In this report we describe the outcome of a consensus meeting that occurred at the National Institutes of Health in Bethesda, Maryland, March 12 through 14, 2005. The meeting brought together 39 specialists from multiple clinical and research disciplines including developmental pediatrics, neurology, neurosurgery, orthopedic surgery, physical therapy, occupational therapy, physical medicine and rehabilitation, neurophysiology, muscle physiology, motor control, and biomechanics. The purpose of the meeting was to establish terminology and definitions for 4 aspects of motor disorders that occur in children: weakness, reduced selective motor control, ataxia, and deficits of praxis. The purpose of the definitions is to assist communication between clinicians, select homogeneous groups of children for clinical research trials, facilitate the development of rating scales to assess improvement or deterioration with time, and eventually to better match individual children with specific therapies. "Weakness" is defined as the inability to generate normal voluntary force in a muscle or normal voluntary torque about a joint. "Reduced selective motor control" is defined as the impaired ability to isolate the activation of muscles in a selected pattern in response to demands of a voluntary posture or movement. "Ataxia" is defined as an inability to generate a normal or expected voluntary movement trajectory that cannot be attributed to weakness or involuntary muscle activity about the affected joints. "Apraxia" is defined as an impairment in the ability to accomplish previously learned and performed complex motor actions that is not explained by ataxia, reduced selective motor control, weakness, or involuntary motor activity. "Developmental dyspraxia" is defined as a failure to have ever acquired the ability to perform age-appropriate complex motor actions that is not explained by the presence of inadequate demonstration or practice, ataxia, reduced selective motor control, weakness, or involuntary motor activity.

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The gait pattern in 10 patients with cerebellar degenerations was studied and the results were compared with 10 matched normal subjects, seeking the principal patterns in this disorder. Gait at natural speed was studied in a biomechanics laboratory using a video-based kinematic data acquisition system for measuring body movements. Patients showed a reduced step and stride length with a trend to reduced cadence. Heel off time, toe off time, and time of peak flexion of the knee in swing were all delayed. Range of motion of ankle, knee, and hip were all reduced, but only ankle range of motion reached significance. Multijoint coordination was impaired, as indicated by a relatively greater delay of plantar flexion of the ankle compared with flexion of the knee and a relatively late knee flexion compared with hip flexion at the onset of swing. The patients also showed increased variability of almost all measures. Although some of the deviations from normal were simply the result of slowness of walking, the gait pattern of patients with cerebellar degeneration shows incoordination similar to that previously described for their multijoint limb motion.

Bipedal locomotion was simulated to generate a pattern of activating muscles for walking using electrical stimulation in persons with spinal cord injury (SCI) or stroke. The simulation presented in this study starts from a model of the body determined with user-specific parameters, individualized with respect to the lengths, masses, inertia, muscle and joint properties. The trajectory used for simulation was recorded from an ablebodied subject while walking with ankle-foot orthoses. A discrete mathematical model and dynamic programming were used to determine the optimal control. A cost function was selected as the sum of the squares of the tracking errors from the desired trajectories, and the weighted sum of the squares of agonist and antagonist activations of the muscle groups acting around the hip and knee joints. The aim of the simulation was to study plausible trajectories keeping in mind the limitations imposed by the spinal cord injury or stroke (e.g., spasticity, decreased range of movements in some joints, limited strength of paralyzed, externally activated muscles). If the muscles were capable of generating the movements required and the trajectory was achieved, then the simulation provided two kinds of information: 1) timing of the onset and offset of muscle activations with respect to the various gait events and 2) patterns of activation with respect to the maximum activation. These results are important for synthesizing a rule-based controller.