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Objective To explore the clinical value of ultrasound guidance combined with C-arm guidance during selective semilunar ganglion radiofrequency thermocoagulation via the foramen ovale for trigeminal neuralgia. Methods This study enrolled 48 patients diagnosed with trigeminal neuralgia between January 2021 and December 2021 in the Department of Pain Management at Xuanwu Hospital. Patients were randomly and equally divided into a C-arm–only group and an ultrasound-combined-with–C-arm (ultrasound+C-arm) group, according to a random number table. After exclusions, 42 patients were analyzed. Of these, 21 patients underwent selective semilunar ganglion radiofrequency thermocoagulation via the foramen ovale guided by the C-arm alone, whereas 21 patients underwent the same procedure guided by ultrasound combined with C-arm. The number of punctures, the amount of time elapsed until the target area of the semilunar ganglion was punctured, the cumulative dose of radiation exposure, and puncture-related complications were recorded during the operation. Numerical rating scale scores and radiofrequency thermocoagulation–related complications were evaluated preoperatively and at 1 day, 3 days, 7 days, 1 month, and 3 months after surgery. Results The number of punctures, the amount of time elapsed until the target area of the semilunar ganglion was punctured, and the cumulative dose of radiation exposure were all lower in the ultrasound+C-arm group than in the C-arm–only group (all P < 0.05). No significant differences were found in numerical rating scale scores and radiofrequency thermocoagulation–related complications between the two groups (P > 0.05). No puncture-related complications occurred in either of the groups. Conclusion Ultrasound guidance combined with C-arm guidance could be safely used for puncturing the semilunar ganglion via the foramen ovale, with more efficiency and less radiation exposure than C-arm guidance alone.

The trigeminal sensory system consists of the trigeminal nerve, the trigeminal ganglion, and the trigeminal sensory nuclei (the mesencephalic nucleus, the principal nucleus, the spinal trigeminal nucleus, and several smaller nuclei). Various sensory signals carried by the trigeminal nerve from the orofacial area travel into the trigeminal sensory system, where they are processed into integrated sensory information that is relayed to higher sensory brain areas. Thus, knowledge of the trigeminal sensory system is essential for comprehending orofacial pain. This review elucidates the individual nuclei that comprise the trigeminal sensory system and their synaptic transmission. Additionally, it discusses four types of orofacial pain and their relationship to the system. Consequently, this review aims to enhance the understanding of the mechanisms underlying orofacial pain.

Abstract BACKGROUND AND IMPORTANCE Hypertrophic interstitial neuropathy (HIN) is an uncommon, non-neoplastic lesion typically affecting peripheral nerves. Cranial nerve (CN) involvement is exceedingly rare. We present a case of isolated trigeminal nerve HIN manifesting with V3 distribution neuralgia. CLINICAL PRESENTATION A 50-yr-old male presented with left sided trigeminal neuralgia refractory to medical management. The patient underwent retromastoid craniectomy for possible microvascular decompression. Intra-operatively, the trigeminal nerve appeared to be focally enlarged with a sausage-like configuration. We selectively resected 1 fascicle which was predominantly involved. Histopathological examination revealed onion bulb formations composed of Schwann cells around centrally placed axons. A diagnosis of HIN was made. Postoperatively, the patient experienced complete resolution of symptoms. CONCLUSION This is the third case of isolated trigeminal nerve HIN in the literature. We performed a selective resection in a patient presenting with trigeminal neuralgia, resulting in complete resolution of symptoms. It is reported here with intraoperative microscope images, along with a review and analysis of this topic as it related to CN.

The trigeminal nerve (V) is the fifth and largest of all cranial nerves, and it is responsible for detecting sensory stimuli that arise from the craniofacial area. The nerve is divided into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3); their cell bodies are located in the trigeminal ganglia and they make connections with second-order neurons in the trigeminal brainstem sensory nuclear complex. Ascending projections via the trigeminothalamic tract transmit information to the thalamus and other brain regions responsible for interpreting sensory information. One of the most common forms of craniofacial pain is trigeminal neuralgia. Trigeminal neuralgia is characterized by sudden, brief, and excruciating facial pain attacks in one or more of the V branches, leading to a severe reduction in the quality of life of affected patients. Trigeminal neuralgia etiology can be classified into idiopathic, classic, and secondary. Classic trigeminal neuralgia is associated with neurovascular compression in the trigeminal root entry zone, which can lead to demyelination and a dysregulation of voltage-gated sodium channel expression in the membrane. These alterations may be responsible for pain attacks in trigeminal neuralgia patients. The antiepileptic drugs carbamazepine and oxcarbazepine are the first-line pharmacological treatment for trigeminal neuralgia. Their mechanism of action is a modulation of voltage-gated sodium channels, leading to a decrease in neuronal activity. Although carbamazepine and oxcarbazepine are the first-line treatment, other drugs may be useful for pain control in trigeminal neuralgia. Among them, the anticonvulsants gabapentin, pregabalin, lamotrigine and phenytoin, baclofen, and botulinum toxin type A can be coadministered with carbamazepine or oxcarbazepine for a synergistic approach. New pharmacological alternatives are being explored such as the active metabolite of oxcarbazepine, eslicarbazepine, and the new Nav1.7 blocker vixotrigine. The pharmacological profiles of these drugs are addressed in this review.

Background Trigeminal neuropathic pain attacks can be excruciating for patients, even after being lightly touched. Although there are rodent trigeminal nerve research models to study orofacial pain, few models have been applied to studies in mice. A mouse trigeminal inflammatory compression (TIC) model is introduced here which successfully and reliably promotes vibrissal whisker pad hypersensitivity. Results The chronic orofacial neuropathic pain model is induced after surgical placement of chromic gut suture in the infraorbital nerve fissure in the maxillary bone. Slight compression and chemical effects of the chromic gut suture on the portion of the infraorbital nerve contacted cause mild nerve trauma. Nerve edema is observed in the contacting infraorbital nerve bundle as well as macrophage infiltration in the trigeminal ganglia. Centrally in the spinal trigeminal nucleus, increased immunoreactivity for an activated microglial marker is evident (OX42, postoperative day 70). Mechanical thresholds of the affected whisker pad are significantly decreased on day 3 after chromic gut suture placement, persisting at least 10 weeks. The mechanical allodynia is reversed by suppression of microglial activation. Cold allodynia was detected at 4 weeks. Conclusions A simple, effective, and reproducible chronic mouse model mimicking clinical orofacial neuropathic pain (Type 2) is induced by placing chromic gut suture between the infraorbital nerve and the maxillary bone. The method produces mild inflammatory compression with significant continuous mechanical allodynia persisting at least 10 weeks and cold allodynia measureable at 4 weeks.

Abstract BACKGROUND Microvascular decompression (MVD) is a potentially curative surgery for drug-resistant trigeminal neuralgia (TN). Predictors of pain freedom after MVD are not fully understood. OBJECTIVE To describe rates and predictors for pain freedom following MVD. METHODS Using preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines, PubMed, Cochrane Library, and Scopus were queried for primary studies examining pain outcomes after MVD for TN published between 1988 and March 2018. Potential biases were assessed for included studies. Pain freedom (ie, Barrow Neurological Institute score of 1) at last follow-up was the primary outcome measure. Variables associated with pain freedom on preliminary analysis underwent formal meta-analysis. Odds ratios (OR) and 95% confidence intervals (CI) were calculated for possible predictors. RESULTS Outcome data were analyzed for 3897 patients from 46 studies (7 prospective, 39 retrospective). Overall, 76.0% of patients achieved pain freedom after MVD with a mean follow-up of 1.7 ± 1.3 (standard deviation) yr. Predictors of pain freedom on meta-analysis using random effects models included (1) disease duration ≤5 yr (OR = 2.06, 95% CI = 1.08-3.95); (2) arterial compression over venous or other (OR = 3.35, 95% CI = 1.91-5.88); (3) superior cerebellar artery involvement (OR = 2.02, 95% CI = 1.02-4.03), and (4) type 1 Burchiel classification (OR = 2.49, 95% CI = 1.32-4.67). CONCLUSION Approximately three-quarters of patients with drug-resistant TN achieve pain freedom after MVD. Shorter disease duration, arterial compression, and type 1 Burchiel classification may predict more favorable outcome. These results may improve patient selection and provider expectations. Graphical Abstract Graphical Abstract

Background Current etiology-centered management guidelines have not brought about satisfactory outcomes for trigeminal neuralgia patients. Therefore, there is an urgent call for pathology-targeted diagnosis and treatment modalities for this intractable disease. Trigeminal root demyelination has been frequently shown or suggested in trigeminal neuralgia patients of diverse etiologies and then naturally regarded as the common pathological cause of this disease. However, this causal relationship has never been validated so far with success in either preclinical or clinical studies. One of the key obstacles is that trigeminal root demyelination per se has not been proven as yet to be sufficient to induce trigeminal neuralgia-like facial pain in animals. Methods Trigeminal root demyelination was directly induced by MRI-informed stereotactic microinjection of (1) myelin-destructive lysophosphatidylcholine into both extrapontine and intrapontine trigeminal roots of adult rats and (2) recombinant adeno-associated virus that genetically ablates myelin-forming oligodendrocytes via apoptosis into trigeminal root entry zones of adult mice. Long-lasting asymmetric eyelid contraction and asymmetric cluster face-stroking were adopted as the affective and motivational behavioral proxies to assess facial pain. More importantly, carbamazepine versus pregabalin treatment and chemical silencing of primary nociceptive afferents were used to ascertain the resemblance of facial pain in rodent models to trigeminal neuralgia in patients. Results Chemically or viral genetically induced demyelination in trigeminal root entry zones were shown to induce facial pain behaviors in adult rats and mice. More importantly, facial pain in these rodent models was shown to resemble patient trigeminal neuralgia in terms of the preferred responsiveness to carbamazepine and the unique requirement of primary nociceptive afferents. Moreover, focal demyelination in adult rat intrapontine trigeminal roots was also shown to induce trigeminal neuralgia-like facial pain. Conclusions Trigeminal root demyelination is sufficient to induce trigeminal neuralgia-like facial pain in adult rodents. Our noteworthy findings would support trigeminal root demyelination as the common pathological cause of trigeminal neuralgia. This advancement will promote pathological conceptualization and clinical management of this etiologically heterogeneous disease as a unified entity of demyelinating disorders. Meanwhile, a group of simple and reliable pathological rodent models were provided for further investigations into trigeminal neuralgia. Graphical Abstract

Calcitonin gene-related peptide (CGRP) and dopamine D2 receptor (D2 receptor) are associated with neuropathic pain. However, their relationship is not well understood. To better establish their relationship in trigeminal neuropathic pain, we examined male rats with infraorbital nerve (ION) ligation. Rats with ION ligation were administered CGRP or anti-CGRP antibody into the trigeminal ganglion (TG). The change in the head-withdrawal threshold was measured using von Frey filament. Immunohistochemical staining for phosphorylated extracellular signal-regulated kinase (pERK) was also performed in the trigeminal spinal subnucleus caudalis (Vc). CGRP was detected in the TG and Vc by immunohistochemical staining, and glial fibrillary acidic protein (GFAP) in the TG and dopamine D2 receptor in the Vc were detected in the same way. Antibody administration restored the head-withdrawal threshold to mechanical stimuli, which had decreased after ION ligation. Furthermore, the number of pERK-immunoreactive (-IR) neurons in the Vc, which increased following ION ligation, declined. The ratio of CGRP-IR TG neurons, large-sized CGRP-IR TG neurons, and TG neurons encircled with the GFAP-IR cells increased after ION ligation and decreased after antibody administration. Moreover, the immunoreactivity of CGRP and D2 receptor in the Vc increased after ION ligation and decreased after antibody administration. There were no significant differences in the head-withdrawal threshold, pERK-IR cell count, ratio of CGRP-IR TG neurons, ratio of size of CGRP-IR TG neurons, ratio of TG neurons encircled with GFAP-IR cells, and immunoreactivity of CGRP and D2 receptor in the Vc between the ION-ligated rats with and without CGRP. These findings suggest that the administration of an anti-CGRP antibody into the TG is involved in the suppression of trigeminal neuropathic pain and the D2 receptor expression in the Vc.

3D-Slicer is an open-source medical image processing and visualization software. In the surgical treatment of trigeminal neuralgia, it is commonly used to predict the responsible vessels. However, there are few reports on the use of 3D-Slicer software to quantitatively measure the bilateral trigeminal nerve volume in patients with primary trigeminal neuralgia (PTN) based on the three-dimensional images. Therefore, this study aims to explore the role of three-dimensional fused images processed by 3D-Slicer in the evaluation of trigeminal nerve atrophy, providing an objective basis for the diagnosis of PTN. 57 PTN patients who underwent microvascular decompression (MVD) or percutaneous balloon compression (PBC) surgery in Hebei general hospital between January 2020 and April 2023 were included. Additionally, 30 patients with facial spasms(HFS) were included as a control group. All patients underwent 3D-TOF-MRA and 3D-FIESTA sequence examinations. Comparisons of bilateral trigeminal nerve volumes within and between groups were conducted by performing image fusion using 3D-slicer. The volume of the affected trigeminal nerve in the MVD group (33.96 mm³±12.61 mm³) and PBC group (23.05 mm³±7.71 mm³) was smaller than that of the unaffected trigeminal nerve in the MVD group (39.61 mm³±12.83 mm³) and PBC group (26.14 mm³±6.42 mm³), as well as the average volume of the trigeminal nerve in the control group (40.27 mm³±10.25 mm³) (P<0.05). The differences in bilateral trigeminal ganglion volume (∆V) was significant between the MVD group (∆V=23.59 %±14.32 %) and the control group (∆V=14.64 %±10.00 %) (P<0.05). There was no statistical difference in the trigeminal nerve volume difference between the MVD group (∆V=23.59 %±14.32 %) and the PBC group (∆V=26.52 %±15.00 %) (P>0.05). Trigeminal nerve atrophy is correlated with primary trigeminal neuralgia. 3D-slicer software can quantitatively measure trigeminal nerve volume and assist in the diagnosis of primary trigeminal neuralgia based on the difference in bilateral trigeminal nerve volumes. However, trigeminal nerve atrophy is not associated with postoperative pain recurrence in patients. •Trigeminal nerve atrophy strongly links to PTN, possibly as a marker for PTN.•Using multimodal image fusion improved the accuracy of nerve volume measurements.•Providing new insights for standardized measurement of nerve volume.•The 3D-Slicer is also highly applicable to primary healthcare institutions.

Abstract BACKGROUND While high-resolution imaging is increasingly used in guiding decisions about surgical interventions for the treatment of trigeminal neuralgia, direct assessment of the extent of vascular contact of the trigeminal nerve is still considered the gold standard for the determination of whether nerve decompression is warranted. OBJECTIVE To compare intraoperative and magnetic resonance imaging (MRI) findings of the prevalence and severity of vascular compression of the trigeminal nerve in patients without classical trigeminal neuralgia. METHODS We prospectively recruited 27 patients without facial pain who were undergoing microvascular decompression for hemifacial spasm and had undergone high-resolution preoperative MRI. Neurovascular contact/compression (NVC/C) by artery or vein was assessed both intraoperatively and by MRI, and was stratified into 3 types: simple contact, compression (indentation of the surface of the nerve), and deformity (deviation or distortion of the nerve). RESULTS Intraoperative evidence of NVC/C was detected in 23 patients. MRI evidence of NVC/C was detected in 18 patients, all of whom had intraoperative evidence of NVC/C. Thus, there were 5, or 28% more patients in whom NVC/C was detected intraoperatively than with MRI (Kappa = 0.52); contact was observed in 4 of these patients and compression in 1 patient. In patients where NVC/C was observed by both methods, there was agreement regarding the severity of contact/compression in 83% (15/18) of patients (Kappa = 0.47). No patients exhibited deformity of the nerve by imaging or intraoperatively. CONCLUSION There was moderate agreement between imaging and operative findings with respect to both the presence and severity of NVC/C.