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Objective: This study evaluates the clinical efficacy and safety of ultrasound-guided long duration, high voltage pulse radiofrequency (PRF) in managing primary glossopharyngeal neuralgia (GPN). Methods: Clinical data were retrospectively analyzed for 13 patients with primary GPN who underwent this treatment between August 2019 and October 2022. Visual Analog Scale (VAS) scores were assessed pre-treatment and at 1 week, 1 month, 3 months, and 6 months post-treatment. Additionally, the rates of discontinuation of oral oxcarbazepine and pregabalin, efficacy, and complication rates at 6 months post-procedure were monitored. Results: Significant post-treatment pain relief, was observed across all patients, with statistically significant improvements in VAS scores (p < 0.05). Discontinuation rates for oxcarbazepine and pregabalin were also high (p < 0.05). At the 6-month follow-up, 69.23% of patients achieved excellent and good efficacy, 84.61% demonstrated overall effectiveness, while 15.38% showed poor efficacy. No critical complications were reported in any case. Conclusion: Ultrasound-guided, long-term, high-voltage PRF effectively relieves primary glossopharyngeal neuralgia and improves quality of life. Featuring ease of operation, high safety and minimal complications making it a promising approach for clinical application. [ABSTRACT FROM AUTHOR]

Diabetic peripheral neuropathic pain (DPNP) is a major complication of diabetes that markedly affects the quality of life and health status of patients. Recent studies have investigated the potential regulatory influence of gut flora and bile acids on DPNP via the TGR5/TRPV1 signaling pathway. Dysbiosis of the gut flora not only directly affects bile acid metabolism but also significantly correlates with diabetes-associated neuropathy through interactions with the bile acid receptor TGR5 and the ion channel TRPV1. This review describes how alterations in the gut flora and bile acid metabolism contribute to the pathogenesis of DPNP through the TGR5/TRPV1 signaling pathway, revealing potential applications for this pathway in DPNP management. Furthermore, experimental and clinical studies have demonstrated the modulation of gut flora and bile acid metabolism as well as targeting the TGR5/TRPV1 signaling pathway as an innovative therapeutic approach. Further studies are warranted to elucidate the underlying mechanism and develop treatment modalities based on gut flora regulation and signaling pathway interventions, thus providing novel insights and approaches for DPNP therapy. [ABSTRACT FROM AUTHOR]

Varicella-zoster virus (VZV) is a deoxyribonucleic acid (DNA) virus that causes both primary and recurrent viral infections. Herpes zoster (HZ), also known as shingles, is a unique condition that is induced by VZV reactivation. Neuropathic pain, malaise, and sleep disruption are prodromal symptoms in such cases. Postherpetic trigeminal neuralgia is a neuropathic pain caused by VZV infection of the trigeminal ganglion or branches, which remains or reappears after herpes crusting. In this report, we present a case of post-herpetic trigeminal neuralgia of the V2 branch, exhibiting findings of unusual involvement of the trigeminal nerve. Notably, the patient was treated using electrodes placed through the foramen ovale. [ABSTRACT FROM AUTHOR]

Trigeminal neuralgia (TN) is a prevalent chronic neuropathic pain syndrome characterized by severe pain, often accompanied by cognitive dysfunction and cerebral degeneration. However, its mechanisms remain poorly understood. Hyperphosphorylation of tau protein (p-tau) is often seen in neurodegenerative disorders such as Alzheimer's disease (AD). LRP1 expression on brain neurons and microglial cells is believed to facilitate the propagation of p-tau. We established a TN rat model via infraorbital nerve chronic constrictive injury (ION-CCI). Once the model was established, we investigated the association between p-tau and cognitive impairment in TN rats by evaluating behavioral and degenerative markers. During the initial phase, we noted an increase in p-tau level in the prefrontal cortex and hippocampal tissues of TN rats. The accompanied impaired learning and memory abilities suggested cognitive dysfunction. Blocking p-tau synthesis by orally administering a protein phosphatase and by injecting adenoviral vectors targeting LRP1 into the lateral ventricle of rats ameliorated cognitive impairment. This suggests that cognitive decline in TN rats is linked to elevated p-tau levels. Our findings show that LRP1-mediated p-tau propagation may drive cognitive impairment associated with neuropathic pain in TN rats., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Trigeminal neuralgia is a common neuropathic pain in the head and face. The pathogenesis of trigeminal neuralgia is complex, and so far, the pathogenesis of trigeminal neuralgia involving peripheral and central nervous inflammation theory has not been explained clearly. The loss of dopamine neurons in striatum may play an important role in the development of trigeminal nerve, but the reason is not clear. C-Abl is a nonreceptor tyrosine kinase, which can be activated abnormally in the environment of neuroinflammation and cause neuron death. We found that in the rat model of infraorbital nerve ligation trigeminal neuralgia, the pain threshold decreased, the expression of c-Abl increased significantly, the downstream activation product p38 was also activated abnormally and the loss of dopamine neurons in striatum increased. When treated with imatinib mesylate (STI571), a specific c-Abl family kinase inhibitor, the p38 expression was decreased and the loss of dopaminergic neurons was reduced. The mechanical pain threshold of rats was also improved. In conclusion, c-abl-p38 signaling pathway may play an important role in the pathogenesis of trigeminal neuralgia, and it is one of the potential targets for the treatment of trigeminal neuralgia.