Evidence has shown that high-intensity laser therapy (HILT) may be beneficial for recovery after peripheral nerve injury (PNI). However, the optimized doses and effective mechanisms remain unclear. The present study sought to explore the effects of various doses of HILT on the recovery of nerve function in sciatic nerve injury (SNI) rats. The potential mechanism of action of HILT alleviating PNI was also assessed. Behavioral testing, polymerase chain reaction, immunoblotting, and immunofluorescence analyses were applied to explore whether HILT promotes the repair of injured nerves and its underlying mechanisms. SNI induces mechanical nociceptive hypersensitivity, disrupts sciatic nerve structure and function, causes gastrocnemius muscle atrophy, and increases oxidative stress and expression levels of inflammatory factors. HILT effectively ameliorated these SNI-induced alterations. Notably, the Bone Morphogenetic Protein 4 (BMP4)-SMAD Family Member 9 (Smad9) pathway mediates the therapeutic effects of HILT on SNI repair. These findings show for the first time that HILT stimulates the BMP4-Smad9 signaling pathway by increasing Smad9 expression to regulate inflammation and oxidative stress, which ultimately ameliorates SNI.

Flexible sensors have emerged as critical interfaces for information exchange between soft biological tissues and machines. Here, we present a dual-mode stretchable sensor system capable of synchronous strain and electromyography (EMG) signal detection, integrated with wireless WIFI transmission for real-time joint movement monitoring. The system consists of two key components: (1) A multi-channel gel electrode array for high-fidelity EMG signal acquisition from target muscle groups, and (2) a novel capacitive strain sensor made of stretchable micro-cracked gold film based on Styrene Ethylene Butylene Styrene (SEBS) that exhibits exceptional performance, including >80% stretchability, >4000-cycle durability, and fast response time (<100 ms). The strain sensor demonstrates position-independent measurement accuracy, enabling robust joint angle detection regardless of placement variations. Through synchronized mechanical deformation and electrophysiological monitoring, this platform provides comprehensive movement quantification, with data visualization interfaces compatible with mobile and desktop applications. The proposed technology establishes a generalizable framework for multimodal biosensing in human motion analysis, robotics, and human-machine interaction systems.

PurposeThis study aims to explore the characteristics of gait initiation in stroke patients with hemiplegia across various phases by proposing a refined gait initiation phase segmentation method tailored to this population. Additionally, the study investigates the correlation between gait initiation parameters and clinical assessment scales to evaluate their clinical value in development of functional assessment and rehabilitation strategies.MethodsA total of 34 patients with hemiparetic stroke and 34 age- and sex-matched healthy controls participated in the study. All participants performed gait initiation with each limb three times. Ground reaction force, center of pressure (COP), and kinematic data were recorded using a gait analysis system. The gait initiation process was divided into four phases based on COP trajectory and movement features. Step length, step width, initial paretic limb loading, duration and COP displacement across various phases, and the peak (Fxmax) and impulse (Impulsex) of the anteroposterior ground reaction force for each limb were calculated. Stroke patients also underwent clinical assessments.ResultsStroke patients exhibited increased step width and total initiation duration (p < 0.05); reduced step length, single-support time of paretic limb, COP displacement in anteroposterior (DCOPX) and mediolateral (DCOPZ) directions during both the first phase (P1) and single-support phase (P3), paretic limb loading, Fxmax and Impulsex (p < 0.05). Compared to non-paretic limb initiation, paretic limb initiation showed shorter duration and reduced DCOPZ of the second phase (P2), as well as longer single-support time and total initiation duration (p < 0.05). In addition, the paretic limb generated lower Fxmax and Impulsex than the non-paretic limb (p < 0.05). DCOPX, Fxmax, and Impulsex were significantly correlated with clinical assessments to varying degrees (p < 0.05). Overall, greater COP displacement, Fxmax, and Impulsex were associated with better clinical function, particularly in the paretic limb.ConclusionRefined phase segmentation provided additional insight: impaired anticipatory postural adjustment capacity during gait initiation after stroke was reflected by prolonged P2 and reduced COP displacement in P1. Biomechanical parameters of gait initiation may serve as objective indicators of motor function and inform rehabilitation strategies in stroke patients.

Purpose: To investigate the analgesic effects and mechanisms of BMSCs-IL-10 + administered via intrathecal injection in CCD rats. Patients and methods: After CCD surgery, rats were administered intrathecal injections of PBS, BMSCs, BMSCs-IL-10 + , BMSCs-IL-10 + +Anti-IL-10, LV-IRF-8, and LV-IRF-8+IL-10. Pain was assessed by measuring the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL). Glial cell activation and M2 microglial polarization were evaluated by immunofluorescence staining of Iba-1, GFAP, and Arg-1, and by WB for Iba-1 and Arg-1. Spinal cord inflammation was assessed by PCR analysis of TGF-β, TNF-α, and IL-1β expression. Results: Compared with the CCD+PBS group, intrathecal injection of both BMSCs and BMSCs-IL-10 + significantly alleviated CCD-induced mechanical and thermal pain. However, the analgesic effect of the BMSCs group markedly decreased after 4 days, while the BMSCs-IL-10 + group lasted at least 14 days. The BMSCs-IL-10 + group significantly upregulated the expression of TGF-β while downregulating TNF-α and IL-1β, inhibiting glial cell activation and promoting M2 microglia polarization. These effects were superior to the BMSCs group and could be abolished by anti-IL-10 antibody. IRF-8 overexpression exacerbated pain and inflammation in CCD rats, but the combined application of IL-10 protein reversed this impact. Conclusion: IL-10 is a key cytokine mediating the analgesic effects of BMSCs. Transplantation of BMSCs-IL-10 + cells reduces glial activation, alleviates neuroinflammation, and relieves neuropathic pain by enhancing IL-10 expression and suppressing IRF-8.

OBJECTIVES:To investigate the electroencephalography (EEG) features in patients with spinal cord injury (SCI) experiencing neuropathic pain (NP) by analyzing the γ (30-80 Hz) frequency band. METHODS:Participants were divided into three groups: the PWP group (SCI patients with pain), the PNP group (SCI patients without pain) and AB group (able-bodied). Then we recorded and preprocessed the EEG data and calculated the power spectral density (PSD). Then, the amplitude of γ band oscillation (GBO) and the strength of brain network connections among the different groups were compared. RESULTS:In the PWP group, early GBO was observed in the FPZ channel in the resting state, and the main effect was concentrated in the 55-60 Hz range. In the high-frequency γ band (55-80 Hz) of the FPZ channel, the PWP group showed a higher GBO than the other groups. Moreover, during motor imagination (MI), the PWP group showed significantly stronger functional connectivity than the AB group, but significantly weaker than the PNP group. CONCLUSION:The GBO related to NP is highly consistent with the frequency domain manifestations of chronic pain. NP causes persistent abnormal increases in the γ-band PSD in multiple brain regions and the GBO changes in the prefrontal cortex have the strongest correlation with NP symptoms.

BACKGROUND:Cardioembolic stroke is the most common cause of ischemic stroke, and patients frequently have motor dysfunction as well as psychological disorders. Both physical and psychological causes can have an impact on a patient's motor function. OBJECTIVES:In this study, we used the fear-avoidance model to examine the impact of patients' illness perception and kinesiophobia (excessive fear of exercise) on their motor function. METHODS:Between June 2021 and February 2022, we conducted a cross-sectional study of 319 participants diagnosed with cardioembolic stroke in the selected hospitals. Correlation analyses and mediation effects tests were used to analyze the relationship between patients' illness perception, kinesiophobia, and motor function. RESULTS:The total motor function score of the patients was (21.39 ± 29.30), the total kinesiophobia score was (48.51 ± 8.33), and the total illness perception score was (53.37 ± 16.82). There was a negative correlation between illness perception and motor function (r = -0.734, P < 0.001), a negative correlation between kinesiophobia and motor function (r = -0.522, P < 0.001), and a positive correlation between illness perception and kinesiophobia (r = 0.508, P < 0.001); kinesiophobia played a mediating role between illness perception and motor function (β = -0.63, P < 0.001). CONCLUSIONS:The findings revealed that individuals with cardioembolic strokes had poor motor function, as well as negative illness perception and kinesiophobia. Negative illness perception had a direct impact on patients' motor function as well as an indirect effect via kinesiophobia. The fear-avoidance model contributes to understanding the process of reduced motor function in cardioembolic stroke patients.

Activation of transient receptor potential vanilloid 4 (TRPV4) in astrocytes is crucial in the occurrence of neuropathic pain (NP). Osthole, a natural herbal component with anti-inflammatory and analgesic effects, can reduce intracellular calcium levels; however, its underlying mechanism remains incompletely understood. Protein kinase C-delta (PKCδ), a serine/threonine protein kinase, regulates calcium levels within the blood-brain barrier (BBB) through its interaction with TRPV4. Astrocytes are integral components of the BBB and play an important role in neuroinflammatory responses. Here, we investigated whether PKCδ is involved in the pharmacological inhibition of NP by osthole. Chronic compression of the dorsal root ganglion (CCD) in rats was used to construct NP animal models. Astrocytes were stimulated using lipopolysaccharide (LPS) to induce NP in vitro. Following CCD surgery, we found that PKCδ protein and its phosphorylated form were upregulated and astrocytes were activated. LPS upregulated intracellular calcium concentration and activated astrocytes, while the PKCδ inhibitors, siRNA of PKCδ, or osthole blocked this effect. In addition, PKCδ-induced astrocyte activation appears to be mediated through its interaction with TRPV4. Overexpression of PKCδ in astrocytes leads to upregulation of TRPV4 expression, increased intracellular calcium levels, and enhanced inflammatory responses-effects that can be reversed by TRPV4 inhibition. There was a positive feedback activation mechanism between PKCδ and TRPV4 during the development of NP. Finally, CCD surgery-induced NP and the associated inflammatory response were significantly alleviated by PKCδ inhibitors, TRPV4 inhibitors, and osthole. Collectively, these findings suggest that astrocyte activation in NP involves the upregulation of pathophysiological processes along the PKCδ/TRPV4/calcium signaling axis. Osthole exerts its potent analgesic effect by effectively inhibiting this pathway.

Aerobic exercise has been recommended as a non-pharmacological treatment for asthma. Previous studies have shown that circMETTL9 regulates cellular inflammation, apoptosis, and oxidative stress levels. However, whether aerobic exercise can modulate the expression of circMETTL9 to alleviate chronic allergic airway inflammation remains unclear. In this study, we established a mouse model of chronic allergic lung inflammation with aerobic exercise intervention to assess its effects. Our results demonstrate that aerobic exercise exerts anti-inflammatory, anti-proliferative, anti-apoptotic, and anti-oxidative stress effects by regulating the circMETTL9/EIF4A3/IGFBP3 axis. Mechanistically, we found that circMETTL9 binding to EIF4A3 does not affect EIF4A3 expression. However, EIF4A3 positively regulates both the protein and mRNA levels of IGFBP3. Specifically, circMETTL9 binds to EIF4A3 to inhibit IGFBP3 transcription and translation. This study identifies a novel potential target and research direction for treating chronic allergic lung inflammation.

Neuroinflammation, which is characterized by glial cell activation and the release of inflammatory factors, is critical for the progression of neuropathic pain. The excessive accumulation of reactive oxygen species (ROS) is related to increased neuroinflammation. Runt-related transcription factor 2 (RUNX2), a regulator of various biological processes, has been reported to regulate the inflammatory response. However, whether RUNX2 participates in neuroinflammation by affecting ROS production remains unclear. In the present study, we investigated the expression pattern of RUNX2 in the context of neuropathic pain induced by chronic compression of the dorsal root ganglion (CCD) and the role of RUNX2 in the development of neuropathic pain. During neuropathic pain, RUNX2 expression was significantly increased in the spinal cord and was mainly localized to astrocytes. Knockdown of RUNX2 attenuated the astrocyte activation and the production of ROS and inflammatory factors induced by CCD surgery, thus relieving neuropathic pain. C-C motif chemokine ligand 2 (CCL2) has been reported to increase ROS generation, thus promoting the inflammatory response. We discovered that RUNX2 transcriptionally activated the expression of Ccl2 by binding to its promoter and that RUNX2 knockdown may inhibit this pathway, thus reducing CCD-induced neuropathic pain. Our study provides the first evidence that RUNX2 contributes to neuropathic pain via the transcriptional activation of Ccl2. A better understanding of the function of RUNX2 in neuropathic pain may be helpful for developing new therapeutic strategies.

Neuropathic pain (NP), a chronic pain condition, is the result of abnormalities in both central and peripheral pain conduction pathways. Here, we investigated the underlying mechanisms associated with this effect. We found that following chronic constriction injury (CCI) surgery, there was an increase of mTOR in astrocytes and an activation of astrocytes within the spinal cord. Pharmacological inhibition of mTOR reversed CCI-induced hyperalgesia and neuroinflammation. Moreover, knockdown of astrocytic mTOR rescued the downregulation of spinal glutamate metabolism-related protein expression, underscoring the pivotal role of mTOR in modulating this pathway. Intriguingly, we observed that overexpression of mTOR, achieved via intrathecal administration of TSC2-shRNA, led to an upregulation of RIP3. Notably, pharmacological inhibition of RIP3, while ineffective in modulating mTOR activation, effectively eliminated the mTOR-induced astrocyte activation. Mechanistically, we found that mTOR controlled the expression of RIP3 in astrocytes through ITCH-mediated ubiquitination and an autophagy-dependent degradation. Taken together, our results reveal an unanticipated link between mTOR and RIP3 in promoting astrocyte activation, providing new avenues of investigation directed toward the management and treatment of NP.

Recent studies have highlighted the critical role of lipid metabolism in macrophages concerning lung inflammation. However, it remains unclear whether lipid metabolism is involved in macrophage extracellular traps (METs). We analyzed the GSE40885 dataset from the GEO database using weighted correlation network analysis (WGCNA) and further selection using the least absolute shrinkage and selection operator (LASSO) regression. We identified ABCA1, SLC44A2, and C3 as key genes jointly involved in lipid metabolism and METs. Additionally, immune infiltration analysis was performed using the Xcell and CIBERSORT algorithms, while single-cell transcriptome analysis was utilized using data from the Tabula Muris database. The expression of key genes was validated in external datasets (GSE42606, GSE27066, GSE137268, and GSE256534). Notably, our results indicated that ABCA1 expression was elevated in patients experiencing acute asthma exacerbations, which aligned with its expression trend in lipopolysaccharide (LPS)-induced macrophages. However, ABCA1 expression was reduced in cases of chronic and severe asthma. Results from immunofluorescence (IF), SYTOX Green staining, and Western blot analyses suggested that ABCA1 may play a role in the formation of METs both in vivo and in vitro. In conclusion, this study indicates that ABCA1 may be involved in METs. ABCA1 may represent a promising therapeutic target for asthma.

Emerging evidence suggests that aerobic exercise exerts beneficial effects on asthma. Previous studies have demonstrated that cell communication can drive the formation of macrophage extracellular traps (METs). However, the potential of aerobic exercise to mediate communication between airway epithelial cells and macrophages, thereby influencing MET formation, remains unexplored. Our data reveal that the upregulation of circular RNA METTL9 (circMETTL9), derived from methyltransferase-like protein 9 (METTL9) in airway epithelial cells, promotes the formation of METs. Notably, aerobic exercise was found to downregulate the expression of circMETTL9, thereby facilitating communication between airway epithelial cells and macrophages and inhibiting METs formation. Mechanistically, circMETTL9 and insulin-like growth factor binding protein 3 (IGFBP3) compete for binding to the DEXDc domain of eukaryotic translation initiation factor 4A3 (EIF4A3), which regulates METs via the C-X-C motif chemokine ligand 12(CXCL12) -C-X-C chemokine receptor type 4(CXCR4) signaling axis. This study provides robust molecular evidence supporting aerobic exercise as a foundational pulmonary rehabilitation strategy for lung protection in asthma. Targeting circMETTL9, mimicking this exercise-mediated pathway, represents a promising therapeutic approach. These insights offer a direct mechanistic rationale for refining exercise-based rehabilitation protocols and developing novel targeted therapies.

Artificial ligaments play a crucial role in replacing injured natural ligaments and facilitating rehabilitation. However, existing artificial ligaments lack real-time strain monitoring capability, which limits personalized rehabilitation guidance. Here, we develop a highly biomimetic and intelligent electronic hydrogel ligament (IEHL) based on polyvinyl alcohol/sodium alginate through a universal directional anneal-casting (DAC) strategy. This innovative approach creates aligned microstructures that overcome conventional hydrogels' limitations of poor structural integrity and inadequate mechanical properties. The IEHL exhibits integrated bionics of microstructure, mechanical parameters and water content closely matching natural ligaments. The efficacy of the IEHL in stabilizing knee joint and monitoring movements is validated through in vivo models, and a wireless monitoring system is developed to detect and analyze ligament strain characteristics in real-time. This IEHL provides a superior intraoperative replacement strategy and quantitative guidance for post-surgical rehabilitation.

Mesenchymal stem cells (MSCs) are multipotent stem cells characterized by their robust proliferative capacity, homing ability, differentiation potential, and low immunogenicity in vitro. MSCs can be isolated from a variety of tissues, primarily including but not limited to bone marrow, adipose tissue, umbilical cord, placenta, and dental pulp. Although there have been a large number of clinical studies on the treatment of diseases by MSCs and MSCs-derived exosomes (MSCs-EXO), the large-scale clinical application of MSCs and MSCs-EXO have been limited due to the heterogeneity of the results among various studies. This review provides a detailed description of the classification and characterization of MSCs and MSCs-EXO, as well as their extraction methods. Furthermore, this review elaborates on three key mechanisms of MSCs and MSCs-EXO: paracrine mechanisms, immunomodulatory and anti-inflammatory effects, as well as their promotion of tissue regeneration. This review also examines the role of MSCs and MSCs-EXO in cardiovascular diseases, neurological disorders, autoimmune diseases, musculoskeletal disorders, and other systemic diseases over the past five years, while discussing the challenges and difficulties associated with their clinical application. Finally, we systematically summarized and analyzed the potential causes of the various heterogeneous results currently observed. Additionally, we provided an in-depth discussion on the challenges and opportunities associated with the clinical translation of disease treatment approaches based on MSCs, MSCs-EXO, and engineered exosomes.

Background Middle-aged and older adults with physical disabilities exhibit more common and severe depressive symptoms than those without physical disabilities. Such symptoms can greatly affect the physical and mental health and life expectancy of middle-aged and older persons with disabilities. Method This study selected 2015 and 2018 data from the China Longitudinal Study of Health and Retirement. After analyzing the effect of age on depression, we used whether middle-aged and older adults with physical disabilities were depressed as the dependent variable and included a total of 24 predictor variables, including demographic factors, health behaviors, physical functioning and socialization, as independent variables. The data were randomly divided into training and validation sets on a 7:3 basis. LASSO regression analysis combined with binary logistic regression analysis was performed in the training set to screen the predictor variables of the model. Construct models in the training set and perform model evaluation, model visualization and internal validation. Perform external validation of the model in the validation set. Result A total of 1052 middle-aged and elderly persons with physical disabilities were included in this study, and the prevalence of depression in the elderly group > middle-aged group. Restricted triple spline indicated that age had different effects on depression in the middle-aged and elderly groups. LASSO regression analysis combined with binary logistic regression screened out Gender, Location of Residential Address, Shortsightedness, Hearing, Any possible helper in the future, Alcoholic in the Past Year, Difficulty with Using the Toilet, Difficulty with Preparing Hot Meals, and Unable to work due to disability constructed the Chinese Depression Prediction Model for Middle-aged and Older People with Physical Disabilities. The nomogram shows that living in a rural area, lack of assistance, difficulties with activities of daily living, alcohol abuse, visual and hearing impairments, unemployment and being female are risk factors for depression in middle-aged and older persons with physical disabilities. The area under the ROC curve for the model, internal validation and external validation were all greater than 0.70, the mean absolute error was less than 0.02, and the recall and precision were both greater than 0.65, indicating that the model performs well in terms of discriminability, accuracy and generalisation. The DCA curve and net gain curve of the model indicate that the model has high gain in predicting depression. Conclusion In this study, we showed that being female, living in rural areas, having poor vision and/or hearing, lack of assistance from others, drinking alcohol, having difficulty using the restroom and preparing food, and being unable to work due to a disability were risk factors for depression among middle-aged and older adults with physical disabilities. We developed a depression prediction model to assess the likelihood of depression in Chinese middle-aged and older adults with physical disabilities based on the above risk factors, so that early identification, intervention, and treatment can be provided to middle-aged and older adults with physical disabilities who are at high risk of developing depression.

ObjectivesTo identify potential treatment targets for spinal cord injury (SCI)-related neuropathic pain (NP) by analysing the differences in electroencephalogram (EEG) and brain network connections among SCI patients with NP or numbness.Participants and methodsThe EEG signals during rest, as well as left- and right-hand and feet motor imagination (MI), were recorded. The power spectral density (PSD) of the θ (4–8 Hz), α (8–12 Hz), and β (13–30 Hz) bands was calculated by applying Continuous Wavelet Transform (CWT) and Modified S-transform (MST) to the data. We used 21 electrodes as network nodes and performed statistical measurements of the phase synchronisation between two brain regions using a phase-locking value, which captures nonlinear phase synchronisation.ResultsThe specificity of the MST algorithm was higher than that of the CWT. Widespread non-lateralised event-related synchronization was observed in both groups during the left- and right-hand MI. The PWP (patients with pain) group had lower θ and α bands PSD values in multiple channels of regions including the frontal, premotor, motor, and temporal regions compared with the PWN (patients with numbness) group (all p < 0.05), but higher β band PSD values in multiple channels of regions including the frontal, premotor, motor, and parietal region compared with the PWN group (all p < 0.05). During left-hand and feet MI, in the lower frequency bands (θ and α bands), the brain network connections of the PWP group were significantly weaker than the PWN group except for the frontal region. Conversely, in the higher frequency bands (β band), the brain network connections of the PWP group were significantly stronger in all regions than the PWN group.ConclusionThe differences in the power of EEG and network connectivity in the frontal, premotor, motor, and temporal regions are potential biological and functional characteristics that can be used to distinguish NP from numbness. The differences in brain network connections between the two groups suggest that the distinct mechanisms for pain and numbness.

Intervertebral disc degeneration (IVDD) is one of the most prevalent causes of chronic low back pain. The role of m6A methylation modification in disc degeneration (IVDD) remains unclear. We investigated immune-related m6A methylation regulators as IVDD biomarkers through comprehensive analysis and experimental validation of m6A methylation regulators in disc degeneration. The training dataset was downloaded from the GEO database and analysed for differentially expressed m6A methylation regulators and immunological features, the differentially regulators were subsequently validated by a rat IVDD model and RT-qPCR. Further screening of key m6A methylation regulators based on machine learning and LASSO regression analysis. Thereafter, a predictive model based on key m6A methylation regulators was constructed for training sets, which was validated by validation set. IVDD patients were then clustered based on the expression of key m6A regulators, and the expression of key m6A regulators and immune infiltrates between clusters was investigated to determine immune markers in IVDD. Finally, we investigated the potential role of the immune marker in IVDD through enrichment analysis, protein-to-protein network analysis, and molecular prediction. By analysising of the training set, we revealed significant differences in gene expression of five methylation regulators including RBM15, YTHDC1, YTHDF3, HNRNPA2B1 and ALKBH5, while finding characteristic immune infiltration of differentially expressed genes, the result was validated by PCR. We then screen the differential m6A regulators in the training set and identified RBM15 and YTHDC1 as key m6A regulators. We then used RBM15 and YTHDC1 to construct a predictive model for IVDD and successfully validated it in the training set. Next, we clustered IVDD patients based on the expression of RBM15 and YTHDC1 and explored the immune infiltration characteristics between clusters as well as the expression of RBM15 and YTHDC1 in the clusters. YTHDC1 was finally identified as an immune biomarker for IVDD. We finally found that YTHDC1 may influence the immune microenvironment of IVDD through ABL1 and TXK. In summary, our results suggest that YTHDC1 is a potential biomarker for the development of IVDD and may provide new insights for the precise prevention and treatment of IVDD.

ObjectiveThe objective of this study was to analyze the changes in connectivity between motor imagery (MI) and motor execution (ME) in the premotor area (PMA) and primary motor cortex (MA) of the brain, aiming to explore suitable forms of treatment and potential therapeutic targets.MethodsTwenty-three inpatients with stroke were selected, and 21 right-handed healthy individuals were recruited. EEG signal during hand MI and ME (synergy and isolated movements) was recorded. Correlations between functional brain areas during MI and ME were compared.ResultsPMA and MA were significantly and positively correlated during hand MI in all participants. The power spectral density (PSD) values of PMA EEG signals were greater than those of MA during MI and ME in both groups. The functional connectivity correlation was higher in the stroke group than in healthy people during MI, especially during left-handed MI. During ME, functional connectivity correlation in the brain was more enhanced during synergy movements than during isolated movements. The regions with abnormal functional connectivity were in the 18th lead of the left PMA area.ConclusionLeft-handed MI may be crucial in MI therapy, and the 18th lead may serve as a target for non-invasive neuromodulation to promote further recovery of limb function in patients with stroke. This may provide support for the EEG theory of neuromodulation therapy for hemiplegic patients.

Background The Pain Relief Motivation Scale (PRMS) was administered to chronic pain sufferers and predicts their psychological well-being. However, the Chinese version of the PRMS has not undergone psychometric validation. Objectives The PRMS will be psychometrically validated in patients with neuropathic pain-induced chronic pain from mainland China. Methods This cross-sectional study involved 340 patients with neuropathic chronic pain from China. The measurability of the Chinese version of the PRMS was determined by the critical ratio between items, and reliability was confirmed by Cronbach's alpha coefficient. The study also examined the validity of the construction and criterion validity of the Chinese PRMS. Results The Chinese version of the PRMS had critical ratio (CR) values ranging from 4.044 to 15.977 (p < 0.05). The Cronbach's alpha coefficient for the scale was 0.821, and the Cronbach's alpha coefficients for the subscales ranged from 0.663 to 0.961. Exploratory Factor Analysis (EFA) showed that five variables accounted for 77.73% of the total variance. The results of the Confirmatory Factor Analysis (CFA) supported the framework for the assessment of the 21-item PRMS. The Chinese version of the PRMS was positively correlated with the General Self-Efficacy Scale in the correlation validity analyses (r = 0.458, p < .001). Conclusion The Chinese version of the PRMS has powerful validity and reliability and can be used to assess the level of the motivation for pain alleviation in people with pain, serving as a reference for the development of intervention programs for healthcare providers.