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Background and Purpose: There are no highly sensitive biomarkers for epilepsy to date. Recently, promising results regarding functional connectivity analysis have been obtained, which may improve epilepsy diagnosis even in the absence of visible abnormality in electroencephalography. We aimed to investigate the differences in functional connectivity after a first unprovoked seizure between patients diagnosed with epilepsy within 1 year due to subsequent seizures and those who were not.Methods: We compared quantitative electroencephalography power spectra and functional connectivity between 12 patients who were diagnosed with epilepsy (two or more unprovoked seizures) within 1 year and 17 controls (those not diagnosed within 1 year) using iSyncBrain® (iMediSync Inc., Suwon, Korea; https://isyncbrain.com/). In the source-level analysis, the current distribution across the brain was assessed using the standardized low-resolution brain electromagnetic tomography technique, to compare relative power values in 68 regions of interest and connectivity (the imaginary part of coherency) between regions of interest.Results: In the epilepsy group, quantitative electroencephalography showed lower alpha2 band power in left frontal, central, superior temporal, and parietal regions and higher beta2 power in both frontal, central, temporal, occipital, and left parietal regions compared with the control group. Additionally, epilepsy patients had significantly lower connectivity in alpha2 and beta2 bands than the controls.Conclusions: Patients experiencing their first unprovoked seizure presented different brain function according to whether they have subsequent seizures and future epilepsy. Our results propose the potential clinical ability to diagnose epilepsy after the first unprovoked seizure in the absence of interictal epileptiform discharges.

Purpose The purpose of this study is to compare and analyze the power spectral changes between subjective cognitive decline (SCD) subjects and normal controls (NC) while checking the preclinical stage of AD in the SCD subjects and to use the derived data for biomarker research that can diagnose early-stage AD in the future. Methods We recruited 23 SCD patients and 23 normal control subjects and QEEG analysis including power spectral density (PSD) and source-level analysis were performed. An automated preprocessing procedure and statistical analysis were performed by iSync Brain ® (iMediSync Inc., Republic of Korea) ( https://isyncbrain.com/ ) using the international standard 10–20 system (19 electrodes). Results Absolute PSD, there was no statistically significant difference in all of the EEG power measurements of the 19 channels. In the relative PSD analysis, the average delta band power of the SCD group was significantly higher in Fp2, F4, and F8 than NC. Alpha1 band power of the O1 channel was 22.56±16.05 for the SCD group and 33.19±19.05 for the NC (p-value Conclusion SCD subjects showed a partial increase of delta waves in the frontal lobe region and a partial decrease in alpha1, a fast wave in the occipital region, compared to the NC. SCD is considered one of the earliest clinical symptoms of AD and it is predicted to be related to minor nerve damage. We were able to observe the power spectral changes in SCD subjects in this cross-sectional study, a large number of subjects and longitudinal studies are needed to evaluate their predictability for future deterioration such as conversion to MCI.

Amlodipine belongs to a class of calcium channel blockers that relax blood vessels to allow easier flow of blood. Higher blood pressure (BP) is associated with cerebrovascular disease and is an important contributor to cognitive decline and dementia.This study aimed to evaluate the effect of 24 weeks of S-amlodipine besylate therapy on cognitive function in patients with hypertension and cerebrovascular disease.The data were obtained from a study of post-market surveillance of S-amlodipine besylate.A total of 545 subjects (mean age 67 ± 9.68 years) with hypertension and ischemic cerebrovascular disease were enrolled. Patients with a baseline Mini-Mental State Examination (MMSE) score above 26 were assigned to the cognitive normal (CN) (n = 294) group, and those with MMSE score less than 26 were in the cognitive decline (CD) (n = 251) group. After 24 weeks of treatment with S-amlodipine besylate 5 mg, MMSE and Global Deterioration Scale (GDS) were evaluated again. Changes in MMSE were compared in the target BP reached (TBPR) and non-reached (NTBPR) groups and for CN and CD groups. Treatment with 5 mg of S-amlodipine besylate for 24 weeks improved MMSE and GDS scores (p 0.001). The CD group showed improvement in MMSE score regardless of whether target BP was obtained (TBPR: p 0.001, NTBPR: p 0.01). However, the CN classification was not significant for either TBPR or NTBPR groups.S-amlodipine besylate improved cognition of the CD group with hypertension and cerebrovascular disease regardless of obtaining target BP.

Background The memory impairments in mild cognitive impairment (MCI) can be classified into encoding (EF) and retrieval (RF) failure, which can be affected by underlying pathomechanism. We explored the differences structurally and functionally. Methods We compared quantitative electroencephalography (qEEG) power spectra and connectivity between 87 MCI patients with EF and 78 MCI with RF using iSyncBrain® (iMediSync Inc., Republic of Korea) (https://isyncbrain.com/). Voxel-based morphometric analysis of the gray matter (GM) in the MCI groups and 71 cognitive normal controls was also done using the Computational Anatomy Toolbox 12 (http://www.neuro.uni-jena.de/cat/). Results qEEG showed higher frontal theta and lower beta2 band power, and higher theta connectivity in the EF. There was no statistically significant difference in GM volume between the EF and RF. However, when compared to normal control, GM volume reductions due to EF in the left thalamus and bilateral hippocampi and reductions due to RF in the left thalamus, right superior frontal lobe, right superior temporal lobe, and right middle cingulum were observed (p Conclusions MCI differs functionally and structurally according to their specific memory impairments. The EF findings are structurally and functionally more consistent with the prodromal Alzheimer’s disease stage than the RF findings. Since this study is a cross-sectional study, prospective follow-up studies are needed to investigate whether different types of memory impairments can predict the underlying pathology of amnestic MCI. Additionally, insufficient sample size may lead to ambiguous statistical findings in direct comparisons, and a larger patient cohort could more robustly identify differences in GM volume reductions between the EF and the RF group.

Background: Memory impairments in mild cognitive impairment can be classified into encoding (EF) and retrieval (RF) failure. We explored differences between the two using quantitative electroencephalography (qEEG) and magnetic resonance imaging volumetry.Methods: We compared qEEG power spectra and connectivity between 87 participants with EF and 78 with RF, and gray matter (GM) volume differences between participants with mild cognitive impairment and 71 controls. Demographic and cognitive assessment results between groups were compared with Student’s t-tests, and obtained qEEG features were analyzed according to statistically significant differences between the groups using iSyncBrain ™. GM volume changes underlying EF and RF in amnestic mild cognitive impairment were compared on processed magnetic resonance images of cognitively normal subjects using Student’s t-tests, with age and total intracranial volume classified as nuisance covariates. We used a voxel-based morphometry analysis to demonstrate significant atrophic GM areas in the two types of patients with amnestic mild cognitive impairment. Results were considered statistically significant at p < 0.05 and were corrected for family-wise errors to avoid multiple-comparison problems.Results: qEEG showed higher frontal theta and lower beta2 band power and higher theta and lower beta connectivity in patients with EF. GM volume reductions due to EF in the left thalamus and bilateral hippocampi and reductions due to RF in the left thalamus, right superior frontal lobe, right superior temporal lobe, and right middle cingulum were observed. Conclusions: Patients with mild cognitive impairment differ functionally and structurally according to their specific memory impairments. EF findings are more consistent with the prodromal Alzheimer's disease stage than RF findings. Since this study is a cross-sectional study, prospective follow-up studies are needed to investigate whether different types of memory impairments can predict the underlying pathology of amnestic MCI. Additionally, insufficient sample size may lead to ambiguous statistical finidings in direct comparisons, a larger patient cohort could more robustly identify differences in GM volume reductions between the EF and the RF group.