Search Results (3,036)

Parkinson’s disease (PD) is characterized by progressive dopaminergic degeneration and maladaptive motor cortical plasticity. However, the cellular pathways underlying cortical surface activity in the primary motor cortex (M1) remain unclear, despite serving as a potential target for electrotherapy. We investigated the excitatory–inhibitory (E-I) balance and synaptic plasticity of superficial M1 circuits in a unilateral 6-hydroxydopamine (6-OHDA)-induced rat model of PD. Using extracellular local field potential and whole-cell patch recordings from the contralateral and ipsilateral M1 hemispheres of hemi-parkinsonian rats, we observed a significantly elevated field excitatory postsynaptic potential (fEPSP) input–output function but unchanged intrinsic neuronal excitability in the M1 superficial layer. An altered relative contribution between alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and N-methyl-D-aspartate receptor (NMDAR)-mediated transmission was reflected by a significantly increased AMPA/NMDA ratio. Markedly reduced inhibitory synaptic tone was also evidenced by the decreased amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs), supporting an E-I imbalance favoring excitation in PD. Furthermore, group I metabotropic glutamate receptor (mGluR_1/5)-dependent long-term depression (LTD) was abolished in the ipsilateral PD hemisphere, whereas NMDAR-dependent LTD remained intact. In summary, dopamine depletion appears to enhance network excitation and disrupt mGluR_1/5-mediated control of M1 surface circuitry. Our findings identify altered cortical surface mGluR-dependent plasticity in the hemi-parkinsonian model; however, the relationship between these electrophysiological alterations and individual motor outcomes remains to be determined. Full article

Depression is often associated with functional disturbances in the visual system. However, the fundamental features underlying these visual system aberrations in depression remain to be fully elucidated. In particular, in the first stage of visual processing, how different retinal output neuron types change their intrinsic properties and output features in response to specific light stimulation remains unclear. Here, by adopting a mouse model of depression induced by chronic unpredictable stress (CUS), we found that depression is associated with reduced blood perfusion in the retinal inner plexiform layer (IPL). The hypoperfusion in the IPL is paralleled by a remarkable reduction of retinal ganglion cell (RGC) density, with more cell loss in ipRGCs than in the general RGCs. The surviving RGCs—particularly, ipRGCs—changed their intrinsic electrical properties, exhibiting decreased membrane input resistance, more depolarized resting membrane potential, and altered spiking properties. Additionally, these cells showed stimulus-size-dependent increases in light-evoked responses. Together, our findings demonstrate that depression is associated with the retinal IPL hypoperfusion and RGC impairments (particularly ipRGCs) and suggest retinal layer- and RGC-type-specific susceptibilities, furthering our understanding of retinal pathophysiology in depression. Full article

Background: Persistent left superior vena cava (PLSVC) is the most common congenital anomaly of the thoracic venous system and is generally considered a benign variant. This study aimed to evaluate arrhythmia-related electrocardiographic parameters in children with isolated PLSVC and to assess the relationship with coronary sinus dimensions. Methods: This retrospective cross-sectional study included 26 children with isolated PLSVC and 26 age- and sex-matched healthy controls. All participants underwent transthoracic echocardiography and electrocardiographic analysis. Coronary sinus diameters were measured and indexed to body surface area. Electrocardiographic parameters reflecting atrial conduction and ventricular repolarization heterogeneity, including P-wave dispersion, QTc dispersion, Tp–e interval, and indices of cardiac electrophysiological balance (QT/QRS and QTc/QRS), were evaluated. Results: P-wave dispersion (62.15 ± 14.78 vs. 35.59 ± 10.02 ms, p < 0.001), QTc dispersion (99.66 ± 30.10 vs. 40.45 ± 10.78 ms, p < 0.001), and Tp–e dispersion (67.29 ± 19.10 vs. 38.42 ± 7.13 ms, p < 0.001) were significantly higher in the PLSVC group. QT/QRS (4.33 ± 0.59 vs. 3.78 ± 0.36, p < 0.001) and QTc/QRS (5.48 ± 0.91 vs. 4.61 ± 0.36, p < 0.001) ratios were also increased. Coronary sinus measurements showed weak and inconsistent correlations with electrocardiographic parameters. Conclusions: Children with isolated PLSVC exhibit significant electrocardiographic alterations reflecting atrial and ventricular electrical heterogeneity. These findings suggest that PLSVC may be associated with subclinical electrophysiological abnormalities beyond a benign anatomical variant. Accordingly, increasing clinical awareness of potential arrhythmic risk during follow-up and considering this aspect in patient evaluation may be appropriate. Full article

Background: Sleep-dependent glymphatic clearance has emerged as a potential mechanism linking sleep disruption with Alzheimer’s Disease (AD) pathology. However, the relationship between objectively measured sleep and glymphatic function across the AD continuum remains unclear. Methods: Four databases (PubMed, Embase, Cochrane Library, and PsycINFO) were systematically searched for studies assessing objective sleep metrics and glymphatic-related biomarkers or clearance measures in humans across the AD continuum. Following peer review of the search strategy, supplementary searches of PubMed and Embase using expanded glymphatic and sleep electrophysiology terminology were undertaken to maximize sensitivity. The final database searches identified 416 records. After removal of 72 duplicates, 344 records were screened, 64 reports underwent full-text assessment, and four studies met the inclusion criteria. Results: Four studies involving participants across the AD continuum were included. Objective sleep assessment was performed using polysomnography or electroencephalography, while brain clearance was evaluated using direct or surrogate imaging measures including diffusion tensor image analysis along the perivascular space (DTI-ALPS), perivascular space burden, blood oxygen level-dependent–cerebrospinal fluid (BOLD-CSF) coupling, or direct tracer-based clearance imaging. Across studies, better preserved slow-wave sleep, slow-wave activity, and sleep oscillatory coupling were generally associated with more favorable glymphatic function or glymphatic-related biomarkers. Conversely, disrupted sleep architecture, reduced sleep efficiency, and altered sleep oscillatory coupling were associated with impaired glymphatic clearance or glymphatic dysfunction. Conclusions: Current evidence suggests that objectively measured sleep architecture, particularly slow-wave sleep and sleep oscillatory dynamics, may be associated with biomarkers of brain clearance across the AD continuum. However, the available evidence remains preliminary, is predominantly cross-sectional, and relies largely on indirect measures of brain clearance. Larger longitudinal studies incorporating standardized sleep assessment and validated measures of cerebral clearance are required to clarify temporal relationships, establish causality, and determine whether sleep-targeted interventions influence brain clearance or disease progression. Summary of findings: Preliminary evidence suggests that preserved slow-wave sleep and sleep oscillatory activity are associated with more favorable biomarkers of brain clearance, whereas disrupted sleep architecture is associated with less favorable clearance-related measures. Full article

Background/Objectives: To describe the genetic resolution rate, molecular findings, and genotype–phenotype correlations of non-ABCA4 and non-BEST1 inherited macular dystrophies (IMDs) within an Irish inherited retinal disease (IRD) registry. Methods: Retrospective review of individuals with a clinical diagnosis of macular or cone dystrophy. Comprehensive phenotyping (dilated ocular biomicroscopy, multimodal retinal imaging, visual electrophysiology) and genetic testing (panel-based next-generation sequencing, single-gene testing, whole exome/genome sequencing, WES/WGS). Variants were interpreted using ACMG AMP criteria, and genotype-phenotype match was confirmed through multidisciplinary review. Results: 232 patients with macular/cone dystrophies were identified. ABCA4 and BEST1 accounted for most molecular diagnoses (47.4%). Removing ABCA4 and BEST1, 59.0% of IMDs were genetically unresolved, higher than the rate in general IRD cohorts. Deep phenotyping enabled diagnostic reclassification in 13/72 (18.1%), namely achromatopsia, congenital stationary night blindness, and oculocutaneous albinism. Further genetic testing resolved 35/72 (48.6%) of those unresolved on first-line testing, with PRPH2 being most prevalent (n = 12), followed by GUCY2D, CRB1, PROM1, and CRX. Characteristic phenotypic signatures—such as CRB1-associated retinal thickening and retinoschisis or PROM1-associated Stargardt-like changes—supported known genotype–phenotype correlations. Conclusions: Genetic resolution rates for rare IMDs remain lower than pan-retinal IRD phenotypes. Beyond ABCA4 and BEST1, IMDs exhibit substantial genetic and phenotypic heterogeneity (24 genotypes in this cohort), with low molecular diagnostic rates despite comprehensive sequencing approaches. Detailed multimodal phenotyping (i.e., structural, functional and extra-ocular) is essential to refine diagnosis, guide genetic testing and interpret candidate variants. Genetic testing is challenging when the retinal phenotype is advanced (i.e., atrophy) or lacks pathognomonic features. Meticulous phenotyping (functional, structural and systemic) and broader genomic strategies (e.g., WES/WGS) may further increase diagnostic yield, though gene panel content is constantly improving. Consistently improving molecular diagnostic rates will ensure equitable access to emerging gene-specific therapies. Full article

Background: Facial nerve regeneration across segmental defects remains challenging despite advances in nerve guidance conduits. Tissue engineering strategies that combine biomaterial scaffolds with bioactive and cellular components may enhance functional and structural nerve repair. This study investigated the regenerative efficacy of a cellulose-based nerve conduit augmented with Matrigel, mesenchymal stem cells (MSCs), and placental extract (PE) in a rat facial nerve gap model. Methods: A 2 mm defect was created at the main trunk of the facial nerve in adult Sprague–Dawley rats. Animals were divided into three groups: control group (Cellulose/Matrigel), group I (Cellulose/Matrigel/MSC), and group II (Cellulose/Matrigel/MSC/PE). Functional recovery was assessed at 2, 4, 6, and 8 weeks postoperatively using slow-motion vibrissa movement analysis, electrically stimulated facial nerve action potential measurements, and facial nerve blood flow by laser Doppler blood flow analysis. Morphological regeneration was evaluated using light microscopy and transmission electron microscopy. Western blotting using facial muscle was performed. Results: All groups exhibited time-dependent facial nerve regeneration. However, group II demonstrated significantly enhanced functional recovery, greater electrophysiological responses, increased nerve blood flow, and superior histological and ultrastructural regeneration compared with the other groups. These improvements were particularly prominent at 6 and 8 weeks postoperatively. Conclusions: The combination of mesenchymal stem cells and PE within a cellulose-based nerve conduit synergistically enhanced facial nerve regeneration. This tissue-engineered strategy may represent an effective approach for improving peripheral nerve repair. Full article

Background: The role of socioeconomic status (SES) in individual intertemporal decision-making has received widespread research attention. However, findings regarding its underlying psychological mechanisms remain inconclusive. This study investigates not only the association between SES and intertemporal decision-making but also the underlying cognitive neural mechanisms from both behavioral and electrophysiological perspectives. Methods: Individuals with high and low SES were recruited. In Experiment 1, a behavioral experiment used the Monetary Choice Questionnaire to measure delay discounting rates using the Kirby method and hierarchical Bayesian modeling, as well as choice consistency using the inverse temperature parameter of the softmax function, to examine differences in decision-making between the two groups. In Experiment 2, event-related potential techniques were employed to examine differences in dynamic neural activity during an intertemporal choice task between the high- and low-SES groups. Results: The behavioral results revealed that, in Experiment 1, the low-SES group exhibited a larger delay discounting rate than the high-SES group. The hierarchical Bayesian modeling further indicated that the low-SES group had lower choice consistency. Experiment 2 found that the low-SES group showed a significantly higher proportion of smaller-sooner (SS) choices than the high-SES group. Electroencephalographic results revealed that, compared with the high-SES group, the low-SES group exhibited larger P200 amplitudes but smaller N2 and P300 amplitudes. Within the high-SES group, the larger-later (LL) option elicited more negative N2 and larger P300 amplitudes than the SS option. Conversely, in the low-SES group, P300 amplitudes did not differ significantly between the SS and LL options during the later stage of intertemporal decision-making. Conclusions: The results showed that the low-SES group was more inclined toward immediate gains, made more random choices, displayed higher variability, relied more on intuitive heuristic strategies, and exhibited weaker cognitive control and reduced cognitive resource allocation during intertemporal decision-making. However, at the later stage, the absence of a significant difference between SS and LL options provided preliminary EEG evidence consistent with the possibility that individuals in the low-SES group did not completely disregard future outcomes. Full article

Spinal cord stimulation (SCS) is a widely used neuromodulatory therapy for chronic neuropathic pain, yet the cellular and molecular mechanisms underlying its clinical efficacy remain incompletely understood. This review synthesizes current literature on the neurophysiology of pain transmission and the mechanistic basis of major SCS paradigms (tonic, high-frequency, burst, and closed-loop stimulation), highlighting how each modality engages distinct dorsal horn circuits, glial and inflammatory pathways, as well as supraspinal networks involved in the affective dimension of pain. Particular attention is given to the evoked compound action potential (ECAP) as an emerging electrophysiological biomarker that enables real-time, feedback-guided stimulation and offers insight into the biophysical determinants of dorsal column activation. We also examine preclinical and clinical evidence linking SCS to modulation of central sensitization, neuroinflammatory signaling, and autonomic regulation, while identifying persistent gaps in mechanistic understanding. Finally, we discuss future directions, including AI-assisted, personalized SCS programming and expanding indications beyond classical neuropathic pain, underscoring the need for multimodal experimental approaches to more precisely define how SCS achieves analgesia. Full article

Under climate warming, bark beetle outbreaks increasingly threaten forest health. Hylurgops longipillus, a native bark beetle in Northeast China, causes patchy mortality in Pinus koraiensis plantations. We developed an integrated emergency control system based on host selection chemical ecology. Damage characterization revealed that adults concentrated on trees with 10–50% crown needle yellowing, and infestations expanded as discrete patches radiating from multiple epicenters. Electrophysiological and behavioral assays of host volatiles and some of their isomers yielded a highly effective attractant (69.4 adults per five-trap set over 5 d, 1.8× control) and a repellent reducing ethanol-baited trap catches by 83.3%. Emergency control techniques consisted of integrated management combining removal and safe disposal of infested trees, chemical stump sealing, push–pull trapping, and tree vigor enhancement. Three-year monitoring showed ~94% decline in trap catches, no subsequent outbreaks, and stable control. This attractant-centered, chemical ecology-based system can rapidly suppress H. longipillus outbreaks and achieve long-term management, providing a scientific basis and operational framework for similar localized bark beetle emergencies under climate warming. Full article

Background/Objectives: Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neuromodulatory approach with potential therapeutic value for cognitive impairment in Alzheimer’s disease (AD). Ferroptosis-related oxidative injury has been implicated in AD-associated neuronal dysfunction, but whether rTMS-induced functional improvement is accompanied by changes in ferroptosis-related oxidative injury remains unclear. This study evaluated the effects of high-frequency rTMS on cognitive function, hippocampal neuronal excitability, and ferroptosis-related oxidative injury in amyloid precursor protein/presenilin-1 (APP/PS1) mice, using Ferrostatin-1 (Fer-1) as a pharmacological comparator. Methods: Six-month-old female mice were used, including age-matched C57BL/6J controls and APP/PS1 mice assigned to the AD + Sham, AD + rTMS, and AD + Fer-1 groups (n = 6 per group). After 14 days of intervention, cognitive performance was assessed using behavioral tests. Whole-cell patch-clamp recordings were performed in hippocampal dentate gyrus granule neurons to evaluate neuronal excitability and voltage-gated sodium (Na⁺) and potassium (K⁺) channel properties. Biochemical assays and transmission electron microscopy were used to assess oxidative, iron-related, and mitochondrial changes, and mitochondrial ultrastructure was examined in an independent cohort (n = 3 per group) using transmission electron microscopy. Results: Compared with AD + Sham mice, high-frequency rTMS improved cognitive performance, increased evoked action potential firing, lowered the elevated action potential threshold, partially restored voltage-gated Na⁺ and K⁺ current amplitudes, and accelerated recovery of Na⁺ currents from inactivation. Fer-1 produced partially overlapping, but not identical, effects across behavioral, electrophysiological, biochemical, and ultrastructural outcomes. Both interventions increased hippocampal glutathione (GSH) levels, reduced malondialdehyde (MDA) and total iron levels, partially restored superoxide dismutase (SOD) activity, and improved mitochondrial ultrastructure and reduced the prevalence of mitochondrial profiles with small cross-sectional areas. Conclusions: High-frequency rTMS improved cognitive and hippocampal neuronal outcomes in female APP/PS1 mice. These improvements were accompanied by biochemical and mitochondrial changes compatible with attenuation of ferroptosis-related injury. However, the findings do not establish ferroptosis inhibition as either necessary or sufficient for the effects of rTMS. Full article

Atrial cardiomyopathy (ACM) is defined as any complex of structural, architectural, functional, electrophysiological, and molecular changes affecting the atria that may result in clinically significant health consequences. ACM can be caused by a variety of factors, including age-related changes, valvular or vascular disease, genetic diseases, congestive heart failure, metabolic diseases, cardiovascular disease (CVD) risk factors such as arterial hypertension (AH) or obesity, obstructive sleep apnea, and other infectious or noninfectious diseases predisposing to chronic inflammation. The diagnosis of ACM relies on several modalities, including electrocardiography, echocardiography, cardiac magnetic resonance imaging (MRI), computed tomography (CT), electroanatomical mapping (EAM), genetic studies, and biomarkers, which can detect and characterize structural, mechanical, and electrical atrial dysfunction. These changes often include structural atrial remodeling (fibrosis), abnormal structure of the atrial wall and its components, and contractile and electrical dysfunctions. When assessing aspects of ACM, structural changes in the atria such as left atrium (LA) size and fibrosis; LA architectural changes such as the expression of remodeling; changes in LA mechanics such as echocardiographic stress indices; changes in reservoir function and changes in contraction; biological factors determining changes in biomarkers; possible genetic predispositions and higher expression of certain genes encoding certain proteins; and arrhythmogenic factors associated with a higher risk of atrial fibrillation (AF) and stroke and a worse short- and long-term prognosis are very important. When considering the challenges of diagnosing ACM, it should be noted that without standardized diagnostics, most ACM diagnostic situations remain primarily research tools rather than practical clinical diagnostic methods. This review critically evaluates the evidence and translational gaps in the diagnosis of ACM, synthesizing the emerging role of advanced diagnostics and their clinical and prognostic implications as a key future tool for individual risk stratification. Full article

Intraoperative neurophysiological monitoring (IONM) is widely used during brainstem surgery to reduce the risk of neurological injury, although its prognostic value in adult brainstem glioma (BSG) surgery remains unclear. We retrospectively analyzed 22 consecutive adults who underwent surgery for BSGs with multimodal IONM between 2010 and 2023. Monitoring included somatosensory evoked potentials (SSEPs), motor evoked potentials (MEPs), brainstem auditory evoked potentials (BAEPs), corticobulbar MEPs (CoMEPs), and cranial nerves electromyography. The primary endpoint was the association between intraoperative neurophysiological changes and postoperative neurological functional status at hospital discharge, assessed with the modified McCormick Scale (mMCS). Secondary endpoints included postoperative complications and length of hospital stay. SSEP warning criteria were met in 10 patients (45.5%), while 10 patients (45.5%) experienced a ≥50% reduction in MEP amplitude in at least one monitored muscle. Despite these findings, neither SSEP nor MEP amplitude changes were significantly associated with postoperative neurological status. Transcranial MEP stimulation thresholds increased significantly during surgery (p = 0.007), and threshold elevation was associated with postoperative complications (Kendall’s τ = 0.498, p = 0.007). BAEP recordings remained stable throughout all procedures. Conventional amplitude-based IONM changes were not associated with early neurological outcome after adult BSG resection. In contrast, increases in MEP stimulation threshold may represent a sensitive indicator of postoperative complications. Further prospective studies are warranted. Full article

Background: To compare the clinical and ultrasonographic effects of pulsed therapeutic ultrasound (US) and pulsed shortwave diathermy (SWD) in patients with mild-to-moderate carpal tunnel syndrome (CTS). Methods: In this randomized controlled trial, 40 patients with electrophysiologically confirmed mild-to-moderate CTS were randomly allocated into two groups. Both groups received wrist splinting and tendon–nerve gliding exercises. The US group received 15 sessions of pulsed ultrasound therapy (3 MHz, 0.8 W/cm²), whereas the SWD group received 15 sessions of pulsed shortwave diathermy (80 Hz, 19.2 W). Outcomes were assessed at baseline, 1 month, and 3 months using ultrasonographic median nerve cross-sectional area (MNCSA) (primary outcome), Boston Carpal Tunnel Questionnaire (BCTQ), Visual Analog Scale (VAS) for pain, Douleur Neuropathique 4 (DN4), and handgrip strength. Results: Baseline demographic characteristics, including age (mean ± SD) and sex distribution, were comparable between groups (p > 0.05), although BCTQ Functional Status and Total scores differed significantly at baseline. Repeated-measures analyses demonstrated significant time effects for MNCSA and all secondary clinical outcomes, including BCTQ scores, VAS pain, DN4 scores, and grip strength (all p < 0.001; partial η² range: 0.51–0.75), indicating moderate-to-large effect sizes. Both the US and SWD groups showed sustained improvements at the 1- and 3-month follow-ups, with no significant differences between treatment modalities (all group × time interaction p > 0.05). Conclusions: In patients with mild-to-moderate CTS, both US and SWD administered alongside splinting and exercise were associated with significant clinical and ultrasonographic improvements over 3 months. No significant difference was observed between the two modalities. Both treatments may be considered adjunctive options within conservative management, although further controlled studies are needed to clarify modality-specific effects. Full article

Microelectrode array (MEA) technology is widely employed in electrophysiological research and, in recent years, has increasingly been applied in the screening of neurotoxicity. In this study, we investigated the neurotoxic effects of different concentrations of Ni²⁺ by analyzing its influence on the mean firing and bursting rates of spontaneous activity, as well as the frequency of electrical-stimulation-evoked activity in the neocortical region in rat brain slices through MEA. Integrating our team’s prior findings on Ni²⁺’s influence on the electrical stimulation threshold of evoked activity, we compared the application effectiveness of the four MEA-based neurotoxicity screening methods in Ni²⁺ neurotoxicity research. Our results demonstrate that all of these methods can effectively assess the neurotoxic effects of Ni²⁺; however, they differ in certain aspects, such as the applicable neuronal networks and data-processing approaches. We also found that Ni²⁺ influences spontaneous and electrical-stimulation-evoked activity in the neocortical region in rat brain slices via distinct mechanisms. Full article

Age-related sarcopenia involves structural and functional neuromuscular changes. Electrophysiological measures from surface electromyography (sEMG) capture activation dynamics, spectral fatigue indices and motor unit properties that may constitute objective signatures of sarcopenia. The objective of this work is to systematically review sEMG features, fatigability metrics and AI-based classification/regression approaches reported for sarcopenia assessment between 2019 and 2026. PRISMA guidelines were followed, and IEEE Xplore, PubMed and Scopus were searched for open access human studies. Extracted information comprised sample characteristics, muscles and tasks, signal acquisition and preprocessing, extracted time/frequency/time–frequency and motor unit features, fatigue metrics, machine learning pipelines, validation schemes and dataset accessibility. Studies were classified into activation, fatigue, ML, and neural control groups; risk of bias was assessed. A total of 12 studies fulfilled the inclusion criteria. Recurrent electrophysiological signatures included reduced distal activation with compensatory proximal recruitment and higher antagonist co-activation; diminished MF/IMDF fatigue slopes indicative of Type II fiber loss and altered motor unit recruitment; motor unit analyses revealed decreased discharge rates and larger MUAP amplitudes. AI-based models combining multidomain features (time, spectral, CWT/EMD, and motor unit metrics) yielded reasonable screening performance (AUC/accuracy 0.73–0.89) when using robust feature selection and explainability tools. Heterogeneity in acquisition, normalization, small cohorts and sparse data sharing limited comparability and external validity. The findings indicate that sEMG-derived electrophysiological signatures are promising for sarcopenia detection and monitoring. To translate signatures into reliable clinical tools, standardized protocols, larger shared datasets, multimodal features, including motor unit metrics, and rigorous external validation of AI models are required. Full article