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

A 35-year-old man was hospitalized after a sudden onset of transient syncopal attack without accompanying complaints of headache or nausea. He was slightly disorientated but neurologically normal. He had a blood pressure of 150/90mmHg and a pulse rate of 40/min. An ECG showed marked sinus brady-cardia with ventricular escaped rhythm followed by advanced atrioventricular (AV) block. Some components of conducted ventricular beats showed aberration. There was no significant ST or T wave abnormality in normally captured QRS components except for prominent T in leads II, III and aVF. At first, we thought that he might require temporary pacing because of Adams-Stokes attack. However, after administration of atropine sulfate, the ECG returned to normal sinus rhythm with heart rate of 88/min. Then he began to complain of headache followed by a convulsive seizure. A CT scan and angiogram revealed a ruptured aneurysm at the top of the basilar artery, which was successfully clipped. A wide spectrum of ECG changes can be demonstrated in practically all patients with subarachnoid hemorrhage (SAH). Prolonged QT interval, ST-T changes, U wave, sinus tachycardia, or ventricular premature complex are the common abnormalities probably caused by increased circulating catecholamine. As bradyarrhythmia in patients with SAH is an uncommon finding, its mechanism has not yet been defined. Transient sinus bradycardia with advanced AV block in this patient might have been caused not by elevated intracranial pressure (Cushing phenomenon) but by drastic discharge of the parasympathetic nerve. This case serves to illustrate the vigilance required in determining whether abnormalities of cardiac rhythm are instrumental in causing neurological symptoms and signs or a disorder of cerebral function.
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PMID:[A case of subarachnoid hemorrhage with sick sinus and advanced AV block]. 151 79

Cardiac arrhythmias are a well known cause of epileptic seizures. Epileptic seizures resulting in cardiac arrhythmias are less well recognised and cardiac arrhythmias are commonly presumed to be of primary cardiac origin. This paper describes a patient with complete AV heart-block during a partial complex seizure. Simultaneous EEG/ECG monitoring was used to show the secondary nature of the bradyarrhythmia.
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PMID:Complete atrio-ventricular conduction block during complex partial seizure. 152 51

The study comprises 10 consecutive medicolegal autopsies of patients treated with intraventricular cardiac pacing who died unexpectedly outside of a hospital. The treatment was indicated by AV-block grade I-III in eight cases, by bradyarrhythmia in one case, and sick sinus syndrome in the last case. Four patients died during a sudden epileptiform seizure, three were found dead, and three died in their sleep. Recent hemorrhages close to the AV-node and His bundle were seen in five cases. The local findings in the vicinity of the pacemaker leads were numerous and multiple consisting of thrombosis of the superior vena cava, tortuous and corroded leads, leads attached to the atrial endocardium, constricted orifice of the coronary sinus, and acute ulcerations, endocarditis, shrinking, and ruptures of the cusps of the tricuspid valve. The right atrium of the pacemaker patients was significantly dilated. The mean value of the ratios between right atrial and ventricular length (AV ratio) of the 10 pacemaker patients was 1.2 in contrast to the mean value of the same ratio of 30 controls, which was 0.6. The AV ratio was particularly increased in patients with lesions of the tricuspid valve and with a long history of cardiac pacing. In 3 of the 10 patients the immediate cause of death was related to anatomical and technical complications of long-term intraventricular pacing. Such complications were clinically unrecognized thrombosis of the superior vena cava, rupture of the chordae tendinae, and cable breakage.
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PMID:Postmortem findings and possible causes of unexpected death in patients treated with intraventricular pacing. 619 10

The behavioral changes associated with seizures induced by auditory stimulation in magnesium (Mg)-deficient rats originate in deep brain structures and secondarily project to neocortex. In the present study, we examined the roles of N-methyl-D-aspartate (NMDA) receptors in this seizure model. The intraperitoneal administration of the competitive NMDA receptor blocker DL-2-amino-7-phosphonoheptanoic acid (36 and 72 mg/kg) and the non-competitive NMDA receptor blocker MK-801 (1.35 and 2.7 mg/kg), completely prevented the induction of seizure and bradyarrhythmia or sudden death resulting from seizure. Therefore, the white-noise-induced seizures in Mg-deficient rats are linked to increased neuronal excitability via the NMDA receptor.
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PMID:In vivo assessment of prevention of white-noise-induced seizure in magnesium-deficient rats by N-methyl-D-aspartate receptor blockers. 801 47

In order to elucidate the mechanism of behavioral alterations in magnesium-deficient rats, changes in the electroencephalogram (EEG) and electrocardiogram (ECG) were studied during auditory stimulation and correlated with the behavioral alterations. Weanling rats were fed either a Mg-deficient diet or a control synthetic diet for 2-3 weeks before the experiment. EEGs were recorded from the hippocampus and the sensorimotor and auditory cortices, and ECGs with a telemetry system. White noise with an intensity of 100 dB was given continuously to induce behavioral changes. The Mg-deficient rats developed consistent and graded behavioral changes in response to the stimulation, showing running-jumping behavior (stage 1), followed by tonic limb convulsion (stage 2) and finally by falling down on the floor (stage 3). The EEGs also showed consistent changes with spike activity, initiating in the hippocampus (stage 2) and then spreading to the neocortices bilaterally (stage 3). These findings indicate that the behavioral changes induced by auditory stimulation in the Mg-deficient rats are due to seizures arising in deeper brain structures, particularly in the limbic system, and projecting secondarily to the neocortices. The ECG changes, mainly consisting of marked bradyarrhythmia, occurred as early as the appearance of the EEG spikes, indicating that they were also related to the seizure. We conclude therefore that Mg deficiency in rats causes increased excitability of the central nervous system, resulting in seizures possibly originated in the limbic system, later developing secondary generalization, and also causing cardiac dysfunctions.
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PMID:Physiological correlates of abnormal behaviors in magnesium-deficient rats. 837 Mar 54

Bradyarrhythmias associated with partial seizures are uncommon, with most reported patients having temporal lobe seizure foci on scalp EEG recordings. We report a patient with bradycardia and sinus arrest during a complex partial seizure documented during bilateral subdural EEG and EEG and simultaneous video and EEG recordings. The seizure began in the left temporal lobe and spread to the right temporal region, with bradycardia occurring 55 seconds after ictal onset and asystole after 60 seconds.
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PMID:Bradycardia and asystole induced by partial seizures: a case report and literature review. 919 93

Little is known about bradycardia and cardiac asystole which occur during partial epileptic seizures, especially whether they relate to ictal involvement of well-defined cortical areas. Several reports based on simultaneous electrocardiographic and intracranial depth electroencephalographic monitoring have shown that either the fronto-orbital cortex or the amygdalohippocampal complex could be responsible for such cardiac variations. We performed stereo-EEG recordings in a patient with refractory localization-related epilepsy associated with a hypothalamic hamartoma. We found that other cortical areas, such as the frontocentral region and the temporal neocortex, can contribute to the genesis of ictal bradyarrhythmia. Second, the lesion per se, although located within the hypothalamus, is not involved with this phenomenon.
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PMID:Ictal bradycardia in a patient with a hypothalamic hamartoma: a stereo-EEG study. 1021 84

Changes in the heart rate during electroconvulsive therapy (ECT) reflect seizure activity at a deeper brain site than shown by electroencephalography and motoric activity. Accordingly, such changes may provide additional information that is helpful in the evaluation of treatment quality. One basic measurement of heart rate change is the duration of ECT-induced tachycardia. In a prospective study, the electrocardiographic ECT records of 24 patients were rated for the abruptness of the endpoint of the seizure-induced elevation in heart rate; 19 showed abrupt endpoints and 5 showed gradual endpoints. The baseline heart rate of patients with abrupt endpoints (88 SD [standard deviation] 10 beats/min) was significantly lower (p = 0.00001) than those with gradual endpoints (118 SD 12 beats/min). A threshold occurred at a baseline heart rate of 100 beats/min, with abrupt endpoints below and gradual endpoints above. The data suggest that patients with low baseline heart rates might be likely to show bradyarrhythmia during the treatment, and corresponding precautions might be considered.
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PMID:Endpoint of ECT-induced elevation in heart rate. 1037 51

Lithium can suppress sinus node function, especially when it is used concomitantly with carbamazepine. We describe a 42-year-old woman who took lithium and carbamazepine for manic-depressive psychosis and seizure disorders, and developed marked sinus node dysfunction. Drug screening showed a toxic serum lithium level of 3.38 mmol/L and a normal serum carbamazepine level of 22.1 mumol/L. An electrophysiologic study showed prolongation of the corrected sinus node recovery time (CSNRT) of up to 9,708 msec. After three sessions of hemodialysis, normal sinus rhythm was resumed. The serum lithium level was 0.1 mmol/L 2 weeks later, and the CSNRT shortened to 309 msec. Because the combination of lithium and carbamazepine in psychiatric patients is not uncommon, recognition of the potential complication of severe bradyarrhythmia is essential in the emergency care of such patients.
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PMID:Sinus node dysfunction in a patient with lithium intoxication. 1074 51

We describe a patient who had cardiac arrhythmia as epileptic manifestation. In a 34-year-old woman who had many episodes of loss of consciousness, the simultaneous ECG and video-EEG monitoring recorded bradycardia with a short episode of asystole (4 seconds) and left temporal rhythmic theta activity on EEG. MRI showed a small mass lesion in the left parahippocampal gyrus. Alterations in cardiac rhythm have been reported in epileptic seizures and tachycardia is the most common finding associated with them; bradyarrhythmia during seizures was uncommon. Many interconnections among insular cortex, limbic system and hypothalamus, may be responsible for vegetative manifestations in temporal lobe epilepsy.
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PMID:[Bradycardia as an epileptic manifestation in temporal epilepsy: report of a case]. 1101 34


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