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The term “spasticity” is commonly used for an upper motor neuron deficit, but it properly refers to a velocity-dependent increase in resistance to passive movement that affects different muscles to a different extent, is not uniform in degree throughout the range of a particular movement, and is commonly associated with other features of pyramidal deficit. It is often a major complication of stroke, cerebral or spinal injury, static perinatal encephalopathy, and multiple sclerosis. Spasticity may be exacerbated by pressure injuries, urinary or other infections, and nociceptive stimuli.
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Physical therapy with appropriate stretching programs is important during rehabilitation after the development of an upper motor neuron lesion and in subsequent management of the patient. The aim is to prevent joint and muscle contractures and perhaps to modulate spasticity.
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Medication management is important also, but treatment may increase functional disability when increased extensor tone is providing additional support for patients with weak legs. Pharmacologic treatment with baclofen (5–10 mg twice daily orally titrated to 80 mg daily), tizanidine (2–8 mg three time daily orally), diazepam (2–10 mg three times daily orally), or dantrolene (25 mg once daily orally, titrated every 3 days as tolerated to a maximum of 100 mg four times daily) is often helpful. Dantrolene is best avoided in patients with poor respiratory function or severe myocardial disease. Cannabinoids are also effective in reducing spasticity, but are associated with side effects, including dizziness, drowsiness, and fatigue. Intramuscular injection of botulinum toxin is used to relax targeted muscles.
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In patients with severe spasticity that is unresponsive to other therapies and is associated with marked disability, intrathecal injection of phenol or alcohol may be helpful. Surgical options include implantation of an intrathecal baclofen pump, rhizotomy, or neurectomy. Severe contractures may be treated by surgical tendon release.