<scp>EEG</scp> – <scp>ECG</scp> correlation in vasovagal syncope triggered by blood‐injection‐injury phobia

A 23-year-old man presented with a 10-year history of recurrent syncope consistently triggered by visual exposure to blood or painful stimuli. Each episode was preceded by palpitations and chest tightness and followed by 3–4 min of loss of consciousness. Transient eye deviation, urinary incontinence, and occasional limb twitching were reported, with full recovery characterized by dizziness and diaphoresis but no postictal confusion or focal deficits. Routine laboratory studies, cardiac evaluation, and brain imaging were unremarkable. Given the highly reproducible trigger, a tilt-table test was performed and reproduced syncope with chest tightness and dizziness, supporting vasovagal syncope (VVS). Ambulatory 24-h ECG recorded sinus pauses up to 5.9 s and brief atrial tachycardia. To clarify the etiology of the episodes and differentiate syncope from possible epileptic seizures, continuous video EEG–ECG monitoring was conducted for 16.5 h using standard 10–20 electrode placement, 10 μV/mm sensitivity, and 0.5–70 Hz filters. Artifact-contaminated EEG segments were excluded by visual inspection, and ECG was used for cardiogenic correlation. Approximately 1.5 h into monitoring, syncope was provoked when the patient viewed blood. EEG showed moderate-to-high amplitude theta slowing with progressively increasing amplitude and decreasing frequency, followed by a gradual normalization. Concurrently, ECG revealed a drop in heart rate from 60 to 30 bpm and a 5.9-s sinus arrest. Critically, no epileptiform discharges—spikes, sharp waves, or ictal rhythmic evolution—were detected throughout the event. The observed diffuse slowing was consistent with transient cerebral hypoperfusion rather than epileptic activity (Figure 1). The rapid recovery without postictal confusion, lack of tongue biting, absence of evolution into rhythmic ictal patterns, and the presence of a significant cardioinhibitory pause all strongly argued against epilepsy. Although brief myoclonic jerks and urinary incontinence occurred, these features are recognized in convulsive syncope and are not seizure-specific. Collectively, the clinical, EEG, and ECG findings confirmed a diagnosis of cardioinhibitory VVS rather than an epileptic seizure. Previous studies have described EEG patterns of syncope as “slow–flat–slow” or showing progressive diffuse slowing secondary to transient cerebral hypoperfusion.1 Simultaneous ECG is essential for correlating cortical slowing with bradycardia or asystole. However, few reports document real-time, blood-triggered syncope with synchronized EEG–ECG recordings capturing both cerebral hypoperfusion and prolonged sinus arrest. This case highlights the diagnostic value of integrated neurophysiological monitoring in distinguishing syncope from epileptic seizures, particularly when convulsive movements raise diagnostic uncertainty. Management decisions for VVS depend on symptom severity, recurrence, and documentation of cardiac involvement. While most patients benefit from conservative therapy, permanent pacemaker implantation may be considered in highly selected individuals with recurrent cardioinhibitory VVS and prolonged asystole during spontaneous or provoked events. The 5.9-s sinus arrest recorded during a symptomatic episode in this patient suggests that pacing could be considered within a multidisciplinary discussion, balancing clinical risk, recurrence likelihood, and patient preference. This study was supported by the National Natural Science Foundation of China (82071364) and Guangdong Natural Science Foundation (2023A1515012525). The authors declare no conflicts of interest. Research data are not shared. Data S1. Appendix S1 Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. In a patient with recurrent syncope triggered by the sight of blood and characterized by eye deviation and limb twitching, which of the following is most essential to differentiate vasovagal syncope (VVS) from epilepsy? What does the presence of moderate to high amplitude theta (θ) activity during a syncopal episode typically represent in the context of simultaneous EEG–ECG monitoring? Based on the clinical vignette, which feature of the patient's syncopal episode might lead to a misdiagnosis of epilepsy? Answers may be found in the supporting information.