Search Results (183)

Physical therapy is a critical component of medical rehabilitation, aiding recovery from conditions such as stroke, spinal cord injuries, and musculoskeletal disorders. Effective rehabilitation requires precise monitoring of patient performance to ensure exercises are executed correctly and progress is accurately assessed. This paper presents a novel automated system for controlling the rehabilitation process and evaluating physical therapy exercise quality using computer vision and a customized Human Skeleton-based Balanced Time Warping algorithm. The proposed method quantitatively assesses the similarity between a physiotherapist and patient performance by analyzing skeletal motion data extracted from RGB-D video sequences without requiring pre-alignment or sensor-specific calibration. A motion-dependent, weighted Euclidean distance between 3D skeletal models is used to compute pose dissimilarity, while a modified DTW approach aligns temporal sequences and evaluates dynamic consistency. The total dissimilarity measure is a balanced combination of posture (DP) and dynamics (DT) components. Evaluated on a custom dataset of 136 video recordings from 23 participants performing exercises in sitting and standing positions under varying performance accuracy levels (“good,” “intermediate,” and “bad”), the system demonstrates the strong clustering of accuracy levels. Proposed dissimilarity, together with a fixed reference element (physiotherapist), induces a natural non-strict order on the set of distances between patients and physiotherapists. A high value of Spearman’s rank correlation coefficient between computed dissimilarity and execution accuracy (0.977) indicates that this method is suitable for assessing exercise performance accuracy and for adequately evaluating the patient’s rehabilitation progress. The method enables objective, real-time feedback, reduces therapist workload, and supports remote monitoring, offering a scalable solution for personalized rehabilitation. Future work will involve clinical validation with post-stroke and cardiac patients. Full article

Spinal cord injury (SCI) is a neurological condition often resulting in permanent motor and sensory deficits, for which effective treatments remain limited. RNA interference (RNAi) is a post-transcriptional mechanism of the downregulation of gene expression mediated by small interfering RNAs. RNAi has demonstrated therapeutic efficacy in various neurological disorders, positioning it as a promising yet underexplored therapeutic strategy for SCI. Here, we provide a focused overview of the key pathological processes in SCI, including primary mechanical injury and secondary cascades such as inflammation, mitochondrial dysfunction, excitotoxicity, oxidative stress, multiple forms of cell death, and others. The potential of RNAi to selectively silence genes implicated in these pathological processes, thereby enhancing neuroprotection and functional recovery, is highlighted. We point out that not only protein-coding genes, but non-coding RNAs (ncRNAs) are suitable targets for RNAi. Novel RNAi tools such as CRISPR-Cas13 might revolutionize the field and offer new opportunities for SCI therapy. However, despite all these promising findings, relevant translational studies of RNAi remain scarce. Challenges related to delivery methods, long-term efficacy, and cell-specific targeting must be addressed. Importantly, combining RNAi with other strategies such as cell- or biomaterial-based therapies may enhance therapeutic outcomes. Future investigations should prioritize systematic comparisons of RNAi targets and delivery systems, ideally at single-cell resolution and in different SCI models, to identify the most relevant molecular pathways for clinical translation. Overall, RNAi represents a compelling but still underdeveloped approach for SCI therapy, requiring continued refinement to reach clinical application. Full article

Background: Animal-assisted activities (AAA) are participative interventions, designed to lower hospitalization-related stress and anxiety, enhance communicative readiness, improve quality of life and encourage human–animal interaction. The aim of the present study was to evaluate AAA effects in the context of intensive rehabilitation of patients with spinal cord injury (SCI), traumatic brain injury (TBI), stroke. Methods: AAA in this study were structured by a local specialized association, for small groups of patients (5/7 a time), biweekly; each session lasted 60 min. Each patient participated in 10 sessions of AAA. Evaluation rating scales were administered at T0 (before the first session) and T1 (after the last session, five weeks later) as follows: Neurobehavioral Rating Scale (NRS) in case of patient with stroke/TBI without disorder of consciousness; Hospital Anxiety and Depression Scale (HADS) for SCI patients. Results: A total of 50 patients concluded the study. NRS score for joined TBI and stroke populations varied from a T0 mean value of 32.34 [C.I. 26.83–37.35] to 17.21 [C.I. 12.66–21.76] (46.7%); this difference proved to be statistically significant (p = 0.000). Stroke patients had a 57.6% NRS lowering by mean 28.10 [C.I. 20.55–35.65] points to 12 [C.I. 6.6–17.36], which was significant (p = 0.000); similarly, TBI patients showed a mean decrease of 35.8% points from the initial 41.6 points [C.I. 37.29–45.93] to 26.76 [C.I. 21.94–31.59] (p = 0.002). As for HADS scores a smaller improvement was found in the cohort of SCI patients: anxiety registered a 1 mean point decrease at T1 (21.5%), from the initial 6.5 points [C.I. 3.80–9.34] to 5.1 ones [C.I. 3.17–7.11]. This variation was near the threshold of significance (p = 0.05). Depression domain, instead, improved by 2.35 mean points (37%), from the 6.35 initial points [C.I. 3.45–9.26] to the final 4 [C.I. 2.15–5.98] with reaching of a significant p value (p = 0.03). ANCOVA did not confirm this last value and showed no influence of age and gender on outcome variations. Discussion: AAA showed preliminary evidence to decrease neurobehavioral disorders in patients with high-complexity neurological diseases, particularly stroke and TBI. The role of AAA in SCI patients remains unclear. Future studies should address confounders’ role for these populations, particularly severity of disease. Furthermore, AAA interventions will have to be studied on larger samples, deepening the exact phase to introduce AAA for neurological patients. Lastly, qualitative studies are needed to explore patients’ lived experiences. Full article

Human induced pluripotent stem cells (hiPSCs) hold great potential for patient-specific therapies. Transplantation of hiPSC-derived neural progenitor cells (NPCs) is a promising reparative strategy for spinal cord injury (SCI), but clinical translation requires efficient differentiation into desired neural lineages and purification before transplantation. Here, differentiated hiPSCs—reprogrammed from human skin fibroblasts using Sendai virus-mediated expression of OCT4, SOX2, KLF4, and C-MYC—into neural rosettes expressing SOX1 and PAX6, followed by neuronal precursors (β-tubulin III⁺/NESTIN⁺) and glial precursors (GFAP+/NESTIN+). Both neuronal and glial precursors expressed the A2B5 surface antigen. A2B5+ NPCs, purified by fluorescence-activated cell sorting (FACS), proliferated in vitro with mitogens, and differentiated into mature neurons and astrocytes under lineage-specific conditions. Then, NOD-SCID mice received a T9 contusion injury followed by transplantation of A2B5+ NPCs, human fibroblasts, or control medium at 8 days post-injury. At two months, grafted NPCs showed robust survival, progressive neuronal maturation (β-tubulin III⁺→doublecortin⁺→NeuN⁺), and astrocytic differentiation (GFAP+), particularly in spared white matter. Transplantation significantly increased spared white matter volume and improved hindlimb locomotor recovery, with no teratoma formation observed. These results demonstrate that hiPSC-derived, FACS-purified A2B5+ NPCs can survive, differentiate into neurons and astrocytes, and enhance functional recovery after SCI. This approach offers a safe and effective candidate cell source for treating SCI and potentially other neurological disorders. Full article

Background: Brachial plexopathies comprise a diverse array of illnesses with multifactorial etiologies, including trauma, inflammation, neoplasia, and iatrogenic damage, frequently manifesting with nonspecific clinical symptoms. Precise and prompt imaging evaluation is essential for diagnosis, treatment planning, and monitoring. Objective: To equip radiologists with interpretative tools for a systematic assessment of the brachial plexus utilizing advanced imaging modalities, specifically ultrasound (US) and magnetic resonance imaging (MRI), while emphasizing techniques, indications, limitations, and critical radiologic signs for differential diagnosis. Imaging Techniques: This narrative review concentrates on US and MRI. High-frequency linear probes with multiplanar dynamic scans provide US visualization of trunks, cords, and terminal branches in superficial areas. Specialized MRI procedures (T1, T2, STIR, DWI, contrast-enhanced) provide comprehensive evaluation of spinal roots and deep tissues, differentiating preganglionic from postganglionic lesions. A combined US–MRI methodology can enhance diagnostic efficacy. Findings: Ultrasound is excellent for superficial and dynamic assessment, especially in post-traumatic and iatrogenic lesions, while MRI is the gold standard for deep structures and complex disorders. The integration of two modalities enhances lesion identification and treatment direction. Emerging methodologies further enhance diagnostic and prognostic capabilities. Conclusions: The synergistic application of US and MRI, emphasizing nerve injury patterns and muscle denervation indicators, facilitates precise and prompt diagnosis of brachial plexopathies. Standardizing imaging standards and incorporating modern techniques are essential for interdisciplinary, customized patient care. Full article

Spinal health depends on the dynamic interplay between mechanical forces, biochemical signaling, and cellular behavior. This review explores how key molecular pathways, including integrin, yeas-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), Piezo, and Wingless/Integrated (Wnt) with β-catenin, actively shape the structural and functional integrity of spinal tissues. These signaling mechanisms respond to physical cues and interact with inflammatory mediators such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α), driving changes that lead to disc degeneration, vertebral fractures, spinal cord injury, and ligament failure. New research is emerging that shows scaffold designs that can directly harness these pathways. Further, new stem cell-based therapies have been shown to promote disc regeneration through targeted differentiation and paracrine signaling. Interestingly, many novel bone and ligament scaffolds are modulating anti-inflammatory signals to enhance tissue repair and integration, as well as prevent scaffold degradation. Neural scaffolds are also arising. These mimic spinal biomechanics and activate Piezo signaling to guide axonal growth and restore motor function. Scientists have begun combining these biological platforms with brain–computer interface technology to restore movement and sensory feedback in patients with severe spinal damage. Although this technology is not fully clinically ready, this field is advancing rapidly. As implantable technology can now mimic physiological processes, molecular signaling, biomechanical design, and neurotechnology opens new possibilities for restoring spinal function and improving the quality of life for individuals with spinal disorders. Full article

Background: Dietary advice for Paralympic athletes (PAs) with a spinal cord injury (PAs-SCI) requires particular attention and has been widely studied. However, currently, no particular attention has been addressed to nutritional guidelines for athletes with an amputation (PAs-AMP). This study aimed at filling up this gap, at least partially, and compared veteran PAs-SCI with PAs-AMP. Methods: A sample of 25 male PAs (12 with SCI and 13 with AMP), recruited during two training camps, was submitted to the following questionnaires: allergy questionnaire for athletes (AQUA), Nordic Musculoskeletal Questionnaire (NMQ), Starvation Symptom Inventory (SSI), neurogenic bowel dysfunction (NBD), orthorexia (ORTO-15/ORTO-7), alcohol use disorders identification test (AUDIT), and Mediterranean diet adherence (MDS). The PAs were also submitted to the following measurements: dietary Oxygen Radical Absorbance Capacity (ORAC) and intakes, body composition, handgrip strength (HGS), basal energy expenditure (BEE), peak oxygen uptake (VO_2peak), peak power, peak heart rate (HR), post-exercise ketosis, and antioxidant response after a cardiopulmonary exercise test (CPET) to voluntary fatigue. Results: Compared to PAs-AMP, PAs-SCI had higher NBD and lower VO_2peak (p < 0.05), peak power, peak HR, peak lactate, phase angle (PhA) of the dominant leg (p < 0.05), and ORTO15 (p < 0.05). The latter was related to NBD (r = −0.453), MDS (r = −0.638), and ORAC (r = −0.529), whereas ORTO7 correlated with PhA of the dominant leg (r = 0.485). Significant differences between PAs-AMP and PAs-SCI were not found in the antioxidant response, glucose, and ketone levels after CPET, nor in dietary intake, AUDIT, AQUA, NMQ, SSI, BEE, HGS, and FM%. Conclusions: The present study showed that PAs-SCI and PAs-AMP display similar characteristics in relation to lifestyle, energy intake, basal energy expenditure, and metabolic response to CPET. Based on both the similarities with PAs-SCI and the consequences of the limb deficiency impairment, PAs-AMP and PAs-SCI require personalized nutritional advice. Full article

Oligodendrocyte precursor cells (OPCs) are a distinct and dynamic glial population that retain proliferative and migratory capacities throughout life. While traditionally recognized for differentiating into oligodendrocytes (OLs) and generating myelin to support rapid nerve conduction, OPCs are now increasingly appreciated for their diverse and non-canonical roles in the central nervous system (CNS), including direct interactions with neurons. A notable feature of OPCs is their expression of diverse ion channels that orchestrate essential cellular functions, including proliferation, migration, and differentiation. Given their widespread distribution across the CNS, OPCs are increasingly recognized as active contributors to the development and progression of various neurological disorders. This review aims to present a detailed summary of the physiological and pathological functions of ion channels in OPCs, emphasizing their contribution to CNS dysfunction. We further highlight recent advances suggesting that ion channels in OPCs may serve as promising therapeutic targets across a broad range of disorders, including, but not limited to, multiple sclerosis (MS), spinal cord injury, amyotrophic lateral sclerosis (ALS), psychiatric disorders, Alzheimer’s disease (AD), and neuropathic pain (NP). Finally, we discuss emerging therapeutic strategies targeting OPC ion channel function, offering insights into potential future directions in the treatment of CNS diseases. Full article

Background/Objectives: This study investigated variations in DNA methylation patterns associated with chronic pain and propensity for recurrent pressure injuries (PrI) in persons with spinal cord injury (SCI). Methods: Whole blood was collected from 81 individuals with SCI. DNA methylation was quantified using Illumina genome-wide arrays (EPIC and EPICv2). Comprehensive clinical profiles collected included secondary health complications, in particular current PrI and chronic pain. Relationships between recurrent PrI and chronic pain and whether the co-occurrence of both traits was mediated by changes in DNA methylation were investigated using R packages limma, DMRcate and mCSEA. Results: Three differentially methylated positions (DMPs) (cg09867095, cg26559694, cg24890286) and one region in the micro-imprinted locus for BLCAP/NNAT are associated with chronic pain in persons with SCI. The study cohort was stratified by PrI status to identify any sites associated with chronic pain and while the same three sites and region were replicated in the group with no recurrent PrI, two novel, hypermethylated (cg21756558, cg26217441) sites and one region in the protein-coding gene FDFT1 were identified in the group with recurrent PrI. Gene enrichment and genes associated with specific promoters using MetaScape identified several shared disorders and ontology terms between independent phenotypes of pain and recurrent PrI and interactive sub-groups. Conclusions: DMR analysis using mCSEA identified several shared genes, promoter-associated regions and CGI associated with overall pain and PrI history, as well as sub-groups based on recurrent PrI history. These findings suggest that a much larger gene regulatory network is associated with each phenotype. These findings require further validation. Full article

Human induced pluripotent stem cells (iPSCs) offer immense potential as a source for cell therapy in spinal cord injury (SCI) and other diseases. The development of hypoimmunogenic, universal cells that could be transplanted to any recipient without requiring a matching donor could significantly enhance their therapeutic potential and accelerate clinical translation. To create off-the-shelf hypoimmunogenic cells, we used CRISPR-Cas9 to delete B2M (HLA class I) and CIITA (master regulator of HLA class II). Double-knockout (DKO) iPSC-derived neural progenitor cells (NPCs) evaded T-cell-mediated immune rejection in vitro and after grafting into the injured spinal cord of athymic rats and humanized mice. However, loss of HLA class I heightened susceptibility to host natural killer (NK) cell attack, limiting graft survival. To counter this negative effect, we engineered DKO NPCs to overexpress macrophage migration inhibitory factor (MIF), an NK cell checkpoint ligand. MIF expression markedly reduced NK cell-mediated cytotoxicity and improved long-term engraftment and integration of NPCs in the animal models for spinal cord injury. These findings demonstrate that MIF overexpression, combined with concurrent B2M and CIITA deletion, generates hiPSC neural derivatives that escape both T- and NK-cell surveillance. This strategy provides a scalable route to universal donor cells for regenerative therapies in SCI and potentially other disorders. Full article

Background: People with spinal cord injury/disorder are at a high risk of pressure injury formation, and, in advanced cases, surgery is mandatory. These patients present specific clinical aspects to consider in order to reduce the risk of complications. This paper is a narrative review and expert opinion based on the authors’ institutional experience of over 10 years in a spinal unit. The specific protocols of treatment based on a multidisciplinary approach, protocols of flap selection, and strategies to prevent and manage complications are reviewed. The specific clinical aspects of each patient that should be considered during treatment to optimize the results and to reduce complication rates are reviewed. Conclusions: A multidisciplinary team approach and specific protocols for patient management allow for a reduction in complication rates in the surgical treatment of pressure injuries in spinal cord injury patients and implement an overall success rate. Complications management protocols should be developed and investigated to further improve the overall success rate. Full article

The gut–brain axis (GBA) refers to the biochemical bidirectional communication between the central nervous system (CNS) and the gastrointestinal tract, linking brain and gut functions. It comprises a complex network of interactions involving the endocrine, immune, autonomic, and enteric nervous systems. The balance of this bidirectional pathway depends on the composition of the gut microbiome and its metabolites. While the causes of neurodegenerative diseases (NDDs) vary, the gut microbiome plays a crucial role in their development and prognosis. NDDs are often associated with an inflammation-related gut microbiome. However, restoring balance to the gut microbiome and reducing inflammation may have therapeutic benefits. In particular, introducing short-chain fatty acid-producing bacteria, key metabolites that support gut homeostasis, can help counteract the inflammatory microbiome. This strong pathological link between the gut and NDDs underscores the gut–brain axis (GBA) as a promising target for therapeutic intervention. This review, by scrutinizing the more recent original research articles published in PubMed (MEDLINE) database, emphasizes the emerging notion that GBA is an equally important pathological marker for neurological movement disorders, particularly in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington’s disease and neurotraumatic disorders such as traumatic brain injury and spinal cord injury. Additionally, the GBA presents a promising therapeutic target for managing these diseases. Full article

Spinal cord injury (SCI) is one of the most frequent causes of disability, accompanied by motor and postural impairments, as well as autonomic and behavioural disorders. Since the beginning of the last century, researchers have been developing and refining experimental models of SCI to study pathogenesis and find therapies. Since the beginning of the 20th century, quite a wide range of methods have been developed for contusion and compression injury, complete and partial transection of the spinal cord, and many others. The choice of model subject in such studies was not limited to mammals, but also included amphibians, lampreys, and even fish. Many functional tests have been proposed to assess functional recovery after injury in laboratory animals, ranging from simple rating scales to locomotion kinematics or recording of spinal neuronal activity. This review describes existing models of SCI in most animal species used in neurobiology. Their key characteristics are discussed, which determine the choice of model and model animals depending on the experimental tasks. Each experimental model of SCI has its own advantages and disadvantages determined by species-specific features of spinal cord anatomy and physiology, the speed of recovery from injury, and the ratio of the necrosis zone to the penumbra. The applicability and availability of the proposed methods for assessing the speed and completeness of recovery is also an important factor. Full article

Neuropathic pain is a chronic disorder that arises from damaged or malfunctioning nerves. Hypersensitivity to stimuli, also known as hyperalgesia, can cause a person to experience pain from non-painful stimuli, termed allodynia. Cannabis-based medicines (CBMs) may provide new treatment options to manage neuropathic pain. A review of the relevant studies was conducted to evaluate the effectiveness of CBMs in treating neuropathic pain. Scientific literature was systematically searched from January 2003 to December 2024 using the Web of Science Core Collection, PubMed, and MEDLINE. A total of 22 randomized controlled trials (RCTs) were identified that considered the use of 1′,1′-dimethylheptyl-Δ⁸-tetrahydrocannabinol-11-oic acid (CT-3), Δ⁹-tetrahydrocannabinol (Δ⁹-THC), cannabidiol (CBD), combinations of Δ⁹-THC with CBD, and cannabidivarin for treatment of neuropathic pain. Significant reductions in pain were reported in 15 studies focused on the treatment of multiple sclerosis, spinal cord injuries, diabetic neuropathy, postherpetic neuralgia, HIV-associated sensory neuropathy, peripheral neuropathic pain, complex regional pain syndrome, chronic radicular neuropathic pain, and peripheral neuropathy of the lower extremities. These positive outcomes often adopted personalized and adjusted dosing strategies. By contrast, seven RCTs observed no significant pain relief compared to placebo, although some had minor improvements in secondary outcomes, such as mood and sleep. Collectively, CBM treatments may improve pain scores, but study limitations such as small sample sizes and study durations, high placebo response rates, and trial unblinding because of the psychoactive effects of cannabinoids all hinder data interpretation and the extrapolation to chronic pain conditions. Hence, future RCTs will need to have larger numbers and be more extended studies that explore optimal dosing and delivery methods and identify patient subgroups that are most likely to benefit. While CBMs show potential, their current use balances modest benefits against possible adverse effects and variable outcomes. Full article

Traumatic spinal cord injury (tSCI) is a devastating neurological disorder with profound effects on physical, psychological, and mental abilities. tSCI affects all age groups, with a higher incidence in elderly patients. There are many causes of tSCI, with motor vehicle accidents (MVA) and falls being the most common. The pathophysiology of tSCI is quite complex and involves primary and secondary injury. The primary injury directly results from the mechanical forces that caused the injury. Secondary injury is caused by long-term changes caused by inflammation, immune changes, and the formation of free radicals. Numerous studies have explored various medical and surgical treatment options that help mitigate long-term damage caused by tSCI and help improve quality of life. Currently, there are no treatments for tSCI that can reverse spinal cord damage or fully restore motor and sensory functions. However, many pharmacological and non-pharmacological options are being studied in tSCI patients. This review will discuss the background, pathophysiology, and clinical presentation of tSCI while also providing a detailed analysis of the recent advancements in treatment options. Full article