Objective: Pharmaceutical intervention targets arm flexor spasticity with an often-unsuccessful goal of improving function. Flexion synergy is a related motor impairment that may be inadvertently neglected. Here, flexor spasticity and flexion synergy are disentangled to determine their contributions to reaching dysfunction.
Methods: Twenty-six individuals participated. A robotic device systematically modulated shoulder abduction loading during ballistic reaching. Elbow muscle electromyography data were partitioned into windows delineated by elbow joint velocity allowing for the separation of synergy- and spasticity-related activation.
Results: Reaching velocity decreased with abduction loading (p<0.001) such that velocity was 30% slower when lifting the arm at 50% of abduction strength compared to when arm weight was supported. Abnormal flexion synergy increased with abduction loading (p<0.001) such that normalized activation ranged from a median (interquartile range) of 0.07 (0.03-0.12) when arm weight was supported to 0.19 (0.12-0.40) when actively lifting (large effect size, d=0.59). Flexor spasticity was detected during reaching (p=0.016) but only when arm weight was supported (intermediate effect size, d=0.33).
Conclusion: Flexion synergy is the predominant contributor to reaching dysfunction while flexor spasticity appears only relevant during unnaturally occurring passively supported movement.
Significance: Interventions targeting flexion synergy should be leveraged in future stroke recovery trials.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5507628 | PMC |
| http://dx.doi.org/10.1016/j.clinph.2017.04.028 | DOI Listing |
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