A magnetorheological knee prosthesis is presented that automatically adapts knee damping to the gait of the amputee using only local sensing of knee force, torque, and position. To assess the clinical effects of the user-adaptive knee prosthesis, kinematic gait data were collected on four unilateral trans-femoral amputees. Using the user-adaptive knee and a conventional, non-adaptive knee, gait kinematics were evaluated on both affected and unaffected sides. Results were compared to the kinematics of 12 age, weight and height matched normals. We find that the useradaptive knee successfully controls early stance damping, enabling amputee to undergo biologically-realistic, early stance knee flexion. These results indicate that a useradaptive control scheme and local mechanical sensing are all that is required for amputees to walk with an increased level of biological realism compared to mechanically passive prosthetic systems.

Abstract-We performed this study to determine the feasibility of controlling and stabilizing seated posture with functional electrical stimulation (FES) after paralysis from spinal cord injury (SCI) using computer simulations and a 3-dimensional model of the hip and trunk. We used the model to approximate the range of postures in the sagittal and transverse planes attainable by a seated subject and to estimate the maximum restorative moment that could be produced in a neutral posture in response to a disturbance. The simulations predicted that approximately 28 degrees of forward flexion in the sagittal plane (combined hip and trunk) and 9 degrees of lateral bending in the transverse plane should be possible with FES and that a maximum disturbance rejection moment of approximately 45 newton meters could be expected with the chosen muscle set. We tested a subject with a motor complete thoracic SCI and implanted electrodes in a subset of the selected muscles to compare the moments the subject required to maintain various hip and trunk positions with those predicted by the model. Although a significant range of seated postures was possible with FES, the data demonstrated that more complete activation of the paralyzed muscles would be needed for the subject to fully achieve the theoretical range of motion. With further refinements, we could apply these techniques to the design of control systems for regulation of seated posture and dynamic motion of the torso.

Abstract-Spastic drop foot is a functional impairment causing significant morbidity and mortality. Multiple treatments are available for this condition, but it is often not clear which treatment or combination of treatments is optimal for a given patient. One relatively recent therapy is the use of functional electrical stimulation to stimulate the peroneal nerve. Another is the use of botulinum toxin injections in the spastic ankle plantar flexors. While reasons exist to think these two treatments might work effectively in combination, there is no clear consensus in the literature. In this article, I review the background of the pathophysiology of spastic drop foot and its treatment options. I present some of the theoretical reasons why functional electrical stimulation and botulinum toxin injections could work synergistically and present a literature review on the topic. Recommendations for future research are discussed.Key words: ankle, botulinum toxins, chemodenervation, drop foot, functional electrical stimulation, gait, muscle spasticity, neurorehabilitation, peroneal nerve stimulation, upper motor neuron syndrome. SPASTIC DROP FOOTSpastic drop foot is a functional impairment causing significant morbidity by impairing gait, limiting activities of daily living, and contributing to injuries [1]. Spastic drop foot exists when, due to a combination of weakness of the ankle dorsiflexors (primarily tibialis anterior) and spasticity of the ankle plantar flexors (primarily gastrocnemius and soleus), the ankle has a predisposition for staying pathologically plantar flexed. Due to associated weakness of ankle evertors (e.g., peroneal musculature) and/or spasticity of invertors (e.g., tibialis posterior), pathological foot inversion is also often associated [2][3].Because ankle dorsiflexion during the swing phase of gait is essential for foot clearance, drop foot can lead to falls and injury [1]. In addition, with drop foot, foot-floor contact in stance phase can happen initially at the forefoot (as opposed to at the heel in nondisabled gait) and limited dorsiflexion can prevent forward progression of the tibia, resulting in hyperextension of the knee and limited forward translation of the body [4]. Those affected often develop pathological compensatory gaits to attempt to compensate for spastic drop foot. One of these, referred to as "steppage gait," involves abnormally flexing the hip and bending the knee to attempt to get the foot to clear the ground [5]. Other patients will hike their hip on the side of the spastic ankle with each swing phase or circumduct the lower limb to aid in foot clearance [6].Abbreviations: AAN = American Academy of Neurology, AFO = ankle-foot orthosis, BTA = botulinum toxin type A, BTB = botulinum toxin type B, BTX = botulinum toxin, CMAP = compound muscle action potential, CNS = central nervous system, FES = functional electrical stimulation, MS = multiple sclerosis, PNS = peroneal nerve stimulation, SCI = spinal cord injury, TBI = traumatic brain injury, UMNS = upper motor neuron syndro...

On the basis of the case presented, BTX may have a limited role in the treatment of pain from muscle spasm in intractable focal seizures. Further study is necessary to see if this use of BTX is generally applicable.