Editorial Views  |   October 2016
Neuropathic Pain: When Nerve Lesion Turns off Peripheral Analgesia
Author Notes
  • From the Department of Biology and Mechanisms of Living Organisms, Université de Montpellier, Place Eugène Bataillon, Montpellier, France; and Institut des Neurosciences de Montpellier, INSERM U1051, Montpellier, France.
  • Corresponding article on page 765.
    Corresponding article on page 765.×
  • Accepted for publication June 28, 2016.
    Accepted for publication June 28, 2016.×
  • Address correspondence to Dr. Rivat: cyril.rivat@umontpellier.fr
Article Information
Editorial Views / Central and Peripheral Nervous Systems / Pain Medicine / Regional Anesthesia
Editorial Views   |   October 2016
Neuropathic Pain: When Nerve Lesion Turns off Peripheral Analgesia
Anesthesiology 10 2016, Vol.125, 627-629. doi:10.1097/ALN.0000000000001262
Anesthesiology 10 2016, Vol.125, 627-629. doi:10.1097/ALN.0000000000001262
PERIPHERAL nerve injury often leads to the development of neuropathic pain that manifests itself in the form of abnormal pain hypersensitivity such as allodynia and hyperalgesia. Pain from damaged or diseased nerves is common worldwide and affects up to 6% of the population.1  The abundant literature dealing with the physiopathologic mechanisms of this disease define numerous alterations in the dorsal root ganglia (DRG) and in the spinal cord and supraspinal structures. These alterations, involving multiple cellular partners, include increased release of pronociceptive molecules, change in gene expression, and remodeling of neural networks. This leads to hyperexcitability of primary nociceptive afferents within the periphery and reorganization of neural networks in the central nervous system. Numerous protein candidates have been suggested as critical for the development of chronic neuropathic pain. However, treatment of neuropathic pain remains unsatisfactory due to the lack of effective pain medications. Importantly, opioids such as morphine cause multiple side effects and have societal consequences. The new report by Zhang et al.,2  is of high interest as it enhances our understanding of the dysregulations that operate after nerve lesion by reporting epigenetic regulation leading to defective endogenous pain inhibition and limited morphine effectiveness. This study may open up novel interventional therapies for the management of neuropathic pain.
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