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Drugs that affect skeletal muscles fall into two major therapeutic groups: those used during surgical procedures and in intensive care units to cause paralysis (i.e., neuromuscular blockers), and those used to reduce spasticity in a variety of neurologic conditions or to reduce muscle spasm following muscle injury or inflammation (i.e., spasmolytics) (Figure 33–1). Neuromuscular blocking drugs interfere with transmission at the neuromuscular end plate and lack central nervous system activity. These compounds are used primarily as adjuncts to general anesthesia. Drugs in the spasmolytic group have traditionally been called “centrally acting” muscle relaxants because most of them act at multiple sites in the central nervous system (CNS) rather than at the neuromuscular end plate. However, two spasmolytic drugs—dantrolene and botulinum toxin—act in or near skeletal muscle with no significant central effects. Spasmolytic drugs (with one exception) do not prevent muscle contraction but rather decrease neuronal excitability. For basic and clinical pharmacology of neuromuscular blocking drugs, see Chapter 5.

Figure 33–1.

Skeletal muscle relaxants in this chapter may be initially divided into those used acutely to reduce muscle spasms, and those used chronically to treat central nervous system (CNS) associated spasticity. The latter group are subsequently divided into those which act within the CNS, and those that act at the muscle.

Spasticity is characterized by an increase in tonic stretch reflexes and flexor muscle spasms (i.e., increased basal muscle tone), together with muscle weakness and a reduction in viscoelastic muscle properties. It is often associated with cerebral palsy, multiple sclerosis, spinal cord injury, and stroke. These conditions often involve abnormal function of the bowel and bladder as well as skeletal muscle. The mechanisms underlying spasticity in these types of neurologic injury appear to involve not only the stretch reflex arc itself but also higher centers in the CNS (upper motor neuron lesions), with damage to descending pathways in the spinal cord, resulting in loss of supraspinal inhibition to the alpha and gamma motor neurons in the anterior horn of the spinal cord. With damage to descending pathways, upper motor neurons from the cerebral cortex and brain stem nuclei no longer modulate spinal reflexes, and no longer activate the spinal cord inhibitory interneuron pools. The decrease in activity in the inhibitory interneurons results in increased excitability of alpha motor neurons in the cord. Some of the components involved in these descending inhibitory pathways are shown in Figure 33–2.

Figure 33–2.

Input to alpha motor neurons. S = sensory primary afferent; I = brain stem interneuron; + = excitatory synapse; – = inhibitory synapse.

Pharmacologic therapy can ameliorate some of the signs and symptoms of neurologic injury spasticity by modifying the stretch reflex arc or, in the case of dantrolene, by interfering directly with skeletal muscle (i.e., excitation-contraction coupling). The ...

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