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At least 19 recordsLinked to original sources

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

Three cases of hypotension and syncope with ventricular pacing: possible role of atrial reflexes.

Hypotension with lightheadedness and near syncope occurred in three patients during effective ventricular pacing. Hemodynamic studies demonstrated a decrease in cardiac output ranging from almost no decrease to 15 percent, presumably related to the loss of effective atrial contraction. The decrease in output was too small to explain by itself the reduced blood pressure, which resulted from paradoxic reduction of total peripheral resistance in one patient and from failure of resistance to increase in two. Baroceptor reflexes (Valsalva response) were normal in all three patients; hence it is suggested that the failure of compensatory increases in total peripheral resistance may be due to a reflex from the sudden atrial distension that occurs during atrioventricular (A-V) dissociation. The fluctuations in arterial pressure during ventricular pacing were synchronous with the appearance of cannon waves in the right atrial pressure tracing. Arterial pressure during A-V dissociation thus appears to be balanced by two opposite reflexes: the baroceptor reflex, which attempts to compensate for reduction in output, and atrial distension, which reduces peripheral resistance.

Blood Pressure

Baroreflex sensitivity in patients with Takayasu's aortitis.

Takayasu's aortitis is an arterial inflammatory disease of arteries of unknown etiology. Fainting is a common symptom and has been attributed to ypersensitivity of the baroreflex. We studied baroreflex sensitivity in 11 patients with Takayasu's aortitis and compared it with that of eight control subjects of comparable age. Baroreflex sensitivity was assessed by determining the slope of a regression line relating the rise of systolic arterial pressure to the prolongation of the R-R interval of the electrocardiogram during a transient rise of arterial pressure induced by an intravenous injection of phenylephrine. The average baroreflex slope of patients with Takayasu's arteritis (4.0 +/- 0.8 msec/mm Hg) was significantly less than that of control subjects (10.7 +/- 0.8 msec/mm Hg, P less than 0.001). Reduced baroreflex sensitivity in patients with Takayasu's aortitis may be due to the hardening of the arteries where baroreceptors lie, or to hypertension and/or cardiac disease which was present in most of the patients included in this study. Patients with Takayasu's aortitis who complained of fainting also showed the reduced baroreflex sensitivity. This indicates that fainting in this disease is not likely to be caused by the hyperreactivity of the baroreceptors as is commonly postulated.

Adult

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

Two types of febrile seizure: anoxic (syncopal) and epileptic mechanisms differentiated by oculocardiac reflex.

The duration of cardiac asystole induced by ocular compression was measured in 100 consecutive children referred for electroencephalographic examination after one or more febrile convulsions (FC). The children were classified into three groups-namely, those with anoxic FCs, those with epileptic FCs, and "others"-according to the appearances of the FC and the electroencephalogram (EEG). In 14 children the description of the FC suggested non-epileptic anoxic cerebral seizures such as are seen after prolonged syncope or breath-holding. In 35 children the FCs were assumed to be epileptic in mechanism on the basis of unilateral (hemiclonic) twitching, known cerebral disease, a family history of epilepsy, or spikes on the EEG. In the 51 "others" the FCs could not be classified. Definitely abnormal asystole (four seconds or over) was induced by ocular compression in half the anoxic group, in 16% of the "others," but in none of the epileptic group. The differences between the degree of asystole induced in each of the three groups was highly significant (P=0.005).These results support the hypothesis that vagal-mediated cerebral ischaemic anoxia is implicated in the genesis of FCs that resemble anoxic seizures and in a substantial number of those without an obvious epileptic mechanism. The significance, genetics, management, and prognosis of FCs must now be re-examined in this light.

Brain Ischemia

Carotid sinus hypersensitivity in patients presenting with syncope.

In 23 patients (ages 44 to 81) presenting with syncope, vertigo, or transient amnesia, carotid sinus massage produced a significant bradycardia in association with symptoms. The 10 most severely symptomatic patients were studied electrophysiologically, including measurement of intracardiac conduction times and corrected sinus node recovery times, as well as with carotid sinus massage before and after atropine. The only detectable abnormality in five of this group was asystole produced by carotid sinus massage; the other five had, in addition, evidence of either sinuatrial disease or an intracardiac conduction defect. Cardiac pacing in these 10 patients completely abolished their symptoms. In a control group of 52 asymptomatic patients (ages 36 to 87), an abnormal response to carotid sinus massage was uncommon (2%).

Adult

Changes in heart rate during administration of local anesthetics in neuropsychiatric patients.

The effects on heart rate of injections of local anesthetics into the oral mucosa were studied in neuropsychiatric patients; these patients, in whom syncope had not occurred, had been hospitalized for a prolonged period. The heart rate in the neuropsychiatric patients decreased by only 3.9% in contrast to an average decrease of 12.6% in healthy adults. Diazepam was also effective in reducing the cardiac response. The lack of responsiveness in the trigeminal-vagal reflex may be a factor in protecting patients from syncope.

Adult

[Vagal tone in symptomatic sinus node dysfunction (author's transl)].

Under investigation in this study were the role of vagal tone in symptomatic sinus node dysfunction and the relationship between hypersensitive carotid sinus reflex (HCSR) and sick sinus syndrome (SSS). In 168 symptomatic patients (pts) resting heart rate (HR), maximal corrected sinus node recovery time (CSRTmax) and maximal carotid sinus pressure results (CSPmax) were determined before and after Atropine, 1 mg i.v. (A). According to test results, 103 pts had HCSR (1), 33 had HCSR + SSS (II), 30 pts had isolated SSS (III) and 20 pts with normal test results served as controls (IV). Mean age was the same in groups I--IV (p greater than 0.05). Groups I--III had a HR less than or equal to 60 bpm, rising 31% after A in groups I--IV, but absolute values were below those in group IV. In groups I--III CSP normalized after A and CSRT remained unchanged (p greater than 0.05). We conclude that increased vagal tone plays but one role in groups I--III and the combination HCSR + SSS seems rather frequent. Specific testing clearly separated HCSR from SSS.

Adult

Carotid sinus syncope induced by malignant tumors in the neck. Emergence of vasodepressor manifestations following pacemaker therapy.

Three patients had carotid sinus syncope secondary to malignant neoplasms in the neck. Pacemaker therapy controlled the cardioinhibitory reflex with bradycardia, but the patients manifested varying episodes of hypotension due to a vasodepressor reflex that most likely resulted from persistent irritation of the carotid sinus by the tumor. These episodes seemed to be self-limiting. Surgical treatment in resistant cases is a possibility.

Carcinoma, Squamous Cell

[The significance of electrophysiologic findings and clinical course in symptomatic sinus node dysfunction (author's transl)].

Under investigation in this study were the relationship between hypersensitive carotid sinus reflex (HCSR) and sick sinus snydrome (SSS), the significance of clinical symptomatology versus electrophysiologic test results and the natural course of both syndromes. In 186 symptomatic patients (pts) resting heart rate, maximal corrected sinus node recovery time (CSRTmax) and maximal carotid sinus pressure results (CSPmax) were determined. According to test results, 103 pts had HCSR (I), 33 had HCSR + SSS (II), 30 pts had SSS (III), and 20 pts with normal test results served as controls (IV). Mean age was the same in groups I--IV (p greater than 0.05). Groups I--III had a heart rate less than or equal to 60 bpm. There was no correlation between patients test data and the occurrence of syncopes in each of groups I--III (p greater than 0.05). In 16 pts with SSS, test results remained unchanged 16 months later (p greater than 0.05). More pts (31%) in group II died in a shorter period of time after pacer application (1.4 +/- 1 year) than pts with AV III degrees block (25%, 1.8 +/- 1.6 years) after pacer application. We conclude that the combination HCSR + SSS seems rather frequent. Specific testing separated HCSR from SSS, but failed to predict syncopes and thereby cannot aid in the indication for pacer application. The 16 months prognosis of SSS proved unfavorable. Mortality after pacer application in HCSR + SSS seems less favorable than in AV III degrees block (p less than 0.05), but depends largely on the severity of associated diseases.

Adult

A patient with repeated syncopal attacks after using isosorbide dinitrate.

The case of a patient with repeated attacks of collapse induced by sublingual isosorbide dinitrate is reported. The patient was an 81 year-old female who was admitted to Yura Hospital because of attacks of precordial pain. Several minutes after the sublingual administration of isosorbide dinitrate (10 mg) for an anginal attack, she developed a sensation of general weakness, and thereafter because unconscious. Arterial blood pressure fell and became unmeasurable. Electrocardiograms recorded during the syncopal attack showed sinus tachycardia and significant elevation of ST-segment in right precordial leads. In response to a drip infusion of noradrenaline, arterial blood pressure returned to normal with recovery of consciousness. Two similar syncopal attacks induced by sublingual isosorbide dinitrate occurred in the next three days. These attacks were not due to augmentation of the vagal reflex. Decrease of venous return probably was the primary etiological factor.

Aged