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Neurally Mediated Syncope in 2 Patients With Extracardiac Disease

Neurally Mediated Syncope in 2 Patients With Extracardiac Disease We describe the cases of 2 patients with repetitive episodes of syncope with profound bradycardia and hypotension. In both patients, the symptoms were initially thought to be neurally mediated and idiopathic but were ultimately determined to be triggered by serious underlying pathologic processes: a massive and locally invasive tumor of the hypopharynx in 1 patient and a gangrenous gallbladder in the other. Appropriate treatment resulted in a resolution of this syndrome in both patients. These cases emphasize the importance of an appropriate evaluation and broad differential diagnoses for patients with severe bradycardia and hypotension.Vasovagal or neurocardiogenic syncope is frequently encountered in medical practice. In most patients, a neurogenic cause of loss of consciousness is apparent after the initial evaluation. Episodes of vasovagal syncope commonly occur in the standing or sitting position and are associated with a prodrome, such as weakness, nausea, diaphoresis, or light-headedness. Loss of consciousness rarely lasts longer than 1 minute. Although the efferent arm of the abnormal reflex responsible for symptoms of neurocardiogenic syncope is relatively well understood, the identification of the mechanism(s) responsible for triggering neurocardiogenic syncope is often difficult. Depending on the trigger mechanism, neurocardiogenic syncope can be classified into 2 distinct syndromes: that of central origin (ie, triggered by emotional stress) and that of peripheral origin (ie, triggered by the stimulation of sensory receptors located in the arterial tree or viscera).The cause of neurocardiogenic syncope of peripheral origin is occasionally difficult to determine. Such cases can become a diagnostic dilemma for which a wide range of possibilities needs to be considered. We present 2 cases of neurocardiogenic syncope, 1 due to a necrotic, polypoid tumor of the hypopharynx and the second due to a gangrenous gallbladder.REPORT OF CASESCASE 1The patient was a 62-year-old man with a history of hypertension, a 90-pack-year smoking history, and daily alcohol intake. On the day before admission, he awoke at 2 AM feeling nauseated and diaphoretic. On returning from the bathroom, he reported feeling dizzy and collapsed, losing consciousness. The following day, he again felt nauseated and light-headed while at work and, minutes later, collapsed. He regained consciousness immediately and was brought to the hospital.In the emergency department, the patient's systolic blood pressure was 130 mm Hg, and his heart rate was 70/min. The findings of the physical examination were unremarkable. A 12-lead electrocardiogram revealed a sinus rhythm with minor ST-segment T-wave abnormalities. While in the emergency department, the patient had light-headedness and diaphoresis and lost consciousness. The cardiac monitor showed sinus bradycardia at a rate of 20 beats per minute. He was given atropine sulfate and improved immediately.During the next several days, the patient had many short episodes of symptomatic bradycardia. Given the abrupt onset of symptoms, preceded by diaphoresis and nausea, and the response to atropine, the bradycardia was thought to be neurally mediated, and β-blocker therapy was started. Symptoms persisted; a scopolamine hydrobromide transdermal patch and disopyramide phosphate were added. The patient was instructed to remain supine and to elevate his legs if symptoms developed. He gradually responded to this combination of therapy with less frequent and less severe episodes and was discharged from the hospital to home.During a follow-up office visit 3 weeks later, the patient reported improvement in his symptoms, although he did have some milder episodes. He denied having any syncope. For the first time, he complained of progressive hoarseness and a dry cough. Evaluation by an otolaryngologist, including direct laryngoscopy, demonstrated a massive, fungating, necrotic, polypoid tumor of the hypopharynx. A computed tomographic scan of the neck confirmed the presence of a large transglottic soft tissue mass with extension through the thyrohyoid membrane into the right side of the neck to involve the soft tissues and glands and with extension along the carotid sheath superiorly to the base of the skull. Biopsy specimens demonstrated a moderately differentiated in situ and invasive squamous cell carcinoma.The tumor was surgically unresectable. In anticipation of further airway and feeding problems, tracheostomy and endotracheal tube placement were performed. The patient was treated with a combination of chemotherapy with a cisplatin-based regimen and radiotherapy that delivered a total of 70 Gy to all sites of gross disease and 54 Gy as "elective neck irradiation."During evaluation, the patient initially had frequent syncopal or near-syncopal episodes, which often occurred during manipulation of his neck for procedures, despite treatment with disopyramide; metoprolol tartrate; ephedrine sulfate (25 mg), theophylline (130 mg), and hydroxyzine hydrochloride (10 mg) (Marax); and sertraline hydrochloride. These episodes became much less frequent during chemotherapy and radiotherapy.On follow-up consultation, the patient had no further episodes of syncope or near-syncope, and he was gradually weaned off all cardiac medications, requiring only low-dose metoprolol for hypertension. He died the following year of extensive metastatic disease.CASE 2The patient, a 67-year-old woman with hypertension, was admitted for elective repair of a descending thoracic aortic aneurysm. She underwent successful repair with the insertion of a 34-mm woven Dacron graft arising in the aorta just distal to the subclavian artery and terminating just above the level of the diaphragm. Her postoperative course was complicated by respiratory failure as a result of diaphragmatic paresis and pneumonia. She gradually improved, and after several days, mechanical ventilation was discontinued. The patient's course was also complicated by atrial fibrillation that converted to sinus rhythm with the administration of procainamide hydrochloride.On the 16th postoperative day, the patient had transient type II second-degree atrioventricular block with pauses of as long as 4.4 seconds. An electrocardiogram was otherwise unchanged, and laboratory results were normal. Digoxin, metoprolol, and procainamide were discontinued. The next day, severe sinus bradycardia developed, and the patient had high-grade atrioventricular block followed by asystole (Figure 1). Cardiopulmonary resuscitation was initiated, but sinus rhythm returned spontaneously before pharmacological intervention could be initiated. Immediately after the episode, the patient was awake but diaphoretic and weak; her heart rate was 95/min, and the systolic blood pressure was 140 mm Hg. The findings of a physical examination were unremarkable. A 12-lead electrocardiogram revealed a sinus rhythm and minor ST-segment T-wave changes. Laboratory results were all normal.Telemetric recording of prolonged asystole in a patient with neurally mediated syncope due to gallbladder inflammation and perforation.A temporary demand pacemaker was placed with an escape rate of 50 beats per minute. When the pacemaker was temporarily disabled to assess rhythm stability, the patient had several episodes of sinus bradycardia, atrioventricular block, and asystole. Episodes lasted 20 to 40 seconds and were associated with weakness, diaphoresis, and loss of consciousness.The abrupt onset of sinus bradycardia and atrioventricular block preceding each episode of asystole, the associated weakness and diaphoresis, and the absence of laboratory test abnormalities or a pharmacological cause suggested a neurally mediated mechanism for these syncopal episodes. The patient was treated with metoprolol with marked improvement, although several milder episodes continued to occur.The development of an unexplained persistent leukocytosis despite the initiation of broad-spectrum antibiotic therapy deferred any further actions. An abdominal computed tomographic scan, performed to identify a possible source of infection, revealed a markedly distended, inflamed gallbladder with thickened walls and evidence of a contained perforation, consistent with severe cholecystitis. Percutaneous drainage was performed.Following percutaneous drainage, the patient had no further episodes of bradyarrhythmias, and temporary pacing was discontinued. She underwent an open cholecystectomy 3 days later. Before and during the operation, pacing was not required. The surgical pathological report revealed a gangrenous gallbladder with changes of severe chronic cholecystitis.Unfortunately, 1 day after the operation, the patient had massive upper gastrointestinal tract bleeding, which rapidly led to death by exsanguination. Autopsy examination showed an aortoesophageal fistula arising 2 cm below the bypass graft.COMMENTLife-threatening bradycardia and asystole may occur as an extreme manifestation of neurally mediated cardioinhibitory syndromeand may even result in asystolic sudden cardiac arrest.The cases presented in this report illustrate the interaction of diverse pathologic processes with the afferent pathway of the autonomic nervous system. In both of our patients, a severe bradycardia leading to cardiovascular collapse was the first manifestation of the pathologic processes not typically implicated in the development of these symptoms. In each patient, the underlying cause of this serious rhythm abnormality was unsuspected and undiagnosed until a comprehensive workup had been performed.The most probable explanation for the first patient's syndrome relates to increased parasympathetic activity resulting from direct carotid sinus stimulation by tumor pressure. The carotid sinus is composed of loosely interwoven nerve endings throughout the outer media of the internal carotid artery, just above the carotid bifurcation .The syndrome of carotid sinus hypersensitivity may be evoked by carotid sinus pressure.The tumor diagnosed in the first patient was large and located on the right side, close to the more sensitive of the carotid sinuses.His symptoms were sometimes triggered by a change in head position, which most likely exerted increased pressure on the carotid sinus, causing a cardioinhibitory response.Glossopharyngeal syncope, a syndrome that occurs in association with tumors of the oropharynx or base of the skull, is a less likely cause of this patient's syndrome. Glossopharyngeal syncope has been previously described.In these patients, severe pain in the throat evoked by chewing, swallowing, or coughing triggers vasovagal syncope.Afferent sensory fibers from the throat and the carotid baroreceptors both run in the glossopharyngeal nerve.Pain impulses are thought to be misdirected and to jump over to baroreceptor fibers somewhere along the nerve.This increased afferent traffic causes reflex parasympathetic outflow with bradycardia and inhibits sympathetic efferent activity. The tumor in the first patient was located in the posterior pharyngeal wall, an area innervated predominantly by the glossopharyngeal nerve. Even though the patient did not have pain, glossopharyngeal nerve overstimulation may have been a cause of his symptoms.In the second patient, cardiac vagal stimulation was thought to be caused by gallbladder inflammation and subacute rupture. Gallbladder distention has been shown to activate spinothalamic tract cells and spinal neurons in the upper thoracic segments of the spinal cord.The spinothalamic tract also receives afferent fibers from the cardiopulmonary baroreceptors at the T1 through T5 level.An increase in reflex sympathetic discharge in the spinothalamic tract caused by gallbladder distention can result in the stimulation of afferent vascular baroreceptor fibers and a reflex increase in vagal tone, resulting in the typical bradycardia response observed in this patient. The average threshold pressure in the gallbladder needed to activate spinothalamic tract cells is 50 mm Hg.Pressures in the gallbladder may approach 60 mm Hg during acute cholecystitis. In this patient, percutaneous drainage of the gallbladder was associated with a complete resolution of the bradycardia-hypotension syndrome, implicating the distended gallbladder as the primary factor leading to the described cascade of events.These cases emphasize the importance of an extensive diagnostic search for nontraditional and unsuspected causes of neurally mediated syncope in patients with repetitive, life-threatening bradycardia and asystole. In this report, we demonstrate a neck malignant tumor and chronic cholecystitis as possible causes. Alternative causes for such a profound syndrome include other gastrointestinal tract disorders, other head and neck malignant tumors, or cerebrovascular disorders.KMSpyerNeural organisation and control of the baroreceptor reflex.Rev Physiol Biochem Pharmacol.1981;88:24-124.GLEngelPsychologic stress, vasodepressor (vasovagal) syncope, and sudden death.Ann Intern Med.1978;89:403-412.SMilsteinJBuetikoferJLesserCardiac asystole.J Am Coll Cardiol.1989;14:1626-1632.DHeathPSmithThe Pathology of the Carotid Body and Sinus.London, England: Edward Arnold; 1985:19, 112.DDSugrueDLWoodMDMcGoonCarotid sinus hypersensitivity and syncope.Mayo Clin Proc.1984;59:637-640.SJSchnellerJWHarthorneCarotid sinus hypersensitivity.Clin Prog Electrophysiol Pacing.1985;3:389-393.TRDykmanEBMontgomeryPDGerstenbergerHEZeigerWEClutterPECryerGlossopharyngeal neuralgia with syncope secondary to tumor.Am J Med.1981;71:165-168.BGWallinCEWesterbergGSundlofSyncope induced by glossopharyngeal neuralgia: sympathetic outflow to muscle.Neurology.1984;34:522-524.HKaufmannNeurally mediated syncope and syncope due to autonomic failure.J Clin Neurophysiol.1997;14:183-196.AGHampton JrJEBeckwithDLWood JrThe relationship between heart disease and gallbladder disease.Ann Intern Med.1959;50:1135-1148.RForemanSpinal cord neuronal regulation of the cardiovascular system.In: Armour JA, Ardell JL, eds. Neurocardiology.Oxford, England: Oxford University Press; 1994:260.Accepted for publication October 21, 1998.We thank Nancy Roistacher, MD, for providing much of the clinical follow-up data on patient 1.Corresponding author: Jonathan S. Steinberg, MD, Arrhythmia Service, Division of Cardiology, St Luke's–Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, 1111 Amsterdam Ave, New York, NY 10025. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Internal Medicine American Medical Association

Neurally Mediated Syncope in 2 Patients With Extracardiac Disease

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American Medical Association
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Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
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2168-6106
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10.1001/archinte.159.6.625
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Abstract

We describe the cases of 2 patients with repetitive episodes of syncope with profound bradycardia and hypotension. In both patients, the symptoms were initially thought to be neurally mediated and idiopathic but were ultimately determined to be triggered by serious underlying pathologic processes: a massive and locally invasive tumor of the hypopharynx in 1 patient and a gangrenous gallbladder in the other. Appropriate treatment resulted in a resolution of this syndrome in both patients. These cases emphasize the importance of an appropriate evaluation and broad differential diagnoses for patients with severe bradycardia and hypotension.Vasovagal or neurocardiogenic syncope is frequently encountered in medical practice. In most patients, a neurogenic cause of loss of consciousness is apparent after the initial evaluation. Episodes of vasovagal syncope commonly occur in the standing or sitting position and are associated with a prodrome, such as weakness, nausea, diaphoresis, or light-headedness. Loss of consciousness rarely lasts longer than 1 minute. Although the efferent arm of the abnormal reflex responsible for symptoms of neurocardiogenic syncope is relatively well understood, the identification of the mechanism(s) responsible for triggering neurocardiogenic syncope is often difficult. Depending on the trigger mechanism, neurocardiogenic syncope can be classified into 2 distinct syndromes: that of central origin (ie, triggered by emotional stress) and that of peripheral origin (ie, triggered by the stimulation of sensory receptors located in the arterial tree or viscera).The cause of neurocardiogenic syncope of peripheral origin is occasionally difficult to determine. Such cases can become a diagnostic dilemma for which a wide range of possibilities needs to be considered. We present 2 cases of neurocardiogenic syncope, 1 due to a necrotic, polypoid tumor of the hypopharynx and the second due to a gangrenous gallbladder.REPORT OF CASESCASE 1The patient was a 62-year-old man with a history of hypertension, a 90-pack-year smoking history, and daily alcohol intake. On the day before admission, he awoke at 2 AM feeling nauseated and diaphoretic. On returning from the bathroom, he reported feeling dizzy and collapsed, losing consciousness. The following day, he again felt nauseated and light-headed while at work and, minutes later, collapsed. He regained consciousness immediately and was brought to the hospital.In the emergency department, the patient's systolic blood pressure was 130 mm Hg, and his heart rate was 70/min. The findings of the physical examination were unremarkable. A 12-lead electrocardiogram revealed a sinus rhythm with minor ST-segment T-wave abnormalities. While in the emergency department, the patient had light-headedness and diaphoresis and lost consciousness. The cardiac monitor showed sinus bradycardia at a rate of 20 beats per minute. He was given atropine sulfate and improved immediately.During the next several days, the patient had many short episodes of symptomatic bradycardia. Given the abrupt onset of symptoms, preceded by diaphoresis and nausea, and the response to atropine, the bradycardia was thought to be neurally mediated, and β-blocker therapy was started. Symptoms persisted; a scopolamine hydrobromide transdermal patch and disopyramide phosphate were added. The patient was instructed to remain supine and to elevate his legs if symptoms developed. He gradually responded to this combination of therapy with less frequent and less severe episodes and was discharged from the hospital to home.During a follow-up office visit 3 weeks later, the patient reported improvement in his symptoms, although he did have some milder episodes. He denied having any syncope. For the first time, he complained of progressive hoarseness and a dry cough. Evaluation by an otolaryngologist, including direct laryngoscopy, demonstrated a massive, fungating, necrotic, polypoid tumor of the hypopharynx. A computed tomographic scan of the neck confirmed the presence of a large transglottic soft tissue mass with extension through the thyrohyoid membrane into the right side of the neck to involve the soft tissues and glands and with extension along the carotid sheath superiorly to the base of the skull. Biopsy specimens demonstrated a moderately differentiated in situ and invasive squamous cell carcinoma.The tumor was surgically unresectable. In anticipation of further airway and feeding problems, tracheostomy and endotracheal tube placement were performed. The patient was treated with a combination of chemotherapy with a cisplatin-based regimen and radiotherapy that delivered a total of 70 Gy to all sites of gross disease and 54 Gy as "elective neck irradiation."During evaluation, the patient initially had frequent syncopal or near-syncopal episodes, which often occurred during manipulation of his neck for procedures, despite treatment with disopyramide; metoprolol tartrate; ephedrine sulfate (25 mg), theophylline (130 mg), and hydroxyzine hydrochloride (10 mg) (Marax); and sertraline hydrochloride. These episodes became much less frequent during chemotherapy and radiotherapy.On follow-up consultation, the patient had no further episodes of syncope or near-syncope, and he was gradually weaned off all cardiac medications, requiring only low-dose metoprolol for hypertension. He died the following year of extensive metastatic disease.CASE 2The patient, a 67-year-old woman with hypertension, was admitted for elective repair of a descending thoracic aortic aneurysm. She underwent successful repair with the insertion of a 34-mm woven Dacron graft arising in the aorta just distal to the subclavian artery and terminating just above the level of the diaphragm. Her postoperative course was complicated by respiratory failure as a result of diaphragmatic paresis and pneumonia. She gradually improved, and after several days, mechanical ventilation was discontinued. The patient's course was also complicated by atrial fibrillation that converted to sinus rhythm with the administration of procainamide hydrochloride.On the 16th postoperative day, the patient had transient type II second-degree atrioventricular block with pauses of as long as 4.4 seconds. An electrocardiogram was otherwise unchanged, and laboratory results were normal. Digoxin, metoprolol, and procainamide were discontinued. The next day, severe sinus bradycardia developed, and the patient had high-grade atrioventricular block followed by asystole (Figure 1). Cardiopulmonary resuscitation was initiated, but sinus rhythm returned spontaneously before pharmacological intervention could be initiated. Immediately after the episode, the patient was awake but diaphoretic and weak; her heart rate was 95/min, and the systolic blood pressure was 140 mm Hg. The findings of a physical examination were unremarkable. A 12-lead electrocardiogram revealed a sinus rhythm and minor ST-segment T-wave changes. Laboratory results were all normal.Telemetric recording of prolonged asystole in a patient with neurally mediated syncope due to gallbladder inflammation and perforation.A temporary demand pacemaker was placed with an escape rate of 50 beats per minute. When the pacemaker was temporarily disabled to assess rhythm stability, the patient had several episodes of sinus bradycardia, atrioventricular block, and asystole. Episodes lasted 20 to 40 seconds and were associated with weakness, diaphoresis, and loss of consciousness.The abrupt onset of sinus bradycardia and atrioventricular block preceding each episode of asystole, the associated weakness and diaphoresis, and the absence of laboratory test abnormalities or a pharmacological cause suggested a neurally mediated mechanism for these syncopal episodes. The patient was treated with metoprolol with marked improvement, although several milder episodes continued to occur.The development of an unexplained persistent leukocytosis despite the initiation of broad-spectrum antibiotic therapy deferred any further actions. An abdominal computed tomographic scan, performed to identify a possible source of infection, revealed a markedly distended, inflamed gallbladder with thickened walls and evidence of a contained perforation, consistent with severe cholecystitis. Percutaneous drainage was performed.Following percutaneous drainage, the patient had no further episodes of bradyarrhythmias, and temporary pacing was discontinued. She underwent an open cholecystectomy 3 days later. Before and during the operation, pacing was not required. The surgical pathological report revealed a gangrenous gallbladder with changes of severe chronic cholecystitis.Unfortunately, 1 day after the operation, the patient had massive upper gastrointestinal tract bleeding, which rapidly led to death by exsanguination. Autopsy examination showed an aortoesophageal fistula arising 2 cm below the bypass graft.COMMENTLife-threatening bradycardia and asystole may occur as an extreme manifestation of neurally mediated cardioinhibitory syndromeand may even result in asystolic sudden cardiac arrest.The cases presented in this report illustrate the interaction of diverse pathologic processes with the afferent pathway of the autonomic nervous system. In both of our patients, a severe bradycardia leading to cardiovascular collapse was the first manifestation of the pathologic processes not typically implicated in the development of these symptoms. In each patient, the underlying cause of this serious rhythm abnormality was unsuspected and undiagnosed until a comprehensive workup had been performed.The most probable explanation for the first patient's syndrome relates to increased parasympathetic activity resulting from direct carotid sinus stimulation by tumor pressure. The carotid sinus is composed of loosely interwoven nerve endings throughout the outer media of the internal carotid artery, just above the carotid bifurcation .The syndrome of carotid sinus hypersensitivity may be evoked by carotid sinus pressure.The tumor diagnosed in the first patient was large and located on the right side, close to the more sensitive of the carotid sinuses.His symptoms were sometimes triggered by a change in head position, which most likely exerted increased pressure on the carotid sinus, causing a cardioinhibitory response.Glossopharyngeal syncope, a syndrome that occurs in association with tumors of the oropharynx or base of the skull, is a less likely cause of this patient's syndrome. Glossopharyngeal syncope has been previously described.In these patients, severe pain in the throat evoked by chewing, swallowing, or coughing triggers vasovagal syncope.Afferent sensory fibers from the throat and the carotid baroreceptors both run in the glossopharyngeal nerve.Pain impulses are thought to be misdirected and to jump over to baroreceptor fibers somewhere along the nerve.This increased afferent traffic causes reflex parasympathetic outflow with bradycardia and inhibits sympathetic efferent activity. The tumor in the first patient was located in the posterior pharyngeal wall, an area innervated predominantly by the glossopharyngeal nerve. Even though the patient did not have pain, glossopharyngeal nerve overstimulation may have been a cause of his symptoms.In the second patient, cardiac vagal stimulation was thought to be caused by gallbladder inflammation and subacute rupture. Gallbladder distention has been shown to activate spinothalamic tract cells and spinal neurons in the upper thoracic segments of the spinal cord.The spinothalamic tract also receives afferent fibers from the cardiopulmonary baroreceptors at the T1 through T5 level.An increase in reflex sympathetic discharge in the spinothalamic tract caused by gallbladder distention can result in the stimulation of afferent vascular baroreceptor fibers and a reflex increase in vagal tone, resulting in the typical bradycardia response observed in this patient. The average threshold pressure in the gallbladder needed to activate spinothalamic tract cells is 50 mm Hg.Pressures in the gallbladder may approach 60 mm Hg during acute cholecystitis. In this patient, percutaneous drainage of the gallbladder was associated with a complete resolution of the bradycardia-hypotension syndrome, implicating the distended gallbladder as the primary factor leading to the described cascade of events.These cases emphasize the importance of an extensive diagnostic search for nontraditional and unsuspected causes of neurally mediated syncope in patients with repetitive, life-threatening bradycardia and asystole. In this report, we demonstrate a neck malignant tumor and chronic cholecystitis as possible causes. Alternative causes for such a profound syndrome include other gastrointestinal tract disorders, other head and neck malignant tumors, or cerebrovascular disorders.KMSpyerNeural organisation and control of the baroreceptor reflex.Rev Physiol Biochem Pharmacol.1981;88:24-124.GLEngelPsychologic stress, vasodepressor (vasovagal) syncope, and sudden death.Ann Intern Med.1978;89:403-412.SMilsteinJBuetikoferJLesserCardiac asystole.J Am Coll Cardiol.1989;14:1626-1632.DHeathPSmithThe Pathology of the Carotid Body and Sinus.London, England: Edward Arnold; 1985:19, 112.DDSugrueDLWoodMDMcGoonCarotid sinus hypersensitivity and syncope.Mayo Clin Proc.1984;59:637-640.SJSchnellerJWHarthorneCarotid sinus hypersensitivity.Clin Prog Electrophysiol Pacing.1985;3:389-393.TRDykmanEBMontgomeryPDGerstenbergerHEZeigerWEClutterPECryerGlossopharyngeal neuralgia with syncope secondary to tumor.Am J Med.1981;71:165-168.BGWallinCEWesterbergGSundlofSyncope induced by glossopharyngeal neuralgia: sympathetic outflow to muscle.Neurology.1984;34:522-524.HKaufmannNeurally mediated syncope and syncope due to autonomic failure.J Clin Neurophysiol.1997;14:183-196.AGHampton JrJEBeckwithDLWood JrThe relationship between heart disease and gallbladder disease.Ann Intern Med.1959;50:1135-1148.RForemanSpinal cord neuronal regulation of the cardiovascular system.In: Armour JA, Ardell JL, eds. Neurocardiology.Oxford, England: Oxford University Press; 1994:260.Accepted for publication October 21, 1998.We thank Nancy Roistacher, MD, for providing much of the clinical follow-up data on patient 1.Corresponding author: Jonathan S. Steinberg, MD, Arrhythmia Service, Division of Cardiology, St Luke's–Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, 1111 Amsterdam Ave, New York, NY 10025.

Journal

JAMA Internal MedicineAmerican Medical Association

Published: Mar 22, 1999

References