The groups differed in elbow extension strength (Contracture, 0.315 ± 0.129; No contracture, 0.559 ± 0.153; p < 0.001) and flexion synergy (0.146 ± 0.186, 0.397 ± 0.229, p = 0.009). The groups did not differ in shoulder abduction strength (0.500 ± 0.174, 0.615 ± 0.199, p = 0.080), flexor spasticity (0.079 ± 0.090, 0.056 ± 0.115, p = 0.523), or reaching function (0.501 ± 0.391, 0.714 ± 0.296, p = 0.082). The findings of this study suggest a relationship between elbow contracture and the concurrent presence of elbow extension weakness and flexion synergy. The quantitative measure of reaching function will likely differentiate individuals with and without contracture if the assessment is modified so that the standardized reaching target is located at 0° of elbow extension (normal range). Future research should use quantitative metrics to further explore the temporal recovery of impairments in order to prevent the development of contracture.