Can You Have a Seizure While Having a Heart Attack

Seizures May Indicate Underlying Cardiac Rhythm Disorder

Feb 5, 2009

Researchers in the United States and kingdom of the netherlands accept reported what appears to exist a seizure phenotype in individuals with congenital long QT syndrome (LQTS), a potentially fatal cardiac conduction disorder that tin be detected only by electrocardiogram (ECG).

PRINTOUT OF ECG recording showing Torsades de pointes. The blue line shows the feature QRS "twist" effectually the isoelectric baseline, demonstrating a rapid, polymorphic ventricular tachycardia.

Because fainting and seizures are common symptoms of LQTS, the disorder is often mistaken for epilepsy and treated with antiepileptic drugs (AEDs) while the underlying cardiac risk goes undetected, according to lead author Michael J. Ackerman, Doctor, PhD, professor and manager of the Long QT Syndrome Dispensary at the Mayo Dispensary in Rochester, MN.

The findings were published in the Jan. xx consequence of Neurology.

Inherited LQTS results from genetic mutations disrupting normal calcium and potassium ion channel regulation in the eye, resulting in a prolonged Q-T interval — the menstruation between electrically stimulated expansion and wrinkle of the ventricles. The disruption causes periodic episodes of fast, chaotic heartbeats and fainting due to ventricular arrhythmia. If the middle does not return to a normal rhythm, ventricular fibrillation can occur, with the possibility of sudden cardiac death. Potassium channel defects in the brain, notably in the hippocampus, have been associated with epileptic seizures.

Different genetic mutations have been identified for 10 types of LQTS. LQT1, the most common blazon, comprises threescore per centum of all cases, and is caused by a mutated KCNQ1 cistron (Run into "More about Long QT Syndrome.") The 2d most mutual blazon, LQT2, which occurs in most 35 percentage percent of cases, is caused by mutations of the man ether-a-go-become related gene (HERG) on chromosome 7. The HERG factor is also known every bit KCNH2.

The disorder can occur in otherwise good for you people, often children or young adults, and especially immature women, and one-half of all cases are asymptomatic.

PROTOCOLS, FINDINGS

Dr. Ackerman and his colleagues at the Mayo Clinic and the Bookish Medical Center, in Amsterdam, reviewed the charts of 343 unrelated patients who had been clinically evaluated and genetically tested for LQTS. Almost (232) were women, diagnosed on average between ages 18 and 27 years. The investigators sought to make up one's mind whether seizures were more mutual in patients with whatsoever of the iii major subtypes of the disorder and whether there were any genetic signatures indicative of potassium channel defects in the brain.

20-nine pct of the patients had a history of seizures, but they were most mutual (at 47 percentage) among patients with LQTS2. A seizure phenotype was conferred if patients had either a personal of family history of seizures or had used AEDs. Patients with LQTS2 who had the KCNH2 gene were more likely to possess the seizure phenotype than those with LQTS1 or LQTS3.

The authors concluded that people with LQT2 may have alterations in KCNH2-encoded cerebral potassium channels resulting in seizure susceptibility, and that the localization of the gene defect to KCNH-2 encoded potassium channels may reside in the hippocampus, resulting in temporal lobe epilepsy.

DR. MICHAEL J. ACKERMAN: "There is a tremendous need to brand neurologists enlightened of LQTS because it is such a profound mimic of epilepsy. At Mayo, nosotros see [epilepsy misdiagnoses] all the fourth dimension in LQTS patients."

"The trademark event for the patient with symptomatic LQTS is the potentially lethal ventricular dysrhythmia known as torsades de pointes (TdP)," the authors noted. "TdP can precipitate syncope, seizures, or sudden decease, depending on whether the heart rhythm spontaneously reverts to normal rhythm or if the patient is defibrillated back to normal rhythm before expiry occurs."

COMMON MISDIAGNOSIS

Once considered a rare congenital disorder, wider ECG testing for other heart conditions has resulted in an increased rate in the past ii decades, Dr. Ackerman told Neurology Today in a telephone interview.

"Just a few years agone the incidence of LQTS was believed to be one in 25,000, but we at present believe it is much more prevalent, perhaps equally mutual every bit 1 person in 2,500," he said. "There is a tremendous need to make neurologists aware of LQTS because information technology is such a profound mimic of epilepsy. At Mayo, we run across [epilepsy misdiagnoses] all the time in LQTS patients."

Misdiagnosis of LQTS every bit epilepsy may explain many cases of sudden unexplained death in epilepsy (SUDEP), he cautioned.

Dr. Ackerman noted that merely one mean solar day before the interview with Neurology Today he saw a 17-year-quondam patient with a history of seizures. Although the patient had been examined by neurologists and was being treated with antiepilepsy drugs, ECG revealed LQTS.

"If she had died during the seizure, it would have been attributed to SUDEP, when it was really due to her heart condition," he said. "In that location is no telling how many cases of SUDEP accept really been caused by long QT syndrome, but neurologists need to be more enlightened of this possibility."

Because information technology is mutual for arrhythmias and subsequent seizures in LQTS patients to be triggered past exercise, excitement or, notably, sudden noise, neurologists can screen for LQTS past asking whether seizures are precipitated past racket, he connected.

"Door bells, alert clocks, and telephones. Ask the patient about them. If the seizures are triggered past such sounds, they should take an ECG to check for long QT syndrome — that's the accept-home message."

Cerebral HYPOXIA?

Orrin Devinsky, Doc, professor of neurology and director of the New York University School of Medicine's Comprehensive Epilepsy Center in New York City, said the findings leave some questions unanswered.

In an due east-mail to Neurology Today, he and colleague Steven V. Pacia, MD, associate professor of neurology and managing director of clinical neurophysiology at the Epilepsy Heart, cited their ain feel with LQTS patients, seizure activity, and epilepsy misdiagnoses, and to a 1994 paper published in Neurology in which they described two such cases and reviewed the medical literature.

"The author's hypothesis that a subset of LQTS patients may also have epilepsy is certainly plausible. However, for the cases we reviewed, there was no proposition of complex partial seizures, fifty-fifty in patients already treated with AEDs, fifty-fifty though the hippocampus is said to be a probable focus of potassium channel dysfunction."

At the time of their publication, however, factor-specific sub-typing was unavailable. All the same, they said, "a unifying historical characteristic was the presence of 'lifelessness' before the convulsive movements, thereby facilitating a diagnosis of convulsive syncope and subsequent evaluation for the presence of a LQTS."

Because the researchers did not provide detailed data almost seizure types or EEG changes, comparisons are difficult, they added.

"Nosotros look forward to a comprehensive video and electroencephalographic study of patients with LQTS to determine whether they are at college risk for epileptic seizures or whether the manifestation of cognitive hypoxia is more 'seizure-like.'"

ARTICLE IN Cursory

Investigators suggest that Long QT syndrome type 2 — a status that typically involves syncope, seizures, or sudden death — may confer susceptibility for recurrent seizures.

MORE Most Built LONG QT SYNDROME

LQTS can be inherited in an autosomal dominant or an autosomal recessive way, depending on the subtype; ten subtypes have been discovered. Investigators take been looking for non-cardiac phenotypic expression in other organs.

The most common blazon, LQT1, is autosomal ascendant and has been associated with profound deafness. Deafness has not been associated with the autosomal recessive LQT2. Patients with LQT3, which comprises fewer than five percent of the cases, have had an increased prevalence of gastrointestinal symptoms.

Triggering events differ by genotype. Patients with LQT1 usually have cardiac events preceded by exercise or pond. Sudden exposure of the patient's face to common cold water is thought to arm-twist a vagotonic reflex. In patients with LQT2, cardiac arrhythmia may be trigged by an emotional outcome, do, or loud sounds. Patients with LQT3 ordinarily have events during nighttime sleep.

For more on LQTS, visit GeneReviews online at www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?volume=cistron&function=rws.

References

Ackerman J, Johnson J. Hofman N, et al. Identification of a possible pathogenic link between built long QT syndrome and epilepsy. Neurology 2009; 72:224–231.

Pacia SV, Devinsky O, Luciano DJ, Vazquez B. The prolonged QT syndrome presenting equally epilepsy: a report of two cases and literature review. Neurology 1994;44(8):1408–1410.

manifoldwhateening01.blogspot.com

Source: https://journals.lww.com/neurotodayonline/Fulltext/2009/02050/Seizures_May_Indicate_Underlying_Cardiac_Rhythm.3.aspx

Share this post