Centrally acting skeletal muscle relaxants

Centrally acting skeletal muscle relaxants

Centrally acting skeletal muscle relaxants, which act on the CNS,are used to treat acute spasms caused by such conditions as:

·                 anxiety

·                 inflammation

·                 pain

·                 trauma.

For intermittent or chronic spasms

A patient with intermittent or chronic spasms may receive tizani-dine.

For acute spasms

A patient with acute muscle spasms may receive one of these drugs:

·                 carisoprodol

·                 chlorzoxazone

·                 cyclobenzaprine

·                 metaxalone

·                 methocarbamol

·                 orphenadrine

·                 tizanidine.

Pharmacokinetics (how drugs circulate)

There’s still a lot we don’t know about how centrally acting skele-tal muscle relaxants circulate within the body. In general, these drugs are absorbed from the GI tract, widely distributed in the body, metabolized in the liver, and excreted by the kidneys.

Cyclobenzaprine sticks around

When these drugs are administered orally, it can take from 30 min-utes to 1 hour for effects to be achieved. The duration of action of most of these drugs varies from 4 to 6 hours; cyclobenzaprine has the longest duration of action, at 12 to 25 hours.

Pharmacodynamics (how drugs act)

The centrally acting drugs don’t relax skeletal muscles directly or depress neuronal conduction, neuromuscular transmission, or muscle excitability. Although their precise mechanism of action is unknown, these drugs are known to be CNS depressants. Their muscle relaxant effects may be related to their sedative effects.

Pharmacotherapeutics (how drugs are used)

Patients receive centrally acting skeletal muscle relaxants to treat acute, painful musculoskeletal conditions. They’re usually pre-scribed along with rest and physical therapy.

Drug interactions

The centrally acting skeletal muscle relaxants interact with other CNS depressants (including alcohol, narcotics, barbiturates, anti-convulsants, tricyclic antidepressants, kava kava, and antianxiety drugs), causing increased sedation, impaired motor function, and respiratory depression. In addition, some of these drugs have oth-er interactions:

o       Cyclobenzaprine interacts with monoamine oxidase inhibitors (MAOIs) and can result in a high body temperature, excitation, and seizures.

o       Cyclobenzaprine can decrease the antihypertensive effects of the blood pressure–lowering drugs guanethidine and clonidine.

o       Orphenadrine and cyclobenzaprine sometimes enhance the ef-fects of cholinergic-blocking drugs.

o       Methocarbamol can antagonize the cholinergic effects of the an-ticholinesterase drugs used to treat myasthenia gravis.

o       Orphenadrine can reduce the effects of phenothiazines.

o       Orphenadrine and propoxyphene taken together can cause addi-tive CNS effects, including mental confusion, anxiety, and tremors. (See Adverse reactions to centrally acting skeletal mus-cle relaxants)

Tizanidine combined with diuretics, central alpha-adrenergic ag-onists, or antihypertensives may increase hypotensive drug ef-fects. Concurrent use of tizanidine with CNS depressants may cause additive CNS depression. Hormonal contraceptives may re-duce the clearance of tizanidine, necessitating a dosage reduction.