Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
, 19 (3), 125-32

Neuropathic Pain: Role of Inflammation, Immune Response, and Ion Channel Activity in Central Injury Mechanisms

Affiliations
Review

Neuropathic Pain: Role of Inflammation, Immune Response, and Ion Channel Activity in Central Injury Mechanisms

Dominic Schomberg et al. Ann Neurosci.

Abstract

Neuropathic pain (NP) is a significant and disabling clinical problem with very few therapeutic treatment options available. A major priority is to identify the molecular mechanisms responsible for NP. Although many seemingly relevant pathways have been identified, more research is needed before effective clinical interventions can be produced. Initial insults to the nervous system, such as spinal cord injury (SCI), are often compounded by secondary mechanisms such as inflammation, the immune response, and the changing expression of receptors and ion channels. The consequences of these secondary effects myriad and compound those elicited by the primary injury. Chronic NP syndromes following SCI can greatly complicate the clinical treatment of the primary injury and result in high comorbidity. In this review, we will describe physiological outcomes associated with SCI along with some of the mechanisms known to contribute to chronic NP development.

Keywords: CB1/CB2; Cannabinoid Receptors; MMPs; Microglia; NKCC-1; Nitric Oxide; TRPV-1.

Conflict of interest statement

Competing interests – None

Figures

Fig. 1:
Fig. 1:
Summary of major NP contributors.

Similar articles

See all similar articles

Cited by 15 PubMed Central articles

See all "Cited by" articles

References

    1. Yezierski RP. Pain following spinal cord injury: the clinical problem and experimental studies. Pain. 1996;68(2–3):185–194. - PubMed
    1. Vranken JH. Mechanisms and treatment of neuropathic pain. Cent Nerv Syst Agents Med Chem. 2009;9(1):71–78. - PubMed
    1. Kumru H, Kofler M, Portell E et al. Alterations in excitatory and inhibitory brainstem interneuronal circuits after severe spinal cord injury. J Neurotrauma. 2010;27(4):721–728. - PubMed
    1. Seltzer Z, Dubner R, Shir Y. A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury. Pain. 1990;43:205–218. - PubMed
    1. Decosterd I, Woolf CJ. Spared nerve injury: an animal model of persistent peripheral neuropathic pain. Pain. 2000;87(2):149–158. - PubMed

LinkOut - more resources

Feedback