Articles: neuralgia.
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Neuropathic pain typically appears in a region innervated by an injured or diseased nerve and, in some instances, also on the contralateral side. This so-called mirror image pain is often observed in mice lacking CB2 receptors after sciatic nerve injury, but the underlying mechanisms for this phenotype largely remain unclear. Here we focused on peripheral leptin signaling, which modulates neuropathic pain development and interacts with the endocannabinoid system. ⋯ Interestingly, an upregulation of leptin receptor expression STAT3 activity and macrophage infiltration was also observed on the non-injured nerve of CB2-KO mice thus reflecting the mirror image pain in CB2-KO animals. Importantly, perineurally-administered leptin-neutralizing antibodies reduced mechanical hyperalgesia, blocked mirror image pain and inhibited the recruitment of F4/80-positive macrophages. These results identify peripheral leptin signaling as an important modulator of CB2 signaling in neuropathic pain.
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Case Reports
Conservative Management of Neuropathic Pain in a Patient With Pancoast-Tobias Syndrome: A Case Report.
Pancoast-Tobias syndrome characterizes the signs and symptoms of a superior pulmonary sulcus tumor, and includes arm and shoulder pain, atrophy of intrinsic hand muscles, and ipsilateral Horner syndrome. The rarity and overall poor prognosis of patients with superior pulmonary sulcus tumors associated with Pancoast-Tobias syndrome has led to few reports detailing pain management strategies with adjunctive therapies, such as continuous infusions of ketamine and lidocaine, chemotherapy, radiation, and multimodal oral medication regimens. This case highlights the diagnosis and treatment of pain in a patient with Pancoast-Tobias syndrome.
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Nerve injury-induced hyperactivity of primary sensory neurons in the dorsal root ganglion (DRG) contributes to chronic pain development, but the underlying epigenetic mechanisms remain poorly understood. Here we determined genome-wide changes in DNA methylation in the nervous system in neuropathic pain. Spinal nerve ligation (SNL), but not paclitaxel treatment, in male Sprague Dawley rats induced a consistent low-level hypomethylation in the CpG sites in the DRG during the acute and chronic phases of neuropathic pain. ⋯ We showed that nerve injury caused DNA methylation changes at 8% of CpG sites with prevailing hypomethylation outside of CpG islands in the dorsal root ganglion. Reducing DNA methylation induced pain hypersensitivity, whereas increasing DNA methylation attenuated neuropathic pain. These findings extend our understanding of the epigenetic mechanism of chronic neuropathic pain and suggest new strategies to treat nerve injury-induced chronic pain.
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Heterogeneity of outcome domains, used in interventional trials and systematic reviews (SRs) for neuropathic pain (NeuP), makes decisions on the comparative effectiveness of available treatments difficult. This study analyzed outcome domains and measures used in SRs of randomized controlled trials on efficacy and safety of interventions for NeuP and compared them with the core outcome set (COS) and core outcome measures (COMs) for chronic pain recommended by the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT). ⋯ Authors of SRs in the field of NeuP insufficiently use relevant recommended COS and COMs for chronic pain. More effort should be put into the implementation of COS to ensure that the study results can be compared and combined. There is a need for defining core outcome domains and measures specific for NeuP.