Carisoprodol is a muscle relaxant that does not directly relax tense skeletal muscles in man. Although not well understood, the mechanism of action of carisoprodol in humans may be related to its sedative properties, either directly or indirectly, via the effects of meprobamate.
In animals, carisoprodol produces muscle relaxation by blocking interneuronal activity in the descending reticular formation and spinal cord. However, it is unknown if this mechanism of action is also present in humans 1. Carisoprodol’s primary metabolite, meprobamate, has barbiturate like modulatory effects on GABA-A receptors . However, it is unclear whether the GABA-A receptor-like effects are from carisoprodol itself or its metabolite meprobamate.
The pharmacological effects of carisoprodol appear to be due to the combination of the effects of carisoprodol and meprobamate. In addition to the desired skeletal muscle-relaxing effects, carisoprodol also produces weak anticholinergic, antipyretic, and analgesic effects. High doses of carisoprodol may induce symptoms that are similar to the symptoms associated with serotonin syndrome .
Muscle relaxant action. It produces muscle relaxation by affecting the central nervous system. It is possible that carisoprodol induced muscle relaxation results from a slight depression of all neurons at synaptic junctions within the central nervous system. It is noteworthy that this agent has a marked depressant effect on hyperactive spinal reflexes in doses that do not affect normal reflexes.
Analgesic action. The pain-relieving properties of carisoprodol are distinctive and in certain respects are different from the actions of either the opium alkaloids, or the antipyretic-analgesics such as aspirin and paracetamol. The analgesic action of any drug may be due to its effect on:
- peripheral pain receptors
- the sensory pain pathways and their synapses
- the centers concerned with pain receptors or sensory pain pathways and that it probably acts upon centers concerned with pain perception.
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