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CASE REPORTS
JOURNAL ARTICLE
Cerebellar ataxia due to Leptospirosis- a case report.
BMC Infectious Diseases 2016 December 13
BACKGROUND: Leptospirosis involves nervous system in around 10-15% of the cases, the commonest presentation being aseptic meningitis. Most of the clinical features of neuroleptospirosis are due to capillary endothelial damage and vasculitis. Ataxia is an extremely uncommon manifestation of Leptospirosis occuring in <5% of cases.
CASE PRESENTATION: A 28 year old female from North India presented with a short febrile illness followed by an acute onset cerebellar ataxia, anemia, thrombocytopenia and transaminitis. Leptospira serology showed high titres of IgM (ELISA) and MAT (microscopic agglutination test titre >1:800) . She was treated with intravenous ceftriaxone for 14 days following which she showed marked recovery.
CONCLUSION: The clinical features of neuroleptospirosis are varied, most of them resulting from endothelial damage and vasculitis. Immune mediated phenomenon with no structural damage is another possible mechanism leading to cerebellar ataxia. Cerebellar ataxia due to common tropical infections should be ruled out in the appropriate setting, as early institution of treatment can abate neurological morbidity. The case report highlights the importance of identifying a reversible cause of cerebellar ataixa due to a tropical infection, possibly due to a immune mediated phenomenon, and would be of interest to both internists and neurologists.
CASE PRESENTATION: A 28 year old female from North India presented with a short febrile illness followed by an acute onset cerebellar ataxia, anemia, thrombocytopenia and transaminitis. Leptospira serology showed high titres of IgM (ELISA) and MAT (microscopic agglutination test titre >1:800) . She was treated with intravenous ceftriaxone for 14 days following which she showed marked recovery.
CONCLUSION: The clinical features of neuroleptospirosis are varied, most of them resulting from endothelial damage and vasculitis. Immune mediated phenomenon with no structural damage is another possible mechanism leading to cerebellar ataxia. Cerebellar ataxia due to common tropical infections should be ruled out in the appropriate setting, as early institution of treatment can abate neurological morbidity. The case report highlights the importance of identifying a reversible cause of cerebellar ataixa due to a tropical infection, possibly due to a immune mediated phenomenon, and would be of interest to both internists and neurologists.
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