Peripheral nerve injuries and diseases often lead to pain persisting beyond the resolution of damage, indicating an active disease-promoting process, which may result in chronic pain. This is regarded as a maladaptive mechanism resulting from neuroinflammation that originally serves to promote regeneration and healing. Knowledge on these physiological and pathophysiological processes has accumulated over the last few decades and has started to yield potential therapeutic targets. Key players are macrophages, T-lymphocytes, cytokines, and chemokines. In the spinal cord and brain, microglia and astrocytes are involved. Recently, data have been emerging on the regulation of these players. MicroRNAs and other noncoding RNAs have been discussed as potential master switches that may link nerve injury, pain, and inflammation. Clinical disorders most intensely studied in the context of neuroinflammation and pain are the complex regional pain syndrome, polyneuropathies, postherpetic neuralgia, and the fibromyalgia syndrome, in which recently a neuropathic component has been described. Research from several groups has shown an important role of both proinflammatory and anti-inflammatory cytokines in neuropathic and other chronic pain states in humans. There is ample evidence of an analgesic action of anti-inflammatory cytokines in animal models. The interplay of anti-inflammatory cytokines and the nociceptive system provides possibilities and challenges concerning treatment strategies based on this concept.
Neuroinflammation plays an important role in pain. Clinical disorders most intensely studied in this context are the complex regional pain syndrome, polyneuropathies, postherpetic neuralgia, and the fibromyalgia syndrome. The interplay of anti-inflammatory cytokines and the nociceptive system provides possibilities and challenges concerning treatment strategies based on this concept.
aDepartment of Neurology, University of Würzburg, Würzburg, Germany
bDepartment of Anesthesiology, Washington University School of Medicine, St. Louis, MO, USA
Corresponding author. Address: Claudia Sommer, MD, Department of Neurology, University of Würzburg, Josef-Schneider-Straße 11, 97080 Würzburg, Germany. Tel.: +49-931-201-23763; fax: +49-931-201-623763. E-mail address: firstname.lastname@example.org.
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Received October 25, 2017
Received in revised form November 19, 2017
Accepted November 22, 2017