What can cause severe bradycardia (abnormally slow heart rate) prior to a seizure?

From the Guidelines

Severe bradycardia prior to a seizure can be caused by ictal bradycardia syndrome, a rare phenomenon where the seizure activity directly affects the cardiac centers in the brain, as well as other potential causes such as vasovagal responses, medication side effects, underlying cardiac conduction disorders, or central nervous system lesions. The exact cause of severe bradycardia prior to a seizure can vary, but it is essential to consider the potential for ictal bradycardia syndrome, which typically occurs due to seizure activity in the temporal lobe, particularly involving the insular cortex or amygdala, which regulate autonomic cardiac function 1. Other potential causes include:

• Vasovagal responses triggered by the pre-ictal state
• Medication side effects, particularly from anti-epileptic drugs like carbamazepine or phenytoin
• Underlying cardiac conduction disorders
• Central nervous system lesions affecting both cardiac regulation and seizure threshold In some cases, this bradycardia-seizure pattern may represent ictal asystole, a potentially dangerous condition where seizure activity causes significant slowing or temporary stopping of the heart. Patients experiencing this phenomenon should undergo comprehensive neurological and cardiac evaluation, including video-EEG monitoring with simultaneous ECG recording, to determine if a cardiac pacemaker might be necessary alongside anti-seizure medications. This pre-seizure bradycardia can be a warning sign of potentially life-threatening cardiac complications during seizures and requires careful management by both neurologists and cardiologists 1. The management of bradycardia, as outlined in the 2018 ACC/AHA/HRS guideline, may involve the use of medications such as atropine, dopamine, isoproterenol, or epinephrine, depending on the underlying cause and severity of the bradycardia 1.

From the FDA Drug Label

Atropine-induced parasympathetic inhibition may be preceded by a transient phase of stimulation, especially on the heart where small doses first slow the rate before characteristic tachycardia develops due to paralysis of vagal control Adequate doses of atropine abolish various types of reflex vagal cardiac slowing or asystole The drug also prevents or abolishes bradycardia or asystole produced by injection of choline esters, anticholinesterase agents or other parasympathomimetic drugs, and cardiac arrest produced by stimulation of the vagus.

Severe bradycardia prior to a seizure can be caused by vagal stimulation. Atropine, which is an antimuscarinic agent, can initially slow the heart rate before causing tachycardia due to paralysis of vagal control. However, the question asks what can cause severe bradycardia, and the label suggests that vagal stimulation or choline esters can cause bradycardia, which atropine can then prevent or abolish. Therefore, vagal stimulation or choline esters can cause severe bradycardia prior to a seizure 2.

From the Research

Causes of Severe Bradycardia Prior to a Seizure

• Severe bradycardia can be caused by various factors, including autonomic nerve activity, as seen in a case report where a patient experienced severe bradycardia during electroconvulsive therapy (ECT) 3.
• Medications such as beta-blockers, calcium channel blockers, and digoxin can contribute to the development of symptomatic bradycardia, as reported in a study where nine patients taking these medications presented with symptomatic bradycardia 4.
• The combined use of beta-blocking agents and sodium channel blockers can lead to severe iatrogenic bradycardia, as demonstrated in a retrospective study of patients hospitalized for drug-related bradycardia 5.
• Bradycardia can also be caused by problems with the conduction system, such as an atrioventricular block, or by sinus, atrial, or junctional bradycardia, as discussed in a review of bradyarrhythmias 6, 7.

Risk Factors and Triggers

• Certain medications, such as beta-blockers and sodium channel blockers, can increase the risk of severe bradycardia 4, 5.
• Autonomic nerve activity, particularly parasympathetic nervous system activity, can contribute to the development of severe bradycardia during ECT 3.
• Underlying cardiac conditions, such as sinoatrial node dysfunction or atrioventricular conduction disturbances, can also increase the risk of bradycardia 6, 7.