A systematic review of brain imaging findings in neurological infection with Japanese encephalitis virus compared with Dengue virus.

OBJECTIVES: Japanese encephalitis virus (JEV) and dengue virus (DENV) represent important causes of encephalitis in Asia. Brain imaging may provide diagnostic clues about the etiology of infectious encephalitis. We performed a systematic review of brain imaging findings in Japanese encephalitis (JE) and DENV neurological infection (dengue) to identify characteristic lesions. METHODOLOGY: Five databases were searched. We included all study types and imaging techniques. Laboratory methods were categorized using diagnostic confidence levels. Imaging data were synthesized, and focal findings are presented as proportions for JE and dengue and for subgroups based on diagnostic confidence. PRINCIPAL FINDINGS: Thalamic lesions were the most reported magnetic resonance imaging finding in both diseases but appeared to occur more often in JE (74% in 23 studies) than dengue (29.4% in 58 studies). In cases diagnosed with antigen or nucleic acid tests, thalamic lesions were reported frequently in both JE (76.5% in 17 studies) and dengue (65.2% in 23 studies). SIGNIFICANCE: The results suggest that thalamic lesions frequently occur in both JE and dengue encephalitis. No radiological findings were found to be pathognomonic of either disease. Although brain imaging may support a diagnosis, laboratory confirmation with highly specific tests remains crucial.

Effects of ketamine on neurogenesis, extracellular matrix homeostasis and proliferation in hypoxia-exposed HT22 murine hippocampal neurons.

Ketamine is a widely used drug in pediatric anesthesia, and both neurotoxic and neuroprotective effects have been associated with its use. There are only a few studies to date which have examined the effects of ketamine on neurons under hypoxic conditions, which may lead to severe brain damage and poor neurocognitive outcomes in neonates. In the present study, the effects of ketamine on cellular pathways associated with neurogenesis, extracellular matrix homeostasis and proliferation were examined in vitro in hypoxia-exposed neurons. Differentiated HT22 murine hippocampal neurons were treated with 1, 10 and 20 µM ketamine and cultured under hypoxic or normoxic conditions for 24 h followed by quantitative PCR analysis of relevant candidate genes. Ketamine treatment did not exert any notable effects on the mRNA expression levels of markers of neurogenesis (neuronal growth factor and syndecan 1), extracellular matrix homeostasis (matrix-metalloproteinase 2 and 9, tenascin C and tenascin R) or proliferation markers (Ki67 and proliferating cell nuclear antigen) compared with the respective untreated controls. However, there was a tendency towards downregulation of multiple cellular markers under hypoxic conditions and simultaneous ketamine treatment. No dose-dependent association was found in the ketamine treated groups for genetic markers of neurogenesis, extracellular matrix homeostasis or proliferation. Based on the results, ketamine may have increased the vulnerability of hippocampal neurons in vitro to hypoxia, independent of the dose. The results of the present study contribute to the ongoing discussion on the safety concerns around ketamine use in pediatric clinical practice from a laboratory perspective.