Practice

Spasticity

Raphael Rush and Dinesh Kumbhare
CMAJ April 07, 2015 187 (6) 436; DOI: https://doi.org/10.1503/cmaj.140405

Spasticity is common in upper motor neuron disorders1

After a stroke, almost 5% of patients are affected by spasticity within 10 days of the event; about 10% of patients are affected after 6 months.2 About one-third of patients with multiple sclerosis have spasticity that limits their ability to perform daily activities.3 Almost 80% of children with cerebral palsy have spasticity.4

Spasticity is a velocity-dependent increase in tone

Spasticity is evoked with quick passive movement of the affected limb. A “spastic catch” is felt and can be overcome with continued force. The effect is diminished at slower speeds.2 The degree of spasticity is quantified by using the Ashworth scale (Appendices 1 and 2, www.cmaj.ca/lookup/suppl/doi:10.1503/cmaj.140405/-/DC1). Hyperreflexia is also present in the affected limb.

Although not all spasticity is problematic, symptoms can be disabling

Resultant clonus can prevent the use of affected limbs, cause pain or falls and impair gait. In addition, bladder spasticity causes incontinence.1,3 Untreated, spasticity can cause contractures, which can be treated with either orthoses or surgery.

Spasticity can be treated with focal or generalized therapy

Focal treatment includes stretching, bracing and injection of botulinum toxin.5 Generalized treatment includes proper seating and positioning, medications administered orally or intrathecal injection of baclofen.6 Clinical trials have shown no consistent improvement in objective measures of spasticity among patients with spinal cord injury, cerebral palsy or stroke who received baclofen, tizanidine or benzodiazepines orally.7 Evidence supporting the use of such agents for patients with multiple sclerosis is mixed.8

If spasticity worsens, the cause of the change should be sought

Neurologic lesions such as a syrinx or disc compression should be considered in patients with worsening symptoms. In addition, a systematic review suggested that pregnancy, infection, heterotopic ossification and sources of pain such as pressure sores, fractures or ingrown toenails can cause spasticity to worsen.9

Footnotes

References

    1. Maynard FM,
    2. Karunas RS,
    3. Waring WP
    . Epidemiology of spasticity following traumatic spinal cord injury. Arch Phys Med Rehabil 1990;71:566–9.
    1. Lundström E,
    2. Smits A,
    3. Terént A,
    4. et al
    . Time-course and determinants of spasticity during the first months following first-ever stroke. J Rehabil Med 2010;42:296–301.
    1. Rizzo MA,
    2. Hadjimichael OC,
    3. Preiningerova J,
    4. et al
    . Prevalence and treatment of spasticity reported by multiple sclerosis patients. Mult Scler 2004;10:589–95.
    1. Yeargin-Allsopp M,
    2. Van Naarden Braun K,
    3. Doernberg NS,
    4. et al
    . Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics 2008;121:547–54.
    1. Baker JA,
    2. Pereira G
    . The efficacy of botulinum toxin A for spasticity and pain in adults: a systematic review and meta-analysis using the Grades of Recommendation, Assessment, Development, and Evaluation approach. Clin Rehabil 2013;27:1084–96.
    1. Olvey EL,
    2. Armstrong EP,
    3. Grizzle AJ
    . Contemporary pharmacologic treatments for spasticity of the upper limb after stroke: a systematic review. Clin Ther 2010;32:2282–303.
    1. Montané E,
    2. Vallano A,
    3. Laporte JR
    . Oral antispastic drugs in nonprogressive neurologic diseases: a systematic review. Neurology 2004;63:1357–63.
    1. Shakespeare DT,
    2. Boggild M,
    3. Young CA
    . Anti-spasticity agents for multiple sclerosis. Cochrane Database Syst Rev 2003;(4):CD001332.
    1. Phadke PP,
    2. Balasubramanian CK,
    3. Ismail F,
    4. et al
    . Revisiting physiologic and psychologic triggers that increase spasticity. Am J Phys Med Rehabil 2013;92:357–69.