Efficacy of the lumbar sympathetic ganglion block in lower limb pain and its application prospects during the perioperative period

Abstract

The sympathetic nervous system is involved in the physiological pathogenesis of many different types of chronic pain. Sympathetic blocks can interrupt the reflex control system by intercepting the noxious afferent fibers accompanying autonomic nerves, resulting in changes in peripheral or central sensory processing. A lumbar sympathetic ganglion block (LSGB), as a treatment method, refers to the injection of nerve blockers into the corresponding lumbar sympathetic nerve segments, usually requiring imaging assistance (CT, X-ray, ultrasound) to guide. At present, LSGB has been widely used in the clinical treatment of lower limb pain, such as neuropathic pain, lower limb ischemic pain, and so on. Its mechanism of action may be through inhibiting sympathetic nerve activity and dilating blood vessels, thereby alleviating pain and inhibiting stress response. However, there are few reports of LSGB during the perioperative period, especially in postoperative pain and gastrointestinal function. Therefore, by studying the literature about LSGB-related studies, this article reviews the anatomy of the lumbar sympathetic nerve (LSN), with its clinical application and possible mechanism. We reviewed the analgesic effect of LSGB in patients with lower limb pain and postoperative pain and the potential application prospects in the recovery of gastrointestinal function, finally providing a reference for its clinical application.

Case report: A combination of mirror therapy and magnetic stimulation to the sacral plexus relieved phantom limb pain in a patient

“…A low frequency (1 Hz) of magnetic stimulation was supposed to inhibit the afferent signals of peripheral nociceptors, thus inhibiting the primary transmission of pain and consequently relieving pain. Surgical interventions of the lumbar sympathetic ganglion block or dorsal root entry zone lesions also can be used to block pain transmission (Zheng et al, 2009;Zhang et al, 2022). But, they are invasive and considered only when other treatments do not work effectively (Subedi and Grossberg, 2011).…”

Advances in the Treatment of Neuropathic Pain by Sympathetic Regulation

“…When the sympathetic nerve is damaged by mechanical, chemical, or high temperature, the sympathetic nerve tension decreases, resulting in relative vasodilation, reduced peripheral vascular resistance, increased collateral and peripheral circulating blood volume, and increased blood perfusion in skin and muscle of extremities through "loss of sympathetic effect" [23][24][25]. Secondly, the sympathetic nerve is involved in the production and release of pain-related mediators, such as nerve growth factor, interleukin-8, bradykinin, calcitonin generelated peptide, and substance P [26]. After the sympathetic nerve is blocked or destroyed, pain stimulation can be blocked to the central nervous system through nerve fibers, and the regeneration of skin vascular cells can be regulated by inhibiting the proliferation of parietal cells and increasing the expression of angiopoietin-1, reducing the inflammatory response in the denervation area of the sympathetic nerve and reducing the release of adrenergic energy in the dorsal root ganglion.…”