Each year, more than 600,000 U.S. citizens experience a major stroke. Following acute care, 30-40% of these survivors sustain permanent motor disabilities. The motor symptoms of stroke include loss of muscle control on one side of the body, spasticity, and loss of coordination ("dyssynergia"). Within days of the stroke, surviving patients begin physical therapy to restore motion, with some recovering completely. However, there are over 5 million individuals in the U.S. alone who have not recovered and are severely incapacitated for the remainder of their lives. Recovery of function typically reaches a plateau within 6-12 months following a stroke. This recovery of function presumably involves "plastic" changes in the cerebral cortex, in which new neural circuits organize to replace those damaged by the injury. The origin of paralysis or paresis (i.e., partial loss of movement) and the cause of spasticity are unclear in many stroke patients. In a small subset, the brain tissue injured by the stroke is localized to the "primary motor cortex", which contains the nerve cells that send movement signals to the muscles. Loss of movement is easy to understand in these individuals. However, in many strokes, the injury is located in other parts of the brain or is more diffuse, and loss of movement is not as easy to explain. In many regions of the brain, sensory information from various sources, including the proprioceptive system, is integrated and then relayed to the motor cortex to produce movement.

Proprioception is the sense of body position and movement, which originates from sensory receptors in muscles, tendons, skin, and joints. Research carried out over the last two decades indicates that proprioception is intimately involved in motor coordination. In fact, individuals who suffer a rapid loss of proprioception they are functionally paralyzed for a period of time. The hypothesis underlying our approach to stroke rehabilitation is that, in many survivors of stroke, the damage to the brain disrupts one or more feedback loops that connect the proprioceptive receiving areas of the primary somatosensory cortex (Areas 1, 2, 3a, and 3b) to the primary and pre-motor cortex (Areas 4 and 6). Without proprioceptive information feeding into the motor output center, the brain cannot "locate" the muscles needed for movement to occur. We hypothesize that the synchronous and repetitive activity of the input and output areas of the cortex stimulates the reorganization of the brain pathways, thereby closing the feedback loop(s) disrupted by the stroke. In this context, the aim of our research is to identify the effect of a wrist/elbow robotic assisted training combined with proprioceptive training provided by repetitive vibratory stimuli in the tendons of the muscles involved in wrist/elbow flexion and extension on voluntary movement like the reaching movements in individuals with chronic stroke.

In this approach to stroke rehabilitation, the investigators aim to enhance plastic changes in the brain following the injury by repetitively causing the nerve cells in the primary somatosensory cortex to fire synchronously with nerve cells in the functionally related parts of the motor cortex. This approach is designed to rebuild the connections between incoming proprioceptive input and outgoing motor output.

The research objective is to develop procedures to rehabilitate participants \> 1 year post-stroke who, through conventional therapies, are not brought to a level of maximal recovery. The aim of the proposed project is to obtain a set of data from a total of 20 chronic stroke participants, all with severe upper extremity disability, between the ages of 18-85, using a robotic therapeutic device placed in a biomechanics laboratory within the Shirley Ryan AbilityLab. This data will allow us to quantify the extent to which a combination of robotic-assisted exercise and tendon vibration induces secondary recovery from stroke in the upper extremity.

The proposed research plan involves a machine with 2 main components, a range of motion sensor and sensory stimulators (i.e., mechanical vibrators). The range-of-motion component of the machine rotates the affected joint (e.g., wrist or elbow) and records position and force. The participant's task involves contracting muscles to assist with the applied motion. Visual feedback of the amount of force or Electromyographic (EMG) activity produced by the participant is displayed on a computer screen. The assisted movement activates the nerve cells in the motor cortex of the brain. While the combined efforts of the robotic device and the participant repeatedly rotate the participant's paretic wrist/elbow into flexion and extension, a pair of vibrators delivers high frequency stimulation (60 pulses per second) to the corresponding tendons on the side of the joint opposite to the agonist muscles. Vibration is known to be an effective stimulus for muscle spindles, the primary sensory receptors that contribute to proprioception. The vibration stimulus increases, by several-fold, the natural response of the muscle spindles to the joint rotation. Only the lengthening tendon is vibrated at any given time. The vibration-induced activation of muscle spindles in the lengthening muscle(s) serve to activate the nerve cells in the somatosensory cortex of the brain. Thus, assisted exercise activates nerve cells in the motor output area of the cortex while vibration simultaneously activates the functionally related nerve cells in the sensory input area, providing a stimulus to develop new, or to enhance existing connections between the two areas.