[Rheoencephalographic examination of patients with syncopal states and syncope-like form of epilepsy].
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Adolescent↗
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Syncope of obscure nature.
One hundred and eleven cases of syncope or loss of consciousness are analyzed. Most are of obscure nature while some illustrate features of syncope that deserve further scrutiny. The cases are divided into six groups: Resembling cardiac syncope (30 cases); vasovagal syncope (22 cases); features of both cardiac and vasovagal syncope (12 cases); orthostatic hypotensive (29 cases); akinetic seizure? (12 cases); and miscellaneous (5 cases). Some groups are subdivided according to the circumstances surrounding the spells, for example, seated eating, nocturnal, associated with bowel movement, response to anticonvulsant therapy, etc. The following conclusions seem warranted: The evidence favors the existence of a type of akinetic seizure resembling cardiac syncope; loss of consciousness while seated eating (prandial syncope) may comprise a syndrome; syncope related to bowel movement or abdominal pain is a striking association; sporadic nocturnal syncope due to temporary hyporeactivity of baroreceptors is not sufficiently recognized; alcohol ingestion may precipitate orthostatic hyporeactivity of baroreceptors is not sufficiently recognized; alcohol ingestion may precipitate orthostatic hypotension. Familial syncope, syncope proneness and cold drink syncope are illustrated.
Adult↗
Superiority of 24-hour outpatient monitoring over multi-stage exercise testing for the evaluation of syncope.
Twenty-four hour outpatient monitoring was compared with maximum multi-stage Treadmill exercise testing for the detection of dysrhythmias producing syncope or near syncope in 119 patients. All patients had cardiovascular disorders; only 21% had coronary artery disease. Patients with obvious cause of syncope and/or significant dysrhythmias by resting electrocardiograms (ECGs) were excluded. A significant dysrhythmia was found which was considered the probable cause of syncope or pre-syncope in 76 patients (64%). A non-cardiac cause was found in tachycardia, exercise testing identified only patients with complex ventricular dysrhythmias and missed 64% of these. Overall, dysrhythmias were found by ambulatory monitoring alone in 63 patients, by exercise testing alone in only three, and by both in 10. It is concluded that: 1) in the majority of patients with syncope or pre-syncope suspected to be of a cardiac origin, a dysrhythmia can be found; 2) ambulatory monitoring is far superior to exercise testing for detection of dysrhythmias; 3) exercise testing increases the yield for complex ventricular dysrhythmias.
Adolescent↗
Electroencephalographic evidence of cortical network disruption preceding overt cardioinhibition during tilt-induced reflex syncope.
OBJECTIVE: Reflex syncope is a common cause of transient loss of consciousness. However, the early cerebral mechanisms underlying cardiovascular changes remain poorly understood. Our objective was to investigate early cerebral changes by quantitatively analyzing EEG activity preceding overt cardioinhibition during tilt-induced reflex syncope. METHODS: EEG recordings from patients undergoing tilt testing were retrospectively analyzed. Patients who experienced reflex syncope were compared to those who did not. Spectral and functional connectivity analyses were performed across baseline, pre-cardioinhibition, and syncopal phases. RESULTS: Prior to the onset of cardioinhibitory pathological reflex, a significant increase in theta-band spectral power was observed in the right temporal region, accompanied by a widespread increase in functional connectivity within the same frequency band. These findings suggest the involvement of brain networks before cardioinhibition. CONCLUSIONS: EEG changes in the theta band (power and functional connectivity) were observed before overt cardioinhibition during tilt-induced reflex syncope. SIGNIFICANCE: Our findings support the hypothesis of cortical processing preceding cardioinhibition in reflex syncope. EEG may represent a valuable complementary tool for improving the understanding and diagnosis of these events.
Humans↗
Carotid sinus hypersensitivity and syncope.
Hyperactivity of the carotid sinus reflex is common in older men. However, an unequivocal diagnosis of carotid sinus syncope is difficult to establish because the symptoms are nonspecific, and both hyperactivity of the carotid sinus reflex and syncope are common. Twenty-one men were evaluated for episodes of lightheadedness or syncope, or both, associated with a hypersensitive carotid sinus reflex. Seventeen patients had the cardioinhibitory type, two the vasodepressor type and two both the cardioinhibitory and vasodepressor types. Patients with the cardioinhibitory type benefited from the insertion of a permanent pacemaker if they had multiple episodes of syncope. A history of syncope associated with some event capable of stimulating the carotid sinus was also helpful in selecting patients for pacemaker treatment. The combination of the cardioinhibitory and vasodepressor types may be missed unless carotid sinus stimulation is repeated after the administration of atropine. The results of electrophysiologic studies in 17 patients with the cardioinhibitory type suggest that intrinsic sinus nodal dysfunction is not the major cause for asystole after carotid sinus stimulation.
Aged↗
Cough syncope: the possible relation to hydrocephalus ex vacuo.
Pneumoencephalographic data in five male patients with cough syncope were compared to those from age-matched patients with syncope from other causes. The 3rd ventricle width was significantly larger in patients with cough syncope than in the control group (p less than 0.01). Theoretically, the most plausible role of hydrocephalus ex vacuo in cough syncope may be: either it causes increased sensitivity to changes normally encountered during coughing, or--which seems less likely--it may abolish mechanisms normally restraining cough.
Asthma↗
[Cardiac syncope].
Clinical cases are presented on the general theme of cardiovascular syncope. A case is cited to illustrate the clinical picture of idiopathic hypertrophic obstructive cardiomyopathy, a frequently disguised and misinterpreted cause of syncope. Chief attention is focused on the concept of fascicular heart block causing syncope. In the light of 3 patients, the various possibilities with respect to etiology, evolution, clinical picture and prognosis of fascicular heart block are outlined. In this context the diagnostic, prognostic and therapeutic significance of His bundle electrocardiography is discussed. Finally, 2 cases are cited to illustrate the sick sinus syndrome as a major cause of syncope. The diagnostic procedure in patients with suspected lazy sinus node is discussed and the results are presented of 16 personally observed cases with this disorder.
Adult↗
Defaecation syncope.
Defaecation syncope is recorded in seven female and two male patients aged between 63 and 78 years seen over a period of nine years. The tendency for defaecation syncope to occur at night contrasts with the rarity of nocturnal defaecation in most old people. The close similarity with micturition syncope is noted.
Aged↗
Vasovagal syncope in aircrew. Psychosocial aspects.
Twenty-four aircrew members with the diagnosis of vasovagal syncope were compared to 26 controls on variables of personality characteristics, psychosocial antecedents to the onset of their conditions, and hyperventilation experience. The syncope group was found to be younger, slightly less adaptable, and to have significantly more negative feelings about their work. The authors argue that syncope in aircrew should be considered from a psychosocial perspective as well as from a medical-neurological perspective.
Adaptation, Psychological↗
Obscure syncope and the sick sinus syndrome.
This report describes a 25-year-old vigorous young man who had a history of eight years of near syncope and syncope of unknown etiology. Repeat in-hospital observation and laboratory electrophysiologic functional testing did not elucidate the origin of the symptoms. Prolonged Holter monitoring finally showed that the syncopal attacks were caused by a sick sinus syndrome (SSS). On electrophysiologic study, a concealed rate-dependent unidirectional antegrade accessory A-V pathway (AP) was found to be present. The AP was an incidental finding and was unrelated to the patient's symptoms. The symptomatic SSS may occur in the young as well as in the elderly. Sinoatrial dysfunction may be intermittent and difficult to detect, may cause severe symptoms, and may even be life-threatening. Prior to definitive therapy (such as the permanent implantation of a pacemaker), the importance of relating symptoms to a rhythm disturbance has been stressed. In cases where the cause of the symptoms is not obvious, this is best accomplished by continuous Holter monitoring.
Adult↗
Serum neurophysins during passive assumption of the erect posture in men and during pregnancy: effect of syncope.
A slight but reproducible increase in serum total immunoreactive neurophysin levels (IRN) occurred 30 minutes following passive assumption of the erect posture (tilt test) in 12 men (17%, 2 P is less than .02) and in 6 pregnant women (20%, 2P=NS) who showed normal cardiovascular adaptation during the test and did not suffer syncope. The increase was much more marked in 4 men in whom there was a fall in blood pressure and syncope in assuming the upright posture. An increase of twice the basal level was also found in a pregnant women who experienced syncope, although she was maintained horizontal. Our results show that it is important to ensure the absence of these intercurrent phenomena in the correct interpretation of dynamic clinical tests of neurohypophysial function.
Adult↗
Psychologic stress, vasodepressor (vasovagal) syncope, and sudden death.
Giving up in the face of emotional arousal and psychologic uncertainty are conditions conducive both to vasodepressor syncope and sudden death. Under such circumstances there may be simultaneous activation of two emergency biologic regulatory systems, flight-fight and conservation-withdrawal. In the healthy person this may result in vasodepressor syncope, benign arrhythmias, or both. In the presence of factors lowering the threshold for conduction disturbances, dangerous arrhythmias and sudden death rather than, or as well as, vasodepressor syncope may result. Although active myocardial damage by itself may provide the necessary and sufficient conditions for lethal arrhythmias, psychic uncertainty must be considered an additional risk factor. The implications of this concept for patient care and prevention of sudden death are a challenge for future research.
Adult↗
[Syncopal attacks and sudden death due to ventricular fibrillation -- a variant of the Jervell or Lange-Nielsen syndrome (author's transl)].
Syncopal attacks due to ventricular fibrillation or -- flutter with elongation of QT in the ECG and deafness are signs of a congenital condition described by Jervell and Lange-Nielsen 18 years ago. Since then we have learned that the range of variation of symptoms is very wide. There are differences genetically and in age-groups. A boy aged 15 years with supposedly cerebral fits is reported on. Since the right diagnosis was missed he had been treated with anticonvulsants for years. But these were syncopal attacks, Effort produced a tendency to bigeminus. -- A knee-bending exercise repeated 13 times lead to his death from ventricular fibrillation. Post-mortem examination showed no pathologic findings except mild left hypertrophy of the ventricle. His sister also had similar attacks without spasms after excitement or mild physical effort. She too had no extension of the QT interval. Their mother and grandmother also had syncopal attacks and died at the ages of 31 and 24 years. A girl-cousin died suddenly at the age of 15. In addition we have seen a neonate with a mild cardiac murmur on whom an ECG was done on the 16th day. The QT interval was significantly prolonged. There were numerous extrasystoles. He died suddenly 2 days later. Post mortem showed no cardiac pathology. One should now be able to explain some cases of unexpected natural death. But ignorance of the pathogenesis does not yet permit definition of the clinical pictures.
Adolescent↗
Holter monitoring in dizziness and syncope.
Holter monitoring was used to detect the underlying mechanism among 53 patients referred for dizziness, fainting and/or syncope. The complaints were unexplained on clinical grounds in 38, suggestive of SSS in 11, and of pacemaker dysfunction in 4 patients who underwent pacemaker implantation for symptomatic A-V block. Occult dysrhythmias were revealed in 24 of 38 (61%) of the first group; the clinical impression of SSS was confirmed in 8 of 11 (72%) in the second, and ineffective pacing confirmed in 2 of 4 in the third group. Thus, the diagnosis was clarified in 34 of 53 (64%) of patients. It is concluded that Holter monitoring is most useful for detecting the underlying mechanism in the above mentioned conditions, especially in elderly subjects whose syncopal attacks remained unexplained despite routine cardiological and neurological examination. Holter monitoring should be carried out for at least 36 hours before ruling out dysrhythmias as a cause of dizziness and/or syncopal attacks.
Adams-Stokes Syndrome↗
Syncope in patients with pulmonary embolism.
A review of 132 consecutive cases of acute pulmonary embolism (PE) documented by pulmonary angiography indicated that syncope was the initial or predominant clinical feature in 17 (13%). When massive PE causes syncope in a nonhospitalized patient, the diagnosis of PE is frequently overlooked. Hypotension after PE may resolve spontaneously after a short interval. In this circumstance, the syncopal episode might easily be attributed to another cause. The appropriate diagnosis can be established only if other clues, suggestive of PE, are sought. Both arterial blood gas determinations and pulmonary scintigraphy are helpful in making this diagnosis.
Adult↗
[Exercise-induced tachyarrhythmic syncopes with sinus bradycardia and normal QT-interval at rest (author's transl)].
Two children with exercise-induced syncopes are described. There was no evidence for congenital or acquired cardiac defects, cardiomyopathy or myocarditis in either of them. Both had sinus bradycardia and a consistently normal QT-interval at rest. In both, exercise induced regularly a multiform ventricular tachycardia, additionally in one on occasion a bidirectional, in the other a supraventricular tachycardia. Beta receptor blocking agents prevented tachyarrhythmias in both. Under treatment with beta receptor blocking agents, one child remained without syncopes, the other died suddenly. These cases underline the possiblility that exercise-induced syncopes may be caused by tachyarrhythmias even if the QT-interval of the resting Ecg is normal. In suspicious cases an exercise-Ecg is indicated.
Bradycardia↗
Syncope with prolonged QT interval.
Four children with syncope had a prolonged QT interval on the electrocardiogram. Neurologic studies were negative. One patient had associated deaf mutism, one had a family history of sudden death and prolonged QT interval, and two had ventricular arrhythmias while being monitored in the hospital. Treatment with propranolol hydrochloride eliminated the syncope in all patients, although the ECGs remained abnormal.
Adolescent↗
Complete heart block as a cause of syncope in asymmetric septal hypertrophy.
This case report presents a young adult with asymmetric septal hypertrophy (ASH) and syncope. Infranodal complete heart block was demonstrated as his cause for syncope. Therapy consisted of implantation of a A-V sequential pacemaker. Cardiac output determinations and systolic time intervals demonstrated the beneficial effects of properly timed atrial contractions.
Adult↗