Most compounds in this group act as simple sedative-hypnotic agents that provide skeletal muscle relaxation indirectly. The drugs commonly used as skeletal muscle relaxants are listed in Table II–55. Carisoprodol (Soma) and baclofen have been abused as recreational drugs.
Table II-55 Skeletal Muscle Relaxants |Favorite Table|Download (.pdf)
Table II-55 Skeletal Muscle Relaxants
Usual Half-life (h)
Usual Daily Adult Dose (mg)
Mechanism of toxicity
Central nervous system. Most of these drugs cause generalized CNS depression.
is an agonist at the GABA(B) receptor and can produce profound CNS and respiratory depression as well as paradoxical muscle hypertonicity and seizure-like activity. Hallucinations, seizures, and hyperthermia have occurred after abrupt withdrawal from baclofen.
Spastic encephalopathy is also common with
Tizanidine, a centrally acting alpha2 agonist, has effects similar to those of clonidine (See Clonidine and Related Drugs).
Cardiovascular effects. Hypotension may occur after overdose.
has caused bradycardia in up to 30% of ingestions. Massive
ingestions have caused supraventricular and ventricular tachycardia.
Pharmacokinetics varies with the drug. Absorption may be delayed because of anticholinergic effects (see also Table II–61).
Toxic dose. The toxic dose varies considerably among drugs, depends largely on individual tolerance, and can be influenced by the presence of other drugs, such as ethanol. For most of these drugs, ingestion of more than 3–5 times the usual therapeutic dose may cause stupor or coma. Death was reported in a 4-year-old who ingested approximately 3500 mg of carisoprodol, and a 2-year-old who ingested two tablets (350 mg each) required intubation. A 2-year-old developed seizures and ventricular tachycardia after ingesting 400 mg of orphenadrine. The lowest dose of tizanidine associated with coma in an adult was between 60 and 120 mg.
Clinical presentation. Onset of CNS depression usually is seen within 30–120 minutes of ingestion. Lethargy, slurred speech, ataxia, coma, and respiratory arrest may occur. Larger ingestions, especially when combined with alcohol, can produce unresponsive coma.
may cause hyperreflexia, opisthotonus, and increased muscle tone.
can produce anticholinergic findings such as tachycardia, dilated pupils, and delirium. Despite its structural similarity to tricyclic antidepressants, cyclobenzaprine has not been reported to cause quinidine-like cardiotoxicity, although it can cause hypotension. Status epilepticus, ventricular tachycardia, and asystolic arrest have been reported after
overdose causes coma, respiratory depression, bradycardia, and paradoxical seizure-like activity. Onset is rapid but may last 12–48 hours. Prolonged delirium with rhabdomyolysis has been reported.
is similar to clonidine and can cause coma, profound hypotension, and bradycardia (See Clonidine and Related Drugs); in addition, sinoatrial (SA) and atrioventricular (AV) nodal dysfunction was reported after an overdose.
Diagnosis usually is based on the history of ingestion and findings of CNS ...