Clinical EEG and neuroscience最新文献

Acceptance, nonjudgmental awareness of the present-moment experiences, is a central component of mindfulness. This study used a pretest-posttest design to examine whether a brief mindfulness intervention (MI) could increase self-reported acceptance and reduce affective reactivity to errors, as indexed by error-related negativity (ERN), error positivity (Pe), and post-error slowing (PES). Meditation-naïve participants (n = 121, ages 18-31 years, 69% female) were randomly assigned to either a mindfulness group, which engaged in 10 min of guided mindful breathing, or a control group, which listened to a Ted talk on green living. Both groups completed a Flanker task before and after the intervention to elicit errors under time pressure. Results showed that participants in the mindfulness group reported greater acceptance following the intervention; however, no corresponding changes were observed in ERN or PES. Instead, both groups showed practice effects, with faster reaction times and larger Pe amplitudes reflecting increased response certainty. These findings suggest that while a brief MI may enhance subjective acceptance, it may not be sufficient to alter neural or behavioral markers of affective error reactivity. Longer or more intensive mindfulness training may be required to influence these deeper cognitive and emotional processes.

ObjectiveAlzheimer's disease (AD) often presents visual hallucinations (VH) in late stages. Visual evoked potentials (VEPs) are noninvasive electrophysiological measures that reflect the functional integrity of the visual conduction pathway. This study uses visual evoked potentials (VEP) to assess visual pathway dysfunction and evaluates VEP as a biomarker for disease progression.MethodsA retrospective study of 112 AD patients (2016-2024) was conducted, categorizing individuals into VH and non-VH groups based on the presence of visual hallucinations. VEP testing assessed P100 latency and amplitude. Baseline characteristics and VEP parameters were compared between groups, and correlations with disease duration were analyzed.ResultsNo significant differences were observed between the two groups in terms of age, sex, years of education, homocysteine (HCY) levels, or Mini-Mental State Examination (MMSE) scores (p > 0.05). However, disease duration was significantly longer in the VH group than in the non-VH group (p = 0.00). VEP findings revealed a significantly prolonged P100 latency (p = 0.01) and reduced P100 amplitude (p = 0.00) in the VH group. Correlation analysis indicated a positive correlation between P100 latency and disease duration (r = 0.21, p = 0.03) and a negative correlation between P100 amplitude and disease duration (r = -0.34, p = 0.00), suggesting progressive impairment of the visual conduction pathway over the course of the disease.ConclusionAD patients with visual hallucinations exhibit more severe impairments in the integrity of the visual conduction pathway than those without hallucinations, as evidenced by prolonged P100 latency and decreased amplitude. These changes are closely associated with disease duration.

ObjectiveSince the pioneering work of Hans Berger in 1929 introducing the utility of human electroencephanlography (EEG) in psychiatry, a considerable amount of work has been devoted to the identification of pathophysiological mechanisms of mental diseases. However, how electrophysiology may be useful in clinical psychiatric settings is still matter of debate. Here we provide a summary of current emerging data and perspectives regarding the promising utility of various EEG tools in the treatment of mental diseases.Methods and ResultsIn this report we focus on new insights reported through the use of various EEG tools (quantitative EEG, QEEG; cognitive event-related potentials, ERPs) and some new EEG-based methods (Mobile Brain/Body Imaging or Artificial Intelligence algorithms) suggesting that their use might be helpful at the clinical level in the management of various forms of mental diseases.ConclusionGiven the encouraging results highlighting how these electrophysiological tools may be used with regard to mental disorders, continued efforts to better implement these EEG tools into psychiatric clinical settings remains one of the most pressing challenges for neurophysiologists.

BackgroundNeurological complications during Extracorporeal membrane oxygenation (ECMO) can result in long-term cognitive deficits. This exploratory study aimed to determine the association between continuous EEG (cEEG) findings and neurological outcome in adult patients undergoing ECMO,MethodsThis retrospective cohort study analyzed EEG characteristics, and clinical outcomes in adult ECMO patients at a tertiary care center. We included all adult ECMO patients from January 1, 2015, to July 31, 2019 including patients in whom cEEG was initiated ASAP with ECMO orders. EEG data were evaluated for association with clinical outcome. Clinical outcomes were assessed using the Glasgow Outcome Scale (GOS), modified Rankin Scale (mRS), and Cerebral Performance Category (CPC) scale at discharge and 6 months.ResultsAmong 329 ECMO encounters, 214 (65%) included cEEG monitoring. Low EEG voltage was associated with poor outcome (CPC, 52.4% vs 64% p = 0.001). EEG reactivity was associated with outcome at 6 months (CPC, 54.8% reactive and good outcome vs 67% unreactive and poor outcomes p = 0.005). The presence of predominant background frequency, normal voltage, was associated with good outcome while higher Mayo EEG grade with poor outcomes. In the limited subset of patients with Sequential Organ Failure Assessment (SOFA) Score, no significant differences were noted between patients with different Mayo EEG grades, EEG reactivity, or background changes. Higher SOFA scores were associated with poor outcomes.ConclusionscEEG monitoring may provide prognostic information for adult ECMO patients. It remains unclear if the EEG findings are solely reflective of underlying severity of illness or not.

This study examined the relationship between alpha activity fluctuations in resting-state electroencephalography (EEG) and the Beck Depression Inventory (BDI) and State-Trait Anxiety Inventory (STAI) scores. A novel approach was introduced using second-order derivatives of the alpha envelope to identify potential functional biomarkers for depression and anxiety conditions. Two 30-s eyes-closed epochs of 64-channel EEG data were collected from open dataset of 113 college-aged participants with the BDI and STAI scores. Metrics including mean positive (Ap) and negative (An) second-order derivatives, the Ap-An ratio, root mean square (RMS), and peak frequency of the alpha envelope were extracted. Correlations between these EEG metrics and scores on the BDI and STAI were analyzed. BDI (Spearman's rank correlation, rs = 0.253-0.304,) and STAI (rs = 0.222-0.339) scores showed significant but weak positive correlations with the Ap-An ratio, in the left frontal regions (P < .05, FDR-corrected). No significant correlation was found between envelope amplitude and either score. The Ap-An ratio at the frontal, temporal, and central electrodes, and peak alpha frequency at the electrodes including the parietal and occipital regions, were significantly higher in participants with BDI scores above 10 compared to those with scores of 10 or below (P < .05, FDR, Mann-Whitney U test). These findings suggest that the second-order derivatives of alpha envelope may serve as functional biomarkers for psychiatric disorders, differently from the frequency and amplitude. Further research is needed to confirm whether these EEG features reflect regional neural activity, such as excitatory and inhibitory activities.

Magnetic resonance imaging (MRI) sequences commonly used in simultaneous electroencephalogram (EEG)-MRI studies include blood oxygenation level-dependent (BOLD) and anatomical T₁-weighted MRI. Safety and electrode heating profiles for these sequences have been well-characterized. However, recent improvements in EEG design may allow for additional sequences to be performed with similar expectations of heating safety, which would expand the EEG-MRI infrastructure for quantitative physiological studies. We evaluated temperature changes ex vivo and in vivo over a wider range of preparation and readout modules with differing specific absorption rate (SAR). A 32-channel EEG cap was used at 3 T and ex vivo heating was assessed for 2D- and 3D-pseudo-continuous-arterial-spin-labeling, 2D-cine, 2D-phase-contrast, 2D T₂-Relaxation-Under-Spin-Tagging, 32-direction b = 1000 s/mm² and b = 2000 s/mm² 2D-diffusion tensor imaging, multiband-BOLD, 3D-T1 MPRAGE, 3D-FLAIR, and 3D-T2. Temperature was monitored with a fiberoptic probe system and plotted over six different electrodes, the amplifier, and battery pack. In vivo assessments were conducted in three participants with the same system. A further in vivo supplemental cohort (n = 10) was used to further evaluate qualitative self-reported heating. Device integrity was evaluated by the manufacturer following experiments. Peak temperature and maximum temperature increases were 23.0°C and 0.4°C respectively ex vivo, and 37.6°C and 0.7°C respectively in vivo. Temperatures did not approach the safety heating threshold of 40°C (defined as a conservative threshold based on manufacturer recommendations and burn injury data). Participants completed in vivo scans without adverse events. No manufacturer-reported device damage was identified. Overall, the tested scans induced heating below critical limits at the clinical field strength of 3 T.

Background: Quantitative electroencephalography (qEEG) data can facilitate the monitoring of treatment progress and the evaluation of therapeutic responses in patients with Major Depressive Disorder (MDD). This study aims to compare the qEEG data of MDD patients and healthy controls, both before and after treatment, to assess the effect of treatment response on neural activity. Methods: A total of 72 patients, aged 18-60, who had not used any psychopharmacological medication for at least two weeks, were included in the study. Based on a minimum 50% reduction in scores on the Hamilton Depression Rating Scale (HDRS-17) and Hamilton Anxiety Rating Scale (HARS), the patients were divided into two groups: responders (n = 51) and non-responders (n = 21). qEEG data were recorded before and after treatment. Results: Responders exhibited a significant shift in cortical activity-particularly in theta, alpha, and high-beta power-toward patterns resembling those observed in the healthy control group (improvement range: 15% to 67%). In contrast, non-responders showed minimal changes in cortical activity (improvement range: 38% to 46%). These findings suggest that while qEEG spectral data reflect marked neural changes in responders, no significant alterations occur in non-responders. Conclusion: The use of qEEG spectral analysis to monitor MDD patients provides valuable insights into treatment efficacy. The distinct patterns of cortical activity observed across most brain regions before treatment, compared to healthy individuals, highlight the potential of qEEG to predict treatment outcomes.

Sleep deprivation has become a severe public health problem in modern societies. Negative consequences of prolonged wakefulness on cognitive abilities have been demonstrated and working memory is one of the main cognitive functions that can be affected by sleep deprivation. This study aims to investigate the effects of sleep deprivation on working memory through EEG event-related oscillations. Thirty healthy young adult university students and graduates were included in this study (15 rested control - 15 sleep-deprived). A 2-back task was used to evaluate working memory, and both groups performed the task during EEG recording. The sleep-deprived (SD) group was required to stay awake for 24 h, and then the EEG session was conducted. The rested control (RC) subjects participated in the morning after a regular night's sleep. Event-related power and phase-locking analyses were applied, and delta (1-3.5 Hz), theta (4-6.5 Hz) and alpha (8-13 Hz) frequencies were investigated in the time-frequency domain. In the 2-back task, significantly prolonged reaction times were observed in the SD group. However, the decrease in accuracy rate was not significant. The EEG analyses revealed that the SD group had decreased frontocentral event-related delta and theta power responses after the presentation of stimuli. Moreover, task accuracy was positively correlated with the left frontocentral delta power in the SD group, and theta power in the RCs. Thus, we propose that the adverse effects of sleep deprivation on working memory can be observed through low-frequency oscillatory responses in the brain.

Background. This study aims to characterize the clinical phenotype of a family with two siblings exhibiting neurological manifestations, utilizing whole exome sequencing (WES) to identify potential pathogenic variants within the NRXN2 gene. Methods. A consanguineous family with two affected siblings displaying developmental delay, severe intellectual disability, epilepsy, and speech delay was examined. WES was performed on DNA samples from affected and unaffected family members, followed by a comprehensive bioinformatics analysis. In-silico tools were employed for variant interpretation and structural modeling of the NRXN2 protein. Clinical and genetic data were integrated to elucidate the potential impact of the identified variant. Results. WES revealed a novel homozygous missense variant (c.1475T>G, p.Leu492Arg) in the NRXN2 gene in both affected siblings. This variant was absent in healthy family members and public databases. In-silico analysis predicted a detrimental effect on protein function. Parental segregation confirmed heterozygous carrier status. The variant was classified as 'Likely Pathogenic' based on ACMG/AMP criteria. Conclusion. This study identifies a novel homozygous missense variant in NRXN2 associated with global developmental delay, severe intellectual disability, speech delay and epilepsy. The findings underscore the critical role of NRXN2 in neurodevelopment and highlight the potential implications of genetic variations within this gene in neurodevelopmental disorders. Further research and functional validation are warranted to deepen our understanding of NRXN2-related disorders and explore potential therapeutic interventions.