Articles: neuropathic-pain.
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The aims of this study were to identify the reasons for explanation of spinal cord stimulator (SCS) devices and to further quantify the proportions and time lines of these causes of explantation in order to determine improvement opportunities for the development of best practices. ⋯ Device removal is not uncommon, and opportunities to enhance the long-term success of SCS devices do exist. These include modification of trialing methods, achieving better paresthesia overlay, using magnetic resonance imaging (MRI) conditional equipment, development of robust technologies and hardware to reduce equipment malfunction, and improving efficacy with new innovative wave forms.
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Aim: We assessed the knowledge and adoption of Initiative on Methods, Measurement and Pain Assessment in Clinical Trials (IMMPACT)-recommended core outcome set (COS) and core outcome measures (COM) among authors of systematic reviews (SR) and randomized controlled trials (RCT) about interventions for neuropathic pain (NeuP). Methods: NeuP SR and RCT authors identified via a systematic literature search were surveyed. ⋯ The main perceived obstacle that prevented the adoption of the COS was the lack of awareness of the full IMMPACT COS. Conclusion: The adoption of IMMPACT-recommended COS and COM among NeuP authors was inadequate and their appropriateness needs to be further evaluated.
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Experimental neurology · Jul 2019
Upregulation of interleukin-6 on Cav3.2 T-type calcium channels in dorsal root ganglion neurons contributes to neuropathic pain in rats with spinal nerve ligation.
The T-type calcium channels Cav3.2, one of the low voltage-activated (LVA) calcium channels, have been found to play important roles in the neuronal excitability. Recently, we and others have demonstrated that accumulation of Cav3.2 channels in the dorsal root ganglion (DRG) neurons and sensory nerves contributes to neuropathic pain after peripheral nerve injury. In the present study, we aimed to further investigate the regulation of Cav3.2 channels by interleukin-6 (IL-6) in DRG neurons in neuropathic pain rats after spinal nerve ligation (SNL). ⋯ Furthermore, inhibition of IL-6 trans-signaling reduced the upregulation of Cav3.2 T-type channel induced by FIL-6 (a fusion protein of IL-6 and sIL-6R) in primary cultured DRG neurons in vitro. In vivo, inhibition of IL-6 trans-signaling reversed the upregulation of Cav3.2, reduced the hyperexcitability of L5 DRG neurons and alleviated mechanical allodynia in SNL rats. Our results suggest that IL-6 upregulates Cav3.2 T-type channels expression and function through the IL-6/sIL-6R trans-signaling pathway in DRG neurons, thus contributes to the development of neuropathic pain in SNL rats.
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To improve patient care and help clinical research, the Neuropathic Pain Special Interest Group of the Italian Neurological Society appointed a task force to elaborate a consensus statement on pharmacoresistant neuropathic pain. The task force included 19 experts in neuropathic pain. ⋯ In the face-to-face meeting the participants discussed the clinical features determining pharmacoresistance. They finally agreed that neuropathic pain is pharmacoresistant when "the patient does not reach the 50% reduction of pain or an improvement of at least 2 points in the Patient Global Impression of Change, having used all drug classes indicated as first, second, or third line in the most recent and widely agreed international guidelines, for at least 1 month after titration to the highest tolerable dose." Our consensus statement might be useful for identifying eligible patients for invasive treatments, and selecting patients in pharmacological trials, thus improving patient care and helping clinical research.
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We aimed to investigate if different protocols of electrical stimulation following nerve injury might improve neuropathic pain outcomes and modify associated plastic changes at the spinal cord level. ⋯ Daily electrical stimulation, especially if frequency-patterned, was effective in ameliorating hyperalgesia after nerve injury, and partially preventing the proinflammatory and hyperalgesic changes in the dorsal horn associated to neuropathic pain.