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Magnesium’s Analgesic Effects are Independent of Serum Concentration

We appreciate the response to our recent article and the opportunity to offer a rebuttal. The commentator’s contention with the inclusion of magnesium deficient and nondeficient patients in trials is rooted in a fundamental misunderstanding of the mechanism. The parallels drawn are nonsensical and unfounded. Such logic would dictate that patients with eclampsia or torsades de pointes should not be treated with magnesium, if they are not known to be deficient. Magnesium’s analgesic effects, when administered as a bolus, are independent of the patient’s serum magnesium level. Magnesium’s analgesic effects are thought to be mediated through antagonism of the N-methyl-daspartate receptor. It is also known to block calcium channels, thereby inhibiting calcium influx and interfering with sensory processing which results in antinociception. In this way, magnesium can alter central hypersensitivity and decrease opioid consumption. Magnesium’s analgesic effects, when administered as a bolus, is independent of the patient’s serum magnesium level. For this reason, it has been utilized as an analgesic for pain of varied etiologies in acute care and perioperative settings. Of note, this is also the proposed reason for the prolonged analgesic effect when administered concomitantly with low dose ketamine for cluster headache. Andrew C. Miller, MD Department of Emergency Medicine, Vidant Medical Center, East Carolina University – Brody School of Medicine, Greenville, NC, USA