BackgroundLumbar adhesive arachnoiditis is a debilitating neuropathic condition and is difficult to diagnose owing to lack of definitive diagnostic criteria. By focusing on the intrathecal mobility of nerve roots, we assessed whether useful diagnostic criteria could be established using MRI.MethodsSeventeen patients with a high risk for lumbar adhesive arachnoiditis and 18 no‐risk patients with chronic low back pain and/or leg pain participated in this study. The patients underwent MRI in both the supine and prone positions. Eleven axial T2‐weighted images between the L2 and L5/S levels were obtained, and the proportion of the low‐intensity area in the dorsal half to the total low‐intensity area in the dural sac was calculated for each axial view.ResultsAt some lumbar levels, the low‐intensity area in the dorsal half of the dural sac was relatively larger in patients with a high risk for lumbar adhesive arachnoiditis than in the no‐risk patients. In the no‐risk group, the proportion of the low‐intensity area in the dorsal half in the supine position was significantly higher than that in the prone position at all lumbar levels. However, in the high‐risk group, at some levels, the proportions were not significantly different in the dorsal half of the dural sac between the supine and prone positions.ConclusionIn patients with a known risk for lumbar adhesive arachnoiditis, nerve roots lose their potential to migrate in the dural sac in the gravitational force direction on MRI.

Aim Cancer pain impairs not only physical functions but also social functions and roles. Consequently, the overall health‐related quality of life of patients with cancer pain deteriorates. Opioid analgesics are recommended for treating moderate to strong cancer pain. Advances in human genome research have fueled a growing interest to understand individual differences in responsiveness to opioid analgesics. This study aimed to explore and identify novel loci for genes predisposing an individual to opioid analgesic responsiveness. Methods A total of 71 cancer patients rated their pain on an 11‐point numerical rating scale twice before and after increasing opioid analgesics. A genomewide association study focusing on single nucleotide polymorphisms (SNPs) was conducted to associate pain decrease with increased dosage of opioid analgesics based on weight (ie, responsiveness to opioid analgesics). A genomewide significance (P < 5E‐8) was set for multiplicity of analyses to control for false positives. Results Two SNPs passed the genomewide threshold for significance. One exonic SNP (rs1641025) was located in the ABAT [4‐aminobutyrate aminotransaminase (GABA transaminase)] gene on chromosome 16. The other SNP (rs12494691) was located on chromosome 3, which was not associated with any known genes. These SNPs were not associated with opioid‐related adverse effects. Conclusions Our results preliminarily suggest that both SNPs might be potential candidate loci for responsiveness to opioid analgesics, and GABA transaminase might be a possible target for developing adjuvant pharmacotherapy with opioid analgesics in adjuvant pharmacotherapy. Our results should be validated in a large‐scale study with a larger sample size.

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