Activation of oxytocin receptor in the trigeminal ganglion attenuates orofacial ectopic pain attributed to inferior alveolar nerve injury.

This study explores the effects of oxytocin receptor (OXTR) in the trigeminal ganglion (TG) on orofacial neuropathic pain. We demonstrate that OXTR activation in the TG relieves the orofacial ectopic pain as well as inhibits the upregulated expression of calcitonin gene-related peptide (CGRP), IL-1ß, and TNFα in the TG and spinal trigeminal nucleus caudalis (SpVc) of rats with inferior alveolar nerve transection. OXTR, a G protein-coupled receptor, has been demonstrated to play a significant role in analgesia after activation by its canonical agonist oxytocin (OXT) in the dorsal root ganglion. However, the role of OXTR in the trigeminal nervous system on the orofacial neuropathic pain is still little known. In the present study, we aimed to investigate the regulation effect and mechanism of OXTR in the TG) and SpVc) on orofacial ectopic pain induced by trigeminal nerve injury. The inferior alveolar nerve (IAN) was transected to establish a ectopic pain model. A behavioral test with electronic von Frey filament demonstrated IAN transection (IANX) evoked mechanical hypersensitivity in the whisker pad from day 1 to at least day 14 after surgery. In addition, administration of OXT (50 and 100 µM) into the TG attenuated the mechanical hypersensitivity induced by IANX, which was reversed by pretreatment with L-368,899 (a selective antagonist of OXTR) into the TG. In addition, immunofluorescence showed the expression of OXTR in neurons in the TG and SpVc. Furthermore, Western blot analysis indicated that the upregulated expression of OXTR, CGRP, IL-1ß, and TNFα in the TG and SpVc after IANX was inhibited by the administration of OXT into the TG. And the inhibition effect of OXT on the expression of CGRP, IL-1ß, and TNFα was abolished by preapplication of OXTR antagonist L-368,899 into the TG.NEW & NOTEWORTHY This study explores the effects of oxytocin receptor (OXTR) in the trigeminal ganglion (TG) on orofacial neuropathic pain. We demonstrate that OXTR activation in the TG relieves the orofacial ectopic pain as well as inhibits the upregulated expression of calcitonin gene-related peptide, IL-1ß, and TNF-α in the TG and spinal trigeminal nucleus caudalis of rats with inferior alveolar nerve transection.

Intranasal self-administration of local anesthetic (ropivacaine) for sphenopalatine ganglion block, for treatment of second trigeminal branch neuralgia secondary to maxillary sinus curettage: A case report. / Autoadministración intranasal de anestésico local (ropivacaína) para bloqueo del ganglio esfenopalatino, para tratamiento de neuralgia de la segunda rama del trigémino secundaria a curetaje del seno maxilar: informe de un caso.

Trigeminal neuralgia (TN) is a severe and often underestimated facial pain that affects quality of life. Pharmacological treatment is insufficient for pain control in 30% of cases and, although intervention techniques may be effective, there is a possibility of relapse and associated complications. The second division of the trigeminal nerve (V2) runs through the sphenopalatine ganglion (SPG), which is anatomically accessible to blocking due to its superficial location in the nasal cavity. We report a clinical case of a patient with uncontrolled V2 TN that was put on ambulatory self-administered SPG block with nasal swabs soaked in 0.75% ropivacaine. In the follow-up visits, we confirmed that this adjuvant treatment provided a significant pain relief over 24hours with a decrease in the number of exacerbations.