Spasticity Medication

Updated: Jun 28, 2019
  • Author: Krupa Pandey, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Medication Summary

Medications used in the treatment of spasticity include the following:

  • Skeletal muscle relaxants (dantrolene sodium, baclofen)

  • Benzodiazepines (diazepam)

  • Alpha2-adrenergic agonists (clonidine, tizanidine)

  • Botulinum toxins (onabotulinumtoxinA, abobotulinumtoxinA, incobotulinumtoxinA)

Because tolerance can occur with medications, drug dosages should regularly be reviewed and implantable devices (pumps, stimulators) should be checked.

Gabapentin, clonazepam, progabide, piracetam, lamotrigine, and cyproheptadine are medications that potentially may affect spasticity. These agents are not indicated for spasticity and currently are under investigation, have undergone little clinical evaluation, or are not available in the United States.

Pharmaceutical cannabinoids and plant-based cannabinoids have been investigated for their therapeutic potential in treating spasticity. There is sufficient evidence that cannabinoids may be effective for symptoms of spasticity in MS but no strong evidence in other conditions. [57, 58]


Skeletal Muscle Relaxants

Class Summary

These agents may be helpful in the treatment of reversible and intractable spasticity

Dantrolene sodium (Dantrium, Revonto, Ryanodex)

This is a peripherally acting medication that prevents calcium release from the sarcoplasmic reticulum. It is particularly effective in cerebral-origin spasticity, such as that occurring in traumatic brain injury (TBI), stroke, or cerebral palsy.

Baclofen (Lioresal, Gablofen)

Baclofen presynaptically inhibits the nerve terminal. It is centrally acting and can be administered intrathecally or orally. Baclofen is the preferred drug for spasticity related to spinal cord injury (SCI) or multiple sclerosis (MS) and is useful in cerebral palsy. Tolerance can occur. Adverse effects are minimized if the drug is given intrathecally.



Class Summary

These agents are skeletal muscle relaxants that can treat convulsive disorders.

Diazepam (Valium, Diastat)

Diazepam acts presynaptically and is a gamma-aminobutyric acid A (GABA-A) agonist. It is centrally acting and is particularly effective in patients with SCI and MS. Tolerance and addiction can occur.


Alpha2-adrenergic Agonists

Class Summary

These agents may reduce sympathetic outflow from the central nervous system (CNS).

Clonidine (Catapres, Kapvay)

Clonidine stimulates alpha-2 adrenoreceptors in the brainstem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow. These effects cause a decrease in vasomotor tone and heart rate. Clonidine is effective in SCI-associated spasticity and possibly in TBI-associated spasticity as well.

Tizanidine (Zanaflex)

Tizanidine is a centrally acting muscle relaxant that is metabolized in the liver and excreted in urine and feces. It is used in patients with predominantly upper motor neuron involvement. It is not a DEA-controlled substance.


Botulinum Toxins

Class Summary

Treatment with botulinum toxins are used to reduce muscle tone and improve passive and/or active function in adults with spasticity. Botulinum toxins are a neurotoxin derived from Clostridium botulinum. Botulinum toxin prevents acetylcholine from the presynaptic membrane, causing temporary calming of muscle contractions by blocking the transmission of nerve impulses.

OnabotulinumtoxinA (Botox)

Binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. It is then internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. Subsequently blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. The toxin does not affect the synthesis or storage of acetylcholine or the conduction of electrical signals along the nerve fiber.

It is approved for upper and lower limb spasticity in adults and children aged 2 years or older.

AbobotulinumtoxinA (Dysport)

Binds to receptor sites on the motor nerve terminals and, after uptake, inhibits release of acetylcholine, blocking transmission of impulses in neuromuscular tissue. At 7-14 days after administration of the initial dose, assess the patient for a satisfactory response. Increase the dose 2-fold over the previously administered dose in patients who experience incomplete paralysis of the target muscle.

It is indicated for treatment of upper and lower limb spasticity in adults. It is also indicated for lower limb spasticity in children aged 2 years or older.

IncobotulinumtoxinA (Xeomin)

IncobotulinumtoxinA is botulinum toxin type A that is free of complexing proteins found in the natural toxin from Clostridium botulinum. This drug inhibits acetylcholine release and elicits neuromuscular blockade. It is indicated for treatment of upper limb spasticity in adults.