Toru Yamamoto

Anatomical terminology research is an important field that seeks to clarify the usage, evolution, and standardization of anatomical terms, thereby promoting consistent scholarly communication in education, research, and clinical practice. Various research approaches, including narrative reviews, systematic reviews, bibliometric studies, and scoping reviews, are used according to the research objectives; however, guidance addressing terminology‐specific methodological decisions across different research approaches remains limited. Although scoping reviews are primarily intended to systematically map key concepts, available evidence, and knowledge gaps within a research field, selected methodological elements derived from scoping reviews—including systematic literature searching, explicit eligibility criteria, standardized data extraction, and reporting of the included literature—may be transferable to anatomical terminology research to enhance its transparency, systematicity, and reproducibility. In contrast, bibliometric studies primarily aim to characterize research trends and knowledge structures through quantitative analyses of bibliographic and citation data, and may also be useful for evaluating the frequency and temporal changes in the use of anatomical terms. These approaches are complementary methodologies that should be selected according to the research objectives, while both require transparent reporting of the research process to support transparency and reproducibility. This article discusses the application of methodological elements derived from scoping reviews to anatomical terminology research, outlines their methodological characteristics in relation to bibliometric studies, and provides a conceptual basis for developing methodological considerations and reporting recommendations for anatomical terminology research.

Cannabinoid 1 and 2 receptor (CB1R and CB2R) agonists alleviate inflammatory and neuropathic pain symptoms. However, central nervous system (CNS) side effects mediated by CB1Rs limit their widespread use. We developed peripherally restricted cannabinoids (PRCBs), which exhibit analgesic efficacy with minimal CNS side effects. Here, we examined PRCB actions in a mouse model of dural acid-induced hypersensitivity. Supradural injections of pH-6.0 (but not pH-7.4) saline (4.5 µL) in five-week-old female C57BL/6J mice induced periorbital allodynia (assessed with von Frey filaments) with recovery by 48 hours. By 72 hours, allodynia was elicited with a supradural pH-7.0 saline injection in pH-6.0 (but not pH-7.4) mice. The CB1R/CB2R agonist PRCB, 4-{2-[(1E)-1-[(4-propylnaphthalen-1-yl) methylidene]-1H-inden-3-yl]ethyl}morpholine (PrNMI) (5 µM) or the selective CB1R agonist arachidonyl-2′-chloroethylamide (ACEA, 5 µM), coapplied with pH-6.0 saline, prevented both the initial and latent allodynia, but coadministering pH 6.0 with the CB2R-selective agonist RNB61 (5 µM) did not. Coadministering pH-6.0/PrNMI with CB1R- or CB2R-selective inverse agonists abolished the preventative effects of PrNMI. Supradural pH-6.0 saline-evoked allodynia followed 72 hours later by coadministration of pH 7.0/PrNMI did not prevent latent allodynia. Patch recordings obtained from dural trigeminal ganglion neurons (dTGNs) acutely isolated from FluoroGold/pH-6.0 (but not pH-7.4)–injected mice had larger acid-induced depolarizations. All dTGNs had electrophysiological properties of Aδ- or C-type nociceptors. PrNMI (1 µM) suppressed acid-induced depolarizations in dTGNs from pH-7.4 (but not pH-6.0)–treated mice, whereas RNB61 (0.5 µM) had no effect. These findings indicate that PrNMI prevents acid-induced sensitization by coactivating neuronal CB1Rs and non-neuronal CB2Rs. Cannabinoid 2 receptor activation alone is insufficient, and once sensitized, combined CB1R/CB2R activation loses efficacy.

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have recently emerged as promising targets for the treatment of neuropathic pain. This study investigated the potential involvement of HCN2 channels in the development of trigeminal neuropathic pain following peripheral nerve injury. Infraorbital nerve chronic constriction injury (ION-CCI) model was adopted to rats, and head withdrawal thresholds (HWT) to mechanical stimulation were assessed pre- and postoperatively, as well as after pharmacological intervention. In the trigeminal ganglion (TG), intracellular cyclic adenosine monophosphate (cAMP) and cytoplasmic protein kinase A (PKA) levels were quantified by Enzyme-Linked Immunosorbent Assay (ELISA), while Hcn2 mRNA expression was evaluated by quantitative Polymerase Chain Reaction (qPCR). Immunohistochemical analysis was performed to assess phosphorylated cAMP response element-binding protein (pCREB) expression in the TG and HCN2 expression in infraorbital nerve (ION) axons. In the TG, cAMP and pCREB levels were elevated, whereas cytoplasmic PKA and Hcn2 mRNA levels were reduced. Axonal HCN2 expression was increased in CCI rats. On day 14, HWT was significantly reduced following CCI but was ameliorated by local administration of the HCN channel blocker ivabradine at the site of axonal injury. Collectively, these findings suggest that CCI-induced alterations in cAMP-PKA-pCREB signaling promote HCN2 accumulation in injured axons, thereby contributing to the development of orofacial neuropathic pain following peripheral nerve injury.

Yamamoto T, et al. J Dent Anesth Pain Med. 2026 ;26:e14. https://doi.org/10.17245/jdapm.2026.26.181

Inoue T, et al. J Dent Anesth Pain Med. 2026 ;26:e12. https://doi.org/10.17245/jdapm.2026.26.155

Yamamoto T, et al. J Dent Anesth Pain Med. 2026 ;26:e9. https://doi.org/10.17245/jdapm.2026.26.146

Yamamoto T, et al. J Dent Anesth Pain Med. 2026 Aug;26(4):365-367. https://doi.org/10.17245/jdapm.2026.26.092

Yamamoto T, et al. J Dent Anesth Pain Med. 2026 Aug;26(4):369-371. https://doi.org/10.17245/jdapm.2026.26.117

Recurrent laryngeal nerve (RLN) paralysis is a rare but clinically significant complication of general anesthesia associated with endotracheal intubation. We report a case of unilateral RLN paralysis that occurred after prolonged neck dissection under general anesthesia. A 77-year-old male patient with a history of hypertension, dyslipidemia, and myocardial infarction underwent right neck dissection and segmental mandibulectomy for mandibular gingival cancer. Tracheostomy was performed after general anesthesia induction, and a spiral endotracheal tube was inserted with the cuff pressure continuously maintained at 28 cmH₂O. The surgery lasted for over 15 h, with the patient’s neck rotated to the right. No intraoperative complications were observed. Postoperatively, the patient presented with hoarseness and was diagnosed with left RLN paralysis. Fiberoptic examination revealed markedly reduced left arytenoid movement with incomplete glottic closure. Improvement in arytenoid mobility was noted on postoperative day (POD) 25 and phonation returned to normal by day 54. The likely mechanisms involve prolonged intubation, neck rotation, and compressive ischemia of the contralateral RLN. This case underscores the importance of careful cuff pressure monitoring and minimization of neck rotation during prolonged surgery to prevent this rare but potentially disabling complication.