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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Syncope is a sudden and temporary loss of consciousness not caused by trauma or seizures. Patients age 65 and older are at elevated risk of syncope-related falls and sudden cardiac death. Cardiovascular causes are generally electrical (ie, arrhythmias) or mechanical (obstruction of central circulation at a cardiac valve or major vascular structure). Noncardiovascular causes include orthostatic hypotension, vasovagal reaction, micturition, carotid sinus hypersensitivity, and neurologic (eg, TIAs). Many causes of syncope can be diagnosed from a thorough history and physical exam. More extensive testing--ECG, Holter monitoring, electrophysiology study--may be indicated for selected patients with unexplained syncope and an unremarkable evaluation.
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PMID:Syncope: diagnosis of cardiac and noncardiac causes. 759 Mar 65

Syncope accounts for approximately 1% to 6% of hospital admissions and 3% of emergency room visits. Syncope is defined as a sudden transient loss of consciousness associated with a loss of postural tone with spontaneous recovery. Patients should not require electrical or chemical cardioversion to regain consciousness. Syncope must be clinically differentiated from other states of altered consciousness, such as dizziness, vertigo, seizures, coma, and nacrolepsy.
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PMID:Workup and management of patients with syncope. 767 89

In the long QT syndrome (LQT), individuals suffer from syncope, seizures and sudden death due to cardiac arrhythmias, specifically torsade de pointes and ventricular fibrillation. Many of these individuals also have prolongation of the QT interval on electrocardiograms, suggesting abnormal cardiac repolarization. To improve our understanding of the mechanisms underlying LQT and to facilitate presymptomatic diagnosis, we have begun to study families with autosomal dominant LQT. In 1991, we reported tight linkage between the LQT phenotype and the Harvey ras-1 gene (HRAS) in several families of Northern European descent. This discovery localized an LQT gene to chromosome 11p15.5 and made presymptomatic diagnosis in some families possible. In initial experiments, no recombination between HRAS and LQT was observed, making this protoncogene a candidate for LQT. This hypothesis was supported by physiologic data; other investigators had shown that ras proteins modulate cardiac potassium channels and an abnormality of potassium homeostasis could explain LQT. We eliminated HRAS as a candidate, however, by sequencing the coding region in 10 unrelated patients and finding no mutations. This indicated that the LQT locus was nearby, but not HRAS. Autosomal dominant LQT was previously thought to be genetically homogeneous and the first seven LQT families we studied were linked to 11p15.5. In 1992, however, several groups, including my laboratory, identified locus heterogeneity for LQT. Recently we identified a second LQT locus, LQT2, on chromosome 7q35-36. Because several families were unlinked, at least one more LQT locus exists. This degree of heterogeneity presents opportunities. It seems likely, for example, that proteins encoded by distinct LQT genes interact to modulate cardiac repolarization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular genetics of long QT syndrome. 767 24

An approach to the pregnant patient with altered consciousness is presented. The unconscious pregnant patient often represents a straightforward simple problem if the event is a minor syncope secondary to physiologic changes of pregnancy. Most loss of consciousness is postictal in nature after either an epileptic or eclamptic seizure. If these are ruled out, other more serious causes must be considered, and the patient must be fully evaluated by appropriate neurologic consultants.
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PMID:The antepartum patient. Sudden changes in central nervous system status and sensorium. 778 34

A 15-year-old female teenager had recurrent syncopes and had been unsuccessfully treated for 6 years for seizures and hysteria. Syncopes were always triggered by emotions, or efforts, but electrocardiograms were normal between the episodes. A 24-hour-monitoring during a syncope, and provocative tests (exercise testing and isoprenaline administration) showed severe ventricular arrhythmias with premature polymorphous beats, followed by ventricular tachycardia and then ventricular fibrillation. These "catecholamine-induced" ventricular tachycardias are very rare but are always fatal without treatment. Syncopes are stress-induced and the diagnosis is almost always delayed, because the patients have a normal electrocardiogram, with normal QT interval. The arrhythmia appears beyond a "threshold" sinus rate and is easily reproducible by exercise testing. Betablockers are the only efficient treatment to prevent sudden death.
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PMID:[Catecholamine induced ventricular tachycardia: a cause of severe syncope during adolescence]. 790 69

Although syncope attacks such as black-out, faint consciousness, and cold sweat are sometimes experienced during leg phlebography, no study of their incidence and mechanism has been reported. We measured blood pressure noninvasively by using a Finapress with ECG monitor during overall examinations (21 cases, 33 limbs; male 8, female 13) following anamnesis. Age, sex, and past history of drug, syncope, leg phlebography, and other diseases were determined. All examinations were done in the upright position. Three cases (14.3%) and four limbs (12.1%) showed syncope attacks during leg phlebography. Syncope occurred after steps taken for the evaluation of venous return in two limbs, during infusion of contrast medium in one, and after infusion in the other. In all cases, the systolic blood pressure measurement during syncope was below 80 mmHg, and the sudden decrease of both systolic blood pressure (-83.0 +/- 22.0 mmHg) and heart rate (-29.5 +/- 5.0/min) suggested vasovagal reaction as a mechanism of syncope. Other causes of syncope including anaphylaxy, hyperventilation syndrome, seizure, and arrhythmia (except for bradycardia) were not found. There were also significant changes in blood pressure and heart rate in the nonsyncope group during leg phlebography that seemed to trigger vasovagal excitation. Premedication, contrast media, and position might be important factors and should be discussed further.
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PMID:[Blood pressure change and syncope during leg phlebography]. 793 82

Recent advances in clinical epilepsy have included improved systems for classifying seizures and epileptic syndromes, better definition of nontemporal seizures, improved methods for distinguishing syncope and pseudoseizures from epilepsy, and new approaches in the management of pregnant women with epilepsy. There has been continued development of the concept that epilepsy is a heterogeneous disorder with many imitators. Treatment is most successful when tailored to the particular seizure type, epileptic syndrome, and special needs of the individual patient.
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PMID:Advances in epilepsy. 801 68

Syncope is a loss of consciousness and postural tone. Although arising suddenly from prolonged recumbency or returning from weightlessness to Earth's gravity can result in syncope from orthostatic or vasovagal effects, there are many other possible causes. These causes can be divided into several groups. Causes listed in the cardiovascular category, especially cardiac causes, are more likely to occur in the elderly; noncardiac causes are more common in the younger population. The cases described herein illustrate the often unexpected mechanisms of syncope in otherwise healthy individuals. Two of the cases emphasize the usefulness of prolonged combined EEG/EKG monitoring. The categories of loss of consciousness experienced by air crew members are reviewed. The most important screening tool in identifying the mechanism(s) of syncope is a detailed history emphasizing a search for underlying disease, the specific associated circumstances, and pre- and post-event symptoms. The type of diagnostic studies, i.e., cardiac or neurologic, undertaken should be based on the historical data. Seizures must be considered as a possible mechanism of otherwise unexplained loss of consciousness in nonelderly persons, including air crew members.
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PMID:The spectrum of syncope. 808 56

Infants and young children cannot describe symptoms of cardiogenic syncope accurately. If the attention in such cases is focused on the seizure activity that may follow, the patient will be treated inappropriately with anticonvulsants. We report such a presentation in 4 infants and young children (ages 6 to 48 months) with idiopathic long QT syndrome. All patients presented with recurrent seizures. All patients had a corrected QT interval (QTc) > or = 0.44 s and none had deafness. The diagnosis was suspected by careful history-taking which revealed episodes of loss of consciousness before convulsions in all patients. All patients were treated successfully with propranolol and remained free of symptoms during the follow-up period of 1-2 years. Screening the other family members revealed a prolonged QTc in 9 out of 16, and a history of 3 sudden and unexplained deaths in two families.
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PMID:Idiopathic long QT syndrome: asking the right question. 809 37

Six female patients with hypoparathyroidism (2 idiopathic and 4 postoperative cases following total thyroidectomy) were examined with brain CT scans; 4 of them underwent MR exams too. Two patients presented with no symptoms, 4 exhibited extrapyramidal syndrome, tetany, fainting seizures or ischemic attacks and only 2 presented with abnormal calcium-phosphorus balance. CT showed calcifications of the basal nuclei in 5 patients. The caudate nucleus was always affected (100%). The calcifications were in the putamen, globus pallidus and thalamus in 4 cases (80%), in the dentate nuclei, centrum semiovale and cerebral cortex in 2 cases (40%) and in the mesencephalic gray matter in 1 case (20%). In one case only CT failed to detect the abnormalities, which were nevertheless depicted by MRI. In the other 3 patients who underwent MRI, CT findings were confirmed as low-signal areas on SE T1- and T2-weighted MR scans where the calcifications were present, but areas of increased signal intensity were also evident on SE T2-weighted images; in one patient, low-signal areas were surrounded by a ring of increased signal intensity on SE T1-weighted scans. Low-signal areas reflect an early stage of calcium deposition; on the other hand, high-signal areas are probably caused by proteins and mucopolysaccharides or by liquid pools secondary to endothelial membrane incompetence. CT better defined the site and extent of the calcifications which may be found in both idiopathic and postoperative hypoparathyroidism, in symptomatic or asymptomatic patients. On the other hand, MRI seems to be capable of depicting the various stages of calcium deposition on the basis of the presence of reduced or increased SE T2 signal intensity.
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PMID:[Calcification of the basal nuclei in hypoparathyroidism. The computed and magnetic resonance tomographic aspects]. 812 14


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