원문정보
초록
영어
Individuals with neurological impairments often develop various compensatory gait strategies that may exacerbate asymmetries and increase fall risk, yet the precise causal relationships between specific muscle deficits and compensatory patterns are not fully understood. This study employed predictive neuromuscular simulation to isolate the pure effects of unilateral plantar flexor weakness on gait compensation mechanisms. Using a three-dimensional musculoskeletal model (9-link, 14-muscle) with reflex-based control, we systematically reduced paretic plantar flexor strength (gastrocnemius and soleus) to 80%, 60%, 40%, and 20% of normal while maintaining all other muscles at full strength. Dynamic optimization algorithms (CMA-ES) generated optimal gait patterns under energy efficiency and stability constraints. Results demonstrated that paretic gastrocnemius activation decreased to 23.5% under severe weakness (20% condition), while paretic soleus exhibited counterintuitive hyperactivation (3-fold increase) under moderate weakness conditions. Kinematic adaptations included increased paretic ankle dorsiflexion (3.7-fold increase) and hip flexion angles reaching 23.5°, consistent with clinical hip strategy patterns. Joint loading analysis revealed systematic distal-to-proximal redistribution, with 36.4% reduction in paretic ankle loading while hip loading remained stable. Bilateral compensations emerged, with non-paretic limb showing 41.3% ankle loading reduction. These simulation results demonstrate that complex gait compensations can emerge solely from plantar flexor weakness, without requiring additional neurological impairments. The threshold-dependent, nonlinear nature of adaptations supports precision rehabilitation approaches targeting individual impairment profiles rather than generic symptomatic treatments.
목차
Ⅰ. Introduction
Ⅱ. Methods
1. Model and controller
2. Objective function
3. Optimization algorithm
4. Experimental conditions
5. Outcome measures
Ⅲ. Results
1. Neuromuscular activation adaptations
2. Phase-specific muscle activation changes
3. Kinematic compensations
4. Joint loading redistribution patterns
Ⅳ. Discussion
Ⅴ. Conclusion
References
