Indications
Methocarbamol is utilized in the United States primarily as an adjunct to rest, physical therapy, and additional interventions aimed at alleviating·h acute, painful musculoskeletal conditions. It is typically administered in oral or intramuscular injection forms. In the U.S., the oral dosage may reach up to 1500 mg, taken four times daily for a period of two to three days. In Canada, methocarbamol is available over the counter in oral formulations for managing·hough combinations containing·harmacodynamics
As a skeletal muscle relaxant, methocarbamol has a mechanism of action that is not fully understood. However, it has been observed to inhibit spinal polysynaptic reflexes, decrease nerve transmission in both spinal and supraspinal polysynaptic pathways, and extend the refractory period of muscle cells. Importantly, methocarbamol does not function as a local anesthetic when administered via injection. Animal studies also indicate its potential in preventing·hock.
Absorption
Methocarbamol reaches peak concentration in approximately 1.1 hours in both healthy individuals and patients undergoing·hemodialysis. The maximum plasma concentrations observed are 21.3 mg/L and 28.7 mg/L, respectively. The area under the curve (AUC) is measured at 52.5 mg/L*hr for healthy individuals and 87.1 mg/L*hr for those on hemodialysis. The percentage AUC based on the terminal elimination half-life is 2% in healthy individuals and 4% in those receiving·hemodialysis treatment. Some older studies have noted maximum plasma concentrations occurring·hin 0.5 hours.
Metabolism
Methocarbamol undergoes hepatic metabolism primarily through demethylation, resulting·hydroxyphenoxy)-1,2-propanediol-1-carbamate, or through hydroxylation, producing·hydroxy-2-methoxyphenoxy)-1,2-propanediol-1-carbamate. Both methocarbamol and its metabolites undergo conjugation via glucuronidation or sulfation pathways.
Mechanism of Action
Methocarbamol operates primarily through its depressant effects on the central nervous system. It is believed that this activity is achieved by inhibiting spinal polysynaptic reflexes and reducing nerve transmission across spinal and supraspinal polysynaptic pathways. Additionally, methocarbamol extends the refractory period of muscle cells. Importantly, it does not influence the contraction of muscle fibers, affect motor end plates, or alter nerve fiber functionality.
