Abstract
BackgroundSpasticity 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.MethodsA 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.ResultsOur 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.ConclusionsOur 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.
Highlights
Spasticity is an important complication after stroke, especially in the anti-gravity muscles, i.e. lower limb extensors
The bottom panes show the reference kinematics, and directional changes with increased length/velocity feedback are qualitatively indicated by arrows
Mean differences between reference and simulated stroke muscle excitations can be found in Additional file 4 (SOL + GAS) and Additional file 5 (VAS + rectus femoris (RF))
Summary
Spasticity is an important complication after stroke, especially in the anti-gravity muscles, i.e. lower limb extensors. 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. The contribution of muscle weakness to an impaired gait pattern has been previously reported in both descriptive and simulation studies. A simulation study by Jonkers et al [6] investigated the causal relationship between muscle weakness and resulting deviations in kinematics. From these studies it is clear that muscle weakness influences the post-stroke gait pattern, the presence of spasticity in specific muscles will reinforce or counteract specific gait deviations. A biomechanical modeling study of Lindberg et al [10] suggested that the neural component is most dominant in resistance to passive stretch
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