The goal of therapy for spasticity is to increase functional capacity and relieve discomfort. As for any symptomatic therapy, the treatment of spasticity should be individualized. Before initiating treatment, one must first evaluate the functional consequences of reducing spasticity. For some patients with proximal leg weakness, increased extensor tone in the legs offers necessary stability and support during transferring and walking. For other patients, hyperreflexia and clonus interfere with normal ambulation. In nonambulatory patients, flexor spasms may be painful and debilitating.
Noxious stimuli (e.g., urinary tract infections) should be excluded before a given therapeutic regimen is altered. Patients with spasticity may exhibit further increase in tone or spontaneous spasm in the setting of such stimuli.
Goals for therapy and realistic expectations should be established by both care provider and patient. Treatment for spasticity should be multimodal. Conservative measures should be incorporated in antispasticity regimens. Physical therapy is an essential component. Stretching, massage, and passive range-of-motion exercises are extremely important in preventing muscle shortening and the formation of contractures. Guidance on proper positioning and posture and on how to avoid specific positions that may elicit clonus or spasms can result in increased function.
Direct effects of muscle relaxation from physiotherapy often are short-lived and, for many patients, these conservative measures alone are insufficient to treat their symptoms. Most patients experience symptomatic improvement with physiotherapy in combination with one or more antispasticity agents.
Patients also should be evaluated for adaptive equipment such as ambulatory aids, reachers, and other devices and should be instructed in the appropriate use of these tools.
Patients whose condition is inadequately controlled by physical therapy and medication may respond to a variety of neurosurgical procedures, both central and peripheral. A practitioner’s understanding of the mechanisms of these therapies should aid in developing individualized regimens for patients.
Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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