zSymptomatic Treatment of Spasticity in Multiple Sclerosis
The etiology of spasticity in multiple sclerosis is either a result of the stiffness of muscle tone over a sustained period of time, or the result of intermittent spasms. The pathophysiology is not completely defined but is thought to involve changes in the afferent and efferent pathways of the alpha motor neurons.
Symptoms of discomfort and pain that occur as a result of spasticity range from sensations of tightness in the musculature to severe pain.. The pain may frequently occur in joints or in the low back, and varies with position, posture, and relaxation. It is typical in multiple sclerosis to see spasticity that varies in degree and location that is affected by fatigue.
Spasticity commonly occurs with other conditions, but must be differentiated from clonus, dystonia, athetoid movement, chorea, rigidity, ballisms, or tremor.
A Proposed Etiology of Spasticity in Multiple Sclerosis
Multiple sclerosis is a disease that causes disruption of neuronal signals due to demyelination of neuronal axons, and spasticity may result from an imbalance in neural signaling. Hyperactive stretch reflexes occur, resulting in either exaggerated muscular tension or involuntary muscular contractions. Exacerbations result from various triggers, including temperature, humidity, or infectious disease processes. External physical triggers may include the impact of something as innocuous as tight clothing.
After obtaining a complete medical history, including current medication regimen, simple physical maneuvers such as active and passive range of motion or the ability to perform simple motor tasks are used to determine the patient’s level of impairment. Treatment for spasticity can range from physical therapy to medication to surgery, in severe cases.
Management of Spasticity
The goals of treatment of spasticity include retention of function, particularly related to mobility and the ability to perform activities of daily living; prevention of any permanent orthopedic deformity or development of pressure ulcers; reduction of pain; and stretching to achieve appropriate fit with orthotics.
Treatment of spasticity will be influenced by severity, location, duration, success of any prior treatment, functional status and future plans, any comorbidities, the likelihood of compliance with treatment, and the availability of a support system and a plan for follow-up. Before spasticity becomes an issue, patients should be managed with preventive measures in place. There is not a stepwise algorithm for treatment of spasticity resulting from MS, and many therapeutic measures may be utilized concurrently or interchangeably.
The first step to attempt to relieve the spasticity includes physical therapy with a focus on lengthening muscles through stretching exercises on a daily basis. Other treatments may include splinting, casting, or bracing as needed, to maintain range of motion or flexibility. Physical therapy may also involve aquatics, hippotherapy, ultrasonography, and biofeedback.
If physical and occupational therapy prove inadequate, then medications such as baclofen or Zanoflex are often prescribed. Valium is an excellent muscle relaxer, and is used in many cases to relieve nighttime spasms. 2
For recalcitrant spasticity that is unresponsive to oral medication, a pump may be implanted to deliver medication locally. A baclofen pump is commonly utilized. Botox injections are another therapy, injected directly into the affected area to relax the muscles that are contracted.
Other Treatment Modalities
Contractures typically occur when the muscle crosses two joints. Spinal cord stimulators are sometimes used for control of pain, rather than reduction of spasticity.
Surgical treatment for spasticity is an option in patients with significant quality-of-life issues and no response to other therapies. These techniques include tendon release, which is performed to resect contracted tendons from the affected muscle. It is interesting to note that surgical procedures do not alter the spasticity of the muscle, but because the ligaments or tendons are resected, the effects of the spasticity are minimized.
The impact of treatment of a spastic muscle must be considered in light of the action of the antagonist muscle group. Consideration should be given to treatment of both agonist and antagonist. Additionally, in some cases spasticity may provide a substitute for strength, and thus has a functional purpose that may diminish with treatment. Certain muscle groups are more frequently targeted for treatment in MS, and they include hip adduction and flexion, knee flexion, and plantar flexion groups. Other involved muscles often include the adductor magnus, iliopsoas, hamstrings, posterior tibialis, soleus, and gastrocnemius.
An additional treatment option, a rhizotomy, consists of resection of the affected spinal nerve, and is used most commonly to relieve spasticity in the lower extremities. Post-surgical physical therapy and occupational therapy optimize the benefits of rhizotomy significantly.
Decisions about treatment must be considered in light of the individual patient’s functional status. Before treatment is undertaken, it is important to rule out any treatable factors, including spinal cord lesions or peripheral nerve impingement. Spasticity may be exacerbated by infection, bladder distension, bowel impaction, cold weather, fatigue or stress, poor positioning, and seizure activity. Spasticity may present in a similar way to seizure activity, but there is neither a postictal period nor a rhythmic or symmetric quality.
Treatment of spasticity in patients with MS is so frequently transient that the risk/benefit ratio must be carefully calculated. Physical and occupational therapy remain extremely important components of treatment.