Drugs for muscle spasm and spasticity

Drugs for muscle spasm and spasticity

In this chapter we consider two groups of drugs that cause skeletal muscle relaxation. One group is used for localized muscle spasm. The other is used for spasticity. With only one exception (dantrolene), these drugs produce their effects through actions in the central nervous system (CNS). As a rule, the drugs used to treat spasticity do not relieve acute muscle spasm and vice versa. Hence, the two groups are not interchangeable.

Drug therapy of muscle spasm: centrally acting muscle relaxants

Muscle spasm is defined as involuntary contraction of a muscle or muscle group. Muscle spasm is often painful and reduces the ability to function. Spasm can result from a variety of causes, including epilepsy, hypocalcemia, acute and chronic pain syndromes, and trauma (localized muscle injury). Discussion here is limited to spasm resulting from muscle injury.

Treatment of spasm involves physical measures as well as drug therapy. Physical measures include immobilization of the affected muscle, application of cold compresses, whirlpool baths, and physical therapy. For drug therapy, two groups of medicines are used: (1) analgesic anti-inflammatory agents (eg, aspirin), and (2) centrally acting muscle relaxants. The analgesic anti-inflammatory agents are discussed in Chapter 71. The centrally acting muscle relaxants are discussed below.

The family of centrally acting muscle relaxants consists of 9 drugs (Table 25–1). All have similar pharmacologic properties. Hence, we will consider these agents as a group.

TABLE 25–1

Drugs for Muscle Spasm: Centrally Acting Muscle Relaxants

Generic Name	Trade Names	Usual Adult Oral Maintenance Dosage
Baclofen	Lioresal	15–20 mg 3 or 4 times/day
Carisoprodol	Soma	350 mg 3 or 4 times/day
Chlorzoxazone	Paraflex, Parafon Forte DSC, Remular-S, Relax-DS	250 mg 3 or 4 times/day
Cyclobenzaprine	Flexeril, Fexmid	10 mg 3 times/day
Cyclobenzaprine ER*	Amrix	15 or 30 mg once daily
Diazepam	Valium	2–10 mg 3 or 4 times/day
Metaxalone	Skelaxin	800 mg 3 or 4 times/day
Methocarbamol	Robaxin	1000 mg 4 times/day
Orphenadrine	Banflex, Flexon, Norflex	100 mg morning and evening
Tizanidine	Zanaflex	4 mg 3 or 4 times/day

^*ER = extended release.

Mechanism of action

For most centrally acting muscle relaxants, the mechanism of spasm relief is unclear. In laboratory animals, high doses can depress spinal motor reflexes. However, these doses are much higher than those used in humans. Hence, many investigators believe that relaxation of spasm results primarily from the sedative properties of these drugs, and not from specific actions exerted on CNS pathways that control muscle tone.

Two drugs—diazepam and tizanidine—are thought to relieve spasm by enhancing presynaptic inhibition of motor neurons in the CNS. Diazepam promotes presynaptic inhibition by enhancing the effects of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter. Tizanidine promotes inhibition by acting as an agonist at presynaptic alpha₂ receptors.

Therapeutic use

The centrally acting muscle relaxants are used to relieve localized spasm resulting from muscle injury. These agents can decrease local pain and tenderness and can increase range of motion. Treatment is almost always associated with sedation. Benefits of treatment equal those of aspirin and the other analgesic anti-inflammatory drugs. Since there are no studies to indicate the superiority of one centrally acting muscle relaxant over another, drug selection is based largely on prescriber preference and patient response. With the exception of diazepam, the central muscle relaxants are not useful for treating spasticity or other muscle disorders resulting from CNS pathology.

Adverse effects

CNS depression.

All of the centrally acting muscle relaxants can produce generalized depression of the CNS. Drowsiness, dizziness, and lightheadedness are common. Patients should be warned not to participate in hazardous activities (eg, driving) if CNS depression is significant. In addition, they should be advised to avoid alcohol and all other CNS depressants.

Hepatic toxicity.

Tizanidine [Zanaflex] and metaxalone [Skelaxin] can cause liver damage. Liver function should be assessed before starting treatment and periodically thereafter. If liver injury develops, these drugs should be discontinued. If the patient has pre-existing liver disease, these drugs should be avoided.

Chlorzoxazone [Paraflex, Parafon Forte DSC, others] can cause hepatitis and potentially fatal hepatic necrosis. Because of this potential for harm, and because the benefits of chlorzoxazone are questionable, the drug should not be used.

Physical dependence.

Chronic, high-dose therapy can cause physical dependence, manifesting as a potentially life-threatening abstinence syndrome if these drugs are abruptly withdrawn. Accordingly, withdrawal should be done slowly.

Drugs for spasticity

The term spasticity refers to a group of movement disorders of CNS origin. These disorders are characterized by heightened muscle tone, spasm, and loss of dexterity. The most common causes are multiple sclerosis and cerebral palsy. Other causes include traumatic spinal cord lesions and stroke. Spasticity is managed with a combination of drugs and physical therapy.

Three drugs—baclofen, diazepam, and dantrolene—can relieve spasticity. Two of these—baclofen and diazepam—act in the CNS. In contrast, dantrolene acts directly on skeletal muscle. With the exception of diazepam, the drugs employed to treat muscle spasm (ie, the centrally acting muscle relaxants) are not effective against spasticity.

Baclofen

Mechanism of action

Baclofen [Lioresal] acts within the spinal cord to suppress hyperactive reflexes involved in regulation of muscle movement. The precise mechanism of reflex attenuation is unknown. Since baclofen is a structural analog of the inhibitory neurotransmitter GABA (Fig. 25–1), it may act by mimicking the actions of GABA on spinal neurons. Baclofen has no direct effects on skeletal muscle.

Figure 25–1 Structural similarity between baclofen and gamma-aminobutyric acid (GABA).

Figure 25–1 Structural similarity between baclofen and gamma-aminobutyric acid (GABA).

Therapeutic use

Baclofen can reduce spasticity associated with multiple sclerosis, spinal cord injury, and cerebral palsy—but not with stroke. The drug decreases flexor and extensor spasms and suppresses resistance to passive movement. These actions reduce the discomfort of spasticity and allow increased performance. Because baclofen has no direct muscle-relaxant action, and hence does not decrease muscle strength, baclofen is preferred to dantrolene when spasticity is associated with significant muscle weakness. Baclofen does not relieve the spasticity of Parkinson’s disease or Huntington’s chorea.

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Tags: Pharmacology for Nursing Care

Jul 24, 2016 | Posted by admin in NURSING | Comments Off

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