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Spasticity: Management

Disease states involving upper motor neuron lesions can cause spasticity and chronic pain. Posturing, muscle spasms, contractures, and loss of mobility all contribute to pain. When addressing how to manage spasticity, consider its origin (cerebral or spinal) and whether it is focal or general in nature. Management should first focus on treating the underlying disease state causing the spasticity and appropriate physical therapy. Only after these are addressed should systemic therapy or interventions be considered.

Oral Therapy

Oral medications are the mainstay of treatment for general or regional spasticity of spinal origin. They are less helpful in cerebral origin spasticity (mediated by disinhibition of oligosynaptic pathways with few synaptic sites for oral medications to act). Spasticity of spinal origin is mediated by polysynaptic pathways and has more synapses for medications to act on.

  • Baclofen is the most commonly utilized oral medication for spasticity. It is a GABA B agonist with inhibitory effects on excitatory neurotransmitter release. Adverse effects include sedation, somnolence, weakness, and psychological disturbances.
  • Tizanidine preferentially inhibits polysynaptic spinal excitatory pathways through stimulating central alpha 2 receptors. It is generally tolerated better than baclofen and diazepam.
  • Diazepam is a GABA A agonist that increases presynaptic inhibition of polysynaptic and monosynaptic reflexes. It is used for spasticity of both cerebral and spinal origin.
  • Dantrolene suppresses release of calcium ions from sarcoplasmic reticulum of the muscle, which inhibits excitation and contraction of the muscle. It is rarely used.


  • Botulinum toxin blocks the release of acetylcholine at the neuromuscular junction of injected muscles to cause focal weakness and decrease spasticity. It is especially useful in the management of focal spasticity of cerebral origin. It affects only the individual muscle that is injected.
  • Neurolysis using phenol or alcohol injections into the perineural space of motor/sensory or motor nerves results in nerve destruction by inducing protein precipitation and Wallerian degeneration. This loss of myelin slows nerve conduction and results in a decrease in spasticity. It affects all muscles supplied by the injected nerve.

If oral medications have been trialed without good effect or poor tolerance of the medication, intrathecal baclofen can be useful for otherwise resistant forms of general spasticity.