稲毛 一秀

Background Symptoms of lumbar spinal stenosis (LSS) are associated with changes in blood flow to lower limbs. These changes in blood flow can be perceived as temperature variations, which can be visualized using thermography. We compared the relationship between the subjective symptoms of LSS and temperature variations before and after surgical intervention and investigated the associated patient factors. Methods Patients who underwent laminectomy for LSS were included. Plantar temperature was measured preoperatively and postoperatively using thermography. Subjective symptoms and patient backgrounds were assessed through interviews and medical records. Temperature differences were evaluated using the parameter ΔT, defined as the temperature of the limb with stronger symptoms minus the temperature of the limb with weaker symptoms. The analyses were performed based on these parameters. Results The symptoms improved following laminectomy, and ΔT showed a significant increase. Pain and ΔT were positively correlated preoperatively, whereas ΔT and numbness and neuropathic pain scores were negatively correlated postoperatively. Cauda equina symptoms were associated with a decrease in ΔT both preoperatively and postoperatively, whereas age and disease duration were associated with a postoperative decrease in ΔT. Conclusion The postoperative increase in ΔT, resulting from the alleviation of nerve compression, suggests a relationship between nerve dysfunction and decreased temperature. The preoperative correlation between pain and ΔT may be attributed to vasodilation mediated by calcitonin gene-related peptide. The postoperative correlation between ΔT and neurological symptoms may reflect an association between the extent of nerve damage and reduced blood flow. In particular, cauda equina symptoms may lead to decreased blood flow through dysfunction of the S region, causing a relatively sympathetic-dominant state due to impaired parasympathetic function. Our findings suggest the potential of using temperature measurements to visualize and objectively evaluate subjective symptoms.

Abstract Diclofenac etalhyaluronate (DF‐HA) sustained diclofenac release with the effects of hyaluronic acid (HA), offering long‐term analgesia in osteoarthritis. In this study, the effects of DF‐HA on pain improvement and osteoarthritis were evaluated in a rat knee monoiodoacetate‐induced osteoarthritis model compared to HA. Eight rats per group had been injected with monoiodoacetate (2.0 mg) or saline in the right knee for 4 weeks and were injected with either DF‐HA (1.25 mg/kg; 0.5 mg), HA (0.5 mg), vehicle which was a substrate without DF‐HA (50 μL), or saline and followed for 4 weeks. Mechanical plantar skin sensitivity was assessed weekly using the von Frey assay. Osteoarthritis changes were monitored with Larsen scores via CT imaging at every 2 weeks. The articular cartilage was analyzed using OARSI scores through H&E, Safranin‐O staining at 8 weeks. The percentage of Iba‐1 positive microglia in the spinal dorsal horn and of FG + CGRP‐labeled cells among FG‐positive cells in the dorsal root ganglion were evaluated by immunohistochemical staining. TNF‐α and IL‐6 mRNA expression levels in the knee synovium were evaluated by PCR. The DF‐HA showed significantly improved pain hypersensitivity compared with the HA at 6–8 weeks. The percentage of Iba‐1‐positive microglia was significantly lower than that in the vehicle and the percentage of FG + CGRP/FG was significantly lower than that in the HA. OARSI scores did not differ among treatment groups, Larsen scores indicated lower in the DF‐HA than in the vehicle. DF‐HA was as effective as HA in joint protection and significantly improved inflammatory pain compared to HA.

Co-administration of mirogabalin besylate and nonsteroidal anti-inflammatory drugs is effective for neuropathic pain; however, mechanism of its action remains unknown. We aimed to evaluate the mechanism of this synergistic effect of the concomitant administration for neuropathic pain using chronic constriction injury model rats. Fifty male Wister rats of 7-week-old were used. Right sciatic nerve ligation was performed in 40 rats and they were sub-divided into four groups: vehicle, mirogabalin, diclofenac sodium and co-administration of them. Ten rats underwent sham surgery. Fluorogold was attached to sciatic nerve during surgery. Von Frey filament and weight bearing tests were performed on postoperative Day 6 as behavioral assessments and drug was administrated intraperitoneally. Half rats in each group underwent behavioral assessment and perfusion fixation using 4% paraformaldehyde on postoperative Day 7 and remaining on postoperative Day 14. Subsequently, dorsal root ganglion at L4 to L6 was collected and examined immunohistochemistry for calcitonin gene-related peptide, and their immunoreactivity in fluorogold-labeled neurons was measured. Spinal cord at lumbar swelling was resected, immunostained for ionized-calcium-binding adapter molecule-1 and glial fibrillary acidic protein, and immunoreactive neurons in dorsal horn of spinal cords were calculated as the occupancy of them. Mirogabalin suppresses the neuropeptide-release from presynaptic afferent neuron directly and it resulted in suppressing glia cells activation. Diclofenac sodium inhibits cyclooxygenase-2 and prostaglandin production, related to allodynia. These effects of mirogabalin and diclofenac sodium, respectively, inhibited glia cells strongly, which is presumed to be one of the mechanisms for the effectiveness of their co-administration for neuropathic pain.