Comparisons of the analgesic effect of different pulsed radiofrequency targets in SNI-induced neuropathic pain

Author:

Liang Ying12,Zhong Shuotao1,Wang Honghua3,Wu Danlei1,Gong Qingjuan1

Affiliation:

1. Department of Pain Medicine, The Second Affiliated Hospital of Guangzhou Medical University

2. Department of Anesthesiology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province

3. Department of Anesthesiology and Perioperative Medicine, The Affiliated Suzhou Science and Technology Town Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, China

Abstract

An injury of the peripheral nerve may lead to neuropathic pain, which could be treated with pulsed radiofrequency to the dorsal root ganglion (DRG) or peripheral nerve [the nerve trunk (NT) or proximal to the injury site (NI)]. However, it is not clear whether there is any difference in analgesic effect or maintenance among the three targets. PRF was applied to the ipsilateral L5 DRG, peripheral nerve (NT or NI) 5 days after spared nerve injury (SNI). Triptolide (10 µg/kg) or vehicle was intrathecally administered 5 days after SNI for 3 days. Mechanical withdrawal thresholds were tested after treatment at different time points. Furthermore, microglia and the P2X7 receptor (P2X7R) in the ipsilateral spinal cord were measured with immunofluorescence and western blotting, respectively. PRF + NI exerted a more remarkable analgesic effect than PRF + DRG and PRF + NT at the early stage, but PRF + DRG had a stronger analgesic effect than PRF + NI and PRF + NT at the end of our study. In addition, PRF + DRG showed no significant difference from intrathecal administration of triptolide. Moreover, SNI-induced microglia activation and upregulation of P2X7R in spinal dorsal horn could be markedly inhibited by PRF + DRG. The results suggest that the analgesic effect of PRF + DRG increased with time whereas the other two not and microglia and P2X7R in the ipsilateral spinal dorsal horn may be involved in the process.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

General Neuroscience

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