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Spasticity is traditionally defined as “a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflexes, as one component of the upper motor neuron syndrome” (Lance 1980). Spasticity is quite commonly confused with tremor, rigidity, clonus, dystonia and various movement disorders (i.e., athetoid, ballisms, and chorea). One of the earliest examples of this confusion is the term “spastic rigidity” used to refer to “excessive muscular contraction” first published in 1843 (Little WJ). Attempts to clarify this confusion have resulted in the most recent definition published by Pandyan et al. (2005) (adapted from Tardieau et al. 1954) as follows: “disordered sensorimotor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscle”.  This definition is intended to be more inclusive of clinical signs and symptoms of “spasticity” but has yet to be validated for clinical relevance.

Regardless of the definitions presented, each eludes to various inter-related components of the upper motor neurone syndrome (i.e., tone, clonus, spasms, spastic dystonia and co-contractions). Therefore, a thorough clinical assessment of spasticity should always be undertaken as follows (Kheder & Nair 2012): 1) differentiate spasticity from other causes of increased tone, 2) identify potential triggers, 3) measure spasticity, 4) assess spasticity’s impact on function, and 5) gather input from individuals, caregivers, therapists and other rehabilitation professionals. Spasticity is not static and therefore, assessments should be done regularly and combined with establishing goals of treatment to make decisions regarding treatment strategy (Rekand et al. 2012).

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