McKenna's Pharmacology for Nursing, 2e

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P A R T 4  Drugs acting on the central and peripheral nervous systems

Myofibrin

KEY POINTS

■■ Movement and muscle control are regulated by spinal reflexes and the upper CNS, including the basal ganglia, cerebellum and cerebral cortex. ■■ Spinal reflexes can be simple, involving an incoming sensory neuron and an outgoing motor neuron, or more complex, involving interneurons that communicate with the related centres in the brain. ■■ The pyramidal tract in the cerebellum coordinates intentional muscle movement, and the extrapyramidal tract in the cerebellum and basal ganglia coordinates involuntary muscle activity. ■■ Muscle or skeletal damage may send a multitude of stimuli to the spinal cord and result in muscle spasms or extended contraction. ■■ Damaged motor neurons can cause muscle spasticity and impaired movement and coordination. CENTRALLY-ACTING SKELETAL MUSCLE RELAXANTS Centrally-acting skeletal muscle relaxants (Table 25.1) include baclofen ( Lioresal ) and orphenadrine ( Norflex ). Diazepam ( Valium ), a drug widely used as an anxiety agent (see Chapter 20), has also been shown to be an effective centrally-acting skeletal muscle relaxant. It may be advantageous in situations in which anxiety may be precipitating the muscle spasm. Other measures in addition to these drugs should be used to alleviate muscle spasm and pain. Such modal- ities as rest of the affected muscle, heat applications to increase blood flow to the area to remove the pain- causing chemicals, physical therapy to return the muscle to normal tone and activity, and anti-inflammatory agents (including non-steroidal anti-inflammatory drugs [NSAIDs]) if the underlying problem is related to injury or inflammation may help. This may be aided by use of a combined product such as orphenadrine and paraceta- mol ( Norgesic ). Therapeutic actions and indications The centrally-acting skeletal muscle relaxants work in the CNS to interfere with the reflexes that are causing the muscle spasm. Because these drugs lyse or destroy spasm, they are often referred to as spasmolytics. Although the exact mechanism of action of these skeletal muscle relax- ants is not known, it is thought to involve action in the upper or spinal interneurons. The primary indication for the use of centrally-acting skeletal muscle agents is the relief of discomfort associated with acute, painful mus- culoskeletal conditions as an adjunct to rest, physical therapy and other measures. Because these drugs work in the upper levels of the CNS, possible depression must

H band I band A band

Sarcomere

Stretched

Myosin Actin

Sarcoplasmic reticulum

Contracted

Transverse tubule

Terminal cisternae

Mitochondria

Muscle fibre

FIGURE 25.2  When stimulation stops, calcium ions are actively transported back into the sarcoplasmic reticulum, resulting in decreased calcium ions in the sarcoplasm. The removal of calcium ions restores the inhibitory action of troponin–tropomyosin; cross-bridge action is impossible in this state.

structures. Because the spasticity is caused by nerve damage in the CNS, it is a permanent condition. Spastic- ity may result from an increase in excitatory influences or a decrease in inhibitory influences within the CNS. The interruption in the balance among all of these higher influences within the CNS may lead to exces- sive stimulation of muscles, or hypertonia , in opposing muscle groups at the same time, a condition that may cause contractures and permanent structural changes. This control imbalance also results in a loss of coordi- nated muscle activity. For example, the signs and symptoms of cerebral palsy and paraplegia are related to the disruption in the nervous control of the muscles. The exact presentation of any chronic neurological disorder depends on the specific nerve centres and tracts that are damaged and how the control imbalance is manifested.