Articles: neuralgia.
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p53 and parkin are involved in mitochondrial quality control. The present study aimed to characterize the functional significance of parkin/p53 in the development of mitochondrial dysfunction and the pathophysiology of neuropathic pain in type I diabetes. Type I diabetes was induced in mice (N = 170) using streptozotocin (STZ). ⋯ Methylglyoxal also decreased mitochondrial membrane potential in cultured DRG neurons. Alteration of p53/parkin expression produces mitochondrial dysfunction and ROS accumulation, leading to pain hypersensitivity in diabetic or methylglyoxal treated mice. Methylglyoxal produces neurological derangements similar to diabetes, via direct mechanisms on DRG neurons.
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Case Reports
Peripheral Nerve Block Efficacy on Refractory Neuralgia Complicating Ramsay Hunt Syndrome: A Case Report.
Several case studies have suggested the usefulness of peripheral nerve blocks in the management of various types of chronic pain that are unresponsive to standard medical treatment. We report here the case of a patient with severe neuralgia, secondary to Ramsay Hunt syndrome that was refractory to standard drug therapy. ⋯ Despite transient facial paralysis, pain was markedly reduced for 3 months with self-reported improved quality of life. To our knowledge, this block has never been described previously.
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Pain is a frequent and disabling symptom in patients with multiple sclerosis (MS); however, the underlying mechanisms of MS-related pain are not fully understood. Here, we demonstrated that cathepsin E (CatE) in neutrophils contributes to the generation of mechanical allodynia in experimental autoimmune encephalomyelitis, an animal model of MS. We showed that CatE-deficient (CatE) mice were highly resistant to myelin oligodendrocyte glycoprotein (MOG35-55)-induced mechanical allodynia. ⋯ Behavioral analyses revealed that sivelestat, a selective neutrophil elastase inhibitor, suppressed mechanical allodynia induced by adoptively transferred MOG35-55-stimulated neutrophils. MOG35-55 directly bound to toll-like receptor 4, which led to increased production of CatE in neutrophils. Our findings suggest that inhibition of CatE-dependent elastase production in neutrophil might be a potential therapeutic target for pain in patients with MS.
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Radicular pain is related to lesions that either directly compromise the dorsal root ganglion (DRG) or indirectly compromise the spinal nerve and its roots by causing ischemia or inflammation of the axons. ⋯ Outcomes after PRF at the DRG did not show strong differences according to electrodiagnostic findings in FBSS patients with chronic intractable lumbosacral radicular pain.
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This comprehensive review of pain in paraneoplastic neurological syndromes focuses on current mechanisms that lead to pain, including autoimmune processes as well as the systemic secretion of factors that sensitize nociceptive nerves. Systemic secretion of functional molecules is a well-recognized phenomenon in endocrine paraneoplastic syndromes; however, cancer pain research has predominantly focused on cytokine-nerve interactions in the tumor microenvironment, and few groups have applied the molecular mechanisms of local pain to study widespread neuropathic pain resulting from systemic secretion. We present a novel perspective in the field of pain research by converging data from clinical oncology with recent molecular pain research on cytokine-mediated sensitization of nociceptive nerves. ⋯ Paraneoplastic neurologic syndromes, chronic pain, neuropathic pain, treatment guidelines, cytokines.