Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although cocaine is one of the leading causes of drug-related deaths, there is little clinical information describing the precise sequence of events leading to death in the cocaine intoxication. Usually, cocaine-related sudden deaths are unwitnessed, its electrocardiographic features are not attainable, and the majority of these patients have a rapidly fatal course and die before arriving at the hospital. We report a patient with massive cocaine ingestion who developed psychomotor agitation and generalized seizures followed by asystolic cardiac arrest. Ventilation with supplemental oxygen by endotracheal intubation immediately restored spontaneous heart beat. After resuscitation, a severe metabolic acidosis (pH 6.65) and cardiac dysrrhythmias consistent with sodium channel poisoning were detected. The electrocardiogram showed accelerated junctional rhythm at 85 beats/min with right bundle branch block and left anterior hemiblock configuration, prolongation of QRS (0.16 sec) and QTc (0.52 sec) intervals, and terminal J wave associated with coved ST-segment elevation in leads V(1) and V(2) resembling the Brugada syndrome. Sodium bicarbonate administration was quickly followed by normalization of the cardiac conduction disturbances. This article discusses the clinical and electrophysiologic implications of these findings.
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PMID:Aborted sudden death, transient Brugada pattern, and wide QRS dysrrhythmias after massive cocaine ingestion. 1159 May 77

A patient who presented with a new apparent seizure was found to have abnormal electrocardiographic findings, with classic features of the Brugada syndrome. He had spontaneous episodes of nonsustained ventricular tachycardia, easily inducible ventricular fibrillation at electrophysiological study in the absence of structural heart disease, and a negative neurological evaluation. These findings suggested that sustained ventricular arrhythmias known to be associated with the Brugada syndrome and resultant cerebral hypoperfusion, rather than a primary seizure disorder, were responsible for the event. Patients with the Brugada syndrome often present with sudden death or with syncope resulting from ventricular arrhythmias. In consideration of its variability in presentation sometimes mimicking other disorders, primary care physicians and internists should be aware of its often transient electrocardiographic features.
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PMID:Brugada syndrome: an unusual cause of convulsive syncope. 1207 42

Since 1992, the Brugada syndrome has been increasingly recognized worldwide, although its incidence and distribution remain unclear. In Asia, several cases have been reported in Japan, Thailand, Singapore, and Vietnam. However, little information is available from the Chinese population. Since June 1997, we have identified 10 patients with the diagnosis of the Brugada syndrome from six hospitals in Taiwan. All patients were male with the mean age of 46 +/- 7 years (range 36-61). They all had a normal chemistry profile, coronary angiography and echocardiography. Clinical presentations varied from seizure and syncope to sudden cardiac death. MRI and ultrafast CT of the heart did not show any abnormalities. Sustained ventricular tachycardia/ventricular fibrillation (VF) was induced in 7 of 8 patients who underwent an electrophysiologic study. The pharmacological provocation test was positive in 4 of 5 patients. One of the 4 patients who had a genetic study showed SCN5A gene mutation. An implantable cardioverter defibrillator (ICD) was implanted in 8 patients. During a mean follow-up of 29 +/- 17 months (range 2-54), 3 of 8 patients who had an ICD received appropriate ICD discharges after implantation. These 3 patients who were subsequently treated with antiarrhythmic agents have had no further recurrent ICD discharges. Two patients who refused ICD implantation are alive and well without taking antiarrhythmic agents. Our study showed that the clinical characteristics of our patients are similar to those described in the literature and that ICD is an effective treatment modality for patients with recurrent VF. However, antiarrhythmic agents may be beneficial for suppressing arrhythmia recurrences in selected patients.
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PMID:Characteristics of Chinese patients with symptomatic Brugada syndrome in Taiwan. 1284 44

Missense mutations in the skeletal muscle sodium channel alpha-subunit gene (SCN4A) are associated with a group of clinically overlapping diseases caused by alterations in the excitability of the sarcolemma. Sodium channel defects may increase excitability and cause myotonic stiffness or may render fibres transiently inexcitable to produce periodic paralysis. A patient with cold-aggravated myotonia did not harbour any of the common SCN4A mutations. We therefore screened all 24 exons by denaturing high-performance liquid chromatography, followed by direct sequencing. Two novel missense changes were found with predicted amino acid substitutions: T323M in the DIS5-S6 loop and F1705I in the intracellular C-terminus. The functional impact of these substitutions was assessed by recording whole-cell Na+ currents from transiently transfected HEK293 cells. T323M currents were indistinguishable from wild-type (WT). Fast inactivation was impaired for F1705I channels, as demonstrated by an 8.6-mV rightwards shift in voltage dependence and a two-fold slowing in the rate of inactivation. Recovery from fast inactivation was not altered, nor was there an increase in the persistent current after a 50- ms depolarization. Activation and slow inactivation were not appreciably affected. These data suggest that T323M is a benign polymorphism, whereas F1705I results in fast inactivation defects, which are often observed for myotonia. This is the first example of a C-terminal mutation in SCN4A associated with human disease. Like the cardiac disorders (long QT syndrome type 3 or Brugada syndrome) and generalized epilepsy with febrile seizures plus (GEFS+) associated with C-terminal mutations in other NaV channels, the primary effect of F1705I was a partial disruption of fast inactivation.
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PMID:A C-terminal skeletal muscle sodium channel mutation associated with myotonia disrupts fast inactivation. 1577 23

Patients presenting with convulsions are sometimes incorrectly treated for epilepsy, as these symptoms may be manifestations of underlying cardiac disease. Brugada syndrome, associated with an elevated risk of developing fatal arrhythmic events, is a rare disorder characterized by a unique electrocardiographic pattern. The typical clinical presentation mainly involves syncope of unclear cause or sudden death. Seizures are uncommon clinical manifestations of Brugada syndrome, and reports of status epilepticus as initial presentation of Brugada syndrome are extremely rare. In this case report, we present a male patient with a typical pattern on 12-lead electrocardiography, following resuscitation for generalized convulsive status epilepticus.
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PMID:Status epilepticus as an initial presentation of Brugada syndrome: a case report. 1615 83

Brugada syndrome is an arrhythmogenetic disease characterized by electrocardiographic ST segment elevation in right precordial leads, which is called "coved type", and an increased risk of sudden death as the result of ventricular fibrillation. We presented a case of Brugada syndrome with a convulsive seizure, during administration of a tricyclic antidepressant for the treatment of a depressive state. A 43-year-old man with bipolar II disorder and obsessive-compulsive disorder was admitted to our hospital for the treatment of a depressive state. There was no medical history of heart failure. Nortriptyline was effective for his depressive as well as for obsessive symptoms. During the treatment, however, he presented a convulsive syncope. Electrocardiography (ECG) showed "coved type" ST segment elevation, and the patient consulted a cardiologist. Electrophysiological study revealed Brugada syndrome, and an implantable cardioverter defibrillator was placed. An overdose of antidepressants has been reported to produce a Brugada-type ECG because of its Na channel antagonism. However, in the present case, the abnormal ECG findings occurred following a usual dosage of nortriptyline. Thus, it is suggested that Brugada syndrome is related to a susceptibility to antidepressants in the present case. Every psychiatrist managing antidepressant therapy should be aware of Brugada syndrome and this ECG pattern, which may be a marker of sudden death.
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PMID:[A case of Brugada syndrome with convulsive seizure during antidepressant administration: relation of antidepressant agents and arrhythmia leading to sudden death]. 1708 31

Fever can precipitate ventricular tachycardia in adults with Brugada syndrome, but such a link has not been reported in children. A 21-month-old white girl presented repeatedly with decreased conscious level and seizures during fever. During a typical episode, rapid ventricular tachycardia was documented. The resting 12-lead electrocardiogram revealed a Brugada electrocardiogram signature. Resting electrocardiograms of the asymptomatic brother and mother were normal, but fever in the mother and pharmacologic stress with ajmaline in the brother revealed Brugada electrocardiogram features. Genetic testing revealed an SCN5A mutation in the affected family members.
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PMID:Brugada syndrome masquerading as febrile seizures. 1742 Feb 62

The emergence of Brugada pattern on electrocardiogram in response to class IA or IC antiarrhythmic agents is widely utilized to diagnose concealed Brugada syndrome and recognized as a risk factor for sudden death. Phenytoin, a class IB antiarrhythmic agent, has not been reported to induce Brugada pattern. We report a patient who presented with Brugada electrocardiogram at supratherapeutic phenytoin level. Considering that patients with syncope may falsely be labeled to have seizures and some epilepsy patients are at increased risk of sudden death, all patients with supratherapeutic phenytoin level should be evaluated with an electrocardiogram for emergence of Brugada pattern.
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PMID:Brugada pattern electrocardiogram associated with supratherapeutic phenytoin levels and the risk of sudden death. 1746 83

Brugada syndrome is a genetic dysfunction of the myocardial sodium channel that leads to ventricular dysrhythmias. The electrocardiographic (ECG) pattern of Brugada syndrome is occasionally seen after tricyclic antidepressant (TCA) ingestion; however, the outcome and complication risk for these patients is not clear. The objective of our study was to describe the incidence of Brugada ECG pattern (BEP) and serious complications of these patients in a large case series of intentional TCA ingestions. We also compared the proportion of complications of patients with BEP versus those without BEP. We evaluated 402 TCA ingestions, of which 9 (2.3%) were associated with the development of BEP. We compared the adverse outcomes of all TCA ingestions versus TCA ingestions with BEP. A increase in the adverse outcomes in the BEP group was found: seizures (relative risk [RR] 4; 95% confidence interval [CI] 1.5 to 10.8), widened QRS (RR 4.8; 95% CI 1.8 to 12.9), and hypotension (RR 3.9; 95% CI 2.1 to 7.4). To reduce confounding ingestants, we also compared all patients with an isolated TCA ingestion versus those with BEP. A significant increase in adverse outcomes was again found with the BEP group: seizures (RR 3; 95% CI 1.1 to 8.6), widened QRS (RR 4.8; 95% CI 1.5 to 15.1), and hypotension (RR 3.4; 95% CI 1.9 to 22.3). No deaths or dysrhythmias were found in the BEP group. In conclusion, BEP after TCA ingestion is rare, and death or dysrhythmias did not occur. However, patients with BEP are likely at increased risk for TCA-induced complications.
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PMID:Incidence of Brugada electrocardiographic pattern and outcomes of these patients after intentional tricyclic antidepressant ingestion. 1769 24

A woman with a past medical history of epilepsy was transferred to our hospital for episodic changes in mental status, jerking movements, and decreased hearing that were thought to represent seizure activity. While in the hospital, she was diagnosed with Brugada syndrome. Her antiepileptic medications were adjusted while she was monitored on constant electroencephalography, video, and cardiac telemetry. It was found that the patient's seizures were not caused by hypoperfusion of her brain secondary to cardiac arrhythmia. Instead, we theorize that she had an underlying systemic, genetic sodium ion channel dysfunction.
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PMID:Woman with Brugada syndrome and epilepsy: a unifying diagnosis? 1908 13


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