This review explores the pathogenetic mechanisms of rotavirus encephalopathy based on two clinical cases.
Rotavirus encephalopathy mechanisms merit clinical consideration in unexplained pediatric cases; leaves open prospective validation of direct and enterotoxin pathways.
Two cases of rotavirus gastroenteritis associated with neurological involvement, one with encephalitis (defined by abnormal neurological signs, cerebrospinal fluid (CSF) pleocytosis and detection of rotavirus genomic nucleic acid in the CSF) and one with a non-inflammatory encephalopathy (defined by abnormal neurological signs, an entirely normal CSF and detection of rotavirus genomic nucleic acid in the CSF), are presented and used as a basis to review and explore potential pathogenetic mechanisms, including direct viral replication within neurons and indirect effects of the newly described rotavirus 'enterotoxin'.
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Goldwater et al. (2001) studied this question.
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