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In Vivo Imaging Systems (IVIS) Detection of a Neuro-Invasive Encephalitic Virus
Published on: December 2, 2012
[Three pediatric cases of group A coxsackievirus-associated encephalitis/encephalopathy]
Koichi Aizaki1, Tomohiko Tsuru, Keiko Okumura
1Department of Pediatric Neurology, Shimada Ryoiku Center Hachioji, Hachioji, Tokyo. k.aizaki@shimada-ryoiku.or.jp
Insights
Group A coxsackievirus can cause severe pediatric encephalitis/encephalopathy, leading to serious outcomes like brain edema and seizures. Some children may experience poor prognoses, highlighting the need for awareness and prompt diagnosis.
Area of Science:
- Neurology
- Infectious Diseases
- Pediatrics
Background:
- Group A coxsackievirus (CA6) is an enterovirus.
- Encephalitis/encephalopathy is inflammation of the brain.
Observation:
- Three pediatric cases of coxsackievirus A6-associated encephalitis/encephalopathy are presented.
- Clinical presentations included fever, exanthem, convulsions, cardiopulmonary arrest, and severe brain edema.
- Neuroimaging revealed brain edema, subcortical white matter lesions, bilateral hippocampal lesions, and diffusion-weighted imaging abnormalities.
Findings:
- Group A coxsackievirus is identified as a causative agent in pediatric encephalitis/encephalopathy.
- Neurological sequelae, including status epilepticus requiring barbiturate treatment, were observed.
- Diagnoses included acute encephalopathy with febrile convulsive status epilepticus and parainfectious limbic encephalitis.
Implications:
- Group A coxsackievirus infection poses a significant risk for severe neurological complications in children.
- The findings underscore the importance of considering coxsackievirus in the differential diagnosis of pediatric encephalitis/encephalopathy.
- Prompt diagnosis and management are crucial, as some cases may have a poor prognosis.
Abstract:
We report three pediatric cases of group A coxsackievirus-associated encephalitis/encephalopathy. A 4-year-old girl with coxsackievirus A6 infection presented with an exanthem on her upper body on the fourth day of fever. The following day, she developed an episode of convulsions, and subsequently experienced sudden cardiopulmonary arrest. A head computed tomography scan revealed severe brain edema. Two patients with neurological sequelae had initially presented with status epilepticus that required intravenous barbiturate treatment. Both cases had high-signal-intensity lesions on their diffusion-weighted brain magnetic resonance images. A 5-year-old girl with subcortical white matter lesions was diagnosed with acute encephalopathy with febrile convulsive status epilepticus, and a 2-year-old boy with bilateral hippocampal lesions was diagnosed with parainfectious limbic encephalitis. These findings indicate that group A coxsackievirus is a causative agent of pediatric encephalitis/encephalopathy; moreover, the prognosis may be poor in some cases.
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