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Skeletal muscle relaxants are used to treat conditions associated with hyperexcitable skeletal muscle—specifically, spasticity and muscle spasms. Although these two terms are often used interchangeably, spasticity and muscle spasms represent two distinct abnormalities. However, the use of relaxant drugs is similar in each condition because the ultimate goal is to normalize muscle excitability without a profound decrease in muscle function.

Skeletal muscle relaxants are important when one considers the large number of rehabilitation patients with muscle hyperexcitability that is associated with either spasm or spasticity. Likewise, certain rehabilitation interventions complement the actions of muscle relaxant drugs. For example, therapists often use therapeutic exercise, physical agents, and other techniques to help reduce muscle spasms and spasticity. These interventions can supplement drug effects, thus enhancing muscle relaxation and enabling the patient to engage more actively in physical rehabilitation. You should therefore understand the actions and effects of skeletal muscle relaxants to take advantage of the synergy between drug therapy and physical interventions.

The drugs discussed in this chapter decrease muscle excitability and contraction by acting at the spinal cord level, at the neuromuscular junction, or within the muscle cell itself. Some texts also classify neuromuscular junction blockers such as curare derivatives and succinylcholine as skeletal muscle relaxants. However, these drugs are more appropriately classified as skeletal muscle paralytics because they eliminate muscle contraction by blocking transmission at the myoneural synapse. This type of skeletal muscle paralysis is used primarily during general anesthesia (see Chapter 11). Skeletal muscle relaxants do not typically prevent muscle contraction; they only attempt to normalize muscle excitability to decrease pain and improve motor function.


Much confusion and consternation often arise from the erroneous use of the terms spasticity and spasm. For the purpose of this text, these terms will be used to describe two different types of increased excitability, which result from different underlying pathologies.

Spasticity occurs in many patients following an injury to the central nervous system (CNS), including cord-related problems (e.g., multiple sclerosis, spinal cord transection) and injuries to the brain (e.g., cerebrovascular accident [CVA], cerebral palsy, acquired brain injury). Although there is considerable controversy about the exact changes in motor control, most clinicians agree that spasticity is characterized primarily by an exaggerated muscle stretch reflex (Fig. 13-1).1,2 This abnormal reflex activity is velocity-dependent, with a rapid lengthening of the muscle invoking a strong contraction in the stretched muscle.

Figure 13-1

Schematic illustration of the basic components of the stretch reflex. Normally, higher CNS centers control the sensitivity of this reflex by inhibiting synaptic connections within the spinal cord. Spasticity is thought to occur when this higher center influence is lost because of cerebral trauma or damage to descending pathways in the spinal cord.

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