Anti-Basal Ganglia Encephalitis Triggered By Krait Envenomation: A Rare Case Report

Krait bites are known for causing acute neurotoxic effects, such as paralysis and bulbar dysfunction. Anti-basal ganglia encephalitis is a rare autoimmune condition that can lead to movement disorders like dystonia and chorea, often triggered by infections or immune responses. This case report describes a 45-year-old female who presented with delayed-onset anti-basal ganglia encephalitis following a krait bite. Initially, the patient developed bilateral ptosis and bulbar dysfunction, typical of krait neurotoxicity, which resolved after a few weeks. However, three weeks post-recovery, she developed progressive encephalopathy with movement disorders, including dystonia and chorea. MRI revealed hyperintensities in the basal ganglia, and cerebrospinal fluid (CSF) analysis showed mild lymphocytic pleocytosis. Extensive workup ruled out infectious, metabolic, and other causes of encephalopathy. The diagnosis of post-krait bite anti-basal ganglia encephalitis was made after excluding other potential etiologies. Although specific autoimmune markers such as anti-dopamine receptor-2 antibodies could not be tested, the clinical presentation and the temporal association with the snakebite supported the diagnosis of an immune-mediated process. The patient was treated with high-dose intravenous methylprednisolone, followed by oral corticosteroids. Over several months, she showed a gradual improvement in both mental status and movement disorders, though residual motor deficits remained at the six-month follow-up. This case highlights the rare but serious delayed neurological complications that can arise after krait envenomation, emphasizing the potential for autoimmune encephalitis in such cases. Despite the known acute neurotoxic effects of krait venom, this report underscores the importance of recognizing post-envenomation immune mechanisms, particularly when neurological symptoms re-emerge weeks after the initial recovery. Early intervention with immunosuppressive therapy can be crucial in improving outcomes in similar cases.

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Publication Details

Journal
Neurology Letters
Published
2025-08-14
DOI
https://doi.org/10.61882/nl.4.2.102
Primary Topic
Geochemistry and Geologic Mapping
Type
article
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article

Anti-Basal Ganglia Encephalitis Triggered By Krait Envenomation: A Rare Case Report

Neurology Letters
Geochemistry and Geologic Mapping
article

Anti-Basal Ganglia Encephalitis Triggered By Krait Envenomation: A Rare Case Report

article en

Abstract

Krait bites are known for causing acute neurotoxic effects, such as paralysis and bulbar dysfunction. Anti-basal ganglia encephalitis is a rare autoimmune condition that can lead to movement disorders like dystonia and chorea, often triggered by infections or immune responses. This case report describes a 45-year-old female who presented with delayed-onset anti-basal ganglia encephalitis following a krait bite. Initially, the patient developed bilateral ptosis and bulbar dysfunction, typical of krait neurotoxicity, which resolved after a few weeks. However, three weeks post-recovery, she developed progressive encephalopathy with movement disorders, including dystonia and chorea. MRI revealed hyperintensities in the basal ganglia, and cerebrospinal fluid (CSF) analysis showed mild lymphocytic pleocytosis. Extensive workup ruled out infectious, metabolic, and other causes of encephalopathy. The diagnosis of post-krait bite anti-basal ganglia encephalitis was made after excluding other potential etiologies. Although specific autoimmune markers such as anti-dopamine receptor-2 antibodies could not be tested, the clinical presentation and the temporal association with the snakebite supported the diagnosis of an immune-mediated process. The patient was treated with high-dose intravenous methylprednisolone, followed by oral corticosteroids. Over several months, she showed a gradual improvement in both mental status and movement disorders, though residual motor deficits remained at the six-month follow-up. This case highlights the rare but serious delayed neurological complications that can arise after krait envenomation, emphasizing the potential for autoimmune encephalitis in such cases. Despite the known acute neurotoxic effects of krait venom, this report underscores the importance of recognizing post-envenomation immune mechanisms, particularly when neurological symptoms re-emerge weeks after the initial recovery. Early intervention with immunosuppressive therapy can be crucial in improving outcomes in similar cases.

Neurology LettersVol. 4(2)
All India Institute of Medical Sciences Raipur (IN), Seema Dental College and Hospital (IN), All India Institute of Medical Sciences Rishikesh (IN), All India Institute of Medical Sciences (IN)
Zero hunger
Openalex Percentile: Top 27%
Geochemistry and Geologic Mapping
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