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Acute transverse myelitis after Japanese B encephalitis vaccination in a 4-year-old girl
Mika Matsui1, Hiroe Kawano, Makoto Matsukura
1Department of Child Development, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto 860-0811, Japan.
Insights
Japanese B encephalitis (JBE) vaccination can trigger acute transverse myelitis (ATM), a severe spinal cord inflammation. Early treatment with methylprednisolone may reduce swelling but long-term neurological deficits can persist.
Area of Science:
- Neurology
- Immunology
- Vaccinology
Background:
- Japanese B encephalitis (JBE) is a serious mosquito-borne viral disease.
- Vaccination is crucial for preventing JBE, but potential adverse effects require monitoring.
Observation:
- A 4-year-old girl developed acute transverse myelitis (ATM) within 24 hours after JBE vaccination.
- Clinical presentation included ascending flaccid paraplegia, sensory disturbance, bladder dysfunction, and meningeal signs.
Findings:
- Cerebrospinal fluid analysis revealed neutrophil pleocytosis and elevated protein.
- MRI showed diffuse cervical and lumbar cord swelling, indicative of meningo-radiculomyelopathy.
- High-dose methylprednisolone therapy led to reduced cord swelling, suggesting anti-inflammatory efficacy.
Implications:
- Despite treatment, the patient experienced persistent neurological deficits, indicating severe spinal cord pathology.
- A potential cellular autoimmune mechanism triggered by JBE vaccination is suspected.
- This case highlights the importance of vigilance for rare neurological complications post-vaccination.
Abstract:
Fourteen days after Japanese B encephalitis (JBE) vaccination, a 4-year-old girl developed the full clinical manifestation of ATM within 24h. She showed acute ascending flaccid paraplegia with sensory disturbance, bladder dysfunction and meningeal sign. Cerebrospinal fluid examination revealed neutrophil pleocytosis and elevated protein level. Magnetic resonance imaging (MRI) showed diffuse swelling of the cervical and lumbar cord with low signal intensity on T1 and high signal intensity on T2-weighted imaging. These findings suggested that she had developed meningo-radiculomyelopathy. Since sequential MRI studies showed prompt reduction of the cord swelling, the high-dose methylprednisolone therapy employed seemed to have been effective for improvement of inflammation. Even with such potent drug treatment, she still has substantial flaccid diplegia and sphincter disorder 1 year later, and so we are convinced that the pathological change of the cord was as severe as in necrotizing myelopathy. Although the pathological process remains unknown, cellular autoimmune mechanism against the JBE vaccination is suspected.
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