Background and objectivesAccess through the foramen ovale (FO) is essential in performing trigeminal ganglion injection, glycerol rhizolysis, balloon compression, and radiofrequency thermocoagulation (RFT) to treat idiopathic trigeminal neuralgia (ITN). However, identification of the FO under fluoroscopy can be difficult and time-consuming, and thus exposes patients to increased radiation and procedure risks. Here we present the ‘H-figure’ as a novel fluoroscopic landmark to quickly visualize the FO.MethodsThe H-figure landmark can be recognized as the medial border of the mandible and the lateral edge of the maxilla as the two vertical lines, and the superior line of petrous ridge of temporal bone (S-P-T line) as the horizontal line, and the FO fluoroscopic view is then optimized at the center of the H-figure immediately above the S-P-T line. We applied this landmark in a clinical cohort of 136 patients with ITN who underwent fluoroscopy-guided RFT of the trigeminal ganglion. We also compared the H-figure method with the traditional method. The primary outcome was the total number of fluoroscopic images required to visualize the FO (as a proxy of radiation exposure). Secondary measures included the procedure time required to finalize the FO view and the sensory testing voltage for paresthesia.ResultsWith the H-figure approach we were able to view the FO with an average of 4.2 fluoroscopic shots at an average time of 6.8 min. When compared with the non-H-figure traditional technique, the H-figure method required almost half the fluoroscopic shots in nearly half the procedure duration time, and paresthesia was evoked with half of the voltage.ConclusionThe H-figure is an easy fluoroscopic landmark that can help to view the FO with less radiation and procedure time, and the needles placed with this approach can be closer to the target for the RFT treatment of patients with ITN.

Microgliosis is a hallmark of many neurological diseases, including Alzheimer’s disease, stroke, seizure, traumatic brain and spinal cord injuries, and peripheral and optic nerve injuries. Recent studies have shown that the newly self-renewed microglia have specific neurological functions. However, the mechanism of adult microglia proliferation remains largely unclear. Here, with single-cell RNA sequencing, flow cytometry, and immunohistochemistry, we demonstrate that the sciatic nerve injury induced two distinct phases of microglia proliferation in mouse spinal cord, each with different gene expression profiles. We demonstrate that the transcription factor Myc was transiently upregulated in spinal cord microglia after nerve injury to mediate an early phase microglia proliferation. On the other hand, we reveal that the tumor-necrosis factor alpha-induced protein 3 (Tnfaip3) was downregulated to mediate the Myc-independent late-phase microglia proliferation. We show that cyclin dependent kinase 1, a kinase with important function in the M phase of the cell cycle, was involved only in the early phase. We reveal that although the early phase was neither necessary nor sufficient for the late phase proliferation, the late-phase suppressed the early phase microglia proliferation in the spinal cord. Finally, we demonstrate that the termination of spinal cord microglia proliferation required both Myc and Tnfaip3 to resume their baseline expression. Thus, we have delineated an interactive signaling network in the proliferation of differentiated microglia.

Chronic pain remains a public health problem and contributes to the ongoing opioid epidemic. Current pain management therapies still leave many patients with poorly controlled pain, thus new or improved treatments are desperately needed. One major challenge in pain research is the translation of preclinical findings into effective clinical practice. The local neuroimmune interface plays an important role in the initiation and maintenance of chronic pain and is therefore a promising target for novel therapeutic development. Neurons interface with immune and immunocompetent cells in many distinct microenvironments along the nociceptive circuitry. The local neuroimmune interface can modulate the activity and property of the neurons to affect peripheral and central sensitization. In this review, we highlight a specific subset of many neuroimmune interfaces. In the central nervous system, we examine the interface between neurons and microglia, astrocytes, and T lymphocytes. In the periphery, we profile the interface between neurons in the dorsal root ganglion with T lymphocytes, satellite glial cells, and macrophages. To bridge the gap between preclinical research and clinical practice, we review the preclinical studies of each neuroimmune interface, discuss current clinical treatments in pain medicine that may exert its action at the neuroimmune interface, and highlight opportunities for future clinical research efforts.

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