Abstract

Several lines of evidence developed in preclinical models suggest that both spontaneous and evoked pain are mediated in part by voltage-sensitive sodium and calcium channels, which are in abundance in both the peripheral and the central nervous system. There is an abundance of research, both preclinical and clinical, on the effects of the sodium and calcium channel antagonists on nociceptive processing. Clinical studies on the efficacy of the sodium channel antagonists in the treatment of acute and chronic pain have had mixed results. Preliminary studies of the N-type calcium channel antagonists for the treatment of acute and chronic pain are promising but too early to enable researchers to make firm conclusions. This review summarizes the current literature on the effects of the sodium and calcium channel antagonists on acute nociceptive processing, facilitated pain, and neuropathic pain.

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