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Multiple human and animal studies suggest that the upregulation of inflammatory cytokines and other pain‐related molecules in degenerated or injured intervertebral discs (IVDs) may cause discogenic low back pain (LBP). We previously reported that macrophages in injured IVD in mice produced inflammatory cytokines, but not other pain‐related molecules. CD14 is a monocyte marker expressed mainly by macrophages. The aim of the current study was to evaluate the role of CD14‐positive cells in inflammatory cytokine and pain‐related molecule expression in human degenerated IVD. IVD samples were harvested from 14 patients, including 10 with lumbar spinal stenosis, four with adult spinal deformity, and one with lumbar disc herniation during spinal interbody fusion surgery. Harvested IVD‐derived mononuclear cells were obtained and CD14‐positive (+) and CD14‐negative (−) cells were separated using CD14 antibody and streptavidin‐labeled magnetic beads. Inflammatory cytokines messenger RNA (mRNA) in the CD14(+) and CD14(−) cells, including tumor necrosis factor ɑ (TNFA), in, terleukin‐1β (IL1B) and IL6, were determined using quantitative polymerase chain reaction (qPCR) and their expression levels were compared. To evaluate factors controlling the regulation of pain‐related molecules mRNA expression, cultured CD14(−) and CD14(+) cells from IVDs were stimulated with recombinant human TNF‐ɑ and IL‐1β and levels of pain‐related molecules, including calcitonin gene‐related peptide (CGRP) and nerve growth factor (NGF) were determined using qPCR. Levels of TNFA, IL1B, IL6, and NGF in CD14(+) cells were significantly increased compared with those in CD14(−) cells (TNFA, p = 0.006; IL1B, p =.017; IL6, p =.010; NGF, p =.027). Following TNFA stimulation, NGF levels were significantly increased in CD14(−) and CD14(+) cells (CD14(−), p =.003; CD14(+), p <.001) and CGRP was significantly increased in CD14(−) IVD cells (p =.040). Following IL1B stimulation, NGF levels were significantly increased in CD14(−) cells (p =.004). CD14(+) cells had higher TNFA, IL1B, IL6, and NGF expressions than CD14(−) cells in human degenerated IVDs. Additionally, TNFA stimulation promoted the upregulation of NGF and CGRP in CD14(−) cells. These findings suggested that CD14(+) cells directly and indirectly contributed to inflammatory cytokine and pain‐related molecule expression in human degenerated IVD. CD14(+) cells might be important in the pathological mechanism of chronic discogenic LBP in humans. [ABSTRACT FROM AUTHOR]

Introduction Patients with lumbar spine disease sometimes complain of nocturnal leg cramps. We sought to investigate the effectiveness of blocking the medial branch of the deep peroneal nerve as treatment for nocturnal leg cramps after spinal surgery for lumbar spine disease. Methods We evaluated 66 postoperative patients in this prospective comparative study of a group of patients with a nerve block ( n = 41) and a control group without ( n = 25). In the block group, the medial branch of the deep peroneal nerve was blocked at the distal two-thirds of the interspace between the first and second metatarsals using 5.0 mL of 1.0% lidocaine. Results Two weeks after the block, the frequency of nocturnal leg cramps was reduced to less than a quarter of pretreatment baseline frequency in 61.0% of patients ( n = 25) and less than half in 80.5% ( n = 33). In the control group, the frequency of the leg cramps was reduced from baseline in 32.0% of patients ( n = 8), and was unchanged or increased in 68.0% ( n = 17) at 2 weeks. Cramp frequency was reduced to less than a quarter or less than half of baseline frequency in a significantly ( P < 0.05 and P < 0.01, respectively) larger percentage of patients in the block group. The severity of each cramp was less in about two-thirds of patients (63.4%; n = 26) in the block group and was unchanged in one-third (31.7%; n = 13). Conclusions Blocking the medial branch of the peroneal nerve can be an effective, long-lasting, and simple treatment with low risk for nocturnal cramps sustained after lumbar spine surgery. [ABSTRACT FROM AUTHOR]