Severe Symptomatic Bradycardia Following First-Dose Oxcarbazepine in a Very Elderly Patient on Long-Term Carbamazepine - A Case Report

Sep 30, 2026

A 91-year-old male patient developed acute, symptomatic bradycardia shortly after his first standard dose of oxcarbazepine for trigeminal neuralgia, despite long-term tolerance to carbamazepine. The timing strongly implicated oxcarbazepine, while alternative causes were systematically ruled out. Baseline ECG showed marked intraventricular conduction delay; after discontinuation, ECG improved QRS duration and revealed intra-atrial conduction slowing with QTc prolongation. Heart rate normalized within 48 hours, highlighting possible cardiac safety risks and the value of ECG monitoring in older adults.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages8

Reading Time20 min

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Introduction

Case Presentation

Laboratory and diagnostic findings

Discussion

Review began 11/28/2025 Review ended 12/03/2025 Published 12/09/2025 © Copyright 2025 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0. , which permits unrestricted use , distribution , and reproduction in any medium , provided the original author and source are credited. DOI: 10.7759/cureus.98837 Open Access Case Report Severe Symptomatic Bradycardia Following FirstDose Oxcarbazepine in a Very Elderly Patient on Long-Term Carbamazepine: A Case Report Yixin Zhang 1, Qinghua Yan 1, Jingyu Li 1, Guangjian Zhang 1 1. Department of Pain Medicine, Yanbian University Hospital, Yanji, CHN Corresponding author: Guangjian Zhang, [qq383683139@163.com](qq383683139@163.com) Abstract We report a 91-year-old male patient who developed acute symptomatic bradycardia shortly after receiving his first standard dose of oxcarbazepine for trigeminal neuralgia, despite prior long-term tolerance to carbamazepine. A clear temporal association between oxcarbazepine administration and the onset of bradycardia was observed, while alternative causes were systematically excluded. Electrocardiography at baseline showed a marked intraventricular conduction delay. A subsequent ECG after drug discontinuation demonstrated an improved QRS duration, as well as new evidence of intra-atrial conduction slowing and QTc prolongation. The patient’s heart rate progressively normalized within 48 hours after oxcarbazepine withdrawal. Although the patient had tolerated high-dose carbamazepine, the occurrence of severe bradycardia after first exposure to oxcarbazepine suggests that structurally related sodium channel blockers can differ in their cardiac conduction effects. Clinicians should consider ECG monitoring when initiating oxcarbazepine in older adults or individuals with pre-existing conduction system disease or vulnerabilities. Categories: Cardiology, Pharmacology, Geriatrics Keywords: adverse drug reaction, bradycardia, conduction abnormalities, elderly, oxcarbazepine, sodium channel blockers Introduction Oxcarbazepine is a newer-generation antiepileptic drug whose primary mechanism of action involves the inhibition of voltage-gated sodium channels, thereby reducing neuronal excitability. Beyond its established role in epilepsy management, oxcarbazepine is widely used in the treatment of neuropathic pain, particularly trigeminal neuralgia, and has demonstrated favorable efficacy and tolerability [1,2] . Although oxcarbazepine is structurally derived from carbamazepine, it differs significantly in its metabolism. Unlike carbamazepine and other sodium-channel blockers, oxcarbazepine is not metabolized by cytochrome P450 enzymes but is instead converted to its active metabolite, the monohydroxy derivative (MHD or 10, 11-dihydro-10-hydroxycarbazepine), and eliminated primarily via renal excretion, with an elimination half-life of approximately 1-3.7 hours [3,4] . This distinctive metabolic profile is believed to contribute to a reduced incidence of drug-drug interactions and certain adverse reactions [3,4] . Common adverse effects of sodium channel blockers include dizziness, somnolence, nausea, ataxia, and hyponatremia [5] . All sodium-channel-blocking antiepileptic drugs carry a potential risk of precipitating cardiac arrhythmias, particularly at higher serum concentrations [5] . However, among this drug class, reports of severe cardiac adverse events, such as symptomatic bradycardia and various forms of cardiac conduction block, remain relatively uncommon. Emerging evidence suggests that these risks may be amplified in elderly individuals or in patients receiving concomitant medications that affect cardiac conduction [6] . Although the United State Food and Drug Administration (USFDA) prescribing information acknowledges the possibility of serious cardiac reactions with oxcarbazepine [7], documented cases directly implicating the drug remain exceedingly r

FAQs

What event occurred after the first dose of oxcarbazepine in this case?

The patient developed acute symptomatic bradycardia shortly after receiving his first standard dose of oxcarbazepine.

How did the ECG findings change after discontinuing oxcarbazepine?

ECG after drug discontinuation showed improved QRS duration, with new evidence of intra-atrial conduction slowing and QTc prolongation.

What clinical recommendation does the case support when starting oxcarbazepine in older adults?

Clinicians should consider ECG monitoring when initiating oxcarbazepine in older adults or those with pre-existing conduction system disease or vulnerabilities.

Sep 30, 2026

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