Articles: neuralgia.
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Chronic headaches are the second most prevalent disease and second most common cause for years lived with disability worldwide. Occipital neuralgia can cause headaches or be present in addition to other more prevalent causes of headache. If these headaches fail to respond to conservative and pharmacological therapy, physicians proceed to more invasive treatments, starting with infiltration of the greater occipital nerve with local anesthetic with or without corticosteroids, followed by nerve ablation or stimulation. Occipital nerve stimulation gained more popularity as the technology improved and more pain physicians received training on interventional procedures. ⋯ Considering the ease of implant and minimal side effects, implant of peripheral nerve stimulators to stimulate the occipital nerve is a promising treatment modality for patients with chronic headache who present with features of occipital neuralgia. However, wider use of this treatment modality is subject to further studies.
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Gabapentinoids are commonly prescribed for the treatment of neuropathic pain but are not recommended for the primary treatment of carpal tunnel syndrome (CTS). We sought (1) to investigate the preoperative use of gabapentinoids for the treatment of CTS and (2) to determine whether preoperative exposure is associated with persistent gabapentinoid and opioid use after carpal tunnel release. ⋯ Prognostic II.
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This study was performed to characterize the effect of microRNA-101 (miR-101) on the pain hypersensitivity in CCI rat models with the involvement of mitogen-activated protein kinase phosphatase 1 (MKP-1) in spinal cord microglial cells. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) in the developed CCI models were determined to assess the hypersensitivity of rats to mechanical stimulation and thermal pain. To assess inflammation, the levels of interleukin (IL)-1β, IL-6 and tumour necrosis factor-α (TNF-α) in the spinal dorsal horns of CCI rats and lipopolysaccharide (LPS)-activated microglial cells were examined. miR-101 and MKP-1 gain- and loss-of-function experiments were conducted in in vivo and in vitro settings to examine the roles of miR-101 and MKP-1 in CCI hypersensitivity and inflammation. ⋯ MiR-101 was shown to target MKP-1, inhibiting its expression. Moreover, miR-101 promoted pain hypersensitivity in CCI rat models by inhibiting MKP-1 expression and activating the mitogen-activated protein kinase (MAPK) signalling pathway. Taken together, miR-101 could potentially promote hypersensitivity and inflammatory response of microglial cells and aggravate neuropathic pain in CCI rat models by inhibiting MKP-1 in the MAPK signalling pathway.
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Brain Behav. Immun. · Aug 2020
In vivo intrathecal IL-1β quantification in rats: Monitoring the molecular signals of neuropathic pain.
Neuropathic pain, or pain after nerve injury, is a disorder with a significant reliance on the signalling of cytokines such as IL-1β. However, quantifying the cytokine release repeatedly over time in vivo is technically challenging. ⋯ For the first time we have established that the SS based immunosensing platform technology can repeatedly sample the intrathecal space for bioactive peptides, such as IL-1β. Using this novel approach, we have been able to establish the correlation of the intrathecal concentration of IL-1β with the extent of mechanical allodynia, providing a molecular biomarker of the degree of the exaggerated pain state.
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Brain Behav. Immun. · Aug 2020
S100A9 plays a pivotal role in a mouse model of herpetic neuralgia via TLR4/TNF pathway.
Herpetic neuralgia is a painful condition following herpes zoster disease, which results from Varicella-zoster virus reactivation in the dorsal or trigeminal sensory ganglia. Nevertheless, the pathophysiological mechanisms involved in herpetic neuralgia are not well understood. Recently, we identified, that neuroimmune-glia interactions in the sensory ganglion is a critical mechanism for the development of herpetic neuralgia. ⋯ Functionally, genetic or pharmacological inhibition of S100A9 impairs the development of HSV-1 infection-induced mechanical pain hypersensitivity. Finally, we found that the pronociceptive role of S100A9 in herpetic neuralgia depends on the TLR4/TNF pathway. These results unraveled previously unknown mechanisms involved in the pathophysiology of herpetic neuralgia and indicate that S100A9 might be an important target for novel therapies aiming acute herpetic neuralgia.