Trigeminal Root Research Articles

Abstracts from the World Federation for Laser Dentistry—Asia Pacific Division Virtual Conference July 16–17, 2021

Abstracts from the World Federation for Laser Dentistry—Asia Pacific Division Virtual Conference July 16–17, 2021

Two Sides to Every Story: Herpes Simplex Type-1 Viral Glycoproteins gB, gD, gH/gL, gK, and Cellular Receptors Function as Key Players in Membrane Fusion.

Herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2) are prototypical alphaherpesviruses that are characterized by their unique properties to infect trigeminal and dorsal root ganglionic neurons, respectively, and establish life-long latent infections. These viruses initially infect mucosal epithelial tissues and subsequently spread to neurons. They are associated with a significant disease spectrum, including orofacial and ocular infections for HSV-1 and genital and neonatal infections for HSV-2. Viral glycoproteins within the virion envelope bind to specific cellular receptors to mediate virus entry into cells. This is achieved by the fusion of the viral envelope with the plasma membrane. Similarly, viral glycoproteins expressed on cell surfaces mediate cell-to-cell fusion and facilitate virus spread. An interactive complex of viral glycoproteins gB, gD/gH/gL, and gK and other proteins mediate these membrane fusion phenomena with glycoprotein B (gB), the principal membrane fusogen. The requirement for the virion to enter neuronal axons suggests that the heterodimeric protein complex of gK and membrane protein UL20, found only in alphaherpesviruses, constitute a critical determinant for neuronal entry. This hypothesis was substantiated by the observation that a small deletion in the amino terminus of gK prevents entry into neuronal axons while allowing entry into other cells via endocytosis. Cellular receptors and receptor-mediated signaling synergize with the viral membrane fusion machinery to facilitate virus entry and intercellular spread. Unraveling the underlying interactions among viral glycoproteins, envelope proteins, and cellular receptors will provide new innovative approaches for antiviral therapy against herpesviruses and other neurotropic viruses.

Intracranial nociception.

Understanding intracranial nociceptive innervation is essential to understand the pathophysiology of headaches. Our knowledge about human intracranial nociception comes from sparse observations during neurosurgical procedures performed in awake patients, from human anatomical studies and from experimental studies in animals. In this article we review the anatomical and functional organization underlying nociceptive innervation. Intracranial nociception is mainly mediated by the trigeminal system, except in the posterior cranial fossa that is innervated by the first cervical roots. For decades, the dura mater, its vessels and major cerebral blood vessels were considered as the only intracranial pain-sensitive structures. Recent animal and human studies have suggested that smaller brain arteries and potentially pia mater might also be pain sensitive. Nociceptive neurons innervating intracranial blood vessels project via the ophthalmic division (V1) to the trigeminal ganglion and store several neurotransmitters including glutamate, substance P and calcitonin gene-related peptide (CGRP). The trigeminal ganglion, root and brainstem nuclei have a specific topographic and functional somatotopy. Progressive transition between the trigeminal spinal nucleus and the dorsal horn of the cervical spinal cord, and convergence of nociceptive inputs from the face, intracranial structures and the occipital area on the so-called "trigemino-cervical complex" may explain some headache features, relations between facial and occipital pain, and efficacy of occipital nerve stimulation in headache. The specific anatomic organization of the trigeminal system, from the primary-order neuron in the trigeminal ganglion, to the second-order neuron is the trigeminal nuclei, may explain a part of the various characteristics of headaches.

Rational Design of Live-Attenuated Vaccines against Herpes Simplex Viruses.

Diseases caused by human herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) affect millions of people worldwide and range from fatal encephalitis in neonates and herpes keratitis to orofacial and genital herpes, among other manifestations. The viruses can be shed efficiently by asymptomatic carriers, causing increased rates of infection. Viral transmission occurs through direct contact of mucosal surfaces followed by initial replication of the incoming virus in skin tissues. Subsequently, the viruses infect sensory neurons in the trigeminal and lumbosacral dorsal root ganglia, where they are primarily maintained in a transcriptionally repressed state termed “latency”, which persists for the lifetime of the host. HSV DNA has also been detected in other sympathetic ganglia. Periodically, latent viruses can reactivate, causing ulcerative and often painful lesions primarily at the site of primary infection and proximal sites. In the United States, recurrent genital herpes alone accounts for more than a billion dollars in direct medical costs per year, while there are much higher costs associated with the socio-economic aspects of diseased patients, such as loss of productivity due to mental anguish. Currently, there are no effective FDA-approved vaccines for either prophylactic or therapeutic treatment of human herpes simplex infections, while several recent clinical trials have failed to achieve their endpoint goals. Historically, live-attenuated vaccines have successfully combated viral diseases, including polio, influenza, measles, and smallpox. Vaccines aimed to protect against the devastation of smallpox led to the most significant achievement in medical history: the eradication of human disease by vaccination. Recently, novel approaches toward developing safe and effective live-attenuated vaccines have demonstrated high efficacy in various preclinical models of herpetic disease. This next generation of live-attenuated vaccines has been tailored to minimize vaccine-associated side effects and promote effective and long-lasting immune responses. The ultimate goal is to prevent or reduce primary infections (prophylactic vaccines) or reduce the frequency and severity of disease associated with reactivation events (therapeutic vaccines). These vaccines’ “rational” design is based on our current understanding of the immunopathogenesis of herpesviral infections that guide the development of vaccines that generate robust and protective immune responses. This review covers recent advances in the development of herpes simplex vaccines and the current state of ongoing clinical trials in pursuit of an effective vaccine against herpes simplex virus infections and associated diseases.

Cavernous Sinus Meningioma: Tumor Decompression for Trigeminal Neuralgia and Anterior Tibial Artery Graft High-Flow Bypass for Brain Ischemia: 2-Dimensional Operative Video.

A 62-yr-old man with left cavernous sinus tumor presented with atypical trigeminal neuralgia refractory to medical treatment. He received Gamma Knife (Elekta) radiation for the tumor. However, the facial pain worsened after radiation. Neuropsychological testing done for memory problems had revealed mild neurocognitive disorder. Neurological examination showed trigeminal distribution numbness and partial abducens nerve paralysis. Imaging revealed an enhancing left cavernous sinus and supra-cavernous mass. Angiography revealed severe stenosis of the left cavernous internal carotid artery (ICA). Computed tomography (CT) perfusion study showed diminished blood flow on the left side, and ischemic changes were seen in fluid-attenuated inversion-recovery (FLAIR) magnetic resonance imaging (MRI). Surgical resection of the tumor was preferred over ablative treatment for trigeminal neuralgia because of its effectiveness in improving cranial nerve (CN) function.1 The patient underwent staged surgeries. In the first stage, the tumor was partially excised with decompression of the trigeminal ganglion and nerve root in the lateral cavernous sinus wall, Meckel's cave. Postoperatively, MR angiography revealed worsening of the left ICA caliber. Therefore, a high-flow bypass from the external carotid artery to the middle cerebral artery (MCA) was performed with an anterior tibial artery graft. The patient recovered initially but developed enterococcus meningitis postoperatively, which was promptly identified and treated with antibiotics. At 1-yr follow-up, the graft was patent, and the patient had significant relief of his facial pain and cognitively improved. This 2-dimensional video demonstrates the technique of partial excision of cavernous sinus meningioma with CN decompression, and the technique of a high-flow bypass from the external carotid artery to M2 MCA segment using an anterior tibial artery graft. The patient gave informed consent for surgery and video recording. All relevant patient identifiers have been removed from the video and accompanying radiology slides.

A patient with probable neuro‐Behçet's disease presenting a unique linear pontine trigeminal root lesion and a linear subcortical white matter lesion

AbstractBackgroundNeuro‐Behçet's disease (NBD) is typically characterized by inflammatory lesions with vasculitis in the brainstem and basal ganglia. Subcortical white matter lesions and linear lesions along the intramedullary trigeminal nerve are rare, and these lesions make NBD difficult to differentiate from other demyelinating diseases, such as multiple sclerosis.Case presentationA 48‐year‐old woman with an 11‐year history of intestinal Behçet's disease was referred to Department of Neurology, Tohoku Medical and Pharmaceutical University Hospital, Sendai, Japan owing to numbness on the left side of her face and oral cavity for 12 days. Neurological examination revealed left facial hypoesthesia. Brain magnetic resonance imaging showed a linearly shaped T2/fluid‐attenuated inversion recovery hyperintense magnetic resonance imaging lesion in the left pons, which corresponded neuroanatomically with the intramedullary trigeminal root. Based on the presumptive diagnosis of NBD, a course of high‐dose intravenous methylprednisolone was administered on the 14th hospital day. Thereafter, the patient's neurological symptoms improved. However, on the 18th hospital day, the patient developed a linear subcortical white matter lesion with vasogenic edema in the right hemisphere that resolved after the re‐administration of high‐dose intravenous methylprednisolone.ConclusionThe case of a patient with NBD presenting with atypical brain lesions is reported. The NBD in this case might have a pathogenetic mechanism that is different from that of typical NBD.

Microsurgical Anatomy of the Endoscopy-Assisted Retrosigmoid Intradural Suprameatal Approach to the Meckel's Cave.

Understanding the microsurgical anatomical features of the endoscopy-assisted retrosigmoid intradural suprameatal approach (RISA) is critical for surgeons treating petroclival tumors or lesions in the cerebellopontine region that extend into Meckel's cave. To evaluate increased exposure for Meckel's cave in the RISA and assess the surgical landmarks for this approach. A standard retrosigmoid craniotomy to the cerebellopontine region was performed in 4 cadaveric specimens (8 hemispheres) with microscope-assisted endoscopy. The length and depth of the drilling region from the suprameatal tubercle to the petrous apex were analyzed. After opening Meckel's cave and mobilizing the trigeminal root completely, the landmarks for this approach were investigated. The endoscopy-assisted RISA facilitates mobilization of the trigeminal root and enhances surgical exposure in the region of Meckel's cave and the petrous apex with increases of 10.1±1.3 mm in depth, 21.4±3.2 mm in length, and 6.4±0.6 mm in height. The posterior and superior semicircular canals, internal auditory canal, superior petrous sinus, and internal carotid artery (petrous segment) served as important landmarks for this approach. One case illustration is presented to describe the application of this approach. The RISA is suitable mainly for lesions in the posterior fossa that extend into Meckel's cave. The endoscopy-assisted reach optimizes accessibility to the petrous apex region, obviates the need for extensive drilling, and decreases the risk of internal carotid artery injury. Better realization and recognition of microsurgical landmarks and parameters of this approach are crucial for successful outcomes.

Using RNA-Seq to Explore the Hub Genes in the Trigeminal Root Entry Zone of Rats by Compression Injury

Mechanical compression on the trigeminal root entry zone (TREZ) by microvascular is the main etiology of primary trigeminal neuralgia (TN). To study the pathogenesis of TN, hub genes screening in the TREZ of TN in an animal model was performed. A double blind, randomized study was designed in a controlled animal trial. The research took place in the Laboratory of Clinical Applied Anatomy at the School of Basic Medical Science of Fujian Medical University. Twelve male rats were randomly divided into a sham operation group and a TN animal model group. TN animal model was induced by chronic compression of trigeminal nerve root (CCT) operation. Gene expression in the TREZ were analyzed by RNA sequencing (RNA-Seq) technique. KEGG analysis, GO analysis, and PPI analysis were performed in the DEGs. Key signaling pathways analyzing by GSEA and the hub genes in the DEGs were also studied. Reverse transcription real-time polymerase chain reaction (RT-qPCR) was used to verify the RNA-Seq results. Transcriptome data showed that 352 genes up-regulated and 59 genes down-regulated in DEGs on post-operation day 21, after CCT operation in the TN group. KEGG analysis revealed that, "neuroactive ligand receptor interaction" and "cytokine cytokine receptor interaction" may be related to the pathogenesis of TN. GO analysis showed "regulation of signing receptor activity", "chemokine activity", and "carbohydrate binging" may be related to TN. The RT-qPCR results were consistent with the test results, indicating that the transcriptome sequencing results were reliable. Although the incidence of TN in female rats was higher than in male rats, we only used male SD rats to establish the TN animal model, to avoid the effect of estrogen on experimental results. This study only presents some respects of RNA-Seq technique and, therefore, did not identify the DEGs at the protein level. The relationship between the DEGs at different levels shoud be done in the future. Based on the results of RNA-seq, this study discovered 6 hub genes in the TREZ that are closely related to the TN animal model, which provide a potential breakthrough point to explore the pathogenesis of TN.

FAM19A5l Affects Mustard Oil-Induced Peripheral Nociception in Zebrafish.

Family with sequence similarity 19 (chemokine (C-C motif)-like) member A5 (FAM19A5) is a chemokine-like secretory protein recently identified as involved in the regulation of osteoclast formation, post-injury neointima formation, and depression. Although roles for FAM19A5 have been described in nervous system development and psychiatric disorders, its role in the nervous system remains poorly understood. Here, we analyzed the evolutionary history of FAM19A genes in vertebrates and identified FAM19A5l, a paralogous zebrafish gene originating from a common ancestral FAM19A5 gene. Further, zebrafish FAM19A5l is expressed in trigeminal and dorsal root ganglion neurons as well as distinct neuronal subsets of the central nervous system. Interestingly, FAM19A5l+ trigeminal neurons are nociceptive neurons that localized with TRPA1b and TRPV1 and respond to mustard oil treatment. Behavioral analysis further revealed that the nociceptive response to mustard oil decreases in FAM19A5l-knockout zebrafish larvae. In addition, TRPA1b and NGFa mRNA levels are down- and upregulated in FAM19A5l-knockout and -overexpressing transgenic zebrafish, respectively. Together, our data suggest that FAM19A5l plays a role in nociceptive responses to mustard oil by regulating TRPA1b and NGFa expression in zebrafish.

Potential Molecular Targets for Treating Neuropathic Orofacial Pain Based on Current Findings in Animal Models.

This review highlights potential molecular targets for treating neuropathic orofacial pain based on current findings in animal models. Preclinical research is currently elucidating the pathophysiology of the disease and identifying the molecular targets for better therapies using animal models that mimic this category of orofacial pain, especially post-traumatic trigeminal neuropathic pain (PTNP) and primary trigeminal neuralgia (PTN). Animal models of PTNP and PTN simulate their etiologies, that is, trauma to the trigeminal nerve branch and compression of the trigeminal root entry zone, respectively. Investigations in these animal models have suggested that biological processes, including inflammation, enhanced neuropeptide-mediated pain signal transmission, axonal ectopic discharges, and enhancement of interactions between neurons and glial cells in the trigeminal pathway, are underlying orofacial pain phenotypes. The molecules associated with biological processes, whose expressions are substantially altered following trigeminal nerve damage or compression of the trigeminal nerve root, are potentially involved in the generation and/or exacerbation of neuropathic orofacial pain and can be potential molecular targets for the discovery of better therapies. Application of therapeutic candidates, which act on the molecular targets and modulate biological processes, attenuates pain-associated behaviors in animal models. Such therapeutic candidates including calcitonin gene-related peptide receptor antagonists that have a reasonable mechanism for ameliorating neuropathic orofacial pain and meet the requirements for safe administration to humans seem worth to be evaluated in clinical trials. Such prospective translation of the efficacy of therapeutic candidates from animal models to human patients would help develop better therapies for neuropathic orofacial pain.

The changing face of trigeminal neuralgia-A narrative review.

This narrative review aims to update the reader on the new classification of trigeminal neuralgia (TN), clinical signs, pathophysiologic evidence, and their implications on management. This review is based on the authors' collective experience and knowledge of the literature in addition to a literature search. In recent years, the phenotype of TN has been intensively studied leading to discrete groups of patients. These include patients with TN with additional continuous pain, and patients with and without neurovascular compression of the trigeminal dorsal root entry zone. A number of associated clinical signs such as tearing and sensory changes need further research. The literature on TN was searched in PubMed with the aims of providing evidence for the recently published third edition of the International Classification of Headache Disorders (ICHD) and update the clinical phenotype and management of the TN subcategories. The ICHD's new classification for TN is based on reliable clinical data, imaging, and neurophysiologic studies. The TN classification reflects current knowledge and has improved the possibility for clinicians to choose adequate management options. However, there is a lack of effective, safe drugs for the management of TN and sparse, robust data on neurosurgical options. Research into all aspects of TN-diagnosis, pharmacotherapy, surgery, long-term management prognosis, and natural history-is needed. Research should adhere to the ICHD's schema for TN. Improved drugs are needed along with rigorous research into surgical options and their efficacy for different subtypes of TN.

Recent, Bioelectricity-Related Articles Selected by Ann M. Rajnicek, Media Editor of Bioelectricity.

Recent, Bioelectricity-Related Articles Selected by Ann M. Rajnicek, Media Editor of Bioelectricity.

A Cadaver Study Confirming the Location of Dye after Trigeminal Ganglion Rhizotomy

Radiofrequency thermal rhizotomy demonstrates an excellent treatment outcome with a high success rate among patients of intractable trigeminal neuralgia. The triangular plexus which is an immediate retrogasserian portion of the trigeminal root is suggested as the best place of lesioning during radiofrequency thermal rhizotomy. However, the anatomy of the triangular plexus has been relatively unrecognized, while the anatomical study related to therapeutic procedure is scarce. The purpose of this study is to confirm with gross and microscopic finding of the trigeminal system whether, if an electrode tip is placed on the petroclival junction in lateral cranial view, it actually arrives at the triangular plexus or not. In relation to therapeutic procedure, we examined the triangular plexus with morphological and histological methods. Human cadaveric study. An anatomical laboratory in South Korea. Percutaneous procedure of radiofrequency thermal rhizotomy under C-arm guidance was performed in 8 cadavers. Final target of the electrode tip was the petroclival junction under true lateral cranial view. The location of the electrode tip was determined under observation of the presence of an injected dye. Triangular plexus size was measured grossly and microscopically. Gross and microscopic evaluation of the triangular plexus was performed. Among 15 trigeminal systems, 8 showed dye appearance in the triangular plexus, while 6 showed it in the trigeminal ganglion. Overall, 53% of radiofrequency thermal rhizotomy could reach the triangular plexus when an electrode tip was placed on the petroclival junction. The grossly measured average triangular plexus vertical and transverse diameters were 0.8 cm and 1.3 cm, respectively. Only radiologic landmark was used to confirm the location of the electrode tip. However, further study confirming the location of the electrode tip under the guidance of electrical stimulation is needed. When an electrode tip was placed on the petroclival junction, 53% of radiofrequency thermal rhizotomy could reach the triangular plexus.

The effect of IL-6/Piezo2 on the trigeminal neuropathic pain.

The nature of trigeminal neuropathic pain (TN) attacks is regarded as the ignition of ectopic action potentials from the trigeminal root following vascular compression, which seemed to be related to transmembrane proteins and inflammation factors. This study focused on the mechanosensitive channel Piezo2 and cytokine IL-6.The chronic constriction injury of infraorbital nerve in SD rats was used to establish the TN model. The trigeminal ganglion was then achieved to perform immunocytochemistry studies.A significant upregulation of Piezo2 and IL-6 was showed in the TN model rats. The Piezo2 positive accounted for 72.3±9.5% in those IL-6 positive neurons. The Piezo2 co-localized with CGRP, IB4 and NF-200 but not with GFAP, which implied that it was expressed in both the C-type and the A-type neurons. After administration of GsMTx4 or anti-rat IL-6 antibody in the TN model, the dynamic allodynia and pinprick hyperalgesia scores as well as the mechanical threshold changed significantly. In the sham-operation rates, with local administration of IL-6, an upregulation of Piezo2 was also exhibited.Our study demonstrated that the up-regulation of Piezo2 in the pain afferent neurons following trigeminal nerve injury may play a role in the development of the neuralgia. Meanwhile, the expression of Piezo2 may be modulated by inflammatory cytokines, such as IL-6.

Nerve Splitting and Vascular Transposition for Trigeminal Neuralgia Attributed to Nerve Penetrating Trigeminocerebellar Artery: 2-Dimensional Operative Video.

The trigeminocerebellar artery (TCA) is an infrequent anatomic anomaly of the branches originating from the basilar artery. It is clinically identifiable by the presence of the ipsilateral superior cerebellar artery and the anterior inferior cerebellar artery, and its course from the basilar artery to the cerebellar hemisphere. Because of its anatomic proximity to the trigeminal nerve root, the TCA often causes trigeminal neuralgia (TGN). Unlike other common arteries, repositioning the TCA is not always feasible when it penetrates the trigeminal nerve root (the intraneural type of TCA). In addition, the rich perforators originating from the TCA may limit its movability. The nerve decompression technique in such a rare condition has not yet been fully assessed. In this video, we present the nerve-splitting method for the intraneural type of TCA, in which sufficient isolation of the sensory root is achieved. The motor root of the trigeminal nerve originates from the brainstem slightly rostral of the root entry zone of the sensory root. Dissecting the motor root from its exit to the porous trigeminus allows mobilization of the root together with penetrating TCA away from the sensory root. The movability of the TCA increases by dissecting its perforators to the nerve root and brain stem. Sufficient separation of the sensory root contributes to ensuring the surgical result of nerve decompression and reducing the risk of recurrence due to adhesion. No complications of motor root retraction, such as masseter weakness and malocclusion, were noted in our experience. All data identifying the patients were anonymized. All procedures performed in this study were in accordance with the ethical standards of our institutional and national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. This study also obtained approval from the ethics committee of our institution. Written informed consent was obtained from all individual participants, as well as their first-degree relatives, included in this study.

Results of percutaneous rhizotomy for trigeminal neuralgia in patients with multiple sclerosis

Introduction. Neuropathic pain in trigeminal neuralgia (TN) is one of the most common and debilitating symptoms in patients with multiple sclerosis (MS). This condition in MS is due to the demyelination of pontine afferent fibers in the sensory root of the trigeminal nerve. The area of demyelination is usually located in the ventrolateral pons between the exit of the trigeminal nerve root and the trigeminal nucleus, which is confirmed on MRI. In some cases, neurovascular compression also plays a role in afferent fiber injury, leading to the so-called double crush effect. Conservative therapy for TN in patients with MS is often insufficiently effective, thus increasing the pertinence of surgical treatment. Materials and methods. The article reviews current pharmacological and surgical approaches to treating TN, findings from the literature, and our data on the safety and efficacy of percutaneous radiofrequency rhizotomy (PRR) for TN, based on the surgical treatment of 52 patients with MS at the Research Center of Neurology. Results. PRR works by interrupting the connection between peripheral receptor zones and the hyperactive trigeminal structures in the brainstem. All patients were discharged from the hospital on day 2–3 after surgery, with complete pain resolution. There were early and late relapses in some instances, which required a repeated PRR. Conclusion. PRR is a symptomatic surgical method that is safe, repeatable, and effective for treating TN in patients with MS, in whom pharmacological therapy has been ineffective or who could not tolerate it. For citation: Tyurnikov V.M., Askarova L.Sh., Trifonova O.V., Zakharova M.N., Gushcha A.O. [Results of percutaneous rhizotomy for trigeminal neuralgia in patients with multiple sclerosis]. Annals of clinical and experimental neurology. 2021; 15(1): 89–94. (In Russ.). https://doi.org/10.25692/ACEN.2021.1.11

Location of the abducens nerve stretched by a tortuous vertebrobasilar artery in trigeminal neuralgia.

Trigeminal neuralgia (TGN) caused by the vertebrobasilar artery (VBA) is uncommon. The abducens nerve root is frequently dislocated by a tortuous VBA near the trigeminal nerve root. This unusual location of the root is not well known. This study aimed to investigate the location of the stretched abducens nerve root. The objective is 26 patients with VBA-related TGN who underwent microvascular decompression (MVD). We retrospectively investigated the course of the abducens nerve root with magnetic resonance imaging (MRI) with three-dimensional (3D) imaging and surgical findings. The displacement of the abducens nerve root on the affected side was compared to the contralateral side. The abducens nerve root was distorted by a tortuous VBA (46.2%) or the anterior inferior cerebellar artery (53.8%). The average length of the cisternal segment was stretched to 23.4 mm versus 12.4 mm on the contralateral side. The peak point of the elevated abducens nerve root was mostly located rostro-medial (65.4%) or caudo-medial (34.6%) to the neurovascular compression site of the trigeminal nerve with a mean distance of 9.1 mm. Contact with the trigeminal nerve root was observed in 7 patients (26.9%). Three-dimensional imaging was consistent with the surgical findings and useful in predicting the location of the abducens nerve root. No abducens nerve palsy was noted in our series. The abducens nerve root is located near the trigeminal nerve root in VBA-related TGN. Preoperative understanding of the unusual course of the abducens nerve root contributes to avoiding accidental nerve injury during MVD.

Petrosal Vein Involvement in Neurovascular Conflict in Trigeminal Neuralgia: Surgical Technique and Clinical Outcomes.

Contact of the main stem of the petrosal vein (PV) to the nerve root is a rare cause of trigeminal neuralgia (TGN). The implication of the PV in relation with neurovascular contact (NVC) is not fully understood. To assess the operative procedures in microvascular decompression (MVD) in patients with PV involvement in the long-term. We retrospectively reviewed 34 cases (7.0%) in 485 consecutive MVDs for TGN, whose PV main stem had contact with the trigeminal nerve root (PV-NVC). PV-NVCs were divided into 2 groups: concomitant arterial contact or no concomitant arterial contact. Surgical techniques, outcomes, complications, and recurrence were assessed. The anatomical relationship of the PV with the trigeminal nerve root was consistent with preoperative 3-dimensional imaging in all patients. Pain relief was obtained in most patients immediately after surgery (97.1%) by separating the PV from the nerve root. Postoperative facial numbness was noted in 9 patients (26.5%). Symptomatic venous infarctions occurred in 2 patients (5.9%). Recurrence of facial pain occurred in 3 patients (8.8%) with a median 48 mo follow-up period. Re-exploration surgery revealed adhesion being the cause of recurrence. The statistical analyses showed no difference in the surgical outcomes of the 2 groups. Separating the PV from the nerve root contributes to pain relief in patients with PV conflict regardless of concomitant arteries. Preserving venous flow is crucial to avoid postoperative venous insufficiency.

Microvascular Transposition Without Teflon: A Single Institution's 17-Year Experience Treating Trigeminal Neuralgia.

Trigeminal neuralgia (TN) refractory to medical management is often treated with microvascular decompression (MVD) involving the intracranial placement of Teflon. The placement of Teflon is an effective treatment, but does apply distributed pressure to the nerve and has been associated with pain recurrence. To report the rate of postoperative pain recurrence in TN patients who underwent MVD surgery using a transposition technique with fibrin glue without Teflon. Patients were eligible for our study if they were diagnosed with TN, did not have multiple sclerosis, and had an offending vessel that was identified and transposed with fibrin glue at our institution. All eligible patients were given a follow-up survey. We used a Kaplan-Meier (KM) model to estimate overall pain recurrence. A total of 102 patients met inclusion criteria, of which 85 (83%) responded to our survey. Overall, 76 (89.4%) participants responded as having no pain recurrence. Approximately 1-yr pain-free KM estimates were 94.1% (n=83), 5-yr pain-free KM estimates were 94.1% (n=53), and 10-yr pain-free KM estimates were 83.0% (n=23). Treatment for TN with an MVD transposition technique using fibrin glue may avoid some cases of pain recurrence. The percentage of patients in our cohort who remained pain free at a maximum of 17 yr follow-up is on the high end of pain-free rates reported by MVD studies using Teflon. These results indicate that a transposition technique that emphasizes removing any compression near the trigeminal nerve root provides long-term pain-free rates for patients with TN.

Trigeminal radiculopathy in vestibular schwannomas

To evaluate the correlation of trigeminal radiculopathy with anatomical relationships of trigeminal nerve root, brainstem, tumors and vessels in patients with vestibular schwannomas. A retrospective analysis included 153 patients (106 females and 47 males aged 22-82 years) with vestibular schwannomas who underwent surgery via retromastoid approach. Preoperative trigeminal radiculopathy (facial pain and sensory disturbances) was examined after microsurgical resection. Brainstem compression was analyzed by comparison of transverse size of contralateral to vestibular schwannoma half of brainstem and ipsilateral side. Tumor-induced brainstem and trigeminal nerve compression was found in 115 cases. Sixty-four of these patients had trigeminal radiculopathy symptoms. Degree of brainstem compression was significantly higher in trigeminal radiculopathy group. Facial hypoesthesia was found in 61patients, trigeminal neuralgia - in 5 cases, neuropathic pain - in 3 patients. Thirty-seven patients without brainstem compression had no trigeminal nerve involvement. One patient had trigeminal neuralgia following compression by superior cerebellar artery. Total resection with brainstem and trigeminal nerve decompression were performed in all cases. Isolated or combined compression of trigeminal nerve root was noted in 9 patients with trigeminal neuralgia and neuropathic pain, in 2 with facial numbness and in 2 patients without trigeminal symptoms. In case of trigeminal neuralgia following compression by superior cerebellar artery, vascular decompression was performed only in patients with facial pain and numbness. Facial pain completely resolved in all patients. Complete or partial sensory restoration was noted in 25 cases. No facial sensory disorders were noted in 26 cases, transient sensory deterioration - in 10 patients. Trigeminal radiculopathy is caused by severe brainstem compression following vestibular schwannomas and usually results sensory disturbances and rarely facial pain. The impact of tumor on trigeminal nerve root and brainstem trigeminal pathways can be accompanied by vascular compression by superior cerebellar artery. Regression of trigeminal radiculopathy symptoms after resection of vestibular schwannoma is caused by decompression of trigeminal nerve root and brainstem. In case of concomitant neurovascular syndrome, vascular decompression is indicated.