Glossopharyngeal neuralgia with cardiac syncope treated by glossopharyngeal rhizotomy and microvascular decompression.

A glossopharyngeal neuralgia case with cardiac asystole is presented. The sinus mode dysfunction and subsequent syncope with pain appears to be the most important life-threatening symptom in the late period of the disease. Because of cardiac symptoms induced by intense vagal stimulation, this case was considered to be vagoglossopharyngeal neuralgia. Several medical and surgical alternatives have been proposed for its treatment. In the presented case the cause of disease was compression of lower cranial nerves in the right cerebello-pontine angle (CPA) by the vertebro-basilar arterial system. Carbamazepine and pacing were determined ineffective, so the patient was treated surgically by cutting the glossopharyngeal nerve and by decompression of the vagal nerve at the CPA. The sinus arrest and paroxysmal pain attacks disappeared and the patient's life returned to normal.     

Syncope due to parapharyngeal space lesions syncope-syndrome]

The clinic association between tumors in the neck and syncopal attacks has been well documented but uncommon. The pathogenesis of this type of syncope has been attributed to an specific sinus node disfunction and several diseases that affect pacemaker activity, cardiac output and blood supply to the brain are able to produce it. The most common reflex cardiovascular sindromes linked to the IX nerve are carotid sinus syndrome and glossopharyngeal neuralgia-asystole syndrome. Some patients with a pathological involvement of the parapharyngeal space also suffers from syncope but the clinical picture of these patients differs so greatly from the other two syndromes, which suggests specific aetiological, clinical and therapeutical features so the term "parapharyngeal space lesiones syncope-syndrome" has been proposed for this entity.We report a case of a patient with a neck tumor in the parapharyngeal space with syncope as the major symptom.     

A new reflex cardiovascular syndrome: recurrent vasodepressive syncope caused by lesions or tumors of the parapharyngeal space. Etiopathogenesis, clinical picture, differential diagnosis with carotid sinus syndrome and glossopharyngeal neuralgia-asystole syndrome. Therapy by intracranial resection of the 9th cranial nerve

An intense vaso-vagal reaction characterizes all the reflex induced cardiovascular syncopes. In these syndromes the vagal cardio-inhibitor effect on heart rate is more evident than the vasodilatation and fall in blood pressure. The vasodepressor mechanism is uncommon even in carotid sinus syndrome. We have studied 6 male patients, age range 56-73 years (mean age: 64) with recurrent vasodepressor syncopes. The following were always present during such episodes: generalized malaise, profound fatigue, pallor, cyanosis, copious sweating, lack of peripheral pulses, severe fall in blood pressure (BP) (systolic BP less than or equal to 50-60 mmHg or unrecordable), mental disorientation and/or syncope. The first diagnosis in our patients was carotid sinus syndrome, but, the clinical picture was quite different from classic carotid sinus syndrome: triggering factors were not present, the vasovagal episodes were longer, the syncopes more frequent and severe, and the VVI pacing uneffective. Further investigations, including computerized axial tomography, showed--in all these patients--a malignant tumour originally localized in or near the parapharyngeal space. We think that the symptoms of our patients can be attributed to parapharyngeal tumour and that the parapharyngeal space lesions are able to cause severe vasovagal attacks and syncope. The pathogenetic mechanism in this syndrome, due to neural irritation of the glossopharyngeal afferent fibres, is similar to the glossopharyngeal neuralgia-asystole syndrome, but it obviously doesn't involve pain-pathways since none of our patients had pain. Therefore, this syndrome differs from glossopharyngeal neuralgia- asystole syndrome in the presence of tumours and in the absence of neuralgia and initiating factors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glossopharyngeal neuralgia associated with cardiac syncope

Glossopharyngeal neuralgia is an uncommon condition that has rarely been described in association with syncope. We report here 2 cases of glossopharyngeal neuralgia in elderly patients. Both were male and underwent temporary pacemaker insertion to prevent syncopal episodes. We discuss the clinical and surgical treatment of glossopharyngeal neuralgia, the role of cardiac stimulation, and the possible physiopathological mechanism of the associated cardiac disturbances.     

Neurogenic hypertension in the Guillain-Barré syndrome

We report a case of Guillain-Barré syndrome associated with hypertension. The hypertension was related to glossopharyngeal and vagal nerve impairment. Plasma noradrenaline concentration (NA) and plasma renin activity (PRA) were elevated. The possible mechanism of the neurogenic hypertension produced by the sino-aortic denervation is discussed.     

显微血管减压治疗脑神经疾病的疗效观察

目的总结显微血管减压术（MVD）治疗原发性脑神经疾病的手术技巧及疗效。 方法选取昆明医科大学第一附属医院微创神经外科自2010年4月至2018年12月采用MVD治疗的832例脑神经疾病患者进行回顾性分析,其中三叉神经痛489例、面肌痉挛338例、舌咽神经痛患者5例,观察其疗效,统计并发症发生率。 结果所有病例随访时间为3~84个月,平均32.5个月,本组无死亡病例及其他严重并发症发生,三叉神经痛患者手术治愈率为98.36%,面肌痉挛手术治愈率为97.93%,舌咽神经痛治愈率为100.00%。 结论MVD是治疗原发性脑神经疾病的可靠方法,熟练的显微外科技术和丰富的手术经验及对于解剖的熟悉程度是手术治疗脑神经疾病的基础。     

Syncope and hypotension due to carcinoma of the breast metastatic to the carotid sinus

Tumors involving the carotid sinus and glossopharyngeal nerve may produce syncope due to bradycardia and hypotension. Carotid sinus syncope unrelated to cancer is usually caused by bradycardia and responds to control of the heart rate. When neoplastic disease involves the carotid sinus, vasodepressor hypotension, with or without bradycardia, is more common. Control of the heart rate alone is not effective. Although this syndrome is not common, it is probably not recognized in milder forms. Most patients in whom this syndrome develops have cancer of the head and neck. A patient with breast carcinoma metastatic to the neck and carotid sinus is described in whom syncope with hypotension and bradycardia developed. Although a temporary cardiac pacemaker controlled bradycardia, severe hypotensive episodes recurred despite treatment with anticholinergic and sympathomimetic drugs. The pathophysiology and therapy of this syndrome in patients with cancer are reviewed.     

Etiopathogenetic differences and therapeutic possibillities of the carotid sinus syndrome. Report of two rare cases (author's transl)

Two cases of carotid sinus syndrome with peculiar clinical and nosological characteristics are presented. The clinical symptoms were characterized by syncope with bradicardia and hypotension, which occurred contemporarily or independently of each other. The most valuable medical therapy to prevent or got over the syncopal attacks has proved to be one associating the sympathicomimetic drugs (high dosage dopamine, particularly on demande pacemaker. Complete decrease of symptoms following was obtained only after surgical treatment: denervation of carotid sinus in one case, intracranical section of the glosspharyngeal nerve and of the two vagal termination nearer to IX in the other case. This last result makes it possible to consider the case in question from an original nosological point of view exploiting the pathogenetic importance of stimulating the afferent nerve-fibres of the glossofaryngeal-nerve.     

Carotid sinus baroreceptor reflex in dogs with experimental heart failure

We have previously demonstrated a decrease in baroreceptor discharge sensitivity in dogs with experimental heart failure. In the present study, we determined the sensitivity of the carotid sinus baroreceptor reflex in dogs with pacing-induced heart failure. The carotid sinus baroreceptor reflex sensitivity was determined by pressurizing one carotid sinus with all other baroreceptor and cardiopulmonary receptor inputs removed. The data were analyzed by plotting carotid sinus pressure-mean arterial pressure curves and carotid sinus pressure-renal sympathetic nerve activity curves in the two groups of dogs. The peak arterial pressure during carotid hypotension was significantly depressed in dogs with heart failure compared with normal dogs (107.1 +/- 5.7 versus 139.8 +/- 7.0 mm Hg, p less than 0.001). Mean arterial pressure range, renal sympathetic nerve activity range, and peak slope were significantly decreased in the heart-failure group. To determine if this depression was completely due to depression of baroreceptor discharge per se, or to alterations in central or end-organ responsiveness, similar experiments were performed by stimulating the carotid sinus nerve and evaluating frequency, voltage, and duration of stimulation on the resultant mean arterial pressure and renal sympathetic nerve activity. As was the case with carotid sinus pressurization, electrical stimulation caused a significantly smaller change in mean arterial pressure in heart-failure dogs compared with the normal dogs. However, there was no significant difference between normal and heart-failure dogs for the renal sympathetic nerve activity-electrical stimulation curves. These data strongly suggest that the depressed carotid sinus baroreceptor reflex in heart failure is not solely the result of depressed baroreceptor responsiveness but may be related to poor end-organ responses and normal central control of renal sympathetic outflow.     

Glossopharyngeal neuralgia with syncope secondary to tumor: Treatment and pathophysiology

A patient with metastatic laryngeal carcinoma had glossopharyngeal neuralgia and syncope due to hypotension and bradycardia. Treatment of bradyarrhythmias failed to prevent hypotension. The administration of carbamazepine failed to prevent pain or syncope in this patient despite previous reports of success. Symptoms did resolve with intracranial section of the glossopharyngeal nerve and the upper two rootlets of the vagus. Plasma catecholamines were studied during a hypotensive episode. The values obtained demonstrated a suppressed sympathetic adrenergic neural response but an intact adrenomedullary response, suggesting that suppression of adrenergic vasoconstriction contributed to episodes of hypotension. The administration of intravenous atropine produced a transient increase in blood pressure suggesting that, in the presence of suppressed adrenergic vasoconstriction, cholinergic vasodilation may have contributed to the hypotension in this patient.     

Isolated trigeminal neuropathy revealing the presence of Sharp's syndrome or MCTD (mixed connective tissue disease) (author's transl)]

Isolated neuropathies of 5th cranial nerves are rare apart from primary facial neuralgia. A case is reported, in which Raynaud's syndrome was also present, that enabled a diagnosis of mixed connective tissue disease to be established. The authors underline the importance of undertaking complete immunological investigations in order to decide whether there is a particular type of systemic disease present, which could be responsible for these special types of trigeminal nerve disorders.     

Dysphagia and micrognathia in a patient with juvenile rheumatoid arthritis

Summary This report describes the case of a 35-year-old man with juvenile rheumatoid arthritis. The patient experienced swallowing difficulties that were initially thought to be a result of the disease affecting the cervical spine. A maxillofacial examination, however, showed a total loss of the mandibular condyles, short rami and bodies, and a retrusion of the jaw. This was considered to be the main cause of the dysphagia, and not a glossopharyngeal nerve compression. The surgical-orthodontic management of these difficult cases is discussed.     

The usefulness of diving reflex--the effect on PSVT

We attempted to use the diving reflex to treat PSVT in five patients, in whom carotid-sinus massage had failed to terminate, PSVT. In three cases PSVT converted to normal sinus rhythm. The patient was seated comfortably, and a pan of ice and water (4 degrees C) was placed on the table in front of the patient. He then took a deep breath and, without expiration, submerged his face in the cold ice and water for about 30 seconds. In case 1, a 68-year-old male, PSVT stopped after facial immersion of 11 seconds. Subsequently, sinus arrest with junctional or ventricular contractions continued for 7 seconds followed by conversion to the sinus rhythm. The duration of facial immersion was 18 seconds. In case 2, a 51-year-old male, PSVT converted to the sinus rhythm in the same way. The duration of facial immersion was 23 seconds. Case 3 was a 27-year-old female with WPW syndrome. PSVT converted to the sinus rhythm after a 6.6 seconds facial immersion. Case 4 and 5 were respectively 72 and 73-year-old males, whose attacks did not respond to the diving reflex for the reason that they could not maintain breath-holding for a sufficient time to activate the reflex adequately. We postulated that apnea might effect the termination of PSVT in case 1 and 2 because relatively long duration of about 20 seconds was necessary to convert PSVT to the sinus rhythm. On the other hand, in case 3, cold water stimulation on the face might play an important role because PSVT converted to the sinus rhythm immediately.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic nonparoxysmal sinus tachycardia in otherwise healthy persons.

Seven patients had chronic, unexplained, nonparoxysmal sinus tachycardia. The clinical, electrocardiographic, and electrophysiologic characteristics of these cases are described. In each case electrocardiographic and electrophysiologic observations suggested that tachycardia was nonparoxysmal and due to increased automaticity of the sinus node (or of an automatic atrial focus located very near the sinus node). The mechanisms of increased sinus node automaticity in these patients were explored using drugs affecting the autonomic nervous system. In each patient these studies suggested a defect in either sympathetic or vagal nerve control of resting heart rate, with or without an abnormality of intrinsic heart rate. Data are also presented on baroreceptor reflex arc function in these patients.     

IgG4-Related Hypertrophic Pachymeningitis with Skull Base Involvement Presenting with Isolated Glossopharyngeal and Vagus Nerve Palsy

We herein report a 70-year-old man diagnosed with IgG4-related hypertrophic pachymeningitis with skull base involvement, who presented with isolated glossopharyngeal and vagus nerve palsy. Contrast-enhanced magnetic resonance imaging (MRI) showed enhanced dural thickening of the posterior clivus and skull base involvement. When a patient with hypertrophic pachymeningitis presents with isolated cranial neuropathy without systemic manifestations or definite MRI abnormalities, it is difficult to make a diagnosis, and the patient may be misdiagnosed. This case suggests that a detailed radiological evaluation including contrast enhancement of the skull base is very important in patients with isolated glossopharyngeal and vagus nerve palsy.     

Cardiovascular manifestations of chemical rhysolisis of the trigeminal nerve

Twelve chemical rhyzolisis (surgical instilation of 10 c.c. of 15% NaCl solution) of trigeminal nerve were performed in 11 patients with trigeminal neuralgia resistent to medical treatment. Before and at least in the first 30 minutes after instilation the following parameters were monitorized: electrocardiogram, electroencephalogram, intrarradial arterial pressure and venous central pressure. In 10 cases after a 2.8 +/- 2.4 seg. latency period the following arrhythmias appeared (in paragraphs number of cases): sinus bradicardia, sinoauricular block, sinus arrest, atrial-ventricular block and atrial pacemaker migration. During sinus arrest (8 episodes in 4 cases; mean duration 17.6 secs.) slow, high voltage waves appeared in the electroencephalographic tracings. Ventricular scapes were not seen at the end of the sinus pauses. In 6 cases after this slow arrhythmic phase the following arrhythmias were observed: ventricular premature beats, atrial premature beats, sinus tachycardia, bidirectional ventricular tachycardia, and nodal tachycardia. All cases exhibited an elevation of mean arterial pressure after instilation of the nerve which was preceded by a short period of hypertension in 4 occasions. Average and standard deviations changes of systolic, diastolic and mean blood pressure (mm of Hg), pulse (beats/minute) and central venous pressure (cms of H2O) during the procedure were 46.7 +/- 29.3, 23.0 +/- 13.3, 34.1 +/- 16.4, 25.8 +/- 16.2 and 6.6 +/- 5.8, respectively (p less than or equal to 0.001) in all changes but the last ones, less than or equal to 0.05). Physiopathologic considerations of this autonomic crises are done.     

Anomalous right coronary artery in a patient with Kartagener's syndrome

We report a case of an anomalous right coronary artery arising from the morphological left sinus of Valsalva in a patient with Kartagener's syndrome. Literature review has revealed only a small number of cases of anomalous coronary arteries in patients with dextrocardia and none previously reported in Kartagener's syndrome. © 1996 Wiley-Liss, Inc.     

Baroreflex sensitivity measured by the phenylephrine pressor test in patients with carotid sinus and sick sinus syndromes

Baroreflex sensitivity was measured by the heart rate response to the transient rise in blood pressure induced by phenylephrine, in 11 patients with carotid sinus syndrome, 6 patients with sick sinus syndrome and nine age and blood pressure matched controls. Patients with carotid sinus syndrome were divided into those with a hypersensitive carotid sinus reflex manifest as sinus arrest (n = 9) and those with a reflex manifest as atrioventricular block (n = 2). The mean gain of the baroreflex sensitivity was significantly increased (p less than 0.001) in patients with carotid syndrome manifest as sinus arrest (12.7 +/- 5.1 ms . mmg-1) compared to that in patients with sick sinus syndrome (3.8 +/- 2.6 ms . mmHg-1) and controls (4.2 +/- 2.1 ms . mmHg-1). Patients with carotid sinus syndrome manifest as atrioventricular block did not have increased baroreflex sensitivity measured by their sinus node response (2.1 +/- 0.5 ms . mmHg-1). There was significant correlation (p less than 0.001) between the corrected carotid sinus inhibitory response to carotid sinus massage and the measurement of baroreflex sensitivity in the carotid sinus syndrome patients. Patients with carotid sinus syndrome manifest as reflex sinus arrest have an increased gain in baroreflex sensitivity for their age, which is not seen in patients with symptomatic sinoatrial disease. This study provides further evidence of a different mechanism of bradycardiac symptoms in patients with carotid sinus and sick sinus syndromes.     

Gasperini syndrome, a report of two cases

We report 2 cases of Gasperini syndrome and consider them with the 11 previously reported cases to describe the clinical characteristics of this rare syndrome: Core neurological signs are peripheral facial nerve palsy and abducens nerve palsy of the affected side: Among all cases, imaging demonstrated a small lesion in the mediolateral tegmental pons (10/13 cases of microinfarction; 2/13 cases of microbleeding). We found that the responsible artery in ischemic Gasperini syndrome is mainly the long circumferential branch of the anterior inferior cerebellar artery; Case 1 is the first case thought to be caused by infarction of the basilar artery's paramedian branch.