MAIN PROBLEM AND METHODS:This review aims to summarize the role of fat mass and obesity-associated protein (FTO) in neurological disorders and neuropathic pain (NP). RESULTS:Key findings suggest that in neurological disorders such as Alzheimer's disease, Parkinson's disease, and depression, FTO-regulated m6A modification plays a critical role in the hippocampus and striatum. FTO-mediated m6A modification is involved in the pathological processes of NP. These findings suggest that FTO may serve as a potential therapeutic target for neurological disorders and NP. Common mechanisms may include the regulation of downstream mTOR and BDNF/TrkB signaling pathways, as well as modulation of neuronal excitability and synaptic plasticity. However, research on the relationship between exercise and m6A modification remains in its early stages. Emerging evidence suggests that exercise reduces FTO expression and increases m6A levels in the hippocampus and hypothalamus, indicating that exercise may serve as an effective intervention for modulating epigenetic modifications in the central nervous system. CONCLUSIONS:This implies that exercise may serve as an effective intervention for modulating epigenetic modifications, potentially by downregulating the demethylase FTO, regulating m6A modification, enhancing synaptic plasticity, modulating neuronal excitability, and providing neuroprotection, thereby contributing to disease mitigation. We hypothesize that exercise may regulate neurological disorders and NP through FTO-mediated m6A modification, with FTO potentially serving as a biomarker.

The pathogenesis of neuropathic pain is complex, and effective treatment methods are lacking in clinical practice. Recent studies have shown that glucose metabolism reprogramming may be involved in the process of neuropathic pain, but its role and molecular regulatory mechanisms in neuropathic pain are still unclear. In this study, a rat model of chronic constriction injury of the sciatic nerve (CCI) was established, and the pain threshold was evaluated through behavioural analysis. Morphological staining, transmission electron microscopy, transcriptome sequencing, Western blotting, immunofluorescence staining, ELISA, and the whole-cell patch clamp technique were used to systematically observe neuropathological changes, identify differentially expressed genes and associated pathways, and measure the expression levels of glycolysis-related indicators and the key regulatory factor fibroblast growth factor 4 (FGF4). The results showed that the pain threshold of rats decreased and that the structure of sciatic nerve tissue was damaged after CCI. Transcriptome sequencing of the sciatic nerve showed a significant increase in the expression levels of glycolysis-related indicators. Subsequent experiments confirmed that FGF4 expression was downregulated in the sciatic nerve and spinal dorsal horn after CCI, whereas the expression of hypoxia-inducible factor-1α (HIF-1α) and its key downstream glycolytic enzymes was upregulated, accompanied by increased levels of lactic acid and proinflammatory cytokines and decreased ATP levels. The spinal dorsal horn exhibited both synaptic structural abnormalities and neuronal hyperexcitability. Inhibiting HIF-1α alleviated pain and suppressed glycolysis, whereas the overexpression of FGF4 specifically reversed the increase in HIF-1α expression, inhibited neuronal glycolysis, and reduced neuroinflammation and central sensitization, ultimately effectively relieving pain. This study reveals the core role of the FGF4/HIF-1α-mediated regulation of neuronal glycolysis in neuropathic pain, providing a new theoretical basis and experimental evidence for a deeper understanding of the metabolic mechanism of neuropathic pain and the development of targeted treatment strategies.

BACKGROUNDS:Associations between adverse childhood experiences (ACEs) and catastrophic health expenditures (CHEs) among middle-aged or older Chinese individuals remain inadequately documented. In addition, the role of chronic diseases is not entirely clear. This study used data from the China Health and Retirement Longitudinal Study (CHARLS) to investigate the association of ACEs with hospital visits and medical expenditures and the mediating effect of chronic diseases. METHODS:Data were collected from CHARLS in 2014 and 2015 (N = 11,072). Zero-inflated negative binomial regression was used to assess associations of the ACEs with the number of outpatient visits and inpatient hospital days. Logistic regression was used to assess associations between the ACEs and CHEs. The influence of chronic diseases was examined through mediation analysis. RESULTS:The prevalence of each ACE indicator ranges from 0.27% (incarcerated household member) to 31.5% (emotional neglect). Our analysis revealed a significant dose-response relationship between cumulative ACE score and CHEs (P for trend < 0.001), but not for the number of outpatient visits and inpatient hospital days. The average causal mediation effects (ACME) and average direct effects (ADE) are presented. Chronic diseases served as a mediating factor between ACEs and CHE (ACME = 0.000904, P = 0.03; ADE = 0.00813, P < 0.001). CONCLUSIONS:ACE has the capacity to predict CHE, and the findings of this study reinforce the potential pathway through which ACE may exert its influence on CHE via the burden of chronic diseases. Measures should be implemented to prevent ACEs and mitigate the risk of chronic diseases to lessen the economic burden on individuals and families as well as the adverse impact of national financial risk.

BACKGROUND CONTEXT:Although laboratory research has revealed altered gait in some individuals with chronic low back pain (CLBP), large-scale studies using wearable sensors to characterize gait patterns of individuals with CLBP in real-world settings are lacking. PURPOSE:To identify key gait parameters from wrist-worn accelerometers that distinguish individuals with CLBP from those without in everyday environments. STUDY DESIGN:Cross-sectional study. PATIENT SAMPLE:A total of 8,093 participants (979 with CLBP and 7,114 asymptomatic controls) from the UK Biobank who wore accelerometers for 5 to 7 days and provided CLBP data. OUTCOME MEASURES:CLBP status was self-reported. Twelve gait parameters related to gait quantity and quality were extracted from wrist-worn accelerometers' data. METHODS:To minimize confounding, the propensity score matching was applied to create 2 balanced comparison groups. Independent t-tests and logistic regression analyses were conducted to identify key gait parameters that best discriminated CLBP status. Effect sizes were expressed as odds ratios (OR), and discriminative performance was assessed using the area under the receiver operating characteristic curve (AUC). RESULTS:After matching, 1,956 participants were included in the final analysis: 978 with CLBP (mean age 61.4±7.7 years, 52.2% female) and 978 controls (61.4±7.6 years, 53.3% female). Compared to controls, those with CLBP displayed significantly lower daily gait quantity (fewer steps per day, shorter longest walking duration, slower maximal walking speed, and lower cadence) and inferior gait quality (higher step-time variability and lower step regularity) (p<.05). Among all gait parameters, step-time variability was the most discriminative parameter, even after adjusting for sociodemographic, psychological, and sleep-related covariates. However, its effect size (OR = 1.18-1.19) and discriminative performance (AUC = 0.52-0.57) were limited. CONCLUSIONS:Wrist-derived gait parameters, particularly step-time variability, reflect functional differences in individuals with CLBP. Wrist-worn accelerometers show promise for remote gait monitoring, although findings are limited by the cross-sectional design, self-reported pain status, and modest effect size and discriminative ability. Future rigorously designed prospective studies should clarify causal relationships and clinical utility.

Osteoarthritis (OA) is a degenerative joint disorder characterized by complex network dysregulation across the entire joint, which significantly compromises the efficacy of single-target therapeutic interventions. Pathological acidosis and magnesium ion (Mg2+) deficiency have been mechanistically associated with cartilage matrix degradation, abnormal subchondral bone remodeling, and chronic inflammation, collectively driving OA progression. In this study, we engineered porous PLGA microspheres (Cur-Mg/PLGA MPs) incorporating curcumin-modified magnesium hydroxide nanosheets to effectively neutralize excessive hydrogen ions and sustained the release of Mg-Cur nanocomplexes through microporous structures. This acid responsive and neutralization delivery system enhanced the therapeutic capacity of metal-phenolic nanomedicine in suppressing inflammatory responses, inhibiting osteoclast differentiation, and reducing chondrocyte catabolic activity, thereby achieving optimal cartilage preservation. Our in vitro experiments revealed that Cur-Mg/PLGA MPs exhibit remarkable chondroprotective effects under both inflammatory and acidic microenvironmental conditions. Moreover, in vivo evaluations demonstrated that this microsphere system can significantly alleviate OA-associated pain, effectively suppress osteoclast activation, and substantially maintain cartilage matrix homeostasis. Mechanistic investigations identified that Cur-Mg/PLGA MPs inhibit macrophage-to-osteoclast differentiation through ACOD1-mediated mitochondrial metabolic rewiring, ultimately disrupting the “acidosis-osteolysis “vicious cycle in OA pathogenesis. These findings present a novel comprehensive therapeutic strategy for OA management, which has demonstrated significant efficacy in rat models and hold promising potential for clinical translation.

Swimming exercise may alleviate neuropathic pain (NP) in spared nerve injury (SNI) mice by regulating pain-related genes, such as miR-183 and Cacna2d2. However, the related upstream mechanism remains unclear. The demethylase fat-mass and obesity-associated protein (FTO) in the dorsal root ganglia (DRG) participates in NP through m6A modification. However, whether FTO-regulated m6A modification contributes to the analgesic effect of swimming remains unknown. This study aimed to investigate the influence of swimming on FTO expression in the DRG of SNI mice and clarify its role in regulating the m6A modification of miR-183 by inhibiting FTO expression. We established a male SNI mouse model, performed intrathecal injections of adeno-associated viruses to knock down or overexpress FTO, and manipulated the expression of FTO in male and female miR-183 knockout mice. In addition, we subjected the above models to six weeks of swimming training and analyzed the effects on pain behavior, m6A modification levels, and the expression of target gene transcription and protein levels. We observed that swimming exercise downregulated FTO mRNA and protein expressions in the injured L4-L6 DRGs of SNI mice, promoted the m6A modification of miR-183, and showed an association with the increased expression levels of miR-183. These outcomes further reduced the downstream target gene Cacna2d2 and the BDNF/TrkB signaling pathway, which alleviated mechanical and cold allodynia. This study suggested that swimming exercise alleviates NP, potentially by downregulating FTO and promoting m6A methylation of miR-183. FTO-regulated m6A modification plays a key role in the mechanism of exercise-induced analgesia.

AIM:To investigate neck pain prevalence and risk factors pain in China. DESIGN:Cross-sectional analysis using data from the China Health and Retirement Longitudinal Study. SETTING:Nationwide study conducted in China. POPULATION:Adults aged 45 years or older. METHODS:The data for the study were from the China Health and Retirement Longitudinal Study. A total of 19816 representative subjects were selected by multi-stage stratified sampling method. Univariable and multivariable logistic regression analyses were conducted to identify potential risk factors for neck pain. RESULTS:The estimated prevalence of neck pain among Chinese people over 45 was 18.93% (95% CI 18.32-19.55). Neck pain prevalence significantly differed according to sex, with an overall rate of 12.26% in men and 25.04% in women (P<0.001 for sex difference). Risk factors for neck pain included female (odds ratio [OR] 1.83, 95% CI 1.61-2.08), depression (1.23, 1.06-1.42), short sleep time (1.48,1.31-1.68), more than one chronic condition (1.18, 1.04-1.35), headache (4.83, 4.28-5.47), poor health status (2.93, 2.18-3.92), limitation of physical activity (1.37,1.21-1.57) and activity of daily living (1.48, 1.31-1.68). A lower risk of neck pain was associated with age over 75 and illiterate. CONCLUSIONS:The Prevalence of neck pain in China is relatively high. These results may help to develop proper prevention and treatment measures for patients with neck pain. CLINICAL REHABILITATION IMPACT:Our study provides insights for rehabilitating neck pain in adults aged 45 or older, aiding targeted interventions and preventive measures.

BACKGROUND:Impaired postural control, attributed to abnormal function of motor-related cortices, has been proven as one of the potential mechanisms of chronic low back pain (CLBP). Based on available evidence, anodal transcranial direct current stimulation over the primary motor cortex (M1-tDCS) can significantly enhance cortical activation and improve postural control. However, the neuromechanism underlying the effect of anodal M1-tDCS on patients with CLBP remains unclear. METHODS:Twenty-six participants with CLBP were randomly assigned to the active tDCS group or sham group. A 20-minute session of anodal M1-tDCS or sham intervention was applied. Before and after the intervention, postural control performance and cortical activity during unipedal standing were assessed by center of pressure displacement and functional near-infrared spectroscopy (fNIRS), respectively. Regions of interest (ROIs) included bilateral primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), frontopolar area (FpA), and supplementary motor area (SMA). Functional connectivity (FC) among these ROIs was also analyzed. RESULTS:Significant interactions (Group × Time) were observed in anterior-posterior (AP) velocity, sway length, left M1 activation, and FC between left M1 and right DLPFC, as well as between the left M1 and bilateral FpA (ps<0.05). Post-hoc comparisons demonstrated that AP velocity and sway length significantly decreased after the anodal M1-tDCS intervention (pFDR<0.001, effect size (d)= 2.060). Additionally, participants in the active tDCS group exhibited significantly reduced left M1 activation (pFDR<0.001, d=1.894), FC between the left M1 and right DLPFC (pFDR=0.008, d=1.420), and FC between the left M1 and bilateral FpA (left: pFDR=0.006, d=1.461; right: pFDR=0.027, d=1.227) after the intervention. CONCLUSION:The improvement in postural control of patients with CLBP following anodal M1-tDCS, accompanied by reduced cortical activation and functional connectivity, suggests enhanced neural efficiency (more efficient neural processing) and reduced compensatory demands within sensorimotor networks.

Chronic pain affects over 30% of the global population, yet non-pharmacological interventions with clear neurophysiological mechanisms remain limited. While virtual reality (VR) and music therapy independently show promise in pain management, the neural oscillatory underpinnings of rhythm-synchronized audiomotor integration in VR therapy remain poorly understood. This study aimed to investigate whether music-synchronized virtual reality (MSVR) enhances analgesia through distinct neural mechanisms compared to conventional distraction-based VR or non-immersive interventions. 90 healthy adults (45 female, 22 ± 2 years) were randomized to a single session of: (1) MSVR (rhythm-synchronized visuomotor tasks with music), (2) conventional VR (identical tasks with white noise), or (3) non-immersive 2D control. Pressure pain thresholds (PPT) were measured at five movement-generating muscle sites. Conditioned pain modulation (CPM) efficiency was assessed using PPT and cold-water stimulation. 64-channel EEG recorded theta, alpha, beta, and gamma oscillations. Outcomes included PPT changes, CPM efficiency, cold pain intensity/unpleasantness, and neural spectral power. MSVR significantly increased PPTs across all sites (15-25% vs. control, P < 0.001; superior to VR in upper limbs, P < 0.05) and enhanced CPM efficiency by 18% (vs. control, P = 0.010; vs. VR, P = 0.046). Cold pain intensity decreased by 22% with MSVR (P < 0.05 vs. both groups). MSVR uniquely enhanced parietal alpha oscillations during and post-intervention (P = 0.001). MSVR also induced greater immersion and realism than VR (P < 0.001). MSVR significantly enhances endogenous pain inhibition and elevates pain thresholds more effectively than conventional VR or 2D interventions, primarily through rhythmic audiomotor integration modulating parietal alpha-oscillation modulation. These findings suggest MSVR as a scalable digital therapeutic strategy for pain management.

Discogenic pain, caused by intervertebral disc degeneration (IVDD), is a prevalent and challenging condition to treat effectively. Macrophage infiltration with neural ectopic in-growth resulting from structural disturbances within the intervertebral disc (IVD) is a major cause of discogenic pain. This work systematically reveals how nanoparticles can synergistically regulate the immune microenvironment and mitochondrial communication to attenuate discogenic pain. The antioxidant metal-polyphenol nanoparticle system can sequentially regulate macrophage phenotype and mitochondrial delivery efficiency. This strategy circumvents the necessity for mitochondrial isolation and preservation techniques that are typically required in conventional mitochondrial transplantation procedures. Furthermore, it facilitates the effective and sustained delivery of mitochondria to damaged cells. In vivo, this nanoparticle formulation effectively preserves the IVD height, maintains the structural integrity of the nucleus pulposus (NP), and restores pain thresholds. Thus, this nanoplatform offers an effective approach to traditional surgical treatments for discogenic pain, with significant potential for clinical application.

Background Nonpharmacological interventions, including music therapy, are widely used for pain management and improving cognitive function and emotional well-being. Music therapy has particularly shown significant benefits in chronic pain management. Objectives This study aimed to evaluate the effectiveness of music therapy in lowering the pressure pain threshold (PPT) and enhancing cognitive function and emotional well-being. The interrelationships among these factors were also investigated. Design A randomized controlled trial was employed in this study. Method A total of 54 participants were recruited, with 40 healthy college students randomly assigned to one of two groups. The music therapy group listened to Mozart’s K. 448 for 20 min, whereas the control group listened to it for 2 min. Each participant’s 50-minute session comprised a pre-session, intervention, and post-session, with 15 min for emotional and cognitive assessments of the pre- and post-sessions and 20 min for the intervention. The outcome measures included the PPT, Color-Word Stroop test (CWST), and self-assessment manikin (SAM) score. Results The average PPT of most muscles significantly increased in the music therapy group (p < 0.05) than in the control group. In the CWST, the music therapy group performed more accurately than the control group did. The increase in the mean of the SAM score of arousal was also statistically significantly higher in the music therapy group than in the control group. Correlation analysis showed a moderate positive correlation between PPT and SAM. Conclusion This study shows that music therapy helps regulate pain sensitivity. It also improves participants’ memory, executive function, and pleasurable and arousal emotions.

Background and Objectives:While intrinsic capacity (IC) impairment and adverse neighborhood environments are established independent risk factors for dementia, their interaction effects and potential mediating pathways remain poorly understood. This study aimed to examine the independent, interactive, and mediating associations of IC, neighborhood environment, and dementia risk among middle-aged and older adults. Research Design and Methods:We analyzed data from 8,107 adults aged 50+ in the China Health and Retirement Longitudinal Study (2011-2020). IC was quantified using a composite impairment score encompassing locomotor, cognitive, sensory, psychological, and vitality domains. Neighborhood environment was classified by resource availability and social provisions (low risk; moderate risk; high risk). Cox proportional hazards models evaluated associations between IC, neighborhood environment, and dementia risk. The four-way decomposition model was used to examine the potential interaction and mediation effects of IC. Results:Over a median follow-up of 9 years, 909 incident dementia cases occurred. Adjusted analyses revealed dose-dependent relationships: each 1-point increase in IC impairment score elevated dementia risk by 26% (hazard ratio [HR] = 1.29, 95% confidence interval [CI]: 1.22-1.36). Compared with low-risk neighborhoods, moderate-risk (HR = 1.26, 95% CI: 1.08-1.47), and high-risk neighborhoods (HR = 1.41, 95% CI: 1.13-1.77) independently increased dementia risk. Four-way decomposition revealed the association between adverse neighborhood environments and increased dementia risk was partially explained by the pure mediation effect of IC, with no significant interaction-only/mediated interaction effects observed. Discussion and Implications:IC impairments and adverse neighborhood environments independently escalate dementia risk, with IC partially mediating the environmental effects. Integrating interventions targeting both individual capacity and community-level infrastructure may optimize dementia prevention strategies.

This study aimed to investigate whether high-definition transcranial direct current stimulation (HD-tDCS) augmented the effect of attentional bias modification (ABM) on pain perception and to explore the potential neuroimaging mechanism by functional infrared spectroscopy (fNIRS). This randomized, single-blind, and parallel-controlled trial enrolled 46 healthy volunteers who were then randomly assigned to two groups, namely active HD-tDCS combined with ABM and sham HD-tDCS combined with ABM groups. The pressure pain threshold (PPT), cold pain threshold, cold pain tolerance, pain intensity, pain unpleasantness, and attentional bias were measured before and after the intervention. fNIRS was used to monitor cerebral hemodynamic responses during repeated cold pain stimulation tasks. Compared to the sham group, the active HD-tDCS plus ABM group demonstrated significantly greater improvements in PPT. Mixed-design ANOVA revealed significant Time × Group interactions for PPT at both the forearm and leg sites. Simple effects analyses showed that PPT significantly increased from pre- to post-intervention in the active group (forearm: p < 0.001; leg: p < 0.001), whereas no significant change was observed in the sham group for the forearm (p = 0.597) and only a small increase was observed at the leg site (p = 0.036). Between-group differences at post-intervention were not significant. Cold pain unpleasantness ratings also demonstrated a significant Time × Group interaction (p = 0.011), with decreases in the active group (p < 0.001) but not in the sham group (p = 0.305); at post-intervention, the active group reported lower unpleasantness than the sham group (p = 0.025). No significant group or interaction effects were observed for cold pain threshold, cold pain tolerance, pain intensity, or attentional bias. Our findings showed that active HD-tDCS combined with ABM training enhanced the analgesic effect of ABM training and reduced pain unpleasantness rating. The analgesic effect may be associated with changes in the activation of prefrontal cortex. However, this effect may not be mediated by modifying the direction of pain attention bias. Further experiments are needed to clarify the analgesic effect of HD-tDCS combined with ABM training on those with clinical pain.

Objective: To investigate the influence of sleep quality and associated factors on balance control in individuals with chronic low back pain (CLBP). Methods: 85 participants (mean age 33.2 ± 12.5 years) with CLBP were recruited. Physical and emotional well-beings were evaluated using a battery of questionnaires. Sleep quality over the last month was assessed using the Pittsburgh Sleep Quality Index (PSQI). Participants were dichotomized into the good sleep quality (GSQ) and poor sleep quality (PSQ) groups if their PSQI scores were ≤ 5 and > 5, respectively. Balance control was measured using the one-leg stance with eyes closed and Y-balance test. Results: The GSQ group included 37 participants, while the PSQ group comprised 48 participants. After controlling for confounds (including gender, age, disability, anxiety, depression, and fear avoidance beliefs), participants with PSQ displayed significantly poorer performance in the one-leg stance with eyes closed and lower normalized posteromedial, posterolateral, and composite scores of the Y-balance test compared with participants with GSQ. Additionally, sleep quality accounted for 16.9%-24.9% of the variance in balance control, while age explained an additional 5.2%-13.2% of the variance. Additionally, higher levels of physical disability and anxiety were associated with poorer balance control. Conclusions: Individuals with concurrent CLBP and PSQ exhibit significantly worse balance control than those with CLBP alone. Future studies should investigate whether improving sleep quality, physical disability, and anxiety can enhance balance in individuals with CLBP.

INTRODUCTION:The causal association between pulmonary function and Alzheimer's disease (AD) remains unclear. This study aimed to investigate whether low pulmonary function has a causal relationship with the risk of AD. METHODS:We conducted prospective cohort and two-sample Mendelian randomization (MR) studies. In the cohort study, 333,816 UK Biobank participants were eligible for analysis. Forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), FEV1/FVC ratio, percentage of predicted normal value of FEV1 (FEV1% pred), and peak expiratory flow (PEF) were measured at baseline. Longitudinal associations were investigated using cox-proportional hazard models. We conducted univariate and multivariable MR analyses on genome-wide association study (GWAS) data from 421,986 Europeans for FEV1, FVC, and PEF. Inverse-variance weighting was employed as the primary MR analysis approach. RESULTS:Over a median follow-up of 12.8 years (10.3-15.0 years), 2275 incident cases of AD were identified in the cohort study. Compared to the highest quartile, the lowest quartile for pulmonary function exhibited a higher risk of incident AD, and hazard ratios (95% CI) were as follows after adjustment for risk factors: 1.81 (1.32-2.48; FEV1), 1.97 (1.44-2.69; FVC), and 1.86 (1.39-2.47; PEF). In the MR study, genetically determined high FEV1 was associated with a decreased risk of AD (odds ratio: 0.68, 95% CI: 0.53-0.88). The results remained robust after sensitivity and multivariable MR analyses. CONCLUSION:Our findings suggest the potential causal association between high FEV1 and decreased risk of AD.

BACKGROUND:Focused-extracorporeal shockwave therapy (fESWT) has recently been applied in the management of chronic pain. However, its effectiveness in reducing muscular stiffness and pain among office workers has not been extensively studied. This study aimed to investigate the effectiveness of fESWT and sham-fESWT in alleviating muscular stiffness, pain, and functional disability. METHODS:Sixty-four office workers (mean age 31.4 ± 9.5 years) with myofascial pain syndrome of the upper trapezius were randomly and equally assigned to receive either the fESWT or sham-fESWT. The interventions were administered once a week for 4 weeks, with 4 Hz frequency and a total energy of 0.10.232 mJ/mm². Measurements were recorded at baseline, immediately after treatment, at two weeks, and at four weeks, assessing shear modulus (tissue stiffness), visual analogue scale (VAS), and the neck disability index (NDI). RESULTS:The result demonstrated a significant acute decrease in shear modulus at the trigger point (6.1 kPa, p = 0.009) and a delayed reduction in muscle stiffness of the lower aponeurosis (5.3 kPa, p = 0.004) following 4 weeks. Additionally, VAS scores decreased at all time points following fESWT (p < 0.05), while the sham-fESWT group also demonstrated reductions during the final two weeks. NDI showed a decrease in both groups after four sessions (p < 0.05), with no group effect. CONCLUSION:fESWT was effective in reducing muscular pain, stiffness, and functional disability in patients. However, the potential psychological effects of sham-fESWT on VAS and function should be considered. Further research is necessary to determine the optimal treatment sessions and intensity of fESWT to better establish its efficacy.