|Year : 2021 | Volume
| Issue : 1 | Page : 73-75
A case report of ictal bradycardia and asystole: An uncommon manifestation of epilepsy
Nambirajan Jayabalan, Harshal Pamecha, Senthil Nallaswamy
Department of Cardiology, Coimbatore Medical College Hospital, Coimbatore, Tamil Nadu, India
|Date of Submission||10-Mar-2021|
|Date of Decision||14-Apr-2021|
|Date of Acceptance||22-Apr-2021|
|Date of Web Publication||30-Jun-2021|
Dr. Harshal Pamecha
Department of Cardiology, 3rd Floor, Superspeciality Block, Coimbatore Medical College Hospital, Coimbatore - 641 018, Tamil Nadu
Source of Support: None, Conflict of Interest: None
The ictal bradycardia syndrome occurs when epileptic discharges disrupt normal cardiac rhythms leading to a reduction of heart rate that is more than 10 beats/min below the baseline. Mostly documented ictal bradycardias are accompanied by complex partial seizures of temporal lobe origin. Sudden unexpected death in epilepsy is often assumed to be associated with a concomitant seizure, but it is almost impossible to prove conclusively. Here, we report the case of a 52-year-old female patient admitted with the complaints of two episodes of generalized tonic–clonic seizures and vomiting followed by presyncope and syncope. The patient was admitted in a drowsy disoriented state with hypotension and electrocardiogram (ECG) illustrating sinus tachycardia. Later during admission, the patient developed complex focal seizures with secondary generalization and cardiac arrest. During video electroencephalogram/ECG, she had another similar episode and cardiac arrest. ECG showed rapid progression to asystole and ventricular pause of 25 s followed by complete heart block with ventricular escape rhythm of 17 beats/min. She was implanted with a temporary pacemaker but later during the hospitalization, sudden unexpected death in epilepsy occurred in spite of cardiac pacing and optimum antiepileptic medication. Most documented pauses are of nonlife-threatening duration (range 3–20 s) with longer pauses being observed. Cardiac pacing may help to reduce the risk of falls, but in the absence of official practice guidelines, cardiac pacing should only be considered for patients in whom conventional antiepileptic therapy has failed to prevent ictal asystole. Early diagnosis, interventions, and optimum antiepileptic dose escalation with occasional epilepsy surgery are the mainstay to prevent mortality and severe prognosis of the ictal bradycardia syndrome.
Keywords: Asystole, cardiac pacing, case report, ictal bradycardia, sudden death in epilepsy, temporal lobe seizures
|How to cite this article:|
Jayabalan N, Pamecha H, Nallaswamy S. A case report of ictal bradycardia and asystole: An uncommon manifestation of epilepsy. Int J Heart Rhythm 2021;6:73-5
|How to cite this URL:|
Jayabalan N, Pamecha H, Nallaswamy S. A case report of ictal bradycardia and asystole: An uncommon manifestation of epilepsy. Int J Heart Rhythm [serial online] 2021 [cited 2022 Jan 24];6:73-5. Available from: https://www.ijhronline.org/text.asp?2021/6/1/73/319973
| Introduction|| |
Seizures, presyncope, and syncope are well-established complications of cardiac arrhythmias, especially bradycardias. However, reverse manifestation of epilepsy causing abnormal heart rate and rhythm is poorly understood. The most common arrhythmia associated with epilepsy is sinus tachycardia, which occurs in 80–100% of seizures and is usually of no consequence. However, ictal bradycardia occurs in <6% of cases only labelled as ictal bradycardia syndrome and is usually dangerous in nature. It is severe enough to cause ictal asystole defined as the absence of ventricular complexes for more than 4 s accompanied with electroencephalogram (EEG) seizure activity. Herein, we report a rare case we encountered – a patient presented with seizures followed by bradycardia managed with temporary cardiac pacing but seizures were refractory to antiepileptics.
| Case Report|| |
A 52-year-old female patient was admitted to emergency medical service (EMS) with complaints of two episodes of generalized tonic–clonic seizures of both upper and lower limbs, uprolling of both eyeballs lasting for 1–2 min associated with two episodes of vomiting followed by presyncope and syncope associated with a fall at home and the patient remained unconscious for about 1h. However, the patient was admitted to EMS in a drowsy disoriented state and on inquiry had no known previous comorbidities or history of any medications. Vitals on admission with blood pressure 80/50 mmHg, pulse rate 112 beats/min, respiratory rate 14 breaths/min, oxygen saturation 97% at room air, and random blood glucose 7.1 mM. Admission electrocardiogram (ECG) suggested sinus tachycardia with a heart rate of 106 beats/min with left bundle branch block and poor R-wave progression [Figure 1]. Loading dose of phenytoin injection was given followed by divided injectable maintenance dose of 100 mg phenytoin per 8 h.
|Figure 1: Sinus tachycardia with left bundle branch block pattern (arrow)|
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Around 4 h later, she developed focal seizures involving right half of the face, chewing type movement, right upper and lower limb dystonia-like movements lasting for 40–50 s followed by sudden cardiac arrest. The patient was managed as per advanced cardiovascular life support guidelines and later in the day extubated and remained hemodynamically stable and symptom-free for the next 24 h. Repetitive ECG was taken and showed no deviation from previous ECG findings and was on continuous ECG monitoring. After this incident, the patient received the treatment with levetiracetam 500 mg twice a day. After stabilization, her neurological examination was normal, magnetic resonance imaging of the brain was normal.
The patient was later next day subjected to video EEG/ECG monitoring after a typical episode resulting in cardiac arrest. While monitored, she had 50 s of left temporal complex partial seizure with alpha frequencies starting from the left temporal region evolving into theta waves involving both hemispheres manifested by similar seizure activities. During this, her heart rate slowed from 88 to 24 beats/min and went to repeat cardiac arrest and revived again. This episode ECG showed rapid progression to asystole with evidence of ventricular pause of 25 s [Figure 2] and followed by complete heart block with ventricular escape rhythm of 17 beats/min [Figure 3]. A temporary pacemaker was implanted in an emergency, while the patient was still on mechanical ventilation and maintained on injectable phenytoin and levetiracetam. Unfortunately, 4 days after admission, sudden unexpected death occurred in spite of cardiac pacing and optimum antiepileptic medication.
|Figure 2: Rapid progression of sinus tachycardia to asystole with long ventricular pause (arrow)|
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|Figure 3: Complete heart block with very slow ventricular escape rhythm (arrows)|
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The ethical approval was waived by the Institutional Ethical Committee of our hospital owing to the retrospective nature of the study and routine treatments performed on this patient in clinical practice. Therefore, the requirement to obtain informed consent from patients was waived.
| Discussion|| |
Epilepsy and arrhythmia share complex relations. A broad range of cardiac abnormalities, including supraventricular tachycardia, sinus tachycardia, sinus bradycardia, sinus arrest, atrioventricular block, and asystole are manifested due to epileptic activity originating in the amygdala, insular cortex, cingulate gyrus, frontopolar region, and frontotemporal region. Ictal bradycardia is postulated to be caused by an increase in parasympathetic activity or disruption of sympathetic activity resulting from propagative ictal activity in the respective autonomic cortical or subcortical networks.
Complex partial seizures involving the temporal lobe and secondarily frontal lobe with postulates said right insular stimulation leads to tachycardia and pressor responses, whereas bradycardia and depressor responses associated with left insular stimulation. However, there is less evidence of lateralization association between seizures and bradycardia. Ictal bradycardias are usually associated with a long history of epilepsy and refractory seizures as it impairs neurocardiac regulatory system and should be ruled out if associated with syncopal episodes.
To distinguish primary cerebrogenic and cardiogenic causes of arrhythmias is always a diagnostic challenge, and simultaneous ECG and video EEG documentation are considered to be the gold standard. Ictal bradycardia mostly begins 10–30 s after the seizure onset, and its bilateral progression can lead to sudden unexpected death in epilepsy patients (SUDEP). SUDEP can hide arrhythmogenic predisposition due to genetic factors such as cardiac channelopathies. There are no guidelines for the management of ictal bradycardias, and the effect of pacemaker implantation on mortality is not yet determined. The patient in our case did not undergo an electrophysiology test, and in spite of optimum antiepileptic medication and cardiac pacing, she developed possible refractory seizures that eventually led to SUDEP.
Conclusively, we postulate that early diagnosis and treatment of ictal bradycardias in patients with refractory epilepsy could prevent SUDEP. We recommend that patients with temporal lobe epilepsy who present with generalized seizures should either be subjected to video EEG/ECG monitoring or referred to a cardiologist for opinion regarding cardiac pacing thereby reducing high morbidities and mortality.
Financial support and sponsorship
The work was supported by the government-funded medical college under the Ministry of Health and Family Welfare, and under this roof bear there was no cost to the patient. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Conflicts of interest
There are no conflicts of interest.
Institutional review board statement
The ethical approval was waived by the Institutional Ethical Committee of our hospital owing to the retrospective nature of the study and routine treatments performed on this patient in clinical practice.
Declaration of patient consent
The authors certify that they have obtained the appropriate patient consent form before the study. In the form, the patient has given her consent for her case images and other clinical information to be reported in the journal. The patient understands that her name and initial will not be published, and due efforts will be made to conceal her identity.
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[Figure 1], [Figure 2], [Figure 3]