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A 59-year-old male patient was admitted for possible reflex syncope following loss of consciousness during urination. During the visit, a malaise with unconsciousness occurred. Holter ECG at that time showed increasing sinus bradycardia with transition to a junctional escape rhythm (30/min); in addition, there were several sinus pauses 2.0 s (the longest almost 10 s). This malaise occurred again during routine EEG, when a focal epileptic seizure on the right fronto-temporal with sinus bradycardia after 15 s was documented. Thus, the diagnosis of ictal asystole was made, anticonvulsant therapy was started, and a cardiac pacemaker was implanted.Ein 59-jähriger Patient wurde nach einer Bewusstlosigkeit beim Wasserlassen bei möglicher Reflexsynkope aufgenommen. Während der Visite kam es zu einem Unwohlsein mit Bewusstlosigkeit. Das Langzeit-EKG (Elektrokardiogramm) zeigte zu dieser Zeit eine zunehmende Sinusbradykardie mit Übergang in einen junktionalen Ersatzrhythmus (30/min), zusätzlich bestanden mehrere Sinuspausen 2,0 s (die längste fast 10 s). In der Routine-EEG (Elektroenzephalographie) kam es erneut zu diesem Unwohlsein, hierbei bestand ein fokaler epileptischer Anfall rechts frontotemporal und ca. 15 s nach Anfallsbeginn eine ausgeprägte Sinusbradykardie. Somit wurde die Diagnose einer iktalen Asystolie gestellt, eine antikonvulsive Therapie begonnen und ein Herzschrittmacher implantiert.

This review discusses important aspects of pathophysiology, diagnosis and therapy of reflex syncope. The autonomic nervous system plays a crucial role in the origin of this frequently observed form of syncope. In most cases, reflex syncopes occur under specific circumstances. Thus, a detailed history is essential. Besides a physical exam und a normal 12-lead ECG, dedicated tests like tilt-table-testing, carotid massage and the implantation of a loop recorder often assist in making the correct diagnosis. The basis of therapy for all patients is reassurance about the benign course of the disease as well as education about adequate measures. Pharmacotherapy is reserved to a minority of patients. In older patients with repeat or severe syncopes and documented asystoles, pacemaker therapy is a valuable option.In dieser Übersicht werden wichtige Aspekte zur Pathophysiologie, Diagnostik und Therapie von Reflexsynkopen diskutiert. Das autonome Nervensystem spielt eine entscheidende Rolle in der Entstehung dieser häufigen Form von Synkopen. Reflexsynkopen sind in den meisten Fällen gekennzeichnet durch spezifische Umstände des Auftretens. Daher stellt die genaue Anamnese einen zentralen Baustein der Diagnostik dar. Neben der normalen körperlichen Untersuchung und einem unauffälligen 12-Kanal-EKG weisen spezielle Tests wie die Kipptischuntersuchung (KTU), die Karotissinusmassage (CSM) und der implantierbare Loop-Rekorder in vielen Fällen den Weg. Therapeutisch stehen die genaue Aufklärung des Patienten und die Schulung von Verhaltensmaßnahmen allen Patienten mit Reflexsynkopen im Vordergrund, während eine Pharmakotherapie nur in Einzelfällen angewendet wird. Eine definierte Gruppe älterer Patienten mit dokumentierten Asystolien profitiert von einer Schrittmachertherapie.

Syncope is a frequently observed symptom in pediatrics with teenagers being the age group most often affected. In contrast to older age, organic cardiac causes of syncope in child-hood are observed in a minority of only 2-5% of cases, in their majority pediatric syncopes thus are neurocardiogenic in origin. The rare organic cardiac causes that may manifest with syncope are all potentially dangerous entities such as cardiomyopathies, genetic primary electrical disease and some forms of structural heart disease, as well as some other rare diseases such as e.g. primary pulmonary hypertension. These diseases have to be actively looked for or excluded. Guidelines recommend patient evaluation including history, physical examination and ECG, which is sufficient to sort out suspect cases after a syncopal episode.

Reflex-mediated syncope is a common cause for syncope. The first step in evaluating the cause of syncope is to assess the risk of a life-threatening cause for syncope, e.g., ventricular arrhythmias. Reflex-mediated syncope has to be differentiated from orthostatic syncope. In orthostatic syncope, there is an insufficient autonomic response. In contrast to a reflex-mediated syncope, in which the autonomic nervous system acts inappropriately, reflex-mediated syncope is classified into the classical vasovagal form, the situational form, or due to carotid sinus hypersensitivity. In the elderly, often a mixed form is present. Treatment is difficult. Most important is educating the patient and avoiding precipitating factors. Physical maneuvers, e.g., counter pressure maneuvers, are more effective than drug treatment. Permanent pacing is rarely needed. However, before indicating a pacemaker, a correlation between bradycardia and syncope should be documented. This is often only possible by implanting a monitoring device at an early stage.

We report on a 76 year old woman who fainted on her way to the restroom during the night. At the emergency department, a prolonged QT-interval was noticed in addition to sinusbradycardia and marginal hypokalemia. The QT-interval normalized promptly after citalopram was discontinued. Taking into account the clinical picture and the ascertained orthostatic dysregulation, a diagnosis of orthostatic syncope was made. Because of the lengthened QT-interval, drug-induced torsade de pointes ventricular arrhythmia was considered as a differential diagnosis. We describe that citalopram was most probably the cause for the prolonged QT-interval. In our article we discuss the pathophysiology of drug-induced long QT syndrome (LQTS), the most important drugs involved, and finally the prophylaxis and treatment of a TdP ventricular arrhythmia.

Syncope may be nothing more than a run of the mill faint, or a precursor of sudden cardiac death. In persons with a healthy heart, it usually has an autonomic-nervous (vasovagal) genesis; when structural heart disease is present it is often rhythmogenic. For diagnostic purposes, the tilt-table is indicated when neurocardiogenic syncope is suspected, and an electrophysiological investigation or long-term monitoring of cardiac rhythm (implantable loop recorder) if rhythmogenic syncope is suspected. Neurocardiogenic syncope is treated by providing the patient with relevant information, orthostatic training, increased intake of fluids and, where necessary, medication. In the case of the prognostically serious rhythmogenic syncope, the underlying rhythm disorders are treated in accordance with current recommendations.

Approximately 15% of children experience a syncope before the age of 18 years. Tilt table testing represents the diagnostic gold standard whenever a neurocardiogenic spell is suspected. Two methods of continuous, non-invasive hemodynamic monitoring during the tilt table test are presented and their usefulness for clinical routine is discussed.4 patients with suspected neurocardiogenic syncope.Tilt table testing according to standard protocol; non-invasive, continuous blood-pressure measurement by finger cuffs; impedance cardiography for the assessment of cardiac output.In 3 patients a syncope occured during the tilt table test. In pt. 4 characteristic symptoms led to diagnosis prior to syncope. Every patient represents a definite type of neurocardiogenic syncope (cardioinhibitory with asystolia, vasodepressory, mixed as well as postural tachycardia syndrome).Both monitoringmethods allow a differentiated analysis of the cardiovascular interactions during the tilt table test. Thus, specific regulatory patterns may be diagnosed and specific treatment strategies may be offered.

Various disorders of autonomic circulatory control are characterized by symptoms of orthostatic intolerance and syncope. Since the introduction of tilt-table testing as a cardiac diagnostic tool by Kenny et al., definition of these disorders has changed significantly. This review summarizes the current knowledge of diagnosis and treatment of the syndromes of orthostatic intolerance.

The study compares the importance of tilt-table testing and Schellong's test for the diagnosis of syncopes.In a prospective clinical trial 100 consecutive patients (45 males, 55 females) were included. The index symptom for inclusion was a former syncope or presyncope in the patients' history. The tilt-table testing procedure was performed according to a modified version of the Westminster protocol. Following this procedure, Schellong's test was performed in 83 of the patients.During tilt-table testing 34 patients suffered from orthostatic dysautonomy with syncope or neuro-cardiogenic syncope. 29 of these symptomatic patients also underwent Schellong's test. However, only four patients showed a borderline positive finding, whereas a clearly positive result was seen in six patients. These patients had shown orthostatic dysautonomies with syncopes during tilt-table testing. No patient suffered from a syncope or presyncope during Schellong's test.Schellong's test is suitable as a diagnostic procedure for orthostatic dysregulation only, and tilt-table testing is highly superior for objectification of the diagnosis and differentiation of syncope.

Pharmacological approaches for the treatment of cardioinhibitory vasovagal syncope are controversially discussed in the literature. In acute treatment of neurocardiogenic syncope, anticholinergics (atropine) are used effectively. Randomised and placebo-controlled clinical trials evaluating the preventive significance of anticholinergic agents in the therapy of cardioinhibitory vasovagal syncope are still missing. We report the case of an 18-year-old male patient with recurrent convulsive, cardioinhibitory neurocardiogenic syncope. Vasovagal syncope occurred predominantly as centrally induced syncope triggered by negative emotions such as fear or by seeing blood. Under resting conditions, the patient revealed increased parasympathetic tone with nocturnal bradycardia of 38 beats/min. In the course of head-up tilt table testing a cardioinhibitory syncope with an asystolic pause of 10 seconds occurred without any prodromes after 10 minutes of upright positioning. In order to inhibit parasympathetic tone, medication with ipratropiumbromide was initiated. Time-variant analysis of heart rate variability (autoregressive model) during head-up tilt table testing showed under the medication with ipratropiumbromide a vagal mediated cardioinhibition to 56 beats/min, but no further sinus arrest. Throughout clinical follow-up of 6 months the patient remained syncope-free under the medication. The usefulness of ipratropiumbromide in inhibiting vagal mediated cardioinhibition will be discussed referring to the case report and to studies evaluating anticholinergic agents in the treatment of neurocardiogenic syncope.

History, physical examination and ECG allow to define the cause of syncope in about 50%. This initial assessment often, in addition, suggests a diagnosis, which is then confirmed with Holter-ECG or echocardiography, stress-ECG, tilt-test, carotissinus test or intracardial electrophysiological testing, rarely neurological or psychiatric evaluations. A stepwise approach is recommended.

Neurocardiogenic convulsive syncope as a disease at the border between cardiovascular and neurologic dysfunction can pose considerable diagnostic challenges. We report on the case of a 19 year-old female patient with recurrent neurocardiogenic convulsive syncope where the time from the onset of symptoms to the correct diagnosis and initiation of an effective therapy spanned more than three years. Based on this case report, we discuss differential diagnosis, pathophysiology and therapy of this disorder of autonomic cardiovascular regulation. Neurocardiogenic convulsive syncope should be considered whenever a patient has both syncope that exhibits a typical cardiovascular pattern (e.g., fainting of short duration with rapid reorientation phase) and prolonged loss of consciousness with characteristic neurological features (e.g., cerebral seizures with postictal state of confusion). Head-up tilt testing, introduced into clinical practice in 1986, is an efficient tool to diagnose neurocardiogenic syncope with comparatively high sensitivity in patients with recurrent syncope of unknown origin. Besides orthostatic training and pharmacotherapy, permanent dual-chamber cardiac pacing has gained increasing importance as treatment for cardioinhibitory forms of neurocardiogenic syncope.

Since the renaissance of tilt table testing in clinical cardiology some 15 years ago, the syndromes of autonomic dysfunction with orthostatic intolerance underwent improved differentiation and classification. In the present review a variant of autonomic dysfunction with orthostatic intolerance--POTS (postural orthostatic tachycardia syndrome)--will be discussed.The affected patients present with orthostatic intolerance, postural tachycardia, exercise intolerance, fatigue, dizziness and in some cases with other dysautonomic symptoms such as gastrointestinal or sudomotor dysfunction. Together with the clinical history, tilt table testing is the cornerstone of diagnostic evaluation by which the syndrome can be distinguished from typical neurocardiogenic disorders. POTS is characterized by different subtypes; accordingly, therapy for relief of symptoms is variable and includes beta blockers for patients with the hyperadrenergic type and alphamimetics for those with partial dysautonomia.Although it is now possible to differ POTS from other forms of autonomic dysfunction, further research is warranted to clarify the pathophysiology of this syndrome and its subtypes and to improve therapeutic interventions.

Patients with recurrent syncope undiagnosed after extensive noninvasive and invasive testing pose a diagnostic and therapeutic dilemma. Holter monitoring is non-diagnostic in 90% of cases. Recent developments in loop recorder technology permit longterm ECG monitoring in patients with recurrent unexplained syncope. The implantable loop recorder monitors a single lead electrogram continuously using 2 sensing electrodes on the device shell. The device was implanted in 20 patients (11 male, 9 female) with the history of recurrent syncope. During a mean follow-up of 12+/-6 months after device implantation, 11 patients (55%) experienced syncope (8 pts) or presyncope (3 pts). In the remaining 9 patients, no syncope occurred. In all 11 patients with syncope or presyncope during follow-up, loop recording definitively determined whether an arrhythmia was the cause of symptoms or not. Diagnosis included bradycardia in one patient, tachycardia in two patients, in one patient two rhythm disturbances were revealed: frequent ventricular premature beats with bigemini and atrial flutter. Two patients had a neurocardiogenic syncope. Syncope was nonarrhythmic in 5 patients. An implantable loop recorder is useful for establishing the diagnosis if symptoms are recurrent but too infrequent for conventional monitoring techniques.

Orthostatic circulatory disorders are frequently the cause of orthostatic intolerance, syncope or dangerous falls. A sufficient therapy should be based on a differential diagnosis by means of an active standing test or a tilt-table test. Three typical pathological reactions of blood pressure and heart rate can be differentiated. The hypoadrenergic orthostatic hypotension is characterised by an immediate drop in blood pressure (systolic drop20 mmHg below base line within 3 min) with or without compensatory tachycardia. It is caused by peripheral or central sympathetic dysfunction. Tachycardia (30 beats per minute above base line within 10 min) without significant blood pressure drop but with a fall of cerebral blood flow indicates a postural tachycardia syndrome. In general, there is no further somatic dysfunction. Increased venous pooling is thought to be the assumed pathomechanism. A reflex mechanism evokes the neurocardiogenic syncope after a certain time of standing: sympathetic inhibition yields a strong blood pressure drop and vagal activation bradycardia. Proved therapies include use of the mineralocorticoide fludrocortison (hypoadrenergic orthostatic hypotension), of the alpha-agonist midodrin (postural tachycardia syndrome) and of beta-blockers (neurocardiogenic syncope).

Stimulated by the widespread use of tilt table testing, disorders of autonomic function with orthostatic hypotension have recently gained attention by clinical cardiologists. At the same time, improved characterization of the underlying circulatory responses have led to a reclassification of these syndromes. In particular, three subgroups of chronic primary dysautonomia have been defined such as Pure Autonomic Dysfunction, Multiple System Atrophy, and the Postural Orthostatic Tachycardia Syndrome. On the other hand, acute dysautonomias represent a rare yet clinically sometimes dramatic form of autonomic disorders. Several diseases as well as enzymatic disorders, and pharmacological drugs may cause secondary dysautonomia. The clinical correlate of all these forms of dysautonomia is orthostatic hypotension and syncope. Thus, a careful history forms the basis of a successful diagnostic workup of the underlying cause of syncope. This review summarizes the current knowledge of autonomic disorders, their classification and diagnostic and therapy strategies.

OBJECTIVE/MATERIAL AND METHODS: In a prospective randomized study, the techniques of stereotactic breast biopsies in prone and sitting position were compared. Part of the data has already been published. A total of 103 women underwent stereotactic breast biopsies, either prone (n = 51; using TRC-Mammotest, Sweden) or in the sitting position (n = 52; using Stereotix 2, General Electric Medical Systems, Milwaukee, Wisconsin, USA). With the help of pre- and post-biopsy questionnaires, anxiety, pain, and subjective experience were recorded in all patients. Vasovagal reactions were scored from 0 to 2 according to their severity. All biopsy results were verified by surgery. The specificities and sensitivities for the two positions were calculated and statistically compared.With regard to overall tolerance no statistically significant difference between biopsies performed in the sitting or the prone position was noted. Significantly more patients (p = 0.04) in the prone position stated they would prefer premedication prior to a repeat biopsy. Three patients (prone; n = 1; sitting; n = 2) fainted during the procedure. There was no statistically significant difference between the two biopsy positions regarding sensitivity (95%) and specificity (100%).More attention should be paid to patient care and, especially, preintervention information. Biopsies in the prone or sitting position are equally well tolerated. Somatic reactions are not a major problem during breast biopsy. Success and validity are independent of the biopsy position.

Confusion between syncope and epileptic seizures is a common problem in clinical practice. Recently, new insights into the phenomenology of transient cerebral hypoxia have been gained from video analysis of experimentally induced syncope. Common elements of syncope include multifocal and generalized myoclonus, tonic body extension, automatisms, vocalizations, eye deviations and hallucinations. Thus, it is not the presence or absence of these features but their specific character that distinguishes syncope from epileptic seizures. Other clues for differential diagnosis include precipitating factors, premonitory symptoms and postictal events, such as tongue bites and postictal confusion, which has been identified as the single most powerful factor discriminating syncope from epileptic seizures. In contrast, incontinence and head injury are common in both conditions. Investigations such as electroencephalogram, tilt testing and postictal prolactin or creatine kinase levels may aid diagnosis but are never diagnostic in isolation. In rare cases, hypoxic and epileptic mechanisms may interact within one attack.

Vasovagal syncope, also called neurocardiogenic syncope, is common with younger people. It results from an inappropriate, excessive autonomic reflex activity. In the elderly patient the syncope may be provoked by massage of the carotid bodies and is then known as carotid sinus syndrome. The pathogenesis of neurocardiogenic syncope is debated. Sudden vasodilation and/or bradycardia have been attributed to the activation of ventricular mechanoreceptors. The use of betablockers is based on this hypothesis. Head-up tilting at 60 degrees is helpful in the evaluation of syncope. In the therapy of recurrent vasovagal syncope, a thorough information of the patient and an adaptation of behaviour are often successful. Some authors have reported goods results with betablockade, etilefrin or mineralocorticoids. The patient with repeated severe syncopal attacks and asystole may benefit from an implantable DDD pacemaker.

Most cases of sudden and temporary loss of consciousness [syncope] are caused by hypoperfusion of the formatio reticularis. more rarely by primary neurologic or metabolic disorders. The most common etiology is vasodepressor (vasovagal) syncope, which is caused by peripheral vasodilation due to acute withdrawal of the efferent sympathetic tone, while the parasympathetic outpour is increased at the same time. Although the efferent limb of the baroreflex manifests in a rather uniform way, the afferent parasympathetic limb is very variable, leading to a variety of clinical presentations and triggers (orthostatic hypotension, pain, fear, cough, micturition, emotions). While vasodepressor syncope mainly occurs in young people with healthy hearts, cardiac syncope caused by arrhythmias or obstructive lesions are more frequently found in elderly patients with organic heart disease. Neurogenic syncope comprises either primary neurologic disorders, such as epilepsia, or hypoperfusion of the vertebrobasilar system (TIA). Rarely, an acute increase of intracerebral pressure may cause syncope. Similarly, metabolic disorders or side effects of drugs are rare causes of syncope; however, drugs may act as important cofactors in the pathogenesis of syncope.