Abstract and Introduction
Abstract
Spasticity is common in many neurological disorders, such as stroke and multiple sclerosis. It is part of the upper motor neurone syndrome manifesting as increased tone, clonus, spasms, spastic dystonia and co-contractions. The impact of spasticity varies from it being a subtle neurological sign to severe spasticity causing pain and contractures. Existing spasticity can be worsened by external factors such as constipation, urinary tract infections or pressure ulcers. Its management involves identification and elimination of triggers; neurophysiotherapy; oral medications such as baclofen, tizanidine and dantrolene; focal injection of botulinum toxin, alcohol or phenol, or baclofen delivered intrathecally through a pump; and surgical resection of selected dorsal roots of the spinal cord. This article reviews the current understanding of pathophysiology, clinical features and management of spasticity.
Introduction
Spasticity is defined as 'disordered sensorimotor control resulting from an upper motor neurone (UMN) lesion, presenting as intermittent or sustained involuntary activation of muscles'. It is a frequent symptom of common neurological disorders, such as multiple sclerosis and stroke. Spasticity seldom exists in isolation and is usually accompanied by one or more components of UMN syndrome (Table 1).
Spasticity varies from being a clinical sign with no functional impact to being a gross increase in tone interfering with mobility, transfers and personal care. Untreated, it can cause shortening of muscles and tendons, leading to contractures (figure 1). Some patients depend on their spasticity to stand, walk and transfer or sit upright. The optimum management of spasticity requires a co-ordinated approach with rehabilitation professionals.
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Figure 1.
Spasticity resulting in flexion contractures of lower limbs.