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Rationale: Syncope caused by head and neck cancer (HNC) is rare. However, syncope caused by tongue cancer (TC) is even rarer. In TC, syncope is caused by tumor-mediated compression of the carotid sinus and stimulation of the glossopharyngeal nerve., Patient Concerns: In this study, we report the case of a 48-year-old male patient who was diagnosed with advanced TC and bilateral cervical lymph node metastasis. On the third day of admission, the patient experienced recurrent syncope with hypotension and bradycardia., Diagnoses: The patient was diagnosed with a well-differentiated squamous cell carcinoma of the tongue along with massive cervical lymph node metastasis and carotid sinus syndrome., Interventions: Initially, symptomatic treatment of syncope boosted the blood pressure and increased the heart rate. Thereafter, a temporary pacemaker was implanted. Finally, chemotherapy was used to control the tumor and relieve syncope., Outcomes: After chemotherapy, the tongue ulcers and cervical lymph node reduced in size; syncope did not recur., Lessons: This case shows that chemotherapy may be a valid treatment option in patients with cancer-related syncope; however, the choice of chemotherapeutic drugs is critical. Intensive care provides life support to patients and creates opportunities for further treatment.

We herein report a case of glossopharyngeal neuralgia with repeated syncope caused by the recurrence of esophageal carcinoma. The typical symptoms of glossopharyngeal neuralgia are paroxysmal, stabbing, electric shock-like pain in the pharynx and/or base of the tongue on swallowing and talking. In addition, syncope can also be caused by glossopharyngeal neuralgia. The diagnosis of glossopharyngeal neuralgia is not always easy because of its rarity. In the present case, we suspected that repeated syncope was caused by glossopharyngeal neuralgia due to the recurrence of esophageal carcinoma. Concurrent chemoradiation therapy was effective in reducing the tumor size, which resulted in the complete resolution of the symptoms.

Introduction: There are various communications between the superior cervical ganglion (SCG) and the vagus and glossopharyngeal nerves. However, little information exists concerning the origin of these sympathetic ganglion branches at the superior, middle, and inferior regions of the human SCG. The aim of this study was to describe the human SCG in a morphometric manner with the communication with cranial and cervical nerves and supply., Methods: This study characterized 72 SCG samples from 54 elderly Japanese human cadavers (30 males, 24 females; 65-100 years old). The SCG size (length, width, and thickness) and location were measured from the jugular foramen. We also defined the communication branches of the SCG to the vagus, glossopharyngeal, cervical, and accessory nerves at three regions (superior, middle, and inferior regions) of the SCG. Finally, we examined the arrangement and origin of the branch communications in detail and confirmed our observations, using histological sections of the SCG., Results: The SCG in all cadaver donors was detected at the C2 and C3 vertebra levels. The number of SCG branches supplied the communicating branches, such as the carotid branch, communicating branch of the vagus nerve, and glossopharyngeal nerve, were frequently detected in the superior region of the SCG (χ 2  = 587.72, df = 26, p  <   .001). The number of ganglion cells with a large number of neurons per unit area (1 mm 2 ) was most often found in the middle region with shrunken neurons of the SCG compared with other regions., Conclusion: The communication branches of the SCG are mainly connected to the vagus and glossopharyngeal nerves. Characterizing these branches can provide useful data for head and neck ganglion block and surgical treatments.

Glossopharyngeal neuralgia is a rare pain syndrome presenting with paroxysms of pain in the region of the glossopharyngeal nerve. Even more uncommon is the association between glossopharyngeal neuralgia and cardiac syncope. In these patients, the cardiovascular consequences may include bradycardia, hypotension and cardiac arrest. We describe the case of a 40-year-old patient who presented with this rare association of glossopharyngeal neuralgia and syncope. Multiple pauses including one lasting 14 s were noted on ambulatory ECG monitoring. In this case, the patient declined pharmacological treatment with carbamazepine or with permanent pacing and so far has been in remission from symptoms for 3 months., (2016 BMJ Publishing Group Ltd.)

Onset of epilepsy can occur at any age, but it is relatively rare in the elderly. Late onset epilepsy is usually secondary to stroke, tumour, trauma or neurodegenerative disorders. A 62-year-old Indian woman presented with frequent drop attacks sometimes leading to unconsciousness and, rarely, associated with seizure. Her epilepsy work up was unremarkable. As the disease progressed, she was diagnosed as having idiopathic epilepsy, syncope or pseudo-seizure, on different occasions, and was treated at length with no response. Finally, detailed history-taking revealed her as having glossopharyngeal neuralgia leading to syncope and seizures. She subsequently improved. In clinical practice, such rare entities should also be considered for proper management of patients' ailments., (2015 BMJ Publishing Group Ltd.)

Glossopharyngeal and/or vagus nerve involvement is infrequent in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We herein report the case of a 69-year-old Japanese woman who presented with muscle weakness and numbness of the extremities with dysphagia. The serum anti-ganglioside GM1 immunoglobulin IgM antibody levels were elevated, and treatment with intravenous immunoglobulin (IVIg) resulted in a dramatic improvement; the weakness, numbness and dysphagia all resolved. However, relapse comprising dysphagia alone occurred on hospital day 26, and treatment with IVIg again proved extremely effective. IVIg therapy can be effective against cranial nerve involvement in cases of CIDP.

Background: Cerebrospinal fluid (CSF) secretion may be increased in the early phases of subarachnoid hemorrhage (SAH), possibly via ischemic glossopharyngeal nerve discharges, and decreased due to glossopharyngeal nerve degeneration in the late phase of SAH; but this reflex pathway has not been definitively investigated. We studied the relationship between petrous ganglion of the glossopharyngeal nerve (GPN) and water vesicles of the choroid plexus (CP) in the early and late phases of SAH., Methods: This study was conducted on 30 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 20 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 4 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 20 days of injections (Group IV). The Petrous Ganglia and CPs of lateral ventricles were removed and stained for stereological analysis., Results: The mean number of follicles per cubic millimeter was 5.3 ± 1.2 the in control group (Group I), 4.5 ± 0.9 in the sham group (Group II), 16.60 ± 3.77 the in early decapitated group (Group III), and 4.30 ± 0.84 in the late decapitated group (Group IV). The mean number of degenerated neuron density of petrous ganglions was 6 ± 2, 50 ± 6, 742 ± 96, and 2.420 ± 350 in the control (Group I), sham (Group II), early decapitated (Group III), and late decapitated group (Group IV), respectively. The mean number of water vesicles was statistically different after SAH between the early decapitated group (group III) and the late decapitated group (group IV) (P < 0.05)., Conclusions: We studied the relationship between petrous ganglion cells of the GPN and water vesicles of CP in the early and late phases of SAH, and found that CP vesicles are increased in the early phase of SAH due to irritation of GPN, and decreased in the late phase due to ischemic insult of the petrous ganglion and parasympathetic innervation of the CP.

The lower cranial nerves innervate the pharynx and larynx by the glossopharyngeal (CN IX) and vagus (CN X) (mixed) nerves, and provide motor innervation of the muscles of the neck by the accessory nerve (CN XI) and the tongue by the hypoglossal nerve (CN XII). The symptomatology provoked by an anomaly is often discrete and rarely in the forefront. As with all cranial nerves, the context and clinical examinations, in case of suspicion of impairment of the lower cranial nerves, are determinant in guiding the imaging. In fact, the impairment may be located in the brain stem, in the peribulbar cisterns, in the foramens or even in the deep spaces of the face. The clinical localization of the probable seat of the lesion helps in choosing the adapted protocol in MRI and eventually completes it with a CT-scan. In the bulb, the intra-axial pathology is dominated by brain ischemia (in particular, with Wallenberg syndrome) and multiple sclerosis. Cisternal pathology is tumoral with two tumors, schwannoma and meningioma. The occurrence is much lower than in the cochleovestibular nerves as well as the leptomeningeal nerves (infectious, inflammatory or tumoral). Finally, foramen pathology is tumoral with, outside of the usual schwannomas and meningiomas, paragangliomas. For radiologists, fairly hesitant to explore these lower cranial pairs, it is necessary to be familiar with (or relearn) the anatomy, master the exploratory technique and be aware of the diagnostic possibilities., (Copyright © 2013 Éditions françaises de radiologie. Published by Elsevier Masson SAS. All rights reserved.)

Previously we demonstrated that chronic hypoxia (CH) induces an inflammatory condition characterized by immune cell invasion and increased expression of inflammatory cytokines in rat carotid body. It is well established that chronic inflammatory pain induces the expression of acid-sensitive ion channels (ASIC) in primary sensory neurons, where they contribute to hyperalgesia and allodynia. The present study examines the effect of CH on ASIC expression in petrosal ganglion (PG), which contains chemoafferent neurons that innervate oxygen-sensitive type I cells in the carotid body. Five isoforms of ASIC transcript were increased ∼1.5-2.5-fold in PG following exposure of rats to 1, 3, or 7 days of hypobaric hypoxia (380 Torr). ASIC transcript was not increased in the sympathetic superior cervical ganglion (SCG). In the PG, CH also increased the expression of channel-interacting PDZ domain protein, a scaffolding protein known to enhance the surface expression and the low pH-induced current density mediated by ASIC3. Western immunoblot analysis showed that CH elevated ASIC3 protein in PG, but not in SCG or the (sensory) nodose ganglion. ASIC3 transcript was likewise elevated in PG neurons cultured in the presence of inflammatory cytokines. Increased ASIC expression was blocked in CH rats concurrently treated with the nonsteroidal anti-inflammatory drug ibuprofen (4 mg·kg(-1)·day(-1)). Electrophysiological recording of carotid sinus nerve (CSN) activity in vitro showed that the specific ASIC antagonist A-317567 (100 μM) did not significantly alter hypoxia-evoked activity in normal preparations but blocked ∼50% of the hypoxic response following CH. Likewise, a high concentration of ibuprofen, which is known to block ASIC1a, reduced hypoxia-evoked CSN activity by ∼50% in CH preparations. Our findings indicate that CH induces inflammation-dependent phenotypic adjustments in chemoafferent neurons. Following CH, ASIC are important participants in chemotransmission between type I cells and chemoafferent nerve terminals, and these proton-gated channels appear to enhance chemoreceptor sensitivity.

Purpose: To assess the most effective magnetic resonance imaging (MRI) sequence for the visualization of the 9th, 10th, and 11th cranial nerves (glossopharyngeal, vagus, and accessory nerves, respectively) in their intraforaminal/canalicular courses., Materials and Methods: Balanced fast-field echo (b-FFE), 3D-T2W DRIVE, T2W 2D TSE and post-contrast T1W MRI sequences were all applied and we tried to get the best sequence for the exact assessment of the 9th, 10th, and 11th cranial nerves. Six hundred nerves of 100 patients without symptoms of neurovascular compression were examined using the above sequences. Imaging analysis was graded as: a) nerves analyzed by certainty (score of 2), b) nerves analyzed partially (score of 1), and c) nerves not identified (score of 0)., Results: In all three nerves, the best sequence for the visualization of the cisternal and intraforaminal course was b-FFE, with 58%, 73%, 62%, and all together 64.3% success in showing the fascicles of the 9th-11th nerves. This sequence with a very short time of repetition, symmetrical and balanced gradient around the echo time allowed very fast imaging and a high signal to noise ratio. T2W TSE sequence was superior to the DRIVE T2W sequence in assessing the cisternal and intraforaminal part of all three nerves. Post-contrast T1W sequence was probably the worst sequence in showing all three nerves., Conclusion: b-FFE gradient echo MRI sequence with high spatial resolution is the optimal sequence for determining the courses of 9th-11th cranial nerves.

Aim: The aim of this study was to determine the relationship between ischemic neurodegeneration, of the petrosal ganglion of the glossopharyngeal nerve, and BP fluctuations, after subarachnoid hemorrhage (SAH)., Material and Methods: Twenty-four rabbits had their blood pressure and heart rhythms studied daily over 20 days. Then, the histopathology of the petrosal ganglion was examined in all animals. Normal and apoptotic neuron density of the petrosal ganglion and blood pressure values were compared statistically., Results: Mean total volume of the petrosal ganglia was calculated as 0.9 ± 0.34/mm3. BP level of control group was 96.1 ± 2.1 mmHg; 116.5 ± 4 mmHg of mild hypertension (HT) group and 128.1 ± 3.6mmHg in the severe HT group. When the groups were compared to each other they were significantly different. The level of normal-apoptotic neuron in control group was 11,240 ± 802/mm³ -40 ± 6.3/mm³; 9730 ± 148.7/mm³ - 1560 ± 256.2/mm³ in the mild HT group and 6870 ± 378.8/mm³-4240 ± 628.2/mm³ in the severe HT group. When the groups were compared to each other there was significantly difference., Conclusion: Blood pressure variability observed in this study may be explained by ischemic neurodegeneration of petrosal ganglia caused by SAH. The results of this study suggest that petrosal ganglion ischemia has potential implications for the development of hypertension. These findings suggest that new treatment strategies should be considered for the treatment of SAH.

Objective: To examine surgical findings and results of microvascular decompression (MVD) for glossopharyngeal neuralgia (GN)., Methods: Between 1990 and 2007, 31 consecutive patients affected by drug-resistant GN underwent MVD through a retromastoid keyhole in the supine position with the head rotated to the opposite side. A retrospective analysis was performed that paid particular attention to the relationship among surgical technique, pain control and side effects., Results: A vascular compression of the glossopharyngeal nerve was found in all cases. Twenty-eight out of 31 patients (90.3%) were found to be pain free without medication at long-term follow-up (1-17 years, mean 7.5 years). Three patients (9.7%) were found to require medication to control pain paroxysms that were less frequent and less severe than those observed preoperatively. Two patients required repeated surgery for a drug-resistant recurrence of pain for a total of 33 MVDs. We observed no mortality and did not find any long-term surgical morbidity. Cranial nerve impairment, when observed, always resolved in the following months., Conclusions: MVD is a safe and effective treatment for GN in patients of all ages.

A 36-year-old woman presented with glossopharyngeal and vagus nerve palsy, which proved to be herpes zoster based on the high titers of Varicella zoster virus antibody in her serum. Thin-section T1-weighted images with contrast media demonstrated swelling and distinct contrast enhancement of the glossopharyngeal and vagus complex, mimicking a tumor. Following MR imaging, the size of the nerve complex returned to normal; however, the contrast enhancement remained longer than the symptoms.

1. To define the role of environmental oxygen in regulating postnatal maturation of the carotid body afferent pathway, light and electron microscopic methods were used to compare chemoafferent neurone survival and carotid body development in newborn rats reared from birth in normoxia (21 % O2) or chronic hyperoxia (60 % O2). 2. Four weeks of chronic hyperoxia resulted in a significant 41 % decrease in the number of unmyelinated axons in the carotid sinus nerve, compared with age-matched normoxic controls. In contrast, the number of myelinated axons was unaffected by hyperoxic exposure. 3. Chemoafferent neurones, located in the glossopharyngeal petrosal ganglion, already exhibited degenerative changes following 1 week of hyperoxia from birth, indicating that even a relatively short hyperoxic exposure was sufficient to derange normal chemoafferent development. In contrast, no such changes were observed in the vagal nodose ganglion, demonstrating that the effect of high oxygen levels was specific to sensory neurones in the carotid body afferent pathway. Moreover, petrosal ganglion neurones were sensitive to hyperoxic exposure only during the early postnatal period. 4. Chemoafferent degeneration in chronically hyperoxic animals was accompanied by marked hypoplasia of the carotid body. In view of previous findings from our laboratory that chemoafferent neurones require trophic support from the carotid body for survival after birth, we propose that chemoafferent degeneration following chronic hyperoxia is due specifically to the loss of target tissue in the carotid body.

Purpose: To determine the clinical usefulness of MR imaging to screen for vascular compression of the lateral medulla, considered by some to be responsible for neurogenic hypertension., Methods: MR images and clinical records of 120 adults who had received brain MR imaging for any reason were divided into two groups: group 1 (n = 60) consisted of patients with essential hypertension and group 2 (n = 60) included patients who lacked a diagnosis of hypertension. No patient manifested symptomatic cranial neuralgias. The root entry zone of cranial nerves IX and X into the left lateral medulla was examined by MR imaging for proximity to the ipsilateral vertebral artery or its branches. Images lacking any contact between visible vascular structures and the root entry zone were recorded as normal. Vascular compression was graded according to the degree of proximity to the root entry zone. Lateral medullary contact only (grade I), contact and depression (grade II), or lower brain stem displacement or rotation (grade III) of the root entry zone were recorded in both hypertensive and normotensive patients. Among hypertensive patients, additional data were gathered from electrocardiographic, echocardiographic, and urinary protein reports., Results: We found compression in 34 (57%) of the patients from group 1 and in 33 (55%) of the patients from group 2. Compressions in group 1 were grade I in 22 (37%) of the patients, grade II in 8 (45%), grade II in 4 (7%), and grade III in 2 (3%). There were no statistically significant differences in MR findings between the two groups. Among group 1 patients, MR grading did not predict end-organ changes in the heart (left axis deviation and left ventricular hypertrophy) or kidneys (proteinuria)., Conclusion: Vascular compression of the root entry zone of cranial nerves IX and X into the left lateral medulla is not an adequate lesion to produce systemic hypertension. This finding is as common among normotensive patients as among hypertensive populations. Neither the presence nor the severity of changes in the root entry zone on MR images increases the occurrence of common end-organ responses in the heart or kidneys among hypertensive patients. MR screening is not warranted among hypertensive patients lacking symptomatic cranial neuralgias.

A morphological study of the human tympanic plexus was performed. The tympanic nerve patterns on the promontory were classified into two types. The first was the single nerve trunk type, the second the type of nerve which divides into anterior and posterior branches. A tubal branch and a caroticotympanic branch on the promontory were both present in about 90% of the ears studied. Many ganglion cells were distributed on the tympanic plexus. It was concluded that these ganglia were autonomic, based on the nature of their fine structure. We speculate that these ganglia are parasympathetic and that they modulate the functions of vasodilators and secretory glands in the mucosa of the middle ear. In addition, we conducted a fiber analysis of the tympanic nerve and the lingual branch of the glossopharyngeal nerve and made a comparison between them.

There are many conditions in which chronic orofacial pain is a major diagnostic and therapeutic problem. It is generally accepted that surgical treatment for these chronic pain problems should be resorted to only when more conservative treatments have been ineffective. Literature concerning selected orofacial pain problems is reviewed and the indications for surgical management are discussed.

In the muscular dystrophic mouse mutant there is an absence of Schwann cells over circumscribed lengths of all cranial nerves except for II (I was not examined) and the lesion involves the sympathetic system. Where present, Schwann cells do not produce myelin of normal thickness. The lesion is similar to that described for the spinal roots. Causation is discussed.