Abstract
Spasticity is generally defined as velocity-dependent increased resistance during passive movement of peripheral joints owing to increased involuntary muscle activity. However, the word spasticity is clinically used to describe a constellation of symptoms that arise secondary to the upper motor neuron (UMN) syndrome associated with a wide variety of neurological conditions. The clinically observed components of spasticity include increased resistance to passive movement, increased phasic-stretch reflexes, clonus, and flexor or extensor spasms (1–3). These features of spasticity clearly can impede functional motor activities. However, the UMN syndrome includes other important components including weakness, co-contraction of agonist and antagonist muscles, the presence of “pattern” movements (mass contraction of groups of muscles across joints when isolated movements are attempted), and lack of fine motor control. These other components of the UMN syndrome usually contribute more to motor impairment than spasticity. Spasticity is actually beneficial in certain situations. For example, increased extensor tone may facilitate standing in some patients. Theoretical benefits of spasticity include maintenance of muscle mass, reduction of edema, decreased risk of deep venous thrombosis (DVT), and prevention of bone demineralization in weakened extremities (1).
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Good, D.C. (2002). Measurement of Spasticity. In: Gelber, D.A., Jeffery, D.R. (eds) Clinical Evaluation and Management of Spasticity. Current Clinical Neurology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-092-6_3
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DOI: https://doi.org/10.1007/978-1-59259-092-6_3
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