Case report reveals ischemic stroke linked to bee sting in a 61-year-old woman, highlighting severe coagulopathy and neurotoxic effects.
Background: Stroke remains one of the leading causes of global morbidity and mortality, with most cases associated with classical vascular risk factors. Neurological complications following bee stings are rarely reported but may trigger ischemic stroke through mechanisms involving toxins, vasospasm, coagulopathy, and endothelial dysfunction. Case Report: We report a 61-year-old female with a history of hypertension who developed left-sided weakness, facial asymmetry, and involuntary movements within eight hours following a single bee sting on her toe. A non-contrast CT scan revealed a lacunar infarct in the right lentiform nucleus. The patient was treated with dual antiplatelet therapy, levodopa, clonazepam, N-acetylcysteine (NAC), and folic acid, resulting in significant clinical improvement by the fifth hospital day. Discussion: Bee-sting–induced stroke is an uncommon phenomenon involving complex interactions between bee venom toxins (melittin, PLA2, and hyaluronidase) and systemic inflammatory, coagulatory, and vasospastic responses. The pathophysiology of ischemic stroke includes excitotoxicity, oxidative stress, and endothelial dysfunction. Management in this case followed standard ischemic stroke protocols, with adjunctive antioxidant and neuromodulatory therapy for symptomatic control. Conclusion: Although rare, bee stings can precipitate ischemic stroke. This case highlights the need for clinical vigilance toward neurological complications after bee stings and underscores the importance of further research into their mechanisms. More comprehensive data are still needed regarding the diagnostic criteria and confirmation process for ischemic stroke secondary to bee sting.
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Katiandagho et al. (2025) studied this question.
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