Articles: neuropathic-pain.
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The Ochsner journal · Jan 2019
Case ReportsLaminoplasty for Cervical Spinal Cord Stimulator Implantation in Patients With Cervical Spondylosis and Fusion: A Technical Note.
Background: Epidural spinal cord stimulator (SCS) implantation is a commonly used strategy for treating refractory neuropathic pain, but the literature on the technical aspects of cervical SCS surgery remains scarce. Degenerative cervical stenosis and prior fusion surgery are relatively frequent conditions in this population, and the optimal method for cervical lead placement among such patients has not been established. Decompressive laminectomy may be required for cervical SCS placement in the presence of spinal stenosis. ⋯ Case Series: We present a surgical technique for cervical SCS implantation and the cases of 3 patients with significant spinal stenosis and/or prior fusion. In these patients, the paddle lead placement was safely achieved using cervical laminoplasty techniques. Conclusion: In addition to stabilizing the epidural paddle lead, laminoplasty offers several potential advantages compared to decompression alone.
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Chronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment for chronic pain. Before advancements in the pharmacological field, an elucidation of the roles of Nav1.7 and Nav1.8 in the pathophysiology of pain states is required. ⋯ Research concerning the genetic links of Nav1.7 and Nav1.8 in acquired neuropathic and inflammatory pain states from the scientific literature in this field is reported. The role of Nav1.7 and Nav1.8 in the generation and maintenance of abnormal neuronal electrogenesis and hyperexcitability highlights the importance of these channels in the development of pathological pain. However, further research in this area is required to fully elucidate the roles of Nav1.7 and Nav1.8 in the pathophysiology of pain for the development of subtype-specific sodium channel blockers.
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Randomized Controlled Trial
Efficacy and Safety of Computed Tomography-Guided Pulsed Radiofrequency Modulation of Thoracic Dorsal Root Ganglion on Herpes Zoster Neuralgia.
Pulsed radiofrequency (PRF) can relieve postherpetic neuralgia (PHN) caused by herpes zoster (HZ) infection. Nevertheless, its curative effect can vary and may be related to the duration of treatment period. The following study investigates the efficacy and safety of CT-guided PRF modulation on HZ neuralgia over different periods and different time points. ⋯ CT-guided PRF targeting thoracic DRG for modulation of HZ neuralgia in different periods is safe and effective. It is recommended to perform early intervention therapy at the acute phase of HZ.
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Chemotherapy-induced peripheral neuropathy (CIPN) is an adverse side effect of many anti-cancer chemotherapeutic treatments. CIPN often causes neuropathic pain in extremities, and oxidative stress has been shown to be a major contributing factor to this pain. In this study, we determined the site of oxidative stress associated with pain (specifically, mechanical hypersensitivity) in cisplatin- and paclitaxel-treated mouse models of CIPN and investigated the neurophysiological mechanisms accounting for the pain. ⋯ Although systemic delivery of phenyl N-tert-butylnitrone, a reactive oxygen species scavenger, alleviated mechanical hypersensitivity in both cisplatin- and paclitaxel-treated mice, intraplantar phenyl N-tert-butylnitrone was effective only in cisplatin-treated mice, and intrathecal phenyl N-tert-butylnitrone, only in paclitaxel-treated mice. In a reactive oxygen species-dependent manner, the mechanosensitivity of Aδ/C fiber endings in the hindpaw skin was increased in cisplatin-treated mice, and the excitatory synaptic strength in the spinal dorsal horn was potentiated in paclitaxel-treated mice. Collectively, these results suggest that cisplatin-induced mechanical hypersensitivity is attributed to peripheral oxidative stress sensitizing mechanical nociceptors, whereas paclitaxel-induced mechanical hypersensitivity is due to central (spinal) oxidative stress maintaining central sensitization that abnormally produces pain in response to Aβ fiber inputs.
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High frequency spontaneous activity in injured primary afferents has been proposed as a pathological mechanism of neuropathic pain following nerve injury. Although spinal infusion of glial cell line-derived neurotrophic factor reduces the activity of injured myelinated A-fiber neurons after fifth lumbar (L5) spinal nerve ligation in rats, the implicated molecular mechanism remains undetermined. The fast-inactivating transient A-type potassium current (IA) is an important determinant of neuronal excitability, and five voltage-gated potassium channel (Kv) alpha-subunits, Kv1.4, Kv3.4, Kv4.1, Kv4.2, and Kv4.3, display IA in heterologous expression systems. ⋯ Among the examined Kv mRNAs, only the change in Kv4.1-expression was parallel with the change in IA after spinal nerve ligation and glial cell line-derived neurotrophic factor treatment. These findings suggest that glial cell line-derived neurotrophic factor should reduce the hyperexcitability of injured A-fiber primary afferents by IA recurrence. Among the five IA-related Kv channels, Kv4.1 should be a key channel, which account for this IA recurrence.