Clinical training and competency guidelines for using robotic devices.

With the increasing popularity of robotic devices in rehabilitation centers worldwide (e.g. Lokomat(®), ZeroG(®), ReoGo, InMotion 2.0, and Biodex System 4), there is a need for guidelines to ensure proper training and evaluation of therapists on the safe and effective use of these devices. Here, we present training tools and guidelines that were based on the recommendations of several device manufacturers and a user-group made up of clinicians and therapists. The training tools consist of a detailed user manual, clinical manual, hand-on training, video training and web based training tools. We also present procedures for evaluating user competency after they have completed detailed training. We believe that the comprehensive training and competency evaluation guidelines presented here will help ensure that rehabilitation robotic devices are used properly. This in turn will lead to more effective interventions and reduce the likelihood of injury.

Functional neuroanatomy of mirroring during a unimanual force generation task.

Performance of a unimanual motor task often induces involuntary mirror electromyographic (EMG) activity in the opposite, resting hand. In spite of the ubiquitous presence of mirroring, little is known regarding the underlying cortical contributions. Here, we used functional magnetic resonance imaging (fMRI) to study brain regions activated in association with parametric increases in right isometric wrist flexion force (10%, 20%, 30%, and 70%) in 12 healthy volunteers. During scanning, EMG activity was recorded bilaterally from flexor carpi radialis (FCR), extensor carpi radialis (ECR), biceps brachii (BB), and triceps brachii (TB). Mirror EMG was observed in left FCR during 20%, 30%, and 70% of force. Left ECR, BB, and TB showed mirror EMG only at 70% of force. Increasing force was associated with a linear increase of blood-oxygen-level-dependent (BOLD) signal in bilateral primary motor cortex (M1), supplementary motor area (SMA), caudal cingulate, and cerebellum. Mirroring in the left FCR correlated with activity in bilateral M1, SMA, and the cerebellum. Overall, our results suggest that activity in these regions might reflect sensorimotor processes operating in association with mirroring and suggest caution when interpreting fMRI activity in studies that involve unilateral force generation tasks in the absence of simultaneous bilateral EMG/kinematics measurements.

Understanding motor impairment in the paretic lower limb after a stroke: a review of the literature.

In addition to muscle weakness caused by injury to supraspinal centers, several mechanisms may contribute to motor impairment in the paretic lower limb following a stroke. Physiological changes in the paretic muscles and their motor units, passive or active restraint of agonist activation, and abnormal muscle activation patterns have been shown to occur after a stroke and to reduce muscle force generation. Other factors such as increased passive tone may impede agonist and antagonist muscle torque generation, while abnormal motor activation and altered motor control of muscles can produce abnormal gait patterns. Co-activation of opposing lower limb muscles contributes to joint stiffness and postural stability; abnormal co-activation in paretic lower limbs can lead to deficits in postural stabilization. Abnormal timing of muscle activation can also yield reduced muscle work output and, in turn, reduced limb function. When sensory deficits accompany muscle weakness, impaired processing of afferent signals may contribute to abnormal muscle activation, abnormal gait patterns, and abnormal responses to perturbation during gait and stance. This article reviews the impact of these various factors, individually and in combination, on impaired motor function in the paretic lower limb after a stroke.

Inverse-dynamics based assessment of gait using a robotic orthosis.

Body-weight supported treadmill training following neurological disorders such as stroke and spinal cord injuries (SCI) has become an integral part of rehabilitation for treating gait disorders. Unfortunately techniques for selecting important training parameters, such as walking speed and body-weight support, have not been established. Here we present a 3-D inverse-dynamics based approach for evaluating an individual's ability to ambulate, in terms of evaluating the magnitude and timing of joint moments at the ankle, knee and hip. This technique, which utilizes an instrumented gait robot, allows clinicians and researchers the ability to determine the training parameters in which subjects generate joint moments at the proper phases of the gait cycle which when combined with electromyographic recordings, can help establish and then progress training parameters for individuals on a subject-by-subject basis. We believe that training subjects at their preferred walking speed and body-weight support will lead to higher functional outcomes.

Limb alignment and kinematics inside a Lokomat robotic orthosis.

The use of robotic gait training systems has become commonplace world-wide. In particular, the Lokomat robotic orthosis (Hocoma AG, Volketswil, Switzerland) is in use at nearly 75 facilities treating patients with spinal cord injury, stroke, and other neurological impairments. Despite the extensive use of the device, no studies have reported the leg kinematic trajectories while walking in the device. Furthermore, because the subject's legs are not rigidly coupled to the device, there is the potential for significant leg movement inside the device which also has not been reported. Here we report differences in kinematic trajectories between walking in the Lokomat and walking on a treadmill, as well as the relative limb motion within the Lokomat for a single representative subject. Using high-speed motion analysis, it was found that while similar knee and hip angle patterns were produced when walking on the treadmill and while walking in the Lokomat, there were significant differences (p<.0.01) in percent time spent in swing phase, maximum hip and knee flexion, and maximum hip extension. There was also a larger amount of misalignment at the hip (18.2 mm) than at the knees (12 mm) when the joint positions in space were compared.

Robotic-assessment of walking in individuals with gait disorders.

Walking deficits are a common bi-product of numerous neurological injuries, such as stroke and spinal cord injury. A number of new therapeutic interventions, such as body-weight supported locomotor training and robotic technologies aim to improve walking function and reduce co-morbidities. Currently, there is no way to determine what the optimal set of training parameters are for maximizing step performance. This paper presents a technique for estimating the walking performance of individuals with gait disorders using a robotic-orthosis. The device, called the Lokomat is coupled to the subject through instrumented leg cuffs, while the split-belt treadmill on which the subject walks is instrumented with piezo-electric force sensors allowing for the calculation of ground reaction forces and center of pressure. Using this data, a real-time inverse dynamics approach can be used to estimate the kinetics and kinematics of the subject, and when combined with electromyographic (EMG) data, the set of training conditions through which the subject generates the most appropriate EMG patterns and joint moments can be identified. The proposed technique will for the first time provide clinicians a way of determining the optimal gait training parameters for each individual, and also track their functional recovery throughout their neurorehabilitation program. It is postulated that training at the conditions that maximizes stepping performance will lead to higher gains in over-ground walking ability.

Limit cycle behavior in spasticity: analysis and evaluation.

We examined ankle clonus in four spastic subjects to determine whether this oscillatory behavior has the properties of a limit cycle, and whether it is driven by peripheral sensory input or by a spinal generator. Using Floquet Theory and Poincare sections to assess reflex stability, we found that cycle-to-cycle variability was small, such that the Floquet multipliers were always less than unity. Furthermore, the steady-state periodic orbit was not dependent on the initial position of the ankle. Both of these findings, coupled with strong correlations between the size of the applied load and the frequency of ankle movements and electromyogram burst frequency suggests that clonus behaves as a locally stable limit cycle driven from peripheral receptors. To better understand how nonlinear elements might produce stable oscillatory motion, we simulated the ankle stretch reflex response. We found that delays in the pathway caused the reflex to come on during the shortening phase of movement, so the additional reflex torque required to sustain oscillatory ankle movements was quite small. Furthermore, because the resistance to stretch is largely due to passive mechanics whose properties are quite stationary, the system is robust to small perturbations within the reflex pathway.

A simulation study of reflex instability in spasticity: origins of clonus.

Clonus is defined as an involuntary rhythmic muscle contraction that generally occurs in people who have sustained lesions involving descending motor pathways in the neuraxis, and is usually accompanied by other signs of reflex hyperexcitability such as spasticity. This paper hypothesizes that clonus arises when two conditions occur simultaneously: 1) the reflex pathway contains long delay times (implying innervation of distal limb muscles, exacerbated when these muscles display slow twitch properties) and 2) the excitability of the motoneurons is enhanced. This paper tested this dual hypothesis by developing a computer model representing the ankle reflex pathway. This model included the ankle muscles, afferent and efferent pathways, and a monosynaptic spinal link between spindle afferents and motoneurons. Simulations show that as the motoneuron current threshold was reduced (reflecting increased excitability of spinal motoneurons), normal reflex responses became unstable and oscillations developed similar to those observed in spastic patients. In parallel, when we choose reflex delay times typical for distal leg muscles in man, system stability is poor, and oscillations occur readily with increasing motoneuron excitability. As simulated pathway delays are reduced, oscillatory behavior is also reduced, and usually damps out. Conversely, as simulated reflex delays are increased, oscillations increase in amplitude and do not decay. Finally, these two phenomena interact, so that increasing motoneuron excitability will induce reflex oscillations for intermediate loop delays. These findings support the hypothesis that unstable oscillatory behavior, such as the oscillations observed in clonus, will occur when the motoneuron excitability increases in a reflex pathway containing long delays. This change in excitability is mediated by a reduction in motoneuron firing threshold, rather than by an increase in feedback gain. Furthermore, we demonstrate that sustained oscillations occur readily through self reexcitation, which reduces the need to propose that a "central oscillator" must be involved in generating clonus.