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Author: Admin | 2025-04-28
Inhibit norepinephrine reuptake in the locus coeruleus, thus providing analgesic effects on chronic nerve and muscle pain at the level of the brainstem.19 Cyclobenzaprine is extensively metabolized by the liver and excreted by the kidneys. Side-effects of cyclobenzaprine include drowsiness, fatigue, dry mouth, headache, dizziness, and blurred vision due to increased intraocular pressure.5 Of note, there is an association of vision damage with long-term use.19 Cyclobenzaprine can cause overdose symptoms of tachycardia, hypertension, widening of the QRS, tremor, slurred speech, confusion, hallucination, and drowsiness.19 Given the structural similarity to TCAs, cyclobenzaprine is contraindicated in patients on or who have taken monoamine oxidase inhibitors (MAOIs) in the past 14 days. If cyclobenzaprine and MAOIs are taken concomitantly, the patient could experience serotonin syndrome, seizures, or even death.19 Other potential drug interactions that may preclude cyclobenzaprine use include other central nervous system depressants (alcohol, barbiturates, etc.), tramadol (due to increased seizure risk), and anti-cholinergic medications.19 Cyclobenzaprine should also be avoided in patients with arrhythmias, conduction disturbances, congestive heart failure, hyperthyroidism and during the recovery period after acute myocardial infarction. There are relative contraindications for cyclobenzaprine in patients with urinary retention, angle-closure glaucoma, or hepatic impairment.19In pediatrics, cyclobenzaprine had been used as a muscle relaxant prior to the 1990s. However, few studies have reviewed the efficacy of cyclobenzaprine in the pediatric population. There have been small sample pediatric studies from the 1990s that demonstrated efficacy of cyclobenzaprine in treatment of fibromyalgia.20,21 The dosing of cyclobenzaprine is extrapolated from adult dosing regimens, with initiation of cyclobenzaprine at 5 mg at bedtime, escalating up to 10 mg, three times a day.19Methocarbamol Methocarbamol is metabolized by the liver, with most of the metabolites excreted in the urine. Notable side-effects include amnesia, confusion, diplopia, dizziness, drowsiness, insomnia, nystagmus, seizures, blurred vision, nasal congestion, metallic taste, rash, bradycardia, hypotension, flushing, thrombophlebitis, dyspepsia, jaundice, and allergic reactions.22 Patients have also noted change in urine coloration, ranging from green to brown to black.1 Overall, methocarbamol can cause significant anticholinergic side-effects that may preclude use. As with other SMRs, methocarbamol can potentiate respiratory depression if combined with benzodiazepines, barbiturates, or opioids. Methocarbamol is contraindicated in patients with myasthenia gravis as methocarbamol can inhibit pyridostigmine and other acetylcholinesterase inhibitors.22 Thus, methocarbamol can worsen symptoms of myasthenia gravis. Of interest, the urinary metabolites can interfere with 5-hydroxyindoleacetic acid (5-HIAA) and vanillylmandelic acid (VMA) testing.22Methocarbamol is available in both PO and IV formulation, permitting the transition from IV to PO regimen in the acute post-operative setting. Methocarbamol has been used frequently in the post-operative pain management setting to reduce post-surgical muscle spasms pain. Adult studies as far back as the 1950s demonstrated the use of methocarbamol for severe paravertebral and trapezius muscle spasm after
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