In the United States, stroke-related illness is the third leading cause of death.  Each year approximately 600,000 individuals in this country suffer a stroke, and for those who survive, it is a major cause of disability.  It has been estimated that, of every 100 persons surviving an acute stroke, only 10 are able to return to their previous activities.  Forty percent of all individuals suffering an acute stroke episode are disabled to the extent that they require special assistance and, of these, 10% need institutional care. 
There are two causes of stroke.  In one, termed “hemorrhagic stroke,” a blood vessel in the brain ruptures, and bleeding into the brain matter surrounding the hemorrhage damages or kills brain cells.  In the other, termed “ischemic stroke,” a clot interrupts blood flow to part of the brain, creating oxygen deprivation to brain cells normally supplied by the blocked blood vessel.  Regardless of the cause, stroke results in a variety of disabilities in survivors, including paralysis or paresis (i.e., partial paralysis), spasticity, loss of cognition, speech disability, emotional disorders, and pain, all of which reduce the individual's capacity for self-care and quality of life. 
In the first few weeks to up to one year following a stroke, there is typically an improvement in function.  After the first year, however, the deficits reach a plateau with a stabilization of the condition. 
Stroke victims typically are treated with a variety of physical and occupational therapies.  Physical therapies used with stroke patients include passive and assisted range of motion exercises, massage, assisted weight bearing, and training in the use of mobility assistance devices, such as walkers, canes, and splints.  Typically, after the typical one-year recovery period following a stroke, little or no further improvement in mobility and manipulation occurs.  At this time, the goal of physical therapy is no longer to obtain an improvement in neurological condition of the patient, but is limited to training the stroke patient to most effectively compensate for the disabilities. 
Voluntary controlled motion of a muscle requires an intact motor pathway connecting a chain of neurons from the upper motoneuron in the cerebral cortex to the lower motoneuron in the spinal cord.  The upper motoneuron is located entirely within the central nervous system, with the cell body in the motor cortex of the cerebrum and the axon within the spinal cord.  The cell body of the lower motoneuron is located in the spinal cord, and its axon innervates a skeletal muscle. 
The motor pathway receives sensory input within the brain via afferent nerves from various receptors.  Several receptors within muscles and tendons provide afferent information contributing to the sense of proprioception: the perception of the relative position of one body part with respect to other body parts and the motion of these parts.  There are two principal types of proprioceptive receptors found in muscle and tendon: muscle spindles, which give rise to both groups Ia and II afferents, and Golgi tendon organs, which give rise to group Ib afferents.  Muscle spindles lie in parallel with their associated muscle and therefore are stretched and excited during muscle lengthening and relaxed during muscle contraction.  Golgi tendon organs lie in series with the muscle and respond primarily to active contraction of the muscle. 
Another type of neurological dysfunction occurs when limbs are immobilized, such as for therapeutic purposes following an injury to the hard or soft tissues of the limb.  Shortly following the onset of immobilization, the neurons in the sensory and motor areas of the brain serving the immobilized limb reorganize to serve non-immobilized portions of the limb or adjacent limbs.  This neurological reorganization, although of benefit to a patient during the period of immobilization, is a detriment to the patient as soon as the immobilization ends.  Because of this reorganization, the patient must “re-learn” how to use the neural and muscular connections of the healed limb.  The need for this re-learning period is especially critical in individuals who have developed high degrees of skill involving their limbs, such as professional athletes or musicians.  For these individuals, the healing process requires not only the actual healing of the tissues of the damaged limb, but also the reconstruction of neural pathways that have been diverted elsewhere during the immobilization. 
A similar reorganization of sensory and/or motor neurons occurs in dystonia.  This condition occurs, for example, when one part of the body, such as a finger or a hand, is repetitively stimulated or trained to perform a task, as in writer's cramp.  Other patterns of dystonia, which affects muscles of the neck and trunk, are either inherited or have no known origin but involve abnormalities of the basal ganglia.  Common to all forms of dystonia is involuntary, long-lasting contracture of muscles that prevents normal movement and everyday function. 
A frequent type of neurological disorder is spasticity.  Spasticity is manifested in many different ways and has been defined in several ways.  A useful definition of spasticity is “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome.”  Young, “Spasticity: A Review,” Neurology, 44 (suppl 9): S12-S20 (1994).  The pathophysiology of spasticity occurs when there is a disease of or injury to the central nervous system with loss of inhibitory input from either supraspinal or spinal centers due to the disease or injury.  Spasticity complicates many neuromuscular diseases and injuries, including spinal cord and traumatic brain injury such as stroke, multiple sclerosis, cerebral vascular accident, and cerebral palsy. 
Several researchers, including the inventor, have studied how the vibration of tendons and muscles affects the proprioceptive receptors.  Vibration of tendons induces small, repetitive stretches in muscle.  See, Cordo et al.,  Electroencephalography and Clinical Neurophysiology, 89:45-53 (1993), incorporated herein by reference.  These studies have focused on using tendon vibration to learn how the nervous system uses proprioceptive input to control normal movements.  Tendon vibration has been shown to be a powerful stimulus for muscle spindle group Ia afferents, which are highly sensitive to small stretches, whereas muscle spindle group II afferents and Golgi tendon organ group Ib afferents are relatively insensitive to tendon vibration.  The design of a vibrator and placement of the vibrator in position on the ankle of a human subject is shown in the Cordo et al. ( 1993) article. 
Cordo et al.,  J. Neurophysiology, 74(4) 1675-1688 (1995), incorporated herein by reference, disclose that stimulation of the muscle spindle receptors by vibration produces illusory sensations of motion and limb displacement.  Tendon vibration distorts the perceptions of the angulation of static joints and of movement of the joints and causes errors in judgment of position and degree of motion of a joint in subjects that were tested.  Cordo et al.  further disclose that vibrating the biceps tendon at a rate of 20 Hz resulted in a perception of decreased angular motion of the forearm.  In contrast, vibrating the biceps tendon at a rate of 40 Hz or 60 Hz resulted in a perception of increased angular motion of the forearm. 
Tendon vibration has been used in an attempt to treat sensory loss and spasticity following stroke, with mixed results.  Tendon vibration alone was determined to decrease spasticity of a joint only transiently, for about 10 minutes following cessation of the vibration.  Ageranioti, S A and Hayes, K C, Effects of Vibration on Hypertonia and Hyperreflexia in the Wrist Joint of Patients with Spastic Hemiparesis, Physiolther.  Can.,  42:24-32 (1990); Hagbarth, K E, The Effects of Muscle Vibration in Normal Man and in Patients with Motor Disorders.  In: New Developments in Electromyography and Clinical Neurophysiology. ( Desmedt, J E, ed.),  Vol.  13, Basel: Karger, 428-442 (1973); Von Kummer, et al.,  Treatment of paraspacticity with Mechanically Produced Vibration Stimuli.  Nervenarzt, 59:185-188 (1988).  To date there are no published reports of the successful non-transient relief of spasticity using tendon vibration or reports investigating the use of tendon or muscle vibration to treat short-term or long-term paresis or paralysis or disuse neuromuscular degeneration associated with stroke or other neurological disorders, limb immobilization, or repetitive use dystonia. 
A pressing need exists, therefore, for more effective means of therapy following the onset of a neurological disorder that will result in a more rapid recovery from the disorder and a lessening of any long-term disabilities. 
Each of the above cited scientific references is incorporated into this specification by reference.