Search Results (129)

Background/Objectives: Physical exercise has been a cornerstone of health and vitality across all age groups; however, while its importance remains undeniable, the complications associated with exercise such as fatigue, muscle damage, inflammation, and oxidative stress are not always effectively managed through conventional strategies. This review aims to highlight the current evidence on the potential role of natural products in alleviating these exercise-induced responses and supporting exercise performance and recovery. Methods: The available preclinical and clinical literature was comprehensively reviewed to evaluate the effects of natural products on exercise performance and recovery. Evidence was categorized according to five major mechanisms: attenuation of muscle fatigue, enhancement of muscular endurance, improvement of muscular strength and neuromuscular function, modulation of inflammation and other physiological benefits. Results: Approximately 164 natural products have been investigated for their potential to improve exercise performance and recovery by targeting fatigue-related markers, improving energy metabolism, and regulating oxidative stress. Conclusions: These findings underscore the potential of natural products as promising agents as complementary strategies for addressing exercise-induced fatigue and improving recovery. Although current findings indicate biological plausibility and therapeutic potential of natural products, further clinical evidence is required before definitive performance related recommendations can be established. Future well-designed clinical trials are essential to establish efficacy, safety and translational applicability. Full article

Background: Emergence delirium (ED) is a common complication in pediatric patients following general anesthesia. Reduced cholinergic neurotransmission is closely associated with cognitive impairment and an increased risk of delirium. This study aimed to compare the effects of a cholinesterase inhibitor versus sugammadex–used as neuromuscular blockade reversal agents–on the incidence of ED following pediatric strabismus surgery. Methods: Seventy-six patients, aged 4–7 years, were enrolled and randomly allocated to either the pyridostigmine group (Group P) or the sugammadex group (Group S). The dose of each agent was determined according to the train-of-four count or ratio. The Pediatric Anesthesia Emergence Delirium (PAED) scale was assessed at 15-min intervals in the post-anesthesia care unit until the score fell below 10. ED was defined as a PAED score ≥ 10. Results: Of the 73 patients who completed the study, 36 were in Group P, and 37 were in Group S. The incidence of ED was 50.0% in Group P and 40.5% in Group S (odds ratio = 0.682; 95% confidence interval = 0.270–1.721; p = 0.417). The peak PAED scores were 10.0 (7.0, 15.5) in Group P and 9.0 (7.5, 11.5) in Group S (median [interquartile range]; p = 0.277). Conclusions: The choice of neuromuscular reversal agent did not significantly affect the incidence of ED in pediatric patients undergoing strabismus surgery. Full article

Background and Clinical Significance: Anti–myelin-associated glycoprotein (MAG) antibody polyneuropathy is a rare, chronic IgM-mediated demyelinating peripheral neuropathy predominantly affecting sensory nerves in older adults, commonly in association with monoclonal gammopathy of undetermined significance. Reports describing anesthetic management in patients with this condition remain extremely limited, and no specific guidelines currently exist regarding neuromuscular blocking agent (NMBA) use or neuromuscular monitoring in this population. Case Presentation: A 79-year-old man with anti-MAG antibody polyneuropathy (diagnosed in 2007) and IgM monoclonal gammopathy of undetermined significance developed disproportionate progressive lower-extremity weakness and became wheelchair-dependent following COVID-19 infection in 2020. Preoperative evaluation revealed mildly reduced left ventricular function (ejection fraction 49%), mild chronic kidney disease, and marked intrinsic hand muscle atrophy with absent deep tendon reflexes. He was scheduled for robot-assisted radical cystectomy with ileal conduit diversion under combined general and thoracic epidural anesthesia. Before NMBA administration, neuromuscular monitoring was systematically attempted at the ulnar nerve (electromyography and acceleromyography, up to 60 mA/300 μs) and the corrugator supercilii; despite visible muscle contractions following peripheral nerve stimulation, neither modality produced reliable responses at either site. Given the inability to establish reliable monitoring, the administration of NMBAs was considered to carry an unacceptable risk of a prolonged, undetectable blockade. Anesthesia was maintained with deep sevoflurane (2.0–2.5% end-tidal) and remifentanil infusion without NMBAs, titrated to a bispectral index of 40–60. Tracheal intubation was accomplished via video laryngoscopy without NMBA. The 7 h and 30 min surgery was completed without patient movement or surgical compromise. Postoperatively, the patient developed transient upper airway obstruction attributed to glossoptosis, managed successfully with head elevation and nasopharyngeal airway insertion; supplemental oxygen was required until postoperative day 3, and the patient was discharged from the high-dependency unit on postoperative day 5. Conclusions: No measurable quantitative neuromuscular response could be obtained in this patient with advanced anti-MAG antibody neuropathy, despite appropriate application of electromyography- and acceleromyography-based monitoring and the presence of visible muscle contractions following peripheral nerve stimulation. In such circumstances, avoiding NMBA administration in favor of deep volatile or intravenous anesthesia with opioid supplementation may represent a reasonable, hypothesis-generating approach in carefully selected patients; this observation does not establish the general superiority of an NMBA-free strategy, and caution is warranted before generalizing it to procedures such as robotic surgery, in which profound neuromuscular blockade is often considered desirable. Full article

Approximately 30% of patients with tremor-dominant Parkinson’s disease (PD) have rest tremor that persists despite optimal dopaminergic therapy. When deep brain stimulation and focused ultrasound are unavailable or declined, the therapeutic options narrow. Botulinum toxin (BoNT) offers a targeted, titratable, reversible approach, but whether a peripheral neuromuscular blocking agent makes sense for a centrally generated tremor is a legitimate question that deserves a direct answer. This narrative critical review appraises what is currently known across PD and non-PD tremor conditions, defines the technical requirements for safe and effective injection, and provides a practical framework for patient selection and clinical management. The PD-specific literature rests on a single positive double-blind randomized controlled trial of 30 patients; all remaining data are open-label or extrapolated from other tremor conditions, and this narrative synthesis combines heterogeneous conditions, outcome scales, and toxin protocols. A recurring technical observation is that, in the available trials, individualized, EMG-guided injection has been associated with substantially lower rates of hand weakness than fixed-dose injection (reported reductions from roughly 30–70% to below 15%) while maintaining tremor reduction, although the degree of benefit and weakness risk vary with the tremor syndrome, injected muscles, baseline impairment, dose, and guidance method. The careful patient selection this approach requires helps the individual clinician and patient achieve tremor relief, but it departs from the unselected real-world PD population and introduces selection bias that makes a large, statistically representative cohort difficult to assemble. In well-selected patients at centers with the appropriate expertise, BoNT may be a clinically useful option, but routine adoption is not yet supported. Full article

Perioperative anaphylaxis, though rare, is a potentially life-threatening complication. While antibiotics and neuromuscular blocking agents are common triggers, benzodiazepine-induced reactions have been considered uncommon. Remimazolam, a novel benzodiazepine sedative, has gained widespread use in Korea due to its rapid onset, short recovery, hemodynamic stability, and availability of flumazenil. However, increasing utilization has coincided with rising reports of hypersensitivity. We report the case of a 62-year-old female undergoing contralateral total knee replacement under spinal anesthesia. Continuous remimazolam infusion was initiated, but within ten minutes the patient developed chest discomfort followed by abrupt hypotension and oxygen desaturation, requiring urgent conversion to general anesthesia. Following a remimazolam bolus and rocuronium administration, sudden cardiac arrest occurred. Return of spontaneous circulation (ROSC) was achieved after approximately 28 min of cardiopulmonary resuscitation with a cumulative intravenous epinephrine dose of approximately 17 mg, and veno-arterial extracorporeal membrane oxygenation (ECMO) was required. Post-ROSC transesophageal echocardiography demonstrated a transient anteroseptal regional wall motion abnormality; subsequent coronary angiography demonstrated no significant coronary disease, and computed tomography pulmonary angiography was negative for embolism, leaving acute hypersensitivity as the most plausible mechanism. Acute serum tryptase was elevated at 11.6 µg/L and normalized to 3.4 µg/L (the patient’s individual baseline) prior to discharge, satisfying the World Allergy Organization (WAO) criterion. A skin prick test performed four weeks later was positive for remimazolam and negative for rocuronium and the other coadministered agents. An expanded multi-database literature review identified 16 prior cases of remimazolam-induced anaphylaxis. Most described cardiovascular collapse as the predominant manifestation. To our knowledge, based on available literature, this is among the first reports of remimazolam-induced anaphylaxis occurring in the setting of high spinal anesthesia with sympathetic blockade. Vigilance and adherence to established anaphylaxis management guidelines are essential. Full article

Diabetic peripheral neuropathy is an important cause of functional disability, and current therapies have limited ability to halt its progression. Uridine, a pyrimidine nucleoside essential for the synthesis of membrane phospholipids and neuronal metabolism, appears to be a potential neuroprotective agent, but its impact on motor behavior and peripheral nerve integrity in diabetes remains insufficiently investigated. Our study investigated the effects of chronic uridine supplementation on locomotor performance, neuromuscular electrophysiological manifestations, and morphological changes in the sciatic nerve in a murine model of streptozotocin-induced diabetes. We used male C57BL/6 mice (n = 8/group) that were assigned to three groups: sham (no diabetes), diabetic (streptozotocin-induced, diabetes mellitus, DM+), and diabetic treated with uridine (DM+U). We observed that uridine did not alter the metabolic status, as the HbA1c values remained comparable between diabetic groups (9.93 ± 0.57% DM+ vs. 9.71 ± 0.55% DM+U; p = 0.72), suggesting effects independent of glycemic control. The open field test revealed that diabetic mice showed a marked reduction in spontaneous locomotion, while uridine-treated mice maintained a significantly higher level of activity (longer total distance traveled 3761.7 ± 789.1 cm vs. 2477.5 ± 1017.6 cm in DM+; p = 0.023). Electrophysiological evaluation revealed near-normal sciatic nerve function in DM+U mice, including higher compound motor action potential (CMAP) amplitudes (10.21 ± 0.64 mV vs. 5.75 ± 0.72 mV; p < 0.0001) and reduced F-wave latency (6.35 ± 0.45 ms vs. 7.29 ± 0.31 ms; p < 0.0001). Histological and immunohistochemical analyses (PGP 9.5) further confirmed reduced nerve degeneration in DM+U mice. Our data suggest that chronic uridine administration may confer both functional and structural neuroprotection in diabetic neuropathy, even in the absence of improved glycemic control. Full article

Medical errors are inevitable and will happen to almost every specialist. In anesthesiology, one of the main concerns is the inappropriate application of muscle relaxants (MRs). As this group of drugs plays a significant role in facilitating endotracheal intubation and optimizing surgical conditions, it is widely and commonly used in the medical field. To prevent residual neuromuscular block, anesthesiologists may pharmacologically reverse the neuromuscular block (NMB) by administering reversal agents. Lately, sugammadex is becoming more popular due to its ability to reverse various levels of NMB more rapidly than traditionally used acetylcholinesterase inhibitors such as neostigmine. The common challenges and errors associated with the administration of neuromuscular blocking agents (NMBAs) and muscle reversal agents include the absence of neuromuscular monitoring, underestimation of the residual block (RB), misinterpretation of DUR25, inappropriate size descriptors for muscle relaxants and reversal agents requiring weight-based dosing, the wrong dosing of rocuronium, poor usage of cisatracurium among patients with renal or hepatic failure, and the wrong usage of succinylcholine. Another source of mistakes may be inaccurate knowledge about the pharmacokinetics and pharmacodynamics of the administered drugs. Medication errors may occur not only when it comes to the usage of muscle relaxants but also with the use of reversal agents, including lack of neuromuscular monitoring, choosing the wrong antagonist strategy, “too early” administration of neostigmine, inappropriate dosing, and insufficient knowledge about drug interactions. Improving the knowledge of administered drugs and adhering to the latest recommendations could prevent many complications. This article aims to review the current challenges in the use of muscle relaxants and reversal agents in anesthesia. Full article

Background: Eosinophilic granulomatosis with polyangiitis (EGPA), formerly Churg–Strauss syndrome, is a rare necrotizing vasculitis characterized by asthma, eosinophilia, and systemic granulomatosis vasculitis. Perioperative risk is primarily driven by airway hyperreactivity, potential cardiac disease, chronic immunosuppressive therapy, and reported alterations in plasma cholinesterase activity. Evidence specifically addressing anesthetic management remains scarce and largely limited to case-based reports. Methods: A focused narrative review was conducted by searching MEDLINE (via PubMed), Scopus, and Embase from inception to January 2026 for publications reporting perioperative anesthetic management in patients with EGPA/Churg–Strauss syndrome. Case reports and case-based descriptions providing explicit anesthetic details were qualitatively synthesized. Results: Available evidence consists predominantly of isolated case reports across heterogeneous surgical settings, including ENT, abdominal, orthopedic, ambulatory, pediatric, and rare cardiac procedures. Recurring perioperative principles include optimization of bronchial disease and continuation of inhaled therapy; minimization of airway stimulation and avoidance of histamine-releasing drugs; selection of induction agents preserving hemodynamic stability in the presence of myocardial involvement; preference for non-depolarizing neuromuscular blockade with quantitative monitoring (and consideration for sugammadex when appropriate); individualized corticosteroid management and multimodal, opioid-sparing analgesia, often supported by regional techniques. Conclusions: In the absence of dedicated perioperative guidelines, anesthetic care for EGPA should be individualized based on clinical phenotype and organ involvement. A structured approach targeting airway protection, cardiovascular stability, safe neuromuscular management, and opioid-sparing analgesia may represent a pragmatic risk-mitigation framework. These considerations are illustrated by an institutional experience in mitral valve surgery. Full article

Skeletal muscle differentiation is tightly regulated by membrane potential dynamics and voltage-dependent ion channel activity. Potassium (K⁺) and calcium (Ca²⁺) currents cooperate to orchestrate the transition of myoblasts into fusion-competent myotubes, and alterations in this process are associated with dystrophic phenotypes. Here, we investigated the electrophysiological remodeling accompanying C2C12 myogenesis and the modulatory effects of the polyphenol resveratrol (RES) on calcium voltage-gated channel subunit alpha 1 S (CACNA1S, Cav1.1, L-type) currents. Whole-cell patch-clamp recordings were performed in proliferating and differentiating C2C12 cells to characterize the temporal expression of K⁺ currents and voltage-dependent Ca²⁺ channels (VDCCs). During differentiation, three electrophysiological subpopulations were identified according to K⁺ current profiles: SK4+/EAG−/Kir−, SK4−/EAG+/Kir−, and SK4−/EAG+/Kir+. This sequence paralleled a progressive membrane hyperpolarization from −20 mV to −70 mV, consistent with the physiological maturation of myogenic cells. In C2C12 myocytes, nimodipine-sensitive L-type currents were the only Ca²⁺ conductance observed. Their activation threshold (~−30 mV) and half-activation voltage (V/2 ≈ −12 mV) indicated the co-expression of embryonic and adult Cav1.1 isoforms. Exposure to RES (30 µM, 48 h) produced a depolarizing shift in activation (ΔV/2 ≈ +9 mV) and a reduction in current amplitude across all voltages, consistent with a transition toward the adult splice variant of Cav1.1. These findings suggest that RES promotes electrophysiological maturation of skeletal muscle cells by modulating calcium channel expression and gating behavior. Given its known ability to correct splicing abnormalities in CACNA1S and related genes, resveratrol emerges as a promising pharmacological agent for restoring calcium homeostasis in neuromuscular disorders such as myotonic dystrophy type 1 (DM1). Full article

Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disorder caused by loss-of-function mutations in the dystrophin gene, leading to progressive muscle degeneration, motor decline, respiratory compromise, and cardiomyopathy. Diagnosis typically occurs in early childhood following recognition of motor delays, markedly elevated creatine kinase, and confirmatory genetic testing. Over the past decade, the therapeutic landscape for DMD has expanded substantially, evolving from exclusively supportive care to patient-centric multifaceted treatment paradigms, including corticosteroids, mutation-specific therapies, small molecule disease-modifying approaches, and gene replacement strategies. Despite these advances, no currently available therapy restores full-length dystrophin or completely halts disease progression. This review provides a clinically oriented comprehensive overview of currently Food and Drug Administration (FDA)-approved medications for DMD, with particular emphasis on corticosteroids, exon-skipping therapies, nonsense mutation readthrough agents, recently approved gene therapy, and select ongoing gene therapy trials. We summarize mechanisms of action, clinical efficacy, safety considerations, regulatory status, and highlight the challenges of integrating these therapies into longitudinal care. Through illustrative clinical vignettes, we highlight the real-world complexity of treatment selection, shared decision-making, and longitudinal care planning in contemporary DMD management. Full article

Background/Objectives: Accurate assessment of neuromuscular reflexes, such as the Hoffmann reflex (H-reflex), plays a critical role in sports science, rehabilitation, and clinical neurology. Conventional interpretation of H-reflex electromyography (EMG) waveforms is subject to inter-rater variability and interpretive bias, limiting reliability and standardization. This study aims to develop an automated, interpretable, and robust agentic AI–driven framework for H-reflex waveform analysis. Methods: We propose a fine-tuned Vision–Language Model (VLM) consortium combined with a reasoning Large Language Model (LLM)–enabled decision support system for automated H-reflex interpretation. Multiple VLMs were fine-tuned on curated datasets of H-reflex EMG waveform images annotated with expert clinical observations, recovery timelines, and athlete metadata. The VLM outputs were aggregated using a consensus-based strategy and further refined by a specialized reasoning LLM to ensure coherent, transparent, and explainable diagnostic assessments. Model fine-tuning employed Low-Rank Adaptation (LoRA) and 4-bit quantization to enable efficient deployment on consumer-grade hardware. Results: Experimental evaluation demonstrated that the proposed hybrid system delivers accurate, consistent, and clinically interpretable assessments of neuromuscular states, including fatigue, injury, and recovery, directly from EMG waveform images and contextual metadata. Compared with baseline models, the fine-tuned VLM consortium exhibited substantially improved precision, consistency, and contextual awareness, while the reasoning LLM enhanced diagnostic coherence through cross-model consensus and structured reasoning, thereby supporting responsible and explainable AI-driven decision making. Conclusions: This work presents, to the authors’ knowledge, the first integration of a responsible and explainable AI-driven decision support system for H-reflex analysis. The proposed framework advances the automation and standardization of neuromuscular diagnostics and establishes a foundation for next-generation AI-assisted decision support systems in sports performance monitoring, rehabilitation, and clinical neurophysiology. Full article

Background: Rapid Sequence Induction (RSI) is a widely used method for emergency airway management in critically ill and clinically unstable patients. Beyond the risks inherent to the procedure itself, RSI is almost exclusively performed in emergency settings where patients present with severe physiological derangement and a high risk of aspiration. In postmortem examinations, forensic toxicology results may be influenced by the patient’s clinical condition, the sampling site, the postmortem interval (PMI), and postmortem drug redistribution (PMR). This review aims to evaluate the existing literature regarding PMR of drugs commonly used during RSI. Methods: PubMed/MEDLINE, Embase and the Cochrane Library were searched for studies on PMR of drugs used in intravenous (IV) RSI (up to November 2025). Human and animal studies, patient populations comparable to critically ill individuals requiring RSI, and forensic case reports of exclusively IV drug administration were included. Studies on recreational use, overdose and non-IV administration were excluded. Results: Data on the PMR of IV-administered RSI drugs remain limited. Most available studies involve Intensive Care Unit (ICU) patients or individuals who underwent RSI in emergency settings. Fentanyl and midazolam appear to demonstrate notable PMR. Several factors influencing postmortem drug concentrations were identified. Although these findings are consistent with the existing literature, the small number of studies and the heterogeneity of data preclude definitive conclusions. Conclusions: Critical patient condition, including frailty due to advanced age, hemodynamic instability (particularly in ICU patients), hypoalbuminemia, body mass index (BMI), and injury and/or trauma, as well as the interval between IV drug administration and death, appear to affect postmortem concentrations of drugs used during RSI. The potential for PMR of certain agents, such as fentanyl and midazolam, adds further complexity. Given the scarcity of consolidated evidence and until further research provides more robust data, postmortem drug levels should not be interpreted as directly reflective of antemortem concentrations. Full article

Background/Objectives: Perioperative neurocognitive disorders (PND), including postoperative delirium and cognitive dysfunction (POCD), represent significant complications in elderly surgical patients undergoing general anesthesia. The choice of neuromuscular blockade reversal agent may influence POCD risk through different mechanisms and side effects. This systematic review and meta-analysis evaluated the comparative effect of neostigmine versus sugammadex on POCD incidence in elderly patients. Methods: A systematic search of PubMed, Web of Science, Scopus, and Google Scholar was conducted from database inception to September 2025, following PRISMA 2020 guidelines with PROSPERO registration (CRD420251058187). Randomized controlled trials involving elderly patients (≥60 years) undergoing general anesthesia with neuromuscular blockade were included, comparing neostigmine and sugammadex for reversal. Primary outcomes included POCD incidence, assessed using validated cognitive tools, including the Mini-Mental State Examination and Montreal Cognitive Assessment. Meta-analysis was performed using Review Manager 5.4.1, with results expressed as odds ratios (ORs) and 95% confidence intervals (CIs). Results: Six randomized controlled trials involving 795 elderly patients published between 2017 and 2024 met the inclusion criteria. Studies encompassed non-cardiac surgery, robotic-assisted radical cystectomy, and pars plana vitrectomy. Pooled meta-analysis showed neostigmine was associated with a higher risk of POCD than sugammadex (OR 1.74, 95% CI 1.00–3.02, p = 0.05), with low heterogeneity (I² = 39%). Secondary outcomes, including prevention of POCD, management strategies, and related complications, were inconsistently reported and unavailable across all six RCTs. Subgroup analysis stratified by neostigmine dosage demonstrated that administration of a higher dose (≥0.04 mg/kg) was associated with reduced POCD incidence compared to a lower dose (<0.04 mg/kg) (OR 0.31, 95% CI 0.15–0.63, p = 0.001), with negligible heterogeneity (I² = 0%). Conclusions: This meta-analysis suggests that sugammadex may be associated with reduced early postoperative neurocognitive disorders compared to neostigmine in elderly patients, likely through rapid neuromuscular blockade reversal that minimizes residual paralysis and respiratory complications. Full article

Background/Objectives: Pediatric cancer survivors frequently experience neuromuscular sequelae related to chemotherapy-induced neurotoxicity. Agents such as vincristine, methotrexate, and platinum compounds can lead to persistent gait alterations and sensorimotor deficits that impair mobility and quality of life. This study aimed to objectively assess gait in pediatric cancer survivors after the completion of oncological pharmacological treatment to identify specific spatiotemporal, kinematic, and kinetic alterations and characterize neuromechanical patterns associated with neurotoxic exposure. Methods: A cross-sectional observational study was conducted including pediatric cancer survivors (6–18 years) who had completed chemotherapy and age- and sex-matched healthy controls. Gait was analyzed using a Vicon^®3D motion capture system, with reflective markers placed on standardized anatomical landmarks. Spatiotemporal, kinematic, and kinetic variables were compared between groups using parametric tests and statistical parametric mapping (SPM) with Holm–Bonferroni correction (α = 0.05). Results: Pediatric cancer survivors showed slower gait velocity (Mean Difference (MD) = 0.17, p = 0.018, Confidence Interval CI95% = 0.04; 0.4), shorter step (MD = 0.1, p = 0.015, CI95% = 0.01; 0.19) and stride length (MD = 0.17, p = 0.018, CI95% = 0.03; 0.31), as well as reduced single support time (MD = 0.1, p = 0.043, CI95% = 0.01; 0.19), along with significant alterations in pelvic, hip, knee, and ankle kinematics compared with controls. Increased pelvic elevation (MD = 0.92, p = 0.018, CI95% = 0.25; 1.58), reduced hip extension during stance (MD = −2.99, p = 0.039, CI95% = −5.19; −0.74), knee hyperextension in mid-stance (MD = −3.84, p < 0.001, CI95% = −6.18; −0.72), and limited ankle dorsiflexion (MAS MD = −4.04, p < 0.001, CI95% = −6.79; −0.86, LAS MD = −3.16, p < 0.001) and plantarflexor moments in terminal stance (MAS MD = −149.65, p = 0.018, CI95% = −259.35; −48.25, LAS MD = −191.81, p = 0.008, CI95% = −323.81; −57.31) were observed. Ground reaction force peaks during loading response (MAS MD = −16.86, p < 0.001, CI95% = −26.12; −0.72 LAS MD = −11.74, p = 0.001, CI95% = −19.68; −3.94) and foot-off (MAS MD = 10.38, p = 0.015, CI95% = 0.41; 20.53, LAS MD = 11.88, p = 0.01, CI95% = 3.15; 22.38) were also reduced. Conclusions: Children who have completed chemotherapy present measurable gait deviations reflecting persistent neuromechanical impairment, likely linked to chemotherapy-induced neurotoxicity and deconditioning. Instrumented gait analysis allows early detection of these alterations and may support the design of targeted rehabilitation strategies to optimize functional recovery and long-term quality of life in pediatric cancer survivors. Full article

Background/Objectives: Fever and pain are among the most common symptoms in pediatric infections and chronic diseases, causing significant discomfort for children and concern for caregivers. Effective management is essential to relieve distress while avoiding overtreatment or undertreatment. Paracetamol and nonsteroidal anti-inflammatory drugs (NSAIDs), particularly ibuprofen, are the primary antipyretic and analgesic agents in pediatric care, but their use in children with chronic conditions might be challenging. Methods: A narrative review and clinical expert judgment were used to synthesize current evidence on the use of paracetamol and NSAIDs (especially ibuprofen) in children with some common chronic diseases. Results: Paracetamol is often considered a first-line option in several chronic conditions. Caution is warranted in children with pre-existing malnutrition, obesity, and neuromuscular disorders as these factors might increase the risk of hepatotoxicity. NSAIDs provide additional anti-inflammatory effects and comparable analgesic efficacy but should be used cautiously in some high-risk populations due to potential gastrointestinal, renal, and bleeding complications. Their use is contraindicated in children with dehydration, renal impairment, nephrotic syndrome relapses, while careful risk-benefit assessment is required in small and vulnerable neonates. Some data also suggests NSAIDs may worsen outcomes in certain acute bacterial and viral infections. Data on chronic infections such as tuberculosis, HIV, and viral hepatitis are limited, highlighting the need for further research. Combination therapy with paracetamol and ibuprofen may enhance analgesia in postoperative settings without significantly increasing adverse events. Overall, available evidence is limited and largely observational. Conclusions: This narrative review synthesizes current evidence and clinical expertise to provide practical guidance on the rational use of paracetamol and NSAIDs in children, emphasizing individualized therapy according to comorbidities, risk factors, and clinical context, particularly in vulnerable populations. A risk-adapted, evidence-based approach ensures optimal symptom control while minimizing harm, supporting safer, more effective, and family-centered care for children with fever and pain. Full article