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, 7 (4), 331-6

Serotonin-norepinephrine Reuptake Inhibitors for Pain Control: Premise and Promise

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Serotonin-norepinephrine Reuptake Inhibitors for Pain Control: Premise and Promise

David M Marks et al. Curr Neuropharmacol.

Abstract

The precise mechanisms of pain perception and transmission in the central nervous system have not been fully elucidated. However, extensive data support a role for the monoamine neurotransmitters, serotonin and norepinephrine, in the modulation of pain. Experiments with animal models of pain indicate that noradrenergic interventions, and to a lesser extent serotonergic interventions, reduce pain-related behavior. This is supported by data from clinical trials in humans in which antidepressants have been shown to reduce pain and functional impairment in central and neuropathic pain conditions. These effects are particularly well-studied in trials with serotonin-norepinephrine reuptake inhibitors (SNRIs), which have provided a useful tool in the clinician's arsenal, particularly considering the limitations of other classes of pain medications such as opioids, anti-inflammatories, and anticonvulsants (i.e., limited efficacy, safety and tolerability issues). Moreover, painful physical symptoms are frequently comorbid with major psychiatric disorders such as major depressive disorder and anxiety disorders. This paper reviewed and summarized the rationale and potential role of SNRIs for the control of pain including clinical and preclinical background. Currently evidence does not definitely support a role of the SNRIs, while limited data propose a putative promise of SNRIs in the treatment of pain related disorders including fibromyalgia and depressed patients with multiple somatic complaints. More researches are warranted to generalize currently available preliminary evidences.

Keywords: Role; SNRIs; modulation; norepinephrine; pain control; pain pathways.; serotonin.

Figures

Fig. (1)
Fig. (1)
Circuit of pain modulatory pathway. Abbreviations: 5-HT, serotonin; NE, norepinephrine. Thick arrow indicates ascending pain pathway and thin arrow represents descending inhibitory pain pathway.

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References

    1. Arnold LM, Lu Y, Crofford LJ, Wohlreich M, Detke MJ, Iyengar S, Goldstein DJ. A double-blind, multicenter trial comparing duloxetine with placebo in the treatment of fibromyalgia patients with or without major depressive disorder. Arthritis Rheum. 2004;50:2974–2984. - PubMed
    1. Arnold LM, Pritchett YL, D'Souza DN, Kajdasz DK, Iyengar S, Wernicke JF. Duloxetine for the treatment of fibromyalgia in women: pooled results from two randomized, placebo-controlled clinical trials. J. Womens Health, (Larchmt) 2007;16:1145–1156. - PubMed
    1. Arnold LM, Rosen A, Pritchett YL, D'Souza DN, Goldstein DJ, Iyengar S, Wernicke JF. A randomized, double-blind, placebo-controlled trial of duloxetine in the treatment of women with fibromyalgia with or without major depressive disorder. Pain. 2005;119:5–15. - PubMed
    1. Beique JC, de Montigny C, Blier P, Debonnel G. Venlafaxine: discrepancy between in vivo 5-HT and NE reuptake blockade and affinity for reuptake sites. Synapse. 1999;32:198–211. - PubMed
    1. Bymaster FP, Dreshfield-Ahmad LJ, Threlkeld PG, Shaw JL, Thompson L, Nelson DL, Hemrick-Luecke SK, Wong DT. Comparative affinity of duloxetine and venlafaxine for serotonin and norepinephrine transporters in vitro and in vivo, human serotonin receptor subtypes, and other neuronal receptors. Neuropsychopharmacology. 2001;25:871–880. - PubMed

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