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Spasticity is a condition in which certain muscles are continuously contracted. This contraction causes stiffness or tightness of the muscles and can interfere with normal movement, speech and gait. Spasticity is usually caused by damage to the portion of the brain or spinal cord that controls voluntary movement. The damage causes a change in the balance of signals between the nervous system and the muscles. This imbalance leads to increased activity in the muscles. Spasticity negatively affects muscles and joints of the extremities and is particularly harmful to growing children.
Other conditions that may cause spasticity include:
In a person with CP, brain damage has occurred. For unknown reasons, the damage tends to be in the area of the brain that controls muscle tone and movement of the arms and legs. Therefore, the brains of people with CP are unable to influence the amount of flexibility muscles should have. The command from the muscle itself dominates the spinal cord and results in muscles that are too tense or spastic. People born with CP do not have deformities of the extremities present at birth, but develop them over time. Spasticity of muscles, along with the limitations on stretching and use of muscles in daily activities, is a major cause of these deformities.
Spasticity is a very common symptom of MS. There are two types of MS-related spasms: flexor and extensor. Flexor spasticity is an involuntary bending of the hips or knees (primarily involving the hamstring muscles on the back of the upper leg). The hips and knees bend up toward the chest. Extensor spasticity is an involuntary straightening of the legs. Extensor spasticity involves the quadriceps (muscles on the front of the upper leg) and the adductors (inner thigh muscles). The hips and knees remain straight with the legs very close together or crossed over at the ankles. Spasticity may also occur in the arms, but is less common in people with MS.
Spasticity may worsen due to sudden movements or position changes, muscle tightness, temperature extremes, humidity or infections. It may even be triggered by tight clothing.
Spastic hypertonia often occurs after a TBI as a result of damage to the brain stem, cerebellum or mid-brain. This damage affects the reflex centers in the brain, interrupting message flow along different nerve pathways. This disruption can cause changes in muscle tone, movement, sensation and reflex. The location of the TBI may determine which areas of the body are affected and what motor deficits occur. The reflex centers in the brain are more complex than those in the spinal cord. This can make the treatment of spastic hypertonia in individuals with TBI more difficult to treat than in persons with spinal cord injuries or neurological disorders.
Shortly after a brain injury, many people experience a period of increased muscle tone in which their body posture becomes very rigid. A common position is elbows held rigidly at the sides, wrists and fingers bent, and fists clenched. The legs are usually extended at the hips and knees with ankles and toes flexed. As a TBI patient recovers, nerve signals that control motor functions may change. Some signals may not reach the reflex centers of the brain, or the brain may send too many signals, causing the muscles to not respond properly.
Spasticity may be as mild as the feeling of tightness in muscles or may be severe enough to produce painful, uncontrollable spasms of the extremities; most commonly the legs and arms. Spasticity may also create feelings of pain or tightness in and around joints and can cause low back pain.
Adverse effects of spasticity include:
There are several types of treatment available that must be evaluated on a case-by-case basis, depending on the underlying cause, age of the patient and severity of the spasticity. Different treatments share the common goals of:
Physical and occupational therapy for spasticity is designed to reduce muscle tone, maintain or improve range of motion and mobility, increase strength and coordination and improve comfort. Therapy may include stretching and strengthening exercises, temporary braces or casts, limb positioning, application of cold packs, electrical stimulation and biofeedback.
The use of oral medications to treat spasticity may be indicated when symptoms interfere with daily functioning or with sleep. Effective medication management may require the use of two or more drugs or a combination of oral medications with another type of treatment. It is very important to work closely with a doctor to devise an individualized treatment plan. Side effects vary greatly by class of medication and patient.
BTA, also known as Botox injections, when used in tiny amounts, have proven effective in paralyzing spastic muscles. Injection sites are carefully determined based on the pattern of spasticity.
When Botox is injected into the muscle(s), the release of acetylcholine is blocked, resulting in a relaxation of overactive muscles. The injection(s) generally take effect within a few days and last about 12-16 weeks, until new nerve endings grow back and the affected muscle(s) recover. Functional benefits may last longer than this. There are limitations in the number of injections that can be administered.
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