Seizures Secondary to Aconitum Plant Poisoning: a case report

Aconitum plant poisoning typically manifests as isolated early cardiotoxicity or late neurotoxicity. However, the dynamic temporal evolution from arrhythmia-driven cardiogenic syncope to true epileptic seizures mediated by direct central nervous system injury remains rarely documented and poorly characterized. We report a 53-year-old Han Chinese male who presented with ventricular tachycardia rapidly degenerating into ventricular fibrillation and cardiac arrest following ingestion of homemade Aconitum kusnezoffii (caowu)-infused liquor. Initial convulsions were tightly coupled with malignant arrhythmias, consistent with cardiogenic syncope. After successful resuscitation, hemoperfusion, and restoration of stable sinus rhythm, the patient developed breakthrough generalized tonic–clonic seizures on hospital days 4–6. Electroencephalography performed during sedation withdrawal revealed bilateral occipital spike-and-slow and sharp-and-slow waves with focal epileptiform discharges, confirming direct central nervous system neurotoxicity rather than recurrent cardiac ischemia. A mechanism-based, staged treatment strategy was employed: early advanced cardiac life support and hemoperfusion targeted cardiotoxicity, while sodium valproate and acetylglutamine were administered for antiepileptic prophylaxis and neuroprotection. The patient was discharged on day 13; antiepileptic therapy was successfully tapered and discontinued at 3 months without seizure recurrence, with normalization of electroencephalography and electrocardiography. This case provides the first systematic documentation, validated by electroencephalography, of the transition from cardiogenic convulsions to true epileptic seizures in Aconitum alkaloid poisoning. The findings highlight the critical role of pharmacokinetic-driven central nervous system retention in delayed seizure onset and underscore the necessity of prolonged neurological monitoring, early electroencephalography evaluation for late-onset convulsions, and sustained antiepileptic prophylaxis to reduce mortality and long-term neurological sequelae. Aconitum plant poisoning may manifest as early cardiogenic syncope and convulsions secondary to malignant arrhythmias, progressing in the late stage to genuine seizures caused by central nervous system (CNS) injury. Effective management requires a staged treatment strategy targeting both cardiotoxicity and neurotoxicity, with a focus on stabilizing cardiac rhythm and providing neuroprotection as needed.