4 research outputs found

    Neuro-musculoskeletal simulation of instrumented contracture and spasticity assessment in children with cerebral palsy

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    BACKGROUND: Increased resistance in muscles and joints is an important phenomenon in patients with cerebral palsy (CP), and is caused by a combination of neural (e.g. spasticity) and non-neural (e.g. contracture) components. The aim of this study was to simulate instrumented, clinical assessment of the hamstring muscles in CP using a conceptual model of contracture and spasticity, and to determine to what extent contracture can be explained by altered passive muscle stiffness, and spasticity by (purely) velocity-dependent stretch reflex. METHODS: Instrumented hamstrings spasticity assessment was performed on 11 children with CP and 9 typically developing children. In this test, the knee was passively stretched at slow and fast speed, and knee angle, applied forces and EMG were measured. A dedicated OpenSim model was created with motion and muscles around the knee only. Contracture was modeled by optimizing the passive muscle stiffness parameters of vasti and hamstrings, based on slow stretch data. Spasticity was modeled using a velocity-dependent feedback controller, with threshold values derived from experimental data and gain values optimized for individual subjects. Forward dynamic simulations were performed to predict muscle behavior during slow and fast passive stretches. RESULTS: Both slow and fast stretch data could be successfully simulated by including subject-specific levels of contracture and, for CP fast stretches, spasticity. The RMS errors of predicted knee motion in CP were 1.1 ± 0.9° for slow and 5.9 ± 2.1° for fast stretches. CP hamstrings were found to be stiffer compared with TD, and both hamstrings and vasti were more compliant than the original generic model, except for the CP hamstrings. The purely velocity-dependent spasticity model could predict response during fast passive stretch in terms of predicted knee angle, muscle activity, and fiber length and velocity. Only sustained muscle activity, independent of velocity, was not predicted by our model. CONCLUSION: The presented individually tunable, conceptual model for contracture and spasticity could explain most of the hamstring muscle behavior during slow and fast passive stretch. Future research should attempt to apply the model to study the effects of spasticity and contracture during dynamic tasks such as gait. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12984-016-0170-5) contains supplementary material, which is available to authorized users

    Passive stiffness of the gastrocnemius muscle in athletes with spastic hemiplegic cerebral palsy

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    The passive properties of the muscle–tendon unit are regularly assessed in individuals with cerebral palsy (CP). However, no information is available on the passive properties of adult muscle, and whether any differences exist between the paretic and control muscles. Eleven ambulant male athletes with spastic hemiplegic CP (21.2 ± 3.0 years) and controls without neurological impairment (age = 21.8 ± 2.2 years) completed two and one passive stretch session, respectively. During each session, the ankle was passively dorsiflexed until end range of motion (ROM), whilst recording passive ankle angle, torque and gastrocnemius medialis (GM) myotendinous junction (MTJ) displacement. In addition, GM cross-sectional area (CSA) and length were measured. Subsequently, in vivo stress and strain were determined to calculate elastic modulus. Passive stiffness, MTJ displacement and ROM of the paretic GM were not different from the control muscles. However, the elastic modulus of the paretic GM was two times stiffer than the control GM muscles. In conclusion, athletes with CP exhibit absolute passive muscle stiffness similar to the controls; however, the elastic modulus of the CP muscle was significantly greater. Therefore, throughout the same ROM a smaller GM CSA in CP athletes has to dissipate larger relative torque compared to the control muscles, consequently causing the muscle to elongate to the same extent as the non-paretic muscle under stretch
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