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Objectives

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OBJECTIVES

After reading this chapter, the reader will be able to:

  • Differentiate among spasticity, tone, hyperreflexia, and rigidity

  • Describe spasticity and its associated signs

  • Discuss ways that spasticity may be beneficial and ways that spasticity can be problematic

  • Explain clinical tests that are used to quantify spasticity

  • Discuss some of the physical treatments that have been shown to reduce spasticity

  • Compare and contrast the medications that are commonly used to treat spasticity

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Introduction

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Tone, Hyperreflexia, and Spasticity

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Damage to the central nervous system frequently results in pathophysiology of the motor control system. One consequence of this pathophysiology is an alteration in the regulation of muscle tone, such that tone is increased (i.e., hypertonia) or decreased (i.e., hypotonia). Muscle tone is the resting tension in a muscle that is evidenced by its resistance to the elongation associated with imposed movement at a joint. Tone reflects both the balance of excitatory and inhibitory influences on the spinal motoneuron innervating the muscle and the intrinsic elastic properties of the muscle itself. When the neuropathology involves damage to the upper motor neurons or their descending pathways, there is a loss of modulation of spinal reflexes such that these reflexes become more responsive to afferent (sensory) input. This increased responsiveness of spinal reflex activity is termed hyperreflexia and contributes to involuntary muscle contractions (spasms) in response to afferent input.

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One form of hyperreflexia, spasticity, has historically been associated with increased responsiveness of the monosynaptic stretch reflex. The monosynaptic stretch reflex (also called the deep tendon reflex, the Ia reflex, and the phasic stretch reflex) is one of many spinal reflexes, but by virtue of being monosynaptic (i.e., having only a single synapse between the afferent and efferent limb of the reflex arc), it gives rise to motor responses to afferent input (in this case the afferent input being muscle stretch) that are among the fastest responses in the nervous system. The classical definition of spasticity as being "a velocity-dependent increase in resistance to passive stretch,"1 reflects the supposed relationship between the monosynaptic stretch reflex and spasticity.

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Characterizing Spasticity

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Despite the historical attribution of spasticity to impaired regulation of the monosynaptic stretch reflex, it is well recognized that the signs associated with spasticity may occur in response to forms of afferent input other than muscle stretch (e.g., cutaneous input such as touch of the skin or prick from a sharp object and mechanical input such as pulling of the hair on the limb). Thus, in the clinic, involuntary contractions and other associated signs (i.e., clonus, clasped-knife phenomenon, flexor reflexes, extensor spasms, irradiation of spasms, unusual co-contractions during movements) have also been labeled as spasticity, thereby extending the classical definition.2,3,4,5,6 This group of signs in combination with muscle weakness due to impaired voluntary control in ...

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