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BACKGROUND:In trigeminal neuralgia type 1 (TN1), neurovascular compression (NVC) is often assumed to be the pain initiating mechanism. NVC can be surgically addressed by microvascular decompression (MVD). However, some patients with TN1 present without NVC (WONVC). OBJECTIVE:To characterize and analyze the clinical spectrum of a TN1 patient population WONVC. METHODS:A retrospective chart review of patients presenting with TN1 between 2007 and 2017 was performed. Patients who were potential candidates for MVD surgery underwent high-resolution imaging with 3-dimensional (3D) reconstruction to address the presence, or absence, of NVC. Demographic data about the populations with NVC (WNVC) and WONVC were collected. RESULTS:Of 242 patients with TN1, 32% did not have NVC. Patients WONVC were on average 10.6 yr younger than those WNVC. TN1 onset in patients WONVC was more frequent below 48.7 yr, and the opposite was found in patients WNVC. Compared to patients WNVC, those WONVC were predominantly female (odds ratio 4.8), on average were 4 yr younger at symptom onset (34.7 yr) and 7.8 yr younger at first clinic visit, and had a 3.7 yr shorter symptom duration. CONCLUSION:Patients presenting with TN1 WONVC were predominantly females in their mid-30s with short symptom duration. In the absence of NVC, this subgroup of TN1 patients has limited surgical options, and potentially a longer condition duration that must be managed medically or surgically. This population WONVC might provide insights into the true pathophysiology of TN1.

Neurovascular compression syndrome is caused by vessels touching a cranial nerve, resulting in clinical manifestations of abnormal sensory or motor symptoms. The most common manifestations are trigeminal neuralgia and hemifacial spasm. However, neurovascular compression of the vestibular nerve or glossopharyngeal nerve are rare. In this article, we describe four typical cases of neurovascular compression syndrome. In addition, we analyze the main features of the etiology, neuroimaging, and treatment of this disease. •Neurovascular compression syndrome (NVCS) is a condition due to compression of the cranial nerve by adjacent vessels.•The most common manifestations are trigeminal neuralgias (TN), hemifacial spasm (HFS), however, reports of vestibular paroxysmia (VP) and glossopharyngeal neuralgia (GPN) are rare.•Moreover, reviews and analyses of the pathology, symptomatology, neuroimaging, and treatment of NVCS are lacking.•Here, we present four typical cases of NVCS and provide a literature review of previously reported cases to guide clinical practice.

Neurovascular compression syndromes (NVC) are challenging disorders resulting from the compression of cranial nerves at the root entry/exit zone. Clinically, we can distinguish the following NVC conditions: trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia. Also, rare cases of geniculate neuralgia and superior laryngeal neuralgia are reported. Other syndromes, e.g., disabling positional vertigo, arterial hypertension in the course of NVC at the CN IX-X REZ and torticollis, have insufficient clinical evidence for microvascular decompression. The exact pathomechanism leading to characteristic NVC-related symptoms remains unclear. Proposed etiologies have limited explanatory scope. Therefore, we have examined the underlying pathomechanisms stated in the medical literature. To achieve our goal, we systematically reviewed original English language papers available in Pubmed and Web of Science databases before 2 October 2021. We obtained 1694 papers after eliminating duplicates. Only 357 original papers potentially pertaining to the pathogenesis of NVC were enrolled in full-text assessment for eligibility. Of these, 63 were included in the final analysis. The systematic review suggests that the anatomical and/or hemodynamical changes described are insufficient to account for NVC-related symptoms by themselves. They must coexist with additional changes such as factors associated with the affected nerve (e.g., demyelination, REZ modeling, vasculature pathology), nucleus hyperexcitability, white and/or gray matter changes in the brain, or disturbances in ion channels. Moreover, the effects of inflammatory background, altered proteome, and biochemical parameters on symptomatic NVC cannot be ignored. Further studies are needed to gain better insight into NVC pathophysiology.

In 2016, the Bárány Society defined new diagnostic criteria for the neurovascular compression syndrome of the eighth nerve, called “vestibular paroxysmia” (VP), differentiating between definite (dVP) and probable (pVP) forms. The aim of this study was (1) to describe clinical symptoms and laboratory findings in a well-diagnosed large patient cohort according to those criteria, and (2) to evaluate the long-term course over years in dVP. We identified 146 patients (73 dVP, 73 pVP) from our tertiary dizziness center registry. Data of structured history-taking, clinical neurological, neuro-ophthalmological/-otological examinations as well as MRI imaging were extracted for analyses. Overall, attack frequency ranged between 5 and 30 attacks per day; spinning vertigo was the most frequent type. In two-thirds of patients, attacks occurred spontaneously; in one-quarter, they were triggered by head movements. The majority (approximately 70%) reported no accompanying symptoms; in those with symptoms, mild unilateral cochlear symptoms prevailed. One-third of patients initially showed hyperventilation-induced nystagmus without specific direction, and a deviation of the subjective visual vertical between 3° and 6°. Complete loss of peripheral vestibular function was never evident. dVP and pVP significantly differed concerning the vertigo type, e.g., spinning vertigo was more frequent in dVP. Fortunately, three-quarters of dVP patients remained attack-free during follow-up (mean 4.8 years, standardized questionnaire), more than half of them even without any medication. Patients with ongoing attacks showed significantly higher attack frequency at baseline, but reported persistent frequency reduction. Overall, the long-term prognosis of VP appears favorable, not necessarily requiring ongoing treatment.

Trigeminal neuralgia (TN) is a common pain syndrome and is characterized by recurrent episodes of intense lancinating pain in one or more divisions of the trigeminal nerve. Neurovascular compression (NVC) has been considered as the main cause of TN in the root entry zone (REZ) of the trigeminal nerve in the cerebellopontine angle cistern. Microvascular decompression (MVD) is the surgical procedure of choice for the treatment of medically refractory TN. MVD has also been shown to provide pain relief even in patients without visible neurovascular compression. Additionally, it has been accepted that MVD can provide the highest rate of long-term patient satisfaction with the lowest rate of pain recurrence. We did, systematic review of the subject and also our own experiences.

Purpose Building on the pioneering observations of Dandy and Gardner and on Jannetta’s establishment of microvascular decompression (MVD) through microsurgical demonstration of vascular compression, MVD has continuously evolved into a safe and durable treatment for neurovascular compression syndromes. Despite advances in radiosurgery and pharmacotherapy, MVD remains widely used as a first-line surgical option for appropriately selected patients with trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia. Methods This selective narrative historical review traces MVD’s modern evolution after its establishment by Jannetta, organized into four pillars: surgical anatomy, optimization of approaches, decompression strategies, and operative support. Results Detailed microsurgical anatomy, including the “Rule of Three” framework for the cerebellopontine angle, has helped guide tailored, minimally invasive approaches (e.g., the lateral supracerebellar-infratentorial route for trigeminal neuralgia and infrafloccular exposure for hemifacial spasm). Decompression strategies have extended from prosthetic interposition toward noncompressive transposition and biologically harmonious fixation. Advances in visualization (endoscopic and exoscopic systems), simulation, and neuronavigation have extended the original visualization ethos and enhanced surgical education. Intraoperative monitoring, including brainstem auditory evoked potentials and lateral spread responses, has improved both complication avoidance and intraoperative confidence. Conclusion Together, these anatomical “maps” and physiological “compasses” help define contemporary MVD practice aimed at safe and durable outcomes across diverse patient anatomies.

Cranial nerves are mechanically irritated by vascular compression in neurovascular compression syndromes. Vagus nerve neuralgia is one of the less prevalent types of Neurovascular Compression Syndromes. It can cause disorders like Hemilaryngopharyngeal Spasm (HeLPS) and Vagus Associated Neurogenic Cough (VANCOUVER syndrome). HeLPS presents with unilateral spasms of the throat and coughing, whereas VANCOUVER syndrome is typified by a chronic cough brought on by vascular encroachment on the rootlet of the vagus nerve. The diseases' clinical manifestations, diagnosis, differential diagnoses, and therapy approaches are discussed, emphasizing the role of microvascular decompression (MVD) in the case of conservative treatment failure. Due to vagus nerve neuralgia's similarities to other diseases, including psychiatric conditions and gastroesophageal reflux disease (GERD), it can be difficult to diagnose and treat. To make the best possible treatment decisions, the effectiveness of both conservative and surgical care modalities including MVD and medication is discussed. •HeLPS and VANCOUVER syndromes are rare vagal nerve neuralgias caused by vascular compression of the vagus rootlet.•Microvascular decompression may cure both syndromes; medications and botulinum toxin offer only partial relief.•High-resolution MRI identifies vagus nerve conflicts, but imaging findings must match clinical symptoms.•VANCOUVER syndrome causes a tickling sensation and chronic cough, unresponsive to standard therapies like antibiotics or anti-reflux therapy.•Untreated, these syndromes impair quality of life and may cause syncope, incontinence, or airway emergencies.

Background Various instruments are used in microvascular decompression (MVD) to mobilize offending vessels. Most instruments have straight tips for safety but provide limited ability to retract vessels toward the surgeon. To address this limitation, we developed a double-faced microprobe, designated as the “SWAN probe,” to enhance maneuverability in confined operative spaces. Methods The instrument has a 2.5-mm upward-bending tip (1.0-mm width) with multiple curved surfaces for controlled vessel manipulation. The inner face (angled at 45° with a narrow hollow) allows secure vessel capture and retraction, whereas the outer face (angled at 60° with a broader hollow) is optimized for advancing the vessel away from the nerve. Flat lateral surfaces enable gentle lateral displacement. The sandblasted surface reduces slippage and minimizes light reflection. The microprobe was used in 51 MVD procedures for trigeminal neuralgia (TN) and hemifacial spasm (HFS). Its utility and safety were assessed based on intraoperative performance across key maneuvers. Results Usability scores were consistently higher than the theoretical baseline representing procedures achievable with conventional straight-tip instruments. Benefits were most apparent during proximal retraction (“pull-out”) maneuvers of the superior cerebellar artery. The probe also aided Teflon sling handling and controlled arachnoid incision. No procedure-related complications attributable to the instrument were observed. Conclusions The double-faced microprobe allows both retraction and displacement of offending vessels, improving intraoperative maneuverability in selected situations. Within the limits of this study, the SWAN probe appears to be a safe and useful adjunct for MVD and may have broader applicability in microsurgery.

This study aimed to explore the risk factors and potential causes of unilateral classical or idiopathic trigeminal neuralgia (C-ITN) by comparing patients and healthy controls (HCs) with neurovascular compression (NVC) using machine learning (ML). A total of 84 C-ITN patients and 78 age- and sex-matched HCs were enrolled. We assessed the trigeminal pons angle and identified the compressing vessels and their location and severity. Machine learning was employed to analyze the cisternal segment of the trigeminal nerve (CN V). Among the C-ITN patients, 53 had NVC on the unaffected side, while 25 HCs exhibited bilateral NVC, and 24 HCs showed unilateral NVC. By comparing the cisternal segment of CN V between C-ITN patients on the affected side and HCs with NVC, we identified the side of NVC, the compressing vessel, and certain texture features as risk factors for C-ITN. Additionally, four texture features differed in the structure of the cisternal segment of CN V between C-ITN patients on the unaffected side and HCs with NVC. Our findings suggest that the side of NVC, the compressing vessel, and the microstructure of the cisternal segment of CN V are associated with the risk of C-ITN. Furthermore, microstructural changes observed in the cisternal segment of CN V on the unaffected side of C-ITN patients with NVC indicate possible indirect effects on the CN V to some extent.

Aim of the present study was to conduct a comprehensive review of surgical strategies that can be offered to patients with trigeminal neuralgia undergoing microvascular decompression (MVD) surgery and without intraoperative evidence of neurovascular conflict, with a high pre-operative suspicion of conflict lacking intraoperative confirmation, or individuals experiencing recurrence after previous treatment. This systematic review followed established guidelines (PRISMA) to identify and critically appraise relevant studies. The review question was formulated according to the PICO (P: patients; I: intervention; C: comparison; O: outcomes) framework as follows. For patients with trigeminal neuralgia (P) undergoing MVD surgery (I) without demonstrable preoperative neurovascular conflict, high suspicion of conflict but no intraoperative confirmation or recurrence after previous treatment (C), do additional surgical techniques (nerve combing, neurapraxia, arachnoid lysis) (O) improve pain relief outcomes (O)? The search of the literature yielded a total of 221 results. Duplicate records were then removed (n = [76]). A total of 143 papers was screened, and 117 records were excluded via title and abstract screening; 26 studies were found to be relevant to our research question and were assessed for eligibility. Upon full-text review, 17 articles were included in the review, describing the following techniques; (1) internal neurolysis ( n  = 6) (2) arachnoid lysis/adhesiolysis ( n  = 2) (3) neurapraxia ( n  = 3) (4) partial rhizotomy of the sensory root ( n  = 4) (5) pontine descending tractotomy ( n  = 2). The risk of bias was assessed using the ROBINS-I (Risk of Bias in Non-randomized Studies - of Interventions) assessment tool. While the described techniques hold promise, further research is warranted to establish standardized protocols, refine surgical approaches, and comprehensively evaluate long-term outcomes.