Modulation of gluteus medius activity reflects the potential of the muscle to meet the mechanical demands during perturbed walking.

Mediolateral stability during walking can be controlled by adjustment of foot placement. Reactive activity of gluteus medius (GM) is modulated during the gait cycle. However, the mechanisms behind the modulation are yet unclear. We measured reactive GM activity and kinematics in response to a mediolateral platform translation during different phases of the gait cycle. Forward simulations of perturbed walking were used to evaluate the isolated effect of the perturbation and the GM response on gait stability. We showed that the potential of GM to adjust lateral foot placement and prevent collisions during swing varies during the gait cycle and explains the observed modulation. The observed increase in stance, swing or combined GM activity causes an outward foot placement and therefore compensates for the loss of stability caused by a perturbation early in the gait cycle. GM activity of the swing leg in response to a platform translation late in the gait cycle counteracts foot placement, but prevents collision of the swing foot with the stance leg. This study provides insights in the neuromechanics of reactive control of gait stability and proposes a novel method to distinguish between the effect of perturbation force and reactive muscle activity on gait stability.

Extended foot-ankle musculoskeletal models for application in movement analysis.

Multibody simulations of human motion require representative models of the anatomical structures. A model that captures the complexity of the foot is still lacking. In the present work, two detailed 3D multibody foot-ankle models generated based on CT scans using a semi-automatic tool are described. The proposed models consists of five rigid segments (talus, calcaneus, midfoot, forefoot and toes), connected by five joints (ankle, subtalar, midtarsal, tarsometatarsal and metatarsophalangeal), one with 15DOF and the other with 8DOF. The calculated kinematics of both models were evaluated using gait trials and compared against literature, both presenting realistic results. An inverse dynamic analysis was performed for the 8DOF model, again presenting feasible dynamic results.

Altering length and velocity feedback during a neuro-musculoskeletal simulation of normal gait contributes to hemiparetic gait characteristics.

BACKGROUND: Spasticity is an important complication after stroke, especially in the anti-gravity muscles, i.e. lower limb extensors. However the contribution of hyperexcitable muscle spindle reflex loops to gait impairments after stroke is often disputed. In this study a neuro-musculoskeletal model was developed to investigate the contribution of an increased length and velocity feedback and altered reflex modulation patterns to hemiparetic gait deficits. METHODS: A musculoskeletal model was extended with a muscle spindle model providing real-time length and velocity feedback of gastrocnemius, soleus, vasti and rectus femoris during a forward dynamic simulation (neural control model). By using a healthy subject's base muscle excitations, in combination with increased feedback gains and altered reflex modulation patterns, the effect on kinematics was simulated. A foot-ground contact model was added to account for the interaction effect between the changed kinematics and the ground. The qualitative effect i.e. the directional effect and the specific gait phases where the effect is present, on the joint kinematics was then compared with hemiparetic gait deviations reported in the literature. RESULTS: Our results show that increased feedback in combination with altered reflex modulation patterns of soleus, vasti and rectus femoris muscle can contribute to excessive ankle plantarflexion/inadequate dorsiflexion, knee hyperextension/inadequate flexion and increased hip extension/inadequate flexion during dedicated gait cycle phases. Increased feedback of gastrocnemius can also contribute to excessive plantarflexion/inadequate dorsiflexion, however in combination with excessive knee and hip flexion. Increased length/velocity feedback can therefore contribute to two types of gait deviations, which are both in accordance with previously reported gait deviations in hemiparetic patients. Furthermore altered modulation patterns, in particular the reduced suppression of the muscle spindle feedback during swing, can contribute largely to an increased plantarflexion and knee extension during the swing phase and consequently to hampered toe clearance. CONCLUSIONS: Our results support the idea that hyperexcitability of length and velocity feedback pathways, especially in combination with altered reflex modulation patterns, can contribute to deviations in hemiparetic gait. Surprisingly, our results showed only subtle temporal differences between length and velocity feedback. Therefore, we cannot attribute the effects seen in kinematics to one specific type of feedback.