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.