Sensory control of normal movement and of movement aided by neural prostheses.

Signals from sensory receptors in muscles and skin enter the central nervous system (CNS), where they contribute to kinaesthesia and the generation of motor commands. Many lines of evidence indicate that sensory input from skin receptors, muscle spindles and Golgi tendon organs play the predominant role in this regard. Yet in spite of over 100 years of research on this topic, some quite fundamental questions remain unresolved. How does the CNS choose to use the ability to control muscle spindle sensitivity during voluntary movements? Do spinal reflexes contribute usefully to load compensation, given that the feedback gain must be quite low to avoid instability? To what extent do signals from skin stretch receptors contribute? This article provides a brief review of various theories, past and present, that address these questions. To what extent has the knowledge gained resulted in clinical applications? Muscles paralyzed as a result of spinal cord injury or stroke can be activated by electrical stimulation delivered by neuroprostheses. In practice, at most two or three sensors can be deployed on the human body, providing only a small fraction of the information supplied by the tens of thousands of sensory receptors in animals. Most of the neuroprostheses developed so far do not provide continuous feedback control. Instead, they switch from one state to another when signals from their one or two sensors meet pre-set thresholds (finite state control). The inherent springiness of electrically activated muscle provides a crucial form of feedback control that helps smooth the resulting movements. In spite of the dissimilarities, parallels can be found between feedback control in neuroprostheses and in animals and this can provide surprising insights in both directions.