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Focal Coxsackie virus B5 encephalitis with synchronous seizure cluster and eruption: Infantile case
Tadashi Shiohama1,2, Taku Omata1, Kaori Muta1
1Division of Child Neurology, Chiba Children's Hospital, Chiba, Japan.
Insights
A rare Coxsackie virus B5 (CVB5) focal encephalitis case in a 9-month-old boy presented with seizures during a roseola-like illness. The child experienced rapid improvement, suggesting local vascular impairment as a potential cause.
Area of Science:
- Neurology
- Virology
- Pediatrics
Background:
- Enterovirus focal encephalitis is a rare neurological condition.
- It typically presents with focal neurological deficits and rapid spontaneous improvement.
Observation:
- A 9-month-old boy developed focal encephalitis with seizure clusters during a roseola infantum-like illness.
- Cerebrospinal fluid analysis revealed pleocytosis and confirmed Coxsackie virus B5 (CVB5) infection via genome sequencing and virus isolation.
- Neuroimaging and electroencephalography showed no abnormalities during the acute phase or at 2-month follow-up.
Findings:
- The case demonstrated a synchronous presentation of seizure clusters and rash.
- Rapid clinical improvement and a benign outcome were observed.
- CVB5 was identified as the causative agent in the cerebrospinal fluid.
Implications:
- This case highlights a unique presentation of CVB5 focal encephalitis in infants.
- The synchronicity of symptoms suggests potential local vascular impairment as a pathogenic mechanism.
- Further research is needed to elucidate the pathogenesis of enterovirus focal encephalitis.
Abstract:
Enterovirus focal encephalitis is a rare clinical entity that is characterized by focal neurological signs including seizure, hemiparesis, hemichorea, and headache, which are mainly followed by rapid spontaneous improvement. We herein describe the case of a 9-month-old boy who developed Coxsackie virus B5 (CVB5) focal encephalitis with seizure clusters in the eruption stage of roseola infantum-like illness, which were followed by rapid improvement and benign outcome. Lumbar puncture indicated pleocytosis, and CVB5 infection in the cerebrospinal fluid was subsequently identified on genome sequencing and virus isolation. Magnetic resonance imaging and electroencephalography showed no abnormal findings at the acute stage or on 2 month follow up. Although the pathogenesis of enterovirus focal encephalitis currently remains unclear, the pure synchronism of seizure cluster and eruption in this case suggests the involvement of local vascular impairment as the underlying pathogenesis.
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