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

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.
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PMID:The neurologic effects of thiopental therapy following experimental cardiac arrest in cats. 709 47

Electrophysiologic and histopathologic correlation has been carried out in a patient with scleroderma heart disease, affected by syncopal seizures, who died of recorded ventricular fibrillation. The electrophysiological investigation disclosed dysfunction of sinoatrial conduction, revealed by sinoatrial blocks and by an abnormal return cycle pattern after premature atrial beats. Atrial effective and functional refractory periods were increased and an unusual 'pseudo-Wenckebach' phenomenon between artificial stimulus and atrium was observed during atrial pacing. Intra-AV nodal conduction time was at normal upper limits and Wenckebach-type AV block was obtained on pacing the atrium at 100 beats/min. HV conduction was moderately prolonged in the presence of left anterior hemiblock. The histopathologic substrates of these electrophysiologic disturbances were fibrosis of the sinus node, disrupted internodal pathways and atrio-AV nodal connections, and left bundle branch atrophy. As far as fatal tachyarrhythmia is concerned, myofibrillar degeneration may have contributed to its pathogenesis. It is suggested that both lesions of the ordinary myocardium and specialized conduction system account for the electrical instability of sclerodermic patients.
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PMID:Clinicopathologic assessment of arrhythmias in a case of scleroderma heart disease with sudden death. 723 56

A 30 year old woman with marked joint hypermobility had severe, progressive lung disease, seizures, aneurysms of the sinuses of Valsalva and myocardial infarction documented during life. She died of intractable ventricular fibrillation, and postmortem examination showed myocardial injury in the distribution of the left coronary artery but no occlusive coronary artery disease. Severe panacinar emphysema was found in the lungs. Cerebral heterotopias with peculiar vascularization were present and were a likely cause of the seizure disorder. Electron microscopy showed dermal collagen fibrils to be heterogeneous in size, reduced in number, and irregular and frayed in appearance. This patient had a form of the Ehlers-Danlos syndrome, different from the 10 distinct variants described thus far, associated with lethal internal manifestations.
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PMID:Ehlers-Danlos syndrome with abnormal collagen fibrils, sinus of Valsalva aneurysms, myocardial infarction, panacinar emphysema and cerebral heterotopias. 731 50

An unusual electrocardiographic (ECG) pattern was observed in five patients who suffered an acute anterior myocardial infarction. Early in their illness and following resuscitation from ventricular fibrillation (three patients), in the midst of recurrent ventricular irritability prior to development of ventricular fibrillation (one patient), and following a period of seizures (one patient), the ECG showed ST-segment elevation, marked increase in the R-wave amplitude, disappearance of S waves and merging of QRS complexes with the elevated ST segments, ECG patterns noted in these patients were similar to the ones recorded from dogs immediately after ligation of a large coronary artery, and from patients with severe episodes of variant angina. Although these early electrocardiographic changes probably reflect either marked regional transmural blood flow deprivation or its aftermath, they could not be taken as indices of eventual massive myocardial necrosis since in most of these patients the alterations were followed by development of nontransmural myocardial infarction. The possible mechanisms and the implications of such discrepancy between early and late electrocardiographic indicators of injury or necrosis is discussed.
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PMID:Transient giant R waves in the early phase of acute myocardial infarction: association with ventricular fibrillation. 732 85

We studied a family with the long QT syndrome. The initial case was in a patient who presented with seizures, ventricular fibrillation, and syncope. After a trial of conventional modalities of treatment including left stellate ganglionectomy, primidone (Mysoline) therapy was initiated. This drug has been successful in suppressing ventricular arrhythmias and shortening the QT interval over a 2-year follow-up period. Two additional family members with QT prolongation have been treated with primidone. During an 8-month follow-up, electrocardiographic and Holter recordings showed shortening of the QT interval.
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PMID:Primidone in the treatment of the long QT syndrome: QT shortening and ventricular arrhythmia suppression. 739 15

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

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

With suicidal intent a 72-year-old man swallowed 5.8 g aminophylline in a non-retard solution. The theophylline plasma level on admission was 120 mg/l. He had to be intubated when respiratory arrest occurred. Within the first hour he developed cerebral seizures, polymorphous ventricular premature systoles, atrial fibrillation with an irregular ventricular rate and, finally, recurrent episodes of ventricular fibrillation with prolonged circulatory shock (heart rate 120-140/min with a systolic blood pressure of 60 mm Hg for 3 hours) and severe metabolic acidosis (potassium 2.28 mmol/l, phosphate 0.21 mmol/l, pH 7.03, base excess -20.8 mmol/l). He was treated with massive fluid replacement (6.2 l in the first 12 hours), electrolyte substitution to counteract the marked hypokalaemia and hypophosphataemia, repeated defibrillation and antiarrhythmic drugs (lidocaine 240 mg/h and metoprolol twice 5 mg), as well as anticonvulsive treatment (diazepam, 10 mg twice, followed by midazolam 5 mg/h). Detoxication measures consisted initially of gastric lavage followed by high-dosage enteric administration of charcoal (210 g over 36 h), as well as haemoperfusion for 4 h. Full recovery was achieved and the patient was discharged in good health after 3 weeks.
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PMID:[The clinical course and therapy of massive theophylline poisoning]. 822 24

The cases of two young patients with repetitive syncopal attacks due to idiopathic long QT syndrome (ILQTS) are reported. Both had been primarily misdiagnosed for seizures. In one of the cases the QT interval in the ECG at rest was normal. The same patient had a previous episode of cardiac arrest with ventricular fibrillation. The treadmill stress test was of great value, revealing polymorphic ventricular tachycardia induced by exercise, and evaluating the efficacy of beta-blocking therapy in the follow-up. The ILQTS should be considered a possible etiology in any patient presenting with new onset seizures, especially in the young. The treatments were different in both cases. In the first one, the treatment with nadolol (100 mg od) revealed to be very effective with total remission of symptoms. The treadmill stress test performed 15 days after the beginning of treatment did not show any ventricular arrhythmias, and it was assumed that the patient was effectively protected against ventricular arrhythmias. After 4.5 months of follow up, no syncopal episodes occurred. In the second case due to young age, the frequency, and the severity of the attacks (cardiac arrest with ventricular fibrillation), and the inefficacy of beta-adrenergic-blocking agents, the implantable cardioversor-defibrillator was the treatment chosen, although the beta blocking therapy was maintained to reduce the number of arrhythmic events. The ILQTS is a rare anomaly related to sudden cardiac death. The ILQTS is characterised by the association of several distinctive electrocardiographic features, among which prolongation of the QT interval is the best known. Life-threatening arrhythmia occurs usually under conditions of physical or psychological stress. Relatively effective therapies do exist and are represented by antiadrenergic interventions: beta-adrenergic-blocking agents are the treatment of choice. When they fail, left sympathetic denervation or the automatic implantable cardioversor-defibrillator have also proved to be effective.
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PMID:[Exertion syncopal crisis in the young, associated with idiopathic long QT syndrome]. 870 3

The use of dobutamine stress echocardiography for the evaluation of coronary artery disease is rapidly expanding. Despite its widespread use, the feasibility and safety of dobutamine stress echocardiography has not been sufficiently documented. Between November 1992 and June 1995, we performed 1000 dobutamine stress echocardiographies. There were 744 men and 256 women with a mean age of 59 +/- 11 years. Anti anginal medication was not routinely withdrawn before the test. The mean maximal dobutamine dose was 41,4 +/- 10 mu g/kg center dot min(-1). Atropine was given additionally in 440 patients, with a mean dose of 0.5 mg. In patients receiving beta-blockers additional atropine was more often necessary as compared to those not receiving beta-blockers (278/457 = 61% versus 162/543 = 30 %, p < 0.0001). Reasons for discontinuing dobutamine infusion were achievement of target heart rate (64 % of cases) and maximal dose (12 % of cases). In 791 (79,1 %) patients no side-effects of dobutamine stress echocardiography were noticed. Termination of the study because of adverse side-effects occurred in 6.6 %. A total of 103 (10,3 %) noncardiac side-effects were observed: dizziness or nausea 6.4 %, headache 1.7 %. In one patient a focal cerebral seizure occurred. 156 cardiac side-effects occurred: blood pressure decrease of more than 20 mm Hg in 25 patients, extreme palpitations in 16 patients and pulmonary edema in one case. Most common cardiac side-effects consisted of arrhythmias (11.4 %): 9.1 % ventricular and 2.3 % supraventricular arrhythmias. Most ventricular arrhythmias were less severe (uniform and multiform premature ventricular beats, ventricular bigeminy or couplets in 71 patients). Nonsustained ventricular tachycardia, with a maximum duration of 20 s, occurred in 18 patients. In one patient sustained ventricular tachycardia developed and progressed towards ventricular fibrillation. This patient could be successfully defibrillated. Supraventricular arrhythmias presented as new atrial fibrillation in 10 patients, supraventricular tachycardia in three patients, junctional rhythm with a short decline in heart rate in nine patients and a second-degree AV block in another case. Dobutamine stress echocardiography has proven to be a safe and feasible method in the diagnosis of coronary heart disease. Minor side-effects are common and sometimes unpleasant for the patient, but do not often require termination of the study. Severe side-effects are seldom (< 1 %), but nevertheless, adequate medical and technical (defibrillator) support should be rapidly available.
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PMID:[Feasibility and safety of dobutamine stress echocardiography: experiences with 1,000 studies]. 871 45


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