Articles: neuropathic-pain.
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Neurorehabil Neural Repair · Sep 2013
Randomized Controlled Trial Comparative StudyEffect of single-session repetitive transcranial magnetic stimulation applied over the hand versus leg motor area on pain after spinal cord injury.
Neuropathic pain often follows spinal cord injury (SCI). ⋯ rTMS applied over the hand or leg motor cortex decreased neuropathic pain regardless of any change in cortical excitability, suggesting that the analgesic effect is not associated with local changes at the motor cortex level itself.
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SUMMARY Neuropathic pain is typically caused by a lesion or dysfunction in the nervous system that results in both negative (i.e., reduced sensitivity) and positive symptoms (i.e., paraesthesia, spontaneous ongoing pain with shooting, electric shock-like sensations and abnormal responses to evoked pain). Intriguingly, chronic pain disorders manifest profound alterations in brain structure and function, and thus, modern nuclear magnetic resonance (NMR) techniques have allowed us to begin to dissect the complexities of how neuropathic pain affects the brain. NMR approaches can be used as an independent measure to improve our understanding of key changes in brain structure, function and chemistry in chronic neuropathic pain. ⋯ Additionally, although at an early stage, NMR methods can also be useful to define clinical metrics to predict chronification of neuropathic pain and responses to drugs. This article provides a review of NMR techniques and their capacity to study spontaneous pain and evoked pain, as well as structural, functional and neurochemical alterations that have repeatedly been associated with chronic neuropathic pain. Finally, the importance for quantifying disease state and treatment efficacy in neuropathic pain using NMR techniques is discussed.
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Ther Adv Neurol Disord · Sep 2013
A review of the high-concentration capsaicin patch and experience in its use in the management of neuropathic pain.
In the European Union, the high-concentration capsaicin patch is licensed for the management of neuropathic pain conditions in nondiabetic patients, including postherpetic neuralgia (PHN) and HIV-associated distal sensory polyneuropathy (HIV-DSP). However, in the USA, the Food and Drug Administration approved its use only in PHN patients. Capsaicin is a transient receptor potential vanilloid-1 agonist, which increases the intracellular calcium ion concentration. ⋯ Efficacy and therapeutic effect has been shown in several clinical studies of PHN and HIV-DSP. The high-concentration capsaicin patch and its practical application are different from low-concentration creams; one application can help for up to 3 months. The process of setting up of a service to use the capsaicin 8% patch is also discussed.
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Experimental neurology · Sep 2013
Interleukin-10 down-regulates voltage gated sodium channels in rat dorsal root ganglion neurons.
The over-expression of voltage-gated sodium channels (VGSCs) in dorsal root ganglion (DRG) neurons following peripheral nerve injury contributes to neuropathic pain by generation of the ectopic discharges of action potentials. However, mechanisms underlying the change in VGSCs' expression are poorly understood. Our previous work has demonstrated that the pro-inflammatory cytokine TNF-α up-regulates VGSCs. ⋯ Consistent with the electrophysiological results, real-time PCR and western blot revealed that IL-10 (200 pg/ml) down-regulated VGSCs in both mRNA and protein levels and reversed the up-regulation of VGSCs by TNF-α. Moreover, repetitive intrathecal administration of rrIL-10 for 3 days (4 times per day) attenuated mechanical allodynia in L5 spinal nerve ligation model and profoundly inhibited the excitability of DRG neurons. These results suggested that the down-regulation of the sodium channels in DRG neurons might contribute to the therapeutic effect of IL-10 on neuropathic pain.
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Lipocalin 2 (LCN2), which is also known as 24p3 and neutrophil gelatinase-associated lipocalin (NGAL), binds small, hydrophobic ligands and interacts with cell surface receptor 24p3R to regulate diverse cellular processes. In the present study, we examined the role of LCN2 in the pathogenesis of neuropathic pain using a mouse model of spared nerve injury (SNI). Lcn2 mRNA levels were significantly increased in the dorsal horn of the spinal cord after SNI, and LCN2 protein was mainly localized in neurons of the dorsal and ventral horns. ⋯ Lcn2-deficient mice showed significantly less microglial activation and proalgesic chemokine (CCL2 and CXCL1) production in the spinal cord after SNI than wild-type mice, and recombinant LCN2 protein induced the expression of these chemokines in cultured neurons. Furthermore, the expression of LCN2 and its receptor was detected in neutrophils and macrophages in the sciatic nerve following SNI, suggesting the potential role of peripheral LCN2 in neuropathic pain. Taken together, our results indicate that LCN2 plays a critical role in the development of pain hypersensitivity following peripheral nerve injury and suggest that LCN2 mediates neuropathic pain by inducing chemokine expression and subsequent microglial activation.