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The purpose of this study was to determine the effect of fludrocortisone in patients with pediatric vasovagal syncope (VVS).

This retrospective observational single-tertiary-center study based on chart reviews included 74 patients who were newly diagnosed with VVS in the head-up tilt-table test (HUTT). Some of the patients had been treated with fludrocortisone. All patients were assessed using a brain and cardiac workup before treatment to rule out the syncope being due to other causes, which resulted in seven of them being excluded two for epilepsy and five for brain pathologies. The remaining 67 patients were analyzed. The effect of fludrocortisone was evaluated based on the results of a follow-up HUTT, with a response to the treatment considered to be present if there was a negative change at the follow-up HUTT. Univariate logistic regression were used for statistical analyses, with the criterion for significance being
<0.05.

There were no significant differences in the characteristic of the patients between the no-medication (
=39) and fludrocortisone (
=28) groups, including age, sex, and duration of treatment. Ivosidenib Dehydrogenase inhibitor The recurrence rate of syncopal or presyncopal events was significantly lower in the fludrocortisone group (39.3%, 11 of 28) than in the no-medication group (64.1%, 25 of 39) (
=0.044), as was the rate of negative change at the follow-up HUTT 57.1% (16 of 28) and 28.2% (11 of 39), respectively (
=0.017).

Our findings suggest that fludrocortisone is more effective than no medication in pediatric patients with VVS.
Our findings suggest that fludrocortisone is more effective than no medication in pediatric patients with VVS.
We investigated
-fluorodeoxyglucose (FDG) uptake levels in the lumbar vertebrae, liver, and spleen of stroke patients with carotid atherosclerosis.

This study analyzed acute ischemic stroke patients with carotid atherosclerosis who underwent whole-body FDG positron-emission tomography between October 2015 and January 2017. FDG uptake in the lumbar vertebrae, liver, and spleen was measured and compared between stroke patients and control subjects without stroke history. Multivariate linear regression analysis was performed to identify independent factors related to FDG uptake in the proximal internal carotid artery (ICA).

Twenty stroke patients aged 75.1±9.0 years (mean±standard deviation; 10 females) and 20 control subjects aged 62.9±10.7 years (6 females) were included. In comparison with the control group, the stroke group showed significantly higher FDG uptake in the proximal ICA (1.16±0.26 vs. 0.87±0.19,
<0.01), but significantly lower FDG uptake in the lumbar vertebrae (1.09±0.26 vs. 1.38±0.38,
=0.007) and liver (1.71±0.30 vs. 2.01±0.34,
=0.005). Multivariate linear regression analysis showed that the lumbar FDG uptake was negatively correlated with FDG uptake in the proximal ICA (standardized coefficient=-0.367,
=0.013) after adjusting for age and hypertension.

Stroke patients showed decreased FDG uptake in the lumbar vertebrae. Further studies are warranted to evaluate the pathophysiological link between cerebral atherosclerosis and bone.
Stroke patients showed decreased FDG uptake in the lumbar vertebrae. Further studies are warranted to evaluate the pathophysiological link between cerebral atherosclerosis and bone.
Dietary therapy (DT), including the ketogenic diet (KD), is one of the nonpharmacological treatment options for patient with drug-resistant epilepsy. However, maintaining DT in patients without seizure reduction is very difficult, so it is critical for clinicians to decide when to stop this intervention.

We retrospectively analyzed early clinical and laboratory findings and the clinical characteristics of children who received DT. The maintenance of DT and the clinical seizure frequency were assessed at 1, 3, 6, 12, and 24 months after KD initiation. Responders were defined as patients showing an overall reduction in seizure frequency of >50% relative to the baseline.

We included 67 patients who received DT, but only 23 (34.3%) of these patients remained on DT at 6 months. Only 1 (5%) of the 20 responders at 1 month became a nonresponder at 6 months. The response rate at 6 months was significantly higher among patients under 2 years of age (15/17, 88.2%) than older patients (2/6, 33.3%;
=0.021). Moreover, the 6-month responders were significantly younger (29.4±38.6 months, mean±SD) than the nonresponders (98.9±84.6 months,
=0.012) at the initiation of the diet. A high blood β-hydroxybutyrate (BHB) level at 1 month predicted a good DT response at 6 months.

Most 1-month responders maintained their response on DT for up to 6 months. The blood BHB level at 1 month was significantly correlated with the 6-month seizure outcome. Confirming clinical and laboratory biomarkers for the efficacy of DT requires further studies with larger cohorts.
Most 1-month responders maintained their response on DT for up to 6 months. The blood BHB level at 1 month was significantly correlated with the 6-month seizure outcome. Confirming clinical and laboratory biomarkers for the efficacy of DT requires further studies with larger cohorts.
Nonconvulsive status epilepticus (NCSE) is challenging to diagnose. This study aimed to describe and classify the clinical features and electroencephalography (EEG) findings of patients with de novo NCSE and to correlate them with clinical outcomes.

We retrospectively reviewed the medical and EEG records of patients admitted to our institution with altered mentation and EEG abnormalities from January 1, 2013 to December 31, 2018. We evaluated premorbid modified Rankin Scale (mRS) scores, underlying disorders, precipitating factors, clinical manifestations, laboratory tests, and outcomes after a 3-month follow-up. Patients who met the Salzburg Consensus Criteria for NCSE were categorized into good-outcome and poor-outcome groups. A good outcome was defined as 1) clinical and electrographic seizures ceasing after treatment, and 2) an mRS score of ≤2 or remaining unchanged during the 3-month follow-up. A poor outcome was defined as 1) death, 2) seizures continuing despite treatment, or 3) a follow-up mRS score of ≥3 in a patient with a premorbid mRS score of ≤2, or a follow-up mRS score that increased in a patient with a premorbid mRS score of ≥3.
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