井上 雅寛

STUDY DESIGN: Experimental animal study. PURPOSE: We aimed to determine the optimal dose of a single direct injection of the tumor necrosis factor (TNF)-α inhibitor, etanercept, by using the rat model of degenerative intervertebral disc from injury. OVERVIEW OF LITERATURE: The pain-related peptide expression was suppressed in the etanercept (100 µg and 1,000 µg)-administered groups in a dose-dependent manner. METHODS: The neurotracer FluoroGold (FG) was applied to the surfaces of L4/5 discs to label their innervating dorsal root ganglion (DRG) neurons (n=50). Ten rats were included in the nonpunctured disc sham surgery control group, whereas the other 40 were included in the experimental group in which intervertebral discs were punctured with a 23-gauge needle. Saline or etanercept (10 µg, 100 µg, or 1,000 µg) was injected into the punctured discs (n=10 for each treatment). After 14 days of surgery, DRGs from L1 to L6 were harvested, sectioned, and immunostained for calcitonin gene-related peptide (CGRP). The proportion of FG-labeled CGRP-immunoreactive DRG neurons was evaluated in all the groups. RESULTS: There were no significant differences between the puncture+saline group and the puncture+10-µg etanercept group (p >0.05). However, a significant decrease in the percentage of FG and CGRP double-positive cells in FG-positive cells was observed in the etanercept (100 µg and 1,000 µg)-administered groups in a dose-dependent manner (p <0.05). CONCLUSIONS: When a low dose of the TNF-α inhibitor (10 µg of etanercept) was directly administered to the rat intervertebral disc in the rat model of degenerative intervertebral disc from injury, no suppressive effect on the pain-related peptide expression was observed. However, when a higher dose of etanercept (100 µg and 1,000 µg) was administered, the pain-related peptide expression was suppressed in a dose-dependent manner.

STUDY DESIGN: Retrospective study. PURPOSE: To determine whether low-dose tramadol plus non-steroidal anti-inflammatory drug combination therapy could prevent the transition of acute low back pain to chronic low back pain. OVERVIEW OF LITERATURE: Inadequately treated early low back pain transitions to chronic low back pain occur in approximately 30% of affected individuals. The administration of non-steroidal anti-inflammatory drugs is effective for treatment of low back pain in the early stages. However, the treatment of low back pain that is resistant to non-steroidal anti-inflammatory drugs is challenging. METHODS: Patients who presented with acute low back pain at our hospital were considered for inclusion in this study. After the diagnosis of acute low back pain, non-steroidal anti-inflammatory drug administration was started. Forty patients with a visual analog scale score of >5 for low back pain 1 month after treatment were finally enrolled. The first 20 patients were included in a non-steroidal anti-inflammatory drug group, and they continued non-steroidal anti-inflammatory drug therapy for 1 month. The next 20 patients were included in a combination group, and they received low-dose tramadol plus non-steroidal anti-inflammatory drug combination therapy for 1 month. The incidence of adverse events and the improvement in the visual analog scale score at 2 months after the start of treatment were analyzed. RESULTS: No adverse events were observed in the non-steroidal anti-inflammatory drug group. In the combination group, administration was discontinued in 2 patients (10%) due to adverse events immediately following the start of tramadol administration. At 2 months, the improvement in the visual analog scale score was greater in the combination group than in the non-steroidal anti-inflammatory drug group (p<0.001). CONCLUSIONS: Low-dose tramadol plus non-steroidal anti-inflammatory drug combination therapy might decrease the incidence of adverse events and prevent the transition of acute low back pain to chronic low back pain.

BACKGROUND: Far-out syndrome was reported by Wiltse et al. in 1984, which is a condition characterized by L5 spinal nerve radiculopathy due to nerve compression between the L5 transverse process and sacral alar. Although many cases of far-out syndrome have been reported, to our knowledge, the present case firstly showed far-out syndrome due to assimilated L4 hemivertebra and L5 vertebra through which abnormal nerve root passed. CASE PRESENTATION: A 71-year-old man presented with left lower back pain and intermittent claudication accompanied by severe left buttock pain. Radiological examination showed assimilation between the L4 hemivertebra and L5 vertebra, which had two pedicles on the right side, with no canal stenosis. However, computed tomography and magnetic resonance imaging of coronal sections showed extraforaminal stenosis between the L5 transverse process and sacral alar, whereby the L5 spinal nerve was pinched ("far-out lesion"), and an abnormal nerve root passage in the assimilated vertebral corpus. We performed transforaminal lumbar interbody fusion, then resected the L5 transverse process to decompress the extraforaminal stenosis, and finally installed pedicle screws, but not at the one of pedicles of the assimilated vertebra in order to prevent nerve injury. Postoperatively, the patient had no symptoms up to 1.5 years after the surgery. CONCLUSION: The current case suggests the importance of detailed preoperative examination of patients with anatomical abnormalities such as assimilated vertebrae, which may result in incorrect diagnosis and failed surgery.

PURPOSE: To evaluate L5 nerve root injuries caused by outwardly misplaced S1 pedicle screws. Pedicle screws remain the criterion standard for fixation of L5-S1 to correct lumbosacral instability. When inserting S1 pedicle screws, it is possible to injure the L5 nerve root if screws are inserted outwardly and the tip of the screw perforates the anterior cortex of the sacrum. Despite this risk, to our knowledge this type of injury has never been reported as a case series. METHODS: We experienced 2 cases of L5 nerve root injury caused by outwardly-inserted S1 pedicle screws. In both cases, bilateral S1 pedicle screws were inserted outwardly using a free-hand technique, and on one side, screws induced severe pain by impinging on an L5 root. Computed tomography after the selective rootgraphy of the injured nerve showed the nerve compressed laterally by screw threads in Case 1 and crushed between the screw threads and the sacral body in Case 2. RESULTS: In both cases, leg pain disappeared immediately after the infiltration of the nerve with lidocaine, but symptoms recurred within a few days in Case 1 and within an hour in Case 2. Conservative treatment of three spinal nerve infiltrations was effective in Case 1, but reinsertion of the rogue screw was necessary in Case 2. CONCLUSIONS: Surgeons should recognize that lateral inclination of S1 pedicle screws can cause L5 nerve root injury, which may require reinsertion of the screw, especially in cases where insertion is difficult because of overlapping surrounding muscle or bony tissue.