Journal of integrative neuroscience最新文献

Background: Previous studies have found that inhibitory priming with continuous theta burst stimulation (cTBS) can enhance the effect of subsequent excitatory conditioning stimuli with intermittent theta burst stimulation (iTBS) in the upper limbs. However, whether this combined stimulation approach elicits a comparable compensatory response in the lower extremities remains unclear. This study aimed to investigate how cTBS preconditioning modulated the effect of iTBS on motor cortex excitability related to the lower limb in healthy individuals.

Methods: Using a randomised cross-over design, a total of 25 healthy participants (19 females, mean age = 24.80 yr) were recruited to undergo three different TBS protocols (cTBS + iTBS, sham cTBS + iTBS, sham cTBS + sham iTBS) in a random order. Each TBS intervention was administered with one-week intervals. cTBS and iTBS were administered at an intensity of 80% active motor threshold (AMT) delivering a total of 600 pulses. Before intervention (T0), immediately following intervention (T1), and 20 min after intervention (T2), the corticomotor excitability was measured for the tibialis anterior muscle of participants' non-dominant leg using a Magneuro100 stimulator and matched double-cone coil. The average amplitude of the motor-evoked potential (MEP) induced by applying 20 consecutive monopulse stimuli at an intensity of 130% resting motor threshold (RMT) was collected and analysed.

Results: Compare with T0 time, the MEP amplitude (raw and normalised) at T1 and T2 showed a statistically significant increase following the cTBS + iTBS protocol (p < 0.01), but no significant differences were observed in amplitude changes following other protocols (sham cTBS + iTBS and sham cTBS + sham iTBS) (p > 0.05). Furthermore, no statistically significant difference was found among the three protocols at any given time point (p > 0.05).

Conclusions: Preconditioning the lower extremity motor cortex with cTBS prior to iTBS intervention can promptly enhance its excitability in healthy participants. This effect persists for a minimum duration of 20 min.

Clinical trial registration: No: ChiCTR2300069315. Registered 13 March, 2023, https://www.chictr.org.cn.

Background: Sleep patterns often shift as people age, a phenomenon frequently associated with the onset of neurodegenerative conditions. Additionally, distinct alterations occur in brain structure as individuals grow older, particularly within the hippocampus, a region known for its role in cognition and sleep regulation. Yet, how exactly do changes in sleep relate to specific subfields within the hippocampus is still unclear.

Methods: We conducted a study involving non-demented healthy adults from the Aiginition Longitudinal Biomarker Investigation Of Neurodegeneration (ALBION) cohort. Participants underwent objective sleep measurements using wrist Actiwatch and WatchPAT devices. Further, all participants underwent the same Magnetic Resonance Imaging (MRI) protocol, including a 3D high resolution T1-weighted sequence, on the same 3.0 Tesla MRI scanner using an eight-channel head coil. The study aimed to examine the relationship between objectively measured sleep metrics and the morphology of twenty-two distinct hippocampal subregions.

Results: In total, 75 non-demented participants with 63 mean years of age were included in the study. Results indicated that a higher frequency of awakenings during sleep was associated with increased volume in the right presubiculum body (beta = 0.630, p False Discovery Rate (FDR) <0.036). Longer sleep duration showed a tendency to be associated with smaller volumes of the right presubiculum body, hinting at a possible negative impact of prolonged sleep on this brain region. Similar trends were observed regarding sleep apnea and the presubiculum body volume. Further analysis based on age stratification revealed that in younger participants, longer sleep duration was linked to decreased volume of the presubiculum body, while a greater number of awakenings was correlated with increased volume of the same region. Among older participants, higher frequencies of awakenings were associated with larger volumes in various hippocampal subfields.

Conclusions: These findings shed light on the complex relationship between sleep characteristics and brain structure, highlighting potential age-related differences. The study provides valuable insights into how sleep disruptions may impact hippocampal morphology and cognitive function of cognitively healthy adults. Further research is warranted to elucidate the underlying mechanisms and implications for neurodegenerative diseases.

Purpose: To investigate the relationship of diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) parameters with dysfunction in acute focal cerebral ischemia (ACI) rabbits.

Methods: The model of ACI in the middle cerebral artery was made using 30 adult male New Zealand rabbits. The dysfunction severities of the ACI rabbits were assessed using Purdy's score. A paired-sample rank sum test was adopted to compare the abnormal signal zone (ASZ) volumes from T₂ weighted imaging (T₂WI), dynamic susceptibility contrast-enhanced (DSC) imaging, and DWI with a relative cerebral blood flow (rCBF) map; correlations were analyzed between the volume of each ASZ and Purdy's score by Spearman's rank correlation coefficient. The degree of necrotic and apoptotic cells was evaluated in the ASZ from DWI and DSC PWI-DWI mismatch (PDM) zone. Correlations were analyzed between the index of cellular damage and Purdy's score, the volume of ASZs by Spearman's rank correlation coefficient.

Results: The ASZ volumes from DSC-PWI and the rCBF maps were larger than those from DWI (p < 0.001 and p < 0.001, respectively); those from the rCBF map (Z = 0.959, p < 0.001) and DSC-PWI (Z = 0.970, p < 0.001) were positively correlated with DWI; a positive correlation was found between Purdy's score and the ASZ volumes from DSC-PWI (Z = 0.889, p < 0.001), DWI (Z = 0.921, p < 0.001), and rCBF (Z = 0.891, p < 0.001). A significant difference was observed between the ASZ from DWI and the PDM zone in terms of the degree of necrotic (p < 0.001) and apoptotic cells (p < 0.001). The degree of cellular damage in the ASZ of DWI and PDM zone had no relationship with Purdy's score and the volumes of ASZs.

Conclusion: The ASZ volumes from DSC-PWI, rCBF, and particularly DWI reflected the level of dysfunction in rabbits with ACI.

Background: Most acute cerebral infarctions (ACI) may develop vascular dementia (VD), which involves almost all types of cognitive impairment. Unfortunately, there is currently no effective treatment for VD. Most patients exhibit mild cognitive impairment (MCI) before the development of VD. N-butyl-phthalide (NBP) is used to treat ACI and improve cognitive function. The oxygen and glucose deprivation (OGD) model of neurons is an in vitro model of ischemia, hypoxia, and cognitive dysfunction.

Methods: We conducted clinical studies and in vitro experiments to investigate the clinical efficacy and mechanism of action of NBP for treating ACI-induced MCI. Patients with ACI-induced MCI were randomly divided into control (Ctrl) and NBP groups. We assessed various indicators, such as clinical efficacy, montreal cognitive assessment scale (MOCA), activities of daily living (ADL), and cerebral infarct size in both groups before and after treatment. We observed the morphology of neurons and detected the survival rate, action potentials (APs), expression of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), and the interaction between TLR4 and HMGB1.

Results: The MOCA and ADL scores increased significantly after treatment in the NBP group. A OGD model of neurons was established, and the neurons were divided into Ctrl and NBP groups. We observed that the survival rate and APs amplitude of the neurons were significantly increased in the NBP group, whereas TNF-α expression was decreased. Furthermore, the interaction between TLR4 and HMGB1 decreased in the NBP group.

Conclusion: NBP plays a neuroprotective role by inhibiting the TLR4/HMGB1 pathway and ameliorating ACI-induced MCI.

Background: Transcranial direct current stimulation (tDCS) is a therapeutic tool for improving post-stroke gait disturbances, with ongoing research focusing on specific protocols for its application. We evaluated the feasibility of a rehabilitation protocol that combines tDCS with conventional gait training.

Methods: This was a randomized, double-blind, single-center pilot clinical trial. Patients with unilateral hemiplegia due to ischemic stroke were randomly assigned to either the tDCS with gait training group or the sham stimulation group. The anodal tDCS electrode was placed on the tibialis anterior area of the precentral gyrus while gait training proceeded. Interventions were administered 3 times weekly for 4 weeks. Outcome assessments, using the 10-meter walk test, Timed Up and Go test, Berg Balance Scale, Functional Ambulatory Scale, Modified Barthel Index, and European Quality of Life 5 Dimensions 3 Level Version, were conducted before and after the intervention and again at the 8-week mark following its completion. Repeated-measures analysis of variance (ANOVA) was used for comparisons between and within groups.

Results: Twenty-six patients were assessed for eligibility, and 20 were enrolled and randomized. No significant differences were observed between the tDCS with gait training group and the sham stimulation group in gait speed after the intervention. However, the tDCS with gait training group showed significant improvement in balance performance in both within-group and between-group comparisons. In the subgroup analysis of patients with elicited motor-evoked potentials, comfortable pace gait speed improved in the tDCS with gait training group. No serious adverse events occurred throughout the study.

Conclusions: Simultaneous anodal tDCS during gait training is a feasible rehabilitation protocol for chronic stroke patients with gait disturbances.

Clinical trial registration: URL: https://cris.nih.go.kr; Registration number: KCT0007601; Date of registration: 11 July 2022.

Background: The adoption of convolutional neural networks (CNNs) for decoding electroencephalogram (EEG)-based motor imagery (MI) in brain-computer interfaces has significantly increased recently. The effective extraction of motor imagery features is vital due to the variability among individuals and temporal states.

Methods: This study introduces a novel network architecture, 3D-convolutional neural network-generative adversarial network (3D-CNN-GAN), for decoding both within-session and cross-session motor imagery. Initially, EEG signals were extracted over various time intervals using a sliding window technique, capturing temporal, frequency, and phase features to construct a temporal-frequency-phase feature (TFPF) three-dimensional feature map. Generative adversarial networks (GANs) were then employed to synthesize artificial data, which, when combined with the original datasets, expanded the data capacity and enhanced functional connectivity. Moreover, GANs proved capable of learning and amplifying the brain connectivity patterns present in the existing data, generating more distinctive brain network features. A compact, two-layer 3D-CNN model was subsequently developed to efficiently decode these TFPF features.

Results: Taking into account session and individual differences in EEG data, tests were conducted on both the public GigaDB dataset and the SHU laboratory dataset. On the GigaDB dataset, our 3D-CNN and 3D-CNN-GAN models achieved two-class within-session motor imagery accuracies of 76.49% and 77.03%, respectively, demonstrating the algorithm's effectiveness and the improvement provided by data augmentation. Furthermore, on the SHU dataset, the 3D-CNN and 3D-CNN-GAN models yielded two-class within-session motor imagery accuracies of 67.64% and 71.63%, and cross-session motor imagery accuracies of 58.06% and 63.04%, respectively.

Conclusions: The 3D-CNN-GAN algorithm significantly enhances the generalizability of EEG-based motor imagery brain-computer interfaces (BCIs). Additionally, this research offers valuable insights into the potential applications of motor imagery BCIs.

Background and purpose: To investigate the abnormal pattern of altered functional activity in the brain and the neuroimaging mechanisms underlying the cognitive impairment of patients with colorectal cancer (CRC) via resting-state functional magnetic resonance imaging (rs-fMRI).

Materials and methods: CRC patients (n = 56) and healthy controls (HCs) (n = 50) were studied. The participants underwent rs-fMRI scans and the Montreal Cognitive Assessment (MoCA). The amplitude of low-frequency fluctuations (ALFF), degree centrality (DC), regional homogeneity (ReHo), and MoCA scores, were calculated for participants.

Results: The scores of executives, visuospatial, memory, language and attention were lower in CRC patients. ReHo and ALFF values in the left postcentral gyrus, ReHo values in the right postcentral gyrus, ALFF and DC values in the left middle occipital gyrus, ReHo and DC values in the right lingual gyrus, DC values in the right angular gyrus and precuneus, and ALFF values in the left middle temporal gyrus decreased conspicuously in the CRC patients.

Conclusion: CRC patients have abnormal resting state function, mainly in the brain areas involved in cognitive function. The overlapping brain regions with abnormal functional indicators are in the middle occipital gyrus, postcentral gyrus, and lingual gyrus. This study reveals the potential biological pathways involved in brain impairment and neurocognitive decline in patients with CRC.

Background: Neonatal seizures are diagnostically challenging and predominantly electrographic-only. Multichannel video continuous electroencephalography (cEEG) is the gold standard investigation, however, out-of-hours access to neurophysiology support can be limited. Automated seizure detection algorithms (SDAs) are designed to detect changes in EEG data, translated into user-friendly seizure probability trends. The aim of this study was to evaluate the diagnostic accuracy of the Persyst neonatal SDA in an intensive care setting.

Methods: Single-centre retrospective service evaluation study in neonates undergoing cEEG during intensive care admission to Great Ormond Street Hospital (GOSH) between May 2019 and December 2022. Neonates with <44 weeks corrected gestational age, who had a cEEG recording duration >60 minutes, whilst inpatient in intensive care, were included in the study. One-hour cEEG clips were created for all cases (seizures detected) and controls (seizure-free) and analysed by the Persyst neonatal SDA. Expert neurophysiology reports of the cEEG recordings were used as the gold standard for diagnostic comparison. A receiver operating characteristic (ROC) curve was created using the highest seizure probability in each recording. Optimal seizure probability thresholds for sensitivity and specificity were identified.

Results: Eligibility screening produced 49 cases, and 49 seizure-free controls. Seizure prevalence within those patients eligible for the study, was approximately 19% with 35% mortality. The most common case seizure aetiology was hypoxic ischaemic injury (35%) followed by inborn errors of metabolism (18%). The ROC area under the curve was 0.94 with optimal probability thresholds 0.4 and 0.6. Applying a threshold of 0.6, produced 80% sensitivity and 98% specificity.

Conclusions: The Persyst neonatal SDA demonstrates high diagnostic accuracy in identifying neonatal seizures; comparable to the accuracy of the standard Persyst SDA in adult populations, other neonatal SDAs, and amplitude integrated EEG (aEEG). Overdiagnosis of seizures is a risk, particularly from cEEG recording artefact. To fully examine its clinical utility, further investigation of the Persyst neonatal SDA's accuracy is required, as well as confirming the optimal seizure probability thresholds in a larger patient cohort.