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Acute Necrotizing Encephalopathy as a Complication of Chikungunya Infection
V V Holla1, Abhishek B Gohel1, N Kartik1
1Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS) Bengaluru, Karnataka, India.
Insights
Acute necrotizing encephalopathy (ANE), a severe neurological condition, can be triggered by Chikungunya virus. This report details two rare cases of ANE following Chikungunya infection, with patients responding well to steroids.
Area of Science:
- Neurology
- Infectious Diseases
- Pediatrics
Background:
- Acute necrotizing encephalopathy (ANE) is a severe neurological disorder.
- It commonly affects children and is often triggered by viral infections like influenza and Human herpes virus-6.
Observation:
- Two cases of ANE following Chikungunya infection are presented.
- A 13-year-old girl and a 42-year-old man exhibited symptoms including fever, seizures, and altered consciousness.
- Both patients tested positive for Chikungunya virus.
Findings:
- Neuroimaging revealed characteristic bilateral symmetrical thalamic lesions with necrosis and hemorrhage.
- Lesions were also observed in the cerebral white matter, brainstem, and cerebellum.
- This is the first documented instance of ANE associated with Chikungunya infection.
Implications:
- Chikungunya virus should be considered as a potential trigger for ANE.
- Early steroid treatment showed excellent response in these rare cases.
- Further research is needed to understand the pathogenesis and long-term outcomes of ANE post-Chikungunya.
Background:
Acute necrotizing encephalopathy (ANE) is a rapidly progressive encephalopathy seen commonly in children triggered by various prodromal viral infections, most common being influenza virus and Human herpes virus-6.
Objective:
We report two rare cases of ANE preceded by Chikungunya infection.
Cases:
A 13-year old girl presented with a three-day history of headache, fever, seizures, and altered sensorium. Another 42-year old man presented with two days history of fever and altered sensorium. Both were suspected to have viral encephalitis. Evaluation revealed serum positivity for Chikungunya virus. In both cases, diagnosis was clinched by characteristic bilateral symmetrical thalamic lesions with central necrosis and hemorrhage along with lesions in cerebral white matter, brainstem, and cerebellum.
Conclusions:
ANE is reported to have high morbidity and mortality. To the best of our knowledge, this is the first report of ANE post-Chikungunya infection. Apart from being rare etiologically, the patients had excellent response to steroids.
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