Muscle spasticity is a serious and sometimes debilitating condition. It is generally considered to result from a loss of inhibition of motor neurons, causing excessive muscle contraction or hyperreflexia. The altered skeletal muscle performance results in often severe contractions, twitching, and involuntary or jerky movements. In addition, those afflicted with the disorder may have joint stiffness, unusual posture, and exaggerated reflexes. Spasticity can cause pain, loss of sleep, joint deformity, macerated skin, loss of coordination, fatigue, and an inability to perform many basic daily activities.
Spastic cerebral palsy is by far the most common form of cerebral palsy (CP), occurring in more than 70% of all cases, affecting approximately 3 children out of every 1,000 people. Spasticity is also a symptom in 78% of multiple sclerosis patients, 35% of those with stroke, 50% of patients with traumatic brain injury (TBI), and 40% of those with spinal cord injury (SCI).
In general, spasticity develops when an imbalance occurs in the excitatory and inhibitory input to alpha motor neurons in the spinal cord, leading to hyper-excitability of the affected muscle or muscles. Possible mechanisms of action include lesions of the upper motor neuron, such as in CP, stroke, TBI, or SCI, where disruption occurs not only in the pyramidal tract, but also in the corticospinal tract involved in voluntary movement. Removal of inhibition on segmental polysynaptic pathways leads to a rise of the excitatory state due to cumulative excitation. In the cerebral model, enhanced excitability of monosynaptic pathways can cause a buildup of reflex activity.
Spasticity is often localized to a particular muscle or muscles in the body. Specific locations in the body communicate with the brain through at least one spinal nerve. 31 pairs of spinal nerves exist in the body, with each one connecting to the spine via its nerve root. Mapping has been performed and published, which allows one to determine the spinal nerve or nerves that communicate with a specific region of the body. One example would be cervical spinal nerves C5 and C6, which pass signals between the deltoid muscle of the shoulder and the brain.
Treatment of spasticity generally includes physical therapy or occupational therapy targeted at reducing muscle tone, improving range of motion, mobility, comfort, and strength of moveable parts of the body. Botulinum toxin (BTX) is often used to interrupt neuronal signaling by destroying nerve tissue. A variety of medications have been used to treat the symptoms of spasticity. For example, dantrolene reduces the release of calcium into the sarcoplasmic reticulum of muscles, which slows muscle fibers. Baclofen binds to GABAB receptors in the spinal cord, decreasing stretch reflexes. Medications often include serious side effects, including dizziness, weakness, malaise, fatigue, and diarrhea. Confusion and cognition problems are also common with certain medications. For some patients, the only treatment available is surgical denervation of muscles and tendons. It is apparent that a non-invasive, drug-free method for providing treatment of spasticity is desirable.
USPTO Backgrounds
USPTO Backgrounds