This case provides the first systematic documentation, validated by electroencephalography, of the transition from cardiogenic convulsions to true epileptic seizures in Aconitum alkaloid poisoning.
Key Findings
Background
Aconitum kusnezoffii (caowu)-infused liquor ingestion caused ventricular tachycardia degenerating into ventricular fibrillation and cardiac arrest in a 53-year-old male.
The patient was a 53-year-old Han Chinese male
Poisoning occurred via ingestion of homemade Aconitum kusnezoffii (caowu)-infused liquor
Cardiac presentation rapidly progressed from ventricular tachycardia to ventricular fibrillation and cardiac arrest
Initial convulsions were tightly coupled with malignant arrhythmias, consistent with cardiogenic syncope rather than primary seizures
Results
Following resuscitation, the patient developed breakthrough generalized tonic-clonic seizures on hospital days 4 through 6, representing delayed neurotoxicity.
Seizures occurred after successful resuscitation, hemoperfusion, and restoration of stable sinus rhythm
Generalized tonic-clonic seizures emerged on hospital days 4-6
The delayed onset of seizures was attributed to pharmacokinetic-driven central nervous system retention of aconitum alkaloids
This temporal pattern distinguished late-onset true epileptic seizures from early cardiogenic convulsions
Results
Electroencephalography performed during sedation withdrawal confirmed direct central nervous system neurotoxicity by revealing bilateral occipital spike-and-slow and sharp-and-slow waves with focal epileptiform discharges.
EEG was performed during sedation withdrawal
Findings included bilateral occipital spike-and-slow waves and sharp-and-slow waves
Focal epileptiform discharges were identified
EEG findings confirmed direct CNS neurotoxicity rather than recurrent cardiac ischemia as the cause of late seizures
Results
A mechanism-based, staged treatment strategy targeting both cardiotoxicity and neurotoxicity was employed and resulted in full recovery with discharge on day 13.
Early treatment included advanced cardiac life support and hemoperfusion targeting cardiotoxicity
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
Electroencephalography and electrocardiography normalized by the 3-month follow-up
Discussion
Aconitum plant poisoning may manifest as a biphasic neurological presentation, with early cardiogenic syncope and convulsions secondary to malignant arrhythmias progressing in the late stage to genuine seizures caused by direct CNS injury.
The dynamic temporal evolution from arrhythmia-driven cardiogenic syncope to true epileptic seizures had previously been rarely documented and poorly characterized
Pharmacokinetic-driven CNS retention of alkaloids was highlighted as critical to delayed seizure onset
The authors emphasize the necessity of prolonged neurological monitoring and early EEG evaluation for late-onset convulsions
Sustained antiepileptic prophylaxis was identified as necessary to reduce mortality and long-term neurological sequelae
What This Means
This research describes a case of severe poisoning from a traditional herbal preparation made with a plant called Aconitum kusnezoffii (known as 'caowu'), which contains toxic compounds called aconitum alkaloids. A 53-year-old man who drank homemade liquor infused with this plant developed dangerous heart rhythm problems — including cardiac arrest — shortly after ingestion. His initial convulsions appeared to be caused by inadequate blood flow to the brain due to these heart problems, not by direct brain injury. After being resuscitated and treated, his heart rhythm stabilized, but several days later (days 4-6 of his hospital stay), he began having true epileptic seizures, which were confirmed by brain wave testing (EEG) to be caused by the toxic compounds directly affecting his brain.
This research suggests that Aconitum poisoning can cause two distinct phases of neurological problems: an early phase where convulsions are driven by heart dysfunction, and a later phase where the toxic compounds — which linger in the nervous system due to how they are processed by the body — cause genuine seizures from direct brain injury. The case is notable because it is described as the first time this two-phase progression has been systematically documented and confirmed with EEG testing. The patient was successfully treated with a staged approach that addressed both heart and brain toxicity, and he recovered fully, with no seizures at a 3-month follow-up.
This research suggests that doctors treating patients with Aconitum poisoning should be aware that dangerous seizures can appear days after the initial heart-related symptoms have resolved, and that ongoing brain monitoring and preventive anti-seizure medication may be important components of care. The findings also highlight the risks associated with homemade herbal preparations containing toxic plants, and the need for careful, prolonged observation even after a patient appears to have stabilized.
Zhao Z, Zhang J, Du J, Liu L, Rao G, Zhou M. (2026). Seizures Secondary to Aconitum Plant Poisoning: a case report.. Journal of medical case reports. https://doi.org/10.1186/s13256-026-06571-1