scholarly journals Clinical and physiopathological aspects of the glossopharyngeal neuralgia

2021 ◽  
pp. 5-11
Author(s):  
Victor Souza ◽  
Maria Passerini ◽  
Bianca Sobral ◽  
Vinicius Baiardi ◽  
Hilton Junior
Keyword(s):  
Case Reports ◽  
Glossopharyngeal Neuralgia ◽  
Clinical Aspects ◽  
Decompression Surgery ◽  
Vascular Compression ◽  
Entry Zone ◽  
Root Entry Zone ◽  
Underlying Causes ◽  
Vagoglossopharyngeal Neuralgia ◽  
Microvascular Decompression Surgery

Introduction Glossopharyngeal neuralgia is a rare syndrome characterized by paroxysms of unilateral and severe stabbing pain occurring in the nerve’s distribution. Although other neuralgias are well described in the medical literature, glossopharyngeal neuralgia and its physiopathology are not. The vascular compression at the nerve root entry zone is the primary explanation for the disease. The first-line treatment is pharmacological, including carbamazepine, oxcarbazepine, and gabapentin. Surgical treatment is offered to medication-refractory patients, and microvascular decompression surgery has the best outcomes. Objective To investigate the pathophysiological and clinical aspects of the different presentations of glossopharyngeal neuralgia. Method: A systematic review of the literature including case reports and clinical trials, was done. Results A search of the literature yielded 31 papers that regarded glossopharyngeal neuralgia or its variants. Eight of these reports regarded vagoglossopharyngeal neuralgia. Seven regarded the glossopharyngeal neuralgia followed by or caused by another disease. Conclusion Glossopharyngeal neuralgia is a rare disease and requires further studies on its mechanism and clinical assessment; the physician needs to know how to distinguish it from its variants and underlying causes.

Glossopharyngeal neuralgia

1977 ◽  
Vol 47 (3) ◽  
pp. 316-320 ◽  
Author(s):  
Ranjit K. Laha ◽  
Peter J. Jannetta
Keyword(s):  
Posterior Inferior Cerebellar Artery ◽  
Cranial Nerves ◽  
Glossopharyngeal Neuralgia ◽  
Vascular Compression ◽  
Entry Zone ◽  
Content Type ◽  
Root Entry Zone ◽  
Cerebellar Artery ◽  
Sporadic Cases ◽  
Fine Print

✓ Various factors have been considered in the etiology and pathogenesis of glossopharyngeal neuralgia. Vascular compression of the involved cranial nerves has been demonstrated in sporadic cases. In this series of six patients, it was noted with the aid of the operating microscope that the ninth and tenth cranial nerves were compressed by a tortuous vertebral artery or posterior inferior cerebellar artery at the nerve root entry zone in five cases. In selected patients, microvascular decompression without section of the nerves may result in a cure.

Pathophysiology of trigeminal neuralgia: new evidence from a trigeminal ganglion intraoperative microneurographic recording

2004 ◽  
Vol 101 (5) ◽  
pp. 872-873 ◽  
Author(s):  
Kim J. Burchiel ◽  
Thomas K. Baumann
Keyword(s):  
Trigeminal Neuralgia ◽  
Trigeminal Ganglion ◽  
Physiological Mechanism ◽  
Vascular Compression ◽  
Entry Zone ◽  
Content Type ◽  
Root Entry Zone ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
New Evidence

✓ The origin of trigeminal neuralgia (TN) appears to be vascular compression of the trigeminal nerve at the root entry zone; however, the physiological mechanism of this disorder remains uncertain. The authors obtained intraoperative microneurographic recordings from trigeminal ganglion neurons in a patient with TN immediately before percutaneous radiofrequency-induced gangliolysis. Their findings are consistent with the idea that the pain of TN is generated, at least in part, by an abnormal discharge within the peripheral nervous system.

Microanatomy of the Central Myelin-Peripheral Myelin Transition Zone of the Trigeminal Nerve

Neurosurgery ◽  
2006 ◽  
Vol 59 (2) ◽  
pp. 354-359 ◽  
Author(s):  
Selçuk Peker ◽  
Özlem Kurtkaya ◽  
İbrahim Üzün ◽  
M Necmettin Pamir
Keyword(s):  
Trigeminal Neuralgia ◽  
Trigeminal Nerve ◽  
Transitional Zone ◽  
Vascular Compression ◽  
Lateral Aspect ◽  
Entry Zone ◽  
Root Entry Zone ◽  
Central Myelin ◽  
Trigeminal Nerves ◽  
Vascular Decompression

Abstract OBJECTIVE: The aim of this study was to evaluate the microanatomy of the central myelin-peripheral myelin transitional zone (TZ) in trigeminal nerves from cadavers. METHODS: One hundred trigeminal nerves from 50 cadaver heads were examined. The cisternal portion of the nerve (from the pons to Meckel's cave) was measured. Horizontal sections were stained and photographed. The photomicrographs were used to measure the extent of central myelin on the medial and lateral aspects of the nerve and to classify TZ shapes. RESULTS: The cisternal portions of the specimens ranged from 8 to 15 mm long (mean, 12.3 mm; median, 11.9 mm). The data from the photomicrographs revealed that the extent of central myelin (distance from pons to TZ) on the medial aspect of the nerve (range, 0.1–2.5 mm; mean, 1.13 mm; median, 1 mm) was shorter than that on the lateral aspect (range, 0.17–6.75 mm; mean, 2.47 mm; median, 2.12 mm). CONCLUSION: The data definitively prove that the root entry zone (REZ, nerve-pons junction) and TZ of the trigeminal nerve are distinct sites and that these terms should never be used interchangeably. The measurements showed that the central myelin occupies only the initial one-fourth of the trigeminal nerve length. If trigeminal neuralgia is caused exclusively by vascular compression of the central myelin, the problem vessel would always have to be located in this region. However, it is well known that pain from trigeminal neuralgia can resolve after vascular decompression at more distal sites. This suggests that the effects of surgical decompression are caused by another mechanism.

scholarly journals Current neurosurgical management of glossopharyngeal neuralgia and technical nuances for microvascular decompression surgery

2013 ◽  
Vol 34 (3) ◽  
pp. E8 ◽  
Author(s):  
Roberto Rey-Dios ◽  
Aaron A. Cohen-Gadol
Keyword(s):  
Microvascular Decompression ◽  
Cranial Nerve ◽  
Cranial Nerves ◽  
Pain Syndrome ◽  
Glossopharyngeal Neuralgia ◽  
Decompression Surgery ◽  
Delay In Diagnosis ◽  
Root Exit Zone ◽  
Microvascular Decompression Surgery

Glossopharyngeal neuralgia (GPN) is an uncommon facial pain syndrome often misdiagnosed as trigeminal neuralgia. The rarity of this condition and its overlap with other cranial nerve hyperactivity syndromes often leads to a significant delay in diagnosis. The surgical procedures with the highest rates of pain relief for GPN are rhizotomy and microvascular decompression (MVD) of cranial nerves IX and X. Neurovascular conflict at the level of the root exit zone of these cranial nerves is believed to be the cause of this pain syndrome in most cases. Vagus nerve rhizotomy is usually reserved for cases in which vascular conflict is not evident. A review of the literature reveals that although the addition of cranial nerve X rhizotomy may improve the chances of long-term pain control, this maneuver also increases the risk of permanent dysphagia and vocal cord paralysis. The risks of this procedure have to be carefully weighed against its benefits. Based on the authors' experience, careful patient selection with a thorough exploratory operation most often leads to identification of the site of vascular conflict, obviating the need for cranial nerve X rhizotomy.

Hemifacial Spasm Caused by a Venule: Case Report

Neurosurgery ◽  
1984 ◽  
Vol 14 (1) ◽  
pp. 89-92 ◽  
Author(s):  
Peter J. Jannetta
Keyword(s):  
Case Report ◽  
Facial Nerve ◽  
Blood Vessels ◽  
Hemifacial Spasm ◽  
Vascular Compression ◽  
Entry Zone ◽  
Root Entry Zone ◽  
Facial Spasm ◽  
Posterior Direction ◽  
Anterior Posterior

Abstract The syndrome of hemifacial spasm occurs as a consequence of compression, almost universally by blood vessels, of the root entry zone of the facial nerve. The vascular compression is usually obvious at operation, but may be subtle. The author describes a case in which a venule running in an anterior-posterior direction across the caudal aspect of the root entry zone of the facial nerve, which was thought to be causing the spasm, was coagulated and divided. A small, more distal arteriole, probably not contributory, was decompressed away from the nerve. After operation, the patient improved gradually, and she remains free of facial spasm or weakness. This is the most subtle vascular compression seen by the author and his colleagues in over 400 microvascular decompressions for hemifacial spasm.

scholarly journals Microvascular Decompression using Muscle Graft for Vertebral Artery Medullary Compression Syndrome

2020 ◽  
Vol 17 (3) ◽  
pp. 55-58
Author(s):  
Prasanna Karki ◽  
Damber Bikram Shah ◽  
Sumit Joshi ◽  
Prakash Poudel ◽  
Jessica Kayastha ◽  
...  
Keyword(s):  
Vertebral Artery ◽  
Medulla Oblongata ◽  
Microvascular Decompression ◽  
Decompression Surgery ◽  
Vascular Compression ◽  
Muscle Graft ◽  
Lateral Medullary Syndrome ◽  
Microvascular Decompression Surgery ◽  
Vertebral Artery Compression ◽  
Graft Interposition

It is well known that brainstem dysfunction may be caused by vascular compression of the medulla oblongata. However, only a limited number of reports have found microvascular decompression surgery to be an effective treatment for symptomatic patients with medulla oblongata dysfunction. This report describes a patient with vertebral artery compression of lateral medulla oblongata who presented with lateral medullary syndrome. Microvascular decompression surgery using the transcondylar fossa approach was effective in relieving patient symptoms. The transcondylar fossa approach and the transposition of vertebral artery along with autologous muscle graft interposition technique is appropriate in microvascular decompression surgery to relieve vertebral artery compression of medulla oblongata.  

scholarly journals Trigeminal Neuralgia associated with Wallenberg Syndrome, a case report

2021 ◽  
Author(s):  
Matheus Goncalves Maia ◽  
Vivian Dias Baptista Gagliardi ◽  
Francisco Tomaz Meneses Oliveira ◽  
Eduardo dos Santos Sousa ◽  
Marina Trombin Marques ◽  
...  
Keyword(s):  
Case Report ◽  
Trigeminal Neuralgia ◽  
Trigeminal Nerve ◽  
Vascular Compression ◽  
Gasserian Ganglion ◽  
Entry Zone ◽  
Root Entry Zone ◽  
Initial Event ◽  
The Right ◽  
The Brain

Context: Trigeminal neuralgia is typically associated with structural lesions that affect the brainstem, pre-ganglionic roots, gasserian ganglion and the trigeminal nerve. The association of trigeminal neuralgia with infarction of the dorsolateral medulla is rare, being more associated with pontine lesions, in the context of brainstem infarction. Methods: Report the case of a 55-year-old male patient, who presented with a left dorsolateral bulbar infarction, and developed a ipsilateral trigeminal neuralgia afterwards. Case report: A 55-year-old man attended to the emergency room referring sudden incoordination of the left limbs, associated with numbness of the contralateral limbs. The neurological examination showed nystagmus, numbness of the left face, ataxia of the left limbs and numbness of the right limbs. The Magnetic Resonance of the Brain revealed an area of recent infarction in the left posterolateral aspect of the medulla. He underwent thrombolysis, evolving with complete resolution of symptoms. In the week after the initial event, he returned to the outpatient clinic, reporting paroxysms of excruciating pain in the upper lip, nose and left zygomatic region, being diagnosed with neuralgia of the maxillary segment of the trigeminal nerve, improving with introduction of Gabapentin. Conclusion: Although most cases of trigeminal neuralgia are determined by vascular compression of the trigeminal nerve root entry zone, other causes must be considered. The association of this condition with dorsolateral medulla infarction is rare, with only 4 cases reported in the last 10 years.

Management of Recurrent Glossopharyngeal Neuralgia Following Microvascular Decompression Surgery

2018 ◽  
Vol 117 ◽  
pp. 339-343 ◽  
Author(s):  
Dhivya Palanisamy ◽  
Miyatani Kyosuke ◽  
Yamada Yasuhiro ◽  
Kawase Tsukasa ◽  
Yoko Kato
Keyword(s):  
Microvascular Decompression ◽  
Glossopharyngeal Neuralgia ◽  
Decompression Surgery ◽  
Microvascular Decompression Surgery

219 A Clinical Analysis on Microvascular Decompression Surgery for Treatment of Hemifacial Spasm: 2500 Cases Review in a Single Institute

Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 259-260
Author(s):  
Myeongki Yeo ◽  
Bong Jin Park ◽  
Hridayesh Pratap Malla ◽  
Bong Arm Rhee ◽  
Young Jin Lim
Keyword(s):  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Clinical Analysis ◽  
Postoperative Outcomes ◽  
Cerebrospinal Fluid Leakage ◽  
Subdural Hemorrhage ◽  
Decompression Surgery ◽  
Vascular Compression ◽  
Root Exit Zone ◽  
Microvascular Decompression Surgery

Abstract INTRODUCTION Hemifacial spasm (HFS) is caused by vascular compression of the facial nerve at its root exit zone from the brainstem. Microvascular decompression (MVD) is the only treatment option that offers the prospect of a definitive cure for HFS. However, this surgery can be risky and the postoperative outcomes might not be good enough sometimes. In order to refine that, we investigated our result of MVDs. METHODS Among 2500 consecutive cases of MVDs have been performed in our institute between January 2000 and December 2015, 2196 patients were enrolled in the current study. They were retrospectively analyzed with emphasis on postoperative outcomes and complications. RESULTS >Postoperatively, the spasm complete cease occurred immediately in 73.4%. The symptoms improved at some degree in 22.7%. The spasm not improved at all in 3.9%. However, the symptom free rate was 88.3% at 6 months after surgery. Eventually, the successful rate was increased by 93.1% at 1 year after MVD. Major complications included permanent hearing disturbance (1.13%), permanent facial palsy (0.4%), vertebral artery injury (0.2%), subdural hemorrhage (0.2%), and epidural hemorrhage (0.1%). Minor complications included transient cerebrospinal fluid leakage (1.3%), infection (0.6%). CONCLUSION MVD is a safe and effective treatment for HFS. A precise recognition of the neurovascular conflict site lead to a successful MVD.

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