Steroid-responsive delayed multifocal encephalopathy following vasculotoxic snakebite with serial MRI evolution: a case report.
Source: PubMed, NCBI / U.S. National Library of Medicine
Snakebite remains a cause of morbidity in tropical regions, with viperid venoms typically causing local tissue injury (edema, bleeding, ecchymoses), vasculotoxicity, coagulopathy, and acute kidney injury. Delayed immune-mediated encephalopathies are uncommon. We report a 49-year-old woman from Birbhum district, West Bengal, India, who sustained a bite from a Russell's viper in June 2025 (rainy season). She developed vasculotoxic envenoming and acute kidney injury requiring hemodialysis for 5 days, followed by apparent systemic recovery and discharge. Seven days later, she developed abrupt scanning dysarthria, gait ataxia, and oscillopsia. Brain MRI on day 14 demonstrated multifocal T2/FLAIR hyperintensities involving the left cerebellar hemisphere, left frontoparietal cortex, bilateral basal ganglia, and periventricular white matter, without diffusion restriction, hemorrhage, or vascular occlusion. Cerebrospinal fluid showed albuminocytologic dissociation. High-dose intravenous methylprednisolone (1 g/day for 5 days) led to improvement by day 3 and independent ambulation by day 20. Follow-up MRI at 16 weeks showed marked resolution of MRI abnormalities, mirroring clinical recovery, although mild nystagmus persisted at 20 weeks. The temporal dissociation from acute envenoming, the absence of systemic illness or metabolic derangement, and the marked radiologic resolution argue against a persistent direct venom effect and instead favor a secondary, immune-mediated, or delayed to
Abstract
Snakebite remains a cause of morbidity in tropical regions, with viperid venoms typically causing local tissue injury (edema, bleeding, ecchymoses), vasculotoxicity, coagulopathy, and acute kidney injury. Delayed immune-mediated encephalopathies are uncommon. We report a 49-year-old woman from Birbhum district, West Bengal, India, who sustained a bite from a Russell's viper in June 2025 (rainy season). She developed vasculotoxic envenoming and acute kidney injury requiring hemodialysis for 5 days, followed by apparent systemic recovery and discharge. Seven days later, she developed abrupt scanning dysarthria, gait ataxia, and oscillopsia. Brain MRI on day 14 demonstrated multifocal T2/FLAIR hyperintensities involving the left cerebellar hemisphere, left frontoparietal cortex, bilateral basal ganglia, and periventricular white matter, without diffusion restriction, hemorrhage, or vascular occlusion. Cerebrospinal fluid showed albuminocytologic dissociation. High-dose intravenous methylprednisolone (1 g/day for 5 days) led to improvement by day 3 and independent ambulation by day 20. Follow-up MRI at 16 weeks showed marked resolution of MRI abnormalities, mirroring clinical recovery, although mild nystagmus persisted at 20 weeks. The temporal dissociation from acute envenoming, the absence of systemic illness or metabolic derangement, and the marked radiologic resolution argue against a persistent direct venom effect and instead favor a secondary, immune-mediated, or delayed toxic phenomenon. Albuminocytologic dissociation may reflect transient barrier dysfunction with increased permeability and, in viper envenoming complicated by acute kidney injury, systemic endothelial injury, including snakebite-associated thrombotic microangiopathy, could be a contributing mechanism. This case highlights the need for vigilance for delayed multifocal encephalopathy after vasculotoxic snakebite and supports prompt MRI and cerebrospinal fluid evaluation of new post-discharge neurological symptoms, as early high-dose corticosteroids may be crucial in this potentially reversible condition.