Modelling Human Locomotion

This report is a coverage of my 16 weeks practical training at the Center for Sensori-Motor Interaction of the Aalborg University (Denmark). One of their research topics is on the ?eld of the biomedical modelling, where they want to answer the question of the functional behavior of the proprioceptive feedback system of the human body. A valid/good biomedical model could support their hypotheses which are results from different measurements. The original intention of the project was to build a complete walking lower body model to ?nd the reason for proprioceptive feedback during walking. In the middle of the project this original goal was a too high, because of the additional work of redesigning previous work of Huber [26]. The goal is adjusted to design the mechanical and muscle model and a well documented report, so a next project can continue immediately. The mechanical and muscle model appeared to work correct and are veri?ed with measured data. The forward activation of the muscle/mechanical model is not completely the same as expected. This is because the used method does not take co-activation of antagonistic muscle into account. For the continuation of this project a complete measured data set is necessary, because the veri?cation is not 100% valid. This performed veri?cation uses data that is not correlated in the sense that is measured at the same conditions and persons

Control of posture with FES systems

One of the major obstacles in restoration of functional FES supported standing in paraplegia is the lack of knowledge of a suitable control strategy. The main issue is how to integrate the purposeful actions of the non-paralysed upper body when interacting with the environment while standing, and the actions of the artificial FES control system supporting the paralyzed lower extremities. In this paper we provide a review of our approach to solving this question, which focuses on three inter-related areas: investigations of the basic mechanisms of functional postural responses in neurologically intact subjects; re-training of the residual sensory-motor activities of the upper body in paralyzed individuals; and development of closed-loop FES control systems for support of the paralyzed joints

The Relationship Between Medial Gastrocnemius Lengthening Properties and Stretch Reflexes in Cerebral Palsy

Stretch reflex hyperactivity in the gastrocnemius of children with spastic cerebral palsy (CP) is commonly evaluated by passively rotating the ankle joint into dorsiflexion at different velocities, such as applied in conventional clinical spasticity assessments. However, surface electromyography (sEMG) collected from the medial gastrocnemius (MG) during such examination reveals unexplained heterogeneity in muscle activation between patients. Recent literature also highlights altered muscle tensile behavior in children with spastic CP. We aimed to document MG muscle and tendon lengthening during passive ankle motion at slow and fast velocity and explore its interdependence with the elicited hyperactive stretch reflex. The ankle of 15 children with CP (11 ± 3 years, GMFCS 9I 6II, 8 bilateral, 7 unilateral) and 16 typically developing children (TDC) was passively rotated over its full range of motion at slow and fast velocity. Ultrasound, synchronized with motion-analysis, was used to track the movement of the MG muscle-tendon junction and extract the relative lengthening of muscle and tendon during joint rotation. Simultaneously, MG sEMG was measured. Outcome parameters included the angular and muscle lengthening velocities 30 ms before EMG onset and the gain in root mean square EMG during stretch, as a measure of stretch reflex activity. Compared to slow rotation, the muscle lengthened less and stretch reflex activity was higher during fast rotation. These velocity-induced changes were more marked in CP compared to TDC. In the CP group, muscle-lengthening velocity had higher correlation coefficients with stretch reflex hyperactivity than joint angular velocity. Muscles with greater relative muscle lengthening during slow rotation had earlier and stronger stretch reflexes during fast rotation. These initial results suggest that ankle angular velocity is not representative of MG muscle lengthening velocity and is less related to stretch reflex hyperactivity than MG muscle lengthening. In addition, muscles that lengthened more during slow joint rotation were more likely to show a velocity-dependent stretch reflex. This interdependence of muscle lengthening and stretch reflexes may be important to consider when administering treatment. However, muscle and tendon lengthening properties alone could not fully explain the variability in stretch reflexes, indicating that other factors should also be investigated

Muscle weakness and lack of reflex gain adaptation predominate during post-stroke posture control of the wrist

Instead of hyper-reflexia as sole paradigm, post-stroke movement disorders are currently considered the result of a complex interplay between neuronal and muscular properties, modified by level of activity. We used a closed loop system identification technique to quantify individual contributors to wrist joint stiffness during an active posture task. Continuous random torque perturbations applied to the wrist joint by a haptic manipulator had to be resisted maximally. Reflex provoking conditions were applied i.e. additional viscous loads and reduced perturbation signal bandwidth. Linear system identification and neuromuscular modeling were used to separate joint stiffness into the intrinsic resistance of the muscles including co-contraction and the reflex mediated contribution. Compared to an age and sex matched control group, patients showed an overall 50% drop in intrinsic elasticity while their reflexive contribution did not respond to provoking conditions. Patients showed an increased mechanical stability compared to control subjects. Post stroke, we found active posture tasking to be dominated by: 1) muscle weakness and 2) lack of reflex adaptation. This adds to existing doubts on reflex blocking therapy as the sole paradigm to improve active task performance and draws attention to muscle strength and power recovery and the role of the inability to modulate reflexes in post stroke movement disorders.Mechanical, Maritime and Materials Engineerin

Muscle and reflex changes with varying joint angle in hemiparetic stroke

<p>Abstract</p> <p>Background</p> <p>Despite intensive investigation, the origins of the neuromuscular abnormalities associated with spasticity are not well understood. In particular, the mechanical properties induced by stretch reflex activity have been especially difficult to study because of a lack of accurate tools separating reflex torque from torque generated by musculo-tendinous structures. The present study addresses this deficit by characterizing the contribution of neural and muscular components to the abnormally high stiffness of the spastic joint.</p> <p>Methods</p> <p>Using system identification techniques, we characterized the neuromuscular abnormalities associated with spasticity of ankle muscles in chronic hemiparetic stroke survivors. In particular, we systematically tracked changes in muscle mechanical properties and in stretch reflex activity during changes in ankle joint angle. Modulation of mechanical properties was assessed by applying perturbations at different initial angles, over the entire range of motion (ROM). Experiments were performed on both paretic and non-paretic sides of stroke survivors, and in healthy controls.</p> <p>Results</p> <p>Both reflex and intrinsic muscle stiffnesses were significantly greater in the spastic/paretic ankle than on the non-paretic side, and these changes were strongly position dependent. The major reflex contributions were observed over the central portion of the angular range, while the intrinsic contributions were most pronounced with the ankle in the dorsiflexed position.</p> <p>Conclusion</p> <p>In spastic ankle muscles, the abnormalities in intrinsic and reflex components of joint torque varied systematically with changing position over the full angular range of motion, indicating that clinical perceptions of increased tone may have quite different origins depending upon the angle where the tests are initiated.</p> <p>Furthermore, reflex stiffness was considerably larger in the non-paretic limb of stroke patients than in healthy control subjects, suggesting that the non-paretic limb may not be a suitable control for studying neuromuscular properties of the ankle joint.</p> <p>Our findings will help elucidate the origins of the neuromuscular abnormalities associated with stroke-induced spasticity.</p

Deficits in peroneal latency and electromechanical delay in patients with functional ankle instability

The purpose of this study was to compare alterations in peroneal latency and electromechanical delay (EMD) following an inversion perturbation during walking in patients with functional ankle instability (FAI) and with a matched control group. Peroneal latency and EMD were measured from 21 patients with unilateral FAI and 21 controls. Latencies were collected during a random inversion perturbation while walking. EMD measures were collected during stance using a percutaneous stimulus. Two-way ANOVAs were used to detect differences between leg (affected, unaffected) and group (FAI, Control). Functionally unstable ankles displayed delayed peroneus longus (PL) latencies and EMD when compared to the unaffected leg and a matched control group. Peroneal latency and EMD deficits could contribute to recurrence of ankle injury in FAI subjects. How these deficits are associated with the chronic symptoms associated with FAI remains unclear, but gamma activation and subsequent muscle spindle sensitivity likely play a role. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:1541–1546, 2009Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/64439/1/20934_ftp.pd

GABAergic and glutamatergic identities of developing midbrain Pitx2 neurons

Pitx2 , a paired-like homeodomain transcription factor, is expressed in post-mitotic neurons within highly restricted domains of the embryonic mouse brain. Previous reports identified critical roles for PITX2 in histogenesis of the hypothalamus and midbrain, but the cellular identities of PITX2-positive neurons in these regions were not fully explored. This study characterizes Pitx2 expression with respect to midbrain transcription factor and neurotransmitter phenotypes in mid-to-late mouse gestation. In the dorsal midbrain, we identified Pitx2 -positive neurons in the stratum griseum intermedium (SGI) as GABAergic and observed a requirement for PITX2 in GABAergic differentiation. We also identified two Pitx2 -positive neuronal populations in the ventral midbrain, the red nucleus, and a ventromedial population, both of which contain glutamatergic precursors. Our data suggest that PITX2 is present in regionally restricted subpopulations of midbrain neurons and may have unique functions that promote GABAergic and glutamatergic differentiation. Developmental Dynamics 240:333–346, 2011. © 2011 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79425/1/22532_ftp.pd