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PubMed | Chiba University and East Chiba Medical Center Chiba
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2015

Spinal cord stimulation (SCS) is sometimes preferable in some refractory chronic lower back pain (LBP) pathologies. SCS involves an insertion of electrode leads into the epidural space in the prone position under local anesthesia, followed by neurostimulator implantation under local/general anesthesia. These continuous procedures can cause transient post-operative LBP exacerbation and to make temporary pockets that will store redundant leads in it with some risk of subcutaneous irritation and infection in addition to making extra incisions. We introduce a modified simpler method for SCS implantation, systematically designed to be performed only under local anesthesia in a decubitus, non-prone position.An 81-year-old patient with FBSS was treated. A physician was able to insert SCS leads with ease while the patient was in a decubitus position. The patient was comfortable, under totally local anesthesia, and the procedure produced no extra subcutaneous pockets.The patient felt almost no LBP and reported no pain exacerbation during the operation. The SCS installation provided the patient with great improvement in both her lower back (NRS from 8 to 0-1) and leg (from 7 to 2) pain with a great improvement in her daily life activities. No adverse events were observed during the perioperative period.The modified SCS insertion method enabled us to achieve both intraoperative pain relief and complete SCS implantation in a minimally invasive manner.

PubMed | Kitasato University, Teikyo University, Chiba University and East Chiba Medical Center Chiba
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2016

The detailed mechanisms of knee osteoarthritis (OA) pain have not been clarified, but involvement of inflammatory cytokines such as tumor necrosis factor-alpha (TNF) has been suggested. The present study aimed to investigate the more detailed neurological involvement of TNF in joint pain using a TNF-knockout mouse OA model.The right knees of twelve-week-old C57BL/6J wild and TNF-deficient knockout (TNF-ko) mice (n=15, each group) were given a single intra-articular injection of 10 g monoiodoacetate in 10 mL sterile saline. The left knees were only punctured as the control. Evaluations were performed immediately after the injection (baseline) and at 7, 14, and 28 days after the injection with a subsequent intra-articular injection of neurotracer into both knees. The animals were evaluated for immunofluorescence of the lumbar dorsal root ganglia (DRG) innervating the knee joints. The injected knees were observed macroscopically and mouse pain-related behaviors were scored.Macroscopic observation showed similar knee OA development in both wild and TNF-ko mice. Calcitonin gene-related peptide (CGRP, a neuropeptide identified as a inflammatory pain-related biomarker) was significantly increased in DRG neurons innervating OA-induced knee joints with significantly less CGRP expression in TNF-ko animals. Pain-related behavior scoring showed a significant increase in pain in OA-induced joints, but there was no significant difference in pain observed between the wild and TNF-ko mice.The result of the present study indicates the possible association of TNF-alpha in OA pain but not OA development.

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