Treatment of spasticity

Spasticity is characterized by an enhanced size and reduced threshold for activation of stretch reflexes and is associated with "positive signs" such as clonus and spasms, as well as "negative features" such as paresis and a loss of automatic postural responses. Spasticity develops over time after a lesion and can be associated with reduced speed of movement, cocontraction, abnormal synergies, and pain. Spasticity is caused by a combination of damage to descending tracts, reductions in inhibitory activity within spinal cord circuits, and adaptive changes within motoneurons. Increased tone, hypertonia, can also be caused by changes in passive stiffness due to, for example, increase in connective tissue and reduction in muscle fascicle length. Understanding the cause of hypertonia is important for determining the management strategy as nonneural, passive causes of stiffness will be more amenable to physical rather than pharmacological interventions. The management of spasticity is determined by the views and goals of the patient, family, and carers, which should be integral to the multidisciplinary assessment. An assessment, and treatment, of trigger factors such as infection and skin breakdown should be made especially in people with a recent change in tone. The choice of management strategies for an individual will vary depending on the severity of spasticity, the distribution of spasticity (i.e., whether it affects multiple muscle groups or is more prominent in one or two groups), the type of lesion, and the potential for recovery. Management options include physical therapy, oral agents; focal therapies such as botulinum injections; and peripheral nerve blocks. Intrathecal baclofen can lead to a reduction in required oral antispasticity medications. When spasticity is severe intrathecal phenol may be an option. Surgical interventions, largely used in the pediatric population, include muscle transfers and lengthening and selective dorsal root rhizotomy.