Eosinophilic meningoencephalitis successfully treated with glucocorticoids and intravenous immunoglobulin: a case report.

Eosinophilic meningoencephalitis is a rare inflammatory condition of the central nervous system. As a limited number of cases has been reported, debate remains on the optimal treatment. We present a case of idiopathic eosinophilic meningoencephalitis successfully treated with glucocorticoids and intravenous immunoglobulin (IVIG). After extensive evaluation to rule out other possible causes, the patient was treated with intravenous (IV) dexamethasone and showed significant improvement within a few days. However, neurologic impairment persisted, and follow-up lumbar puncture results showed only a mild decrease in pleocytosis. Even after an additional 5 days of IV methylprednisolone, cerebrospinal fluid (CSF) pleocytosis persisted, and brain magnetic resonance imaging (MRI) showed an increase in enhanced lesions, implying persistent neuroinflammation. The patient was maintained on high-dose oral prednisolone for 2 months, and additional immune-modulatory effects were treated with IVIG. Follow-up MRI at 2 months showed a significant decrease in the extent of multiple enhanced lesions and a normalized CSF profile. The patient was maintained on regular maintenance doses of IVIG for an additional 6 months without any neurologic signs or symptoms. Inflammation is the key pathophysiology underlying neurological damage in eosinophilic meningoencephalitis. A literature review revealed that corticosteroid treatment is the only anti-inflammatory treatment used in cases of idiopathic meningoencephalitis, resulting in sufficient response in most patients but only partial response or death in a few cases. This is the first case report of IVIG use in idiopathic eosinophilic meningoencephalitis, suggesting the possibility of a new treatment modality for refractory cases.

Gut microbiome diversity in a febrile seizure mouse model.

Purpose: Febrile seizures at a young age can provoke late-onset temporal lobe epilepsy. Since recent evidence has suggested that the gut microbiome affects central nervous system pathology across the blood-brain barrier, we hypothesized that febrile seizures alter the composition of the gut microbiome to provoke epilepsy. Methods: Third-generation C57BL/6 mice were separated into two groups (n = 5 each), and hot air was applied to only one group to cause febrile seizures. After two weeks of heat challenge, the fecal pellets acquired from each group were analyzed. Results: The gut microbiota of fecal pellets from each group revealed five taxa at the genus level and eight taxa at the species level that were significantly different in proportion between the groups. Conclusion: Although there was no significant difference in the overall diversity of the gut microbiota between the two groups, the identified heterogeneity may imply the pathognomonic causative relevance of febrile seizures and the development of epilepsy.

Cognitive function improvement effects of gintonin-enriched fraction in subjective memory impairment: An assessor- and participant-blinded placebo-controlled study.

Background: Gintonin is a new material of ginseng that acts through the ginseng-derived lysophosphatidic acid (LPA) receptor ligand. The gintonin-enriched fraction (GEF) inhibits amyloid plaque accumulation in the cortex and hippocampus, improves cognitive dysfunction by increasing acetylcholine levels, and promoted hippocampal neurogenesis in an animal model of Alzheimer's disease. We evaluated the effect of the GEF on the cognitive performance of subjects with subjective memory impairment (SMI). Methods: In this eight-week, randomized, assessor- and participant-blinded, placebo-controlled study, participants with SMI were assigned to three groups receiving placebo, GEF 300 mg/day or GEF 600 mg/day. The Korean versions of the Alzheimer's Disease Assessment Scale (K-ADAS), Mini-Mental State Examination (K-MMSE), and Stroop color-word test (K-SCWT) were also evaluated along with the safety profiles. Results: One hundred thirty-six participants completed the study. After eight weeks, we analyzed intergroup differences in primary or secondary outcome score changes. When we compared the GEF group with the placebo group, we observed significant improvements in the K-ADAS and K-SCWT scores. The GEF group did not show a significant improvement in K-MMSE and BDI scores compared to the placebo group. No adverse events were observed in the gintonin and placebo groups for eight weeks. Conclusion: The GEF is safe and effective in improving subjective cognitive impairment related to both the K-ADAS and K-SCWT in this study. However, further large-scale and randomized controlled studies are warranted to secure other cognitive function tests besides the K-ADAS and K-SCWT, and to confirm the findings of the current study.