Compression Injury Research Articles

The use of electrical stimulation to enhance recovery following peripheral nerve injury.

Peripheral nerve injury is common and can have devastating consequences. In severe cases, functional recovery is often poor despite surgery. This is primarily due to the exceedingly slow rate of nerve regeneration at only 1-3 mm/day. The local environment in the distal nerve stump supportive of nerve regrowth deteriorates over time and the target end organs become atrophic. To overcome these challenges, investigations into treatments capable of accelerating nerve regrowth are of great clinical relevance and are an active area of research. One intervention that has shown great promise is perioperative electrical stimulation. Postoperative stimulation helps to expedite the Wallerian degeneration process and reduces delays caused by staggered regeneration at the site of nerve injury. By contrast, preoperative "conditioning" stimulation increases the rate of nerve regrowth along the nerve trunk. Over the past two decades, a rich body of literature has emerged that provides molecular insights into the mechanism by which electrical stimulation impacts nerve regeneration. The end result is upregulation of regeneration-associated genes in the neuronal body and accelerated transport to the axon front for regrowth. The efficacy of brief electrical stimulation on patients with peripheral nerve injuries was demonstrated in a number of randomized controlled trials on compressive, transection and traction injuries. As approved equipment to deliver this treatment is becoming available, it may be feasible to deploy this novel treatment in a wide range of clinical settings.

Review of the treatment options and results of earthquake-related pelvic injuries after the Türkiye earthquake on 6th February.

The aim of this study was to review the characteristics and classifications of pelvic injuries due to earthquake trauma, to determine the treatment options and outcomes, and to present the experiences of our single trauma center. Sixty patients (23 male, 37 female) who underwent surgical treatment for pelvic ring injuries after the earthquake were analyzed in this study. Demographic data, such as age and gender, operations, and fracture details were recorded. Laboratory results and the amount of blood used were included in the analysis. Fractures were classified according to the Young-Burgess classification. Surgical treatment methods, side of injury, accompanying injuries, and treatment results were analyzed using SPSS software. Left-sided trauma was the most common mechanism of injury, with 36 patients (60%) sustaining left-sided pelvic fractures. Pelvic ring fractures were detected in 78.3% of patients, and combined acetabulum and pelvic ring fractures were identified in 21.7% of patients. Thoracic trauma and extra-pelvic fractures were seen in 12 (20%) and 18 (30%) patients, respectively. Twenty percent of patients underwent emergency abdominal surgery prior to pelvic surgery. Complications were observed in 7 patients (11.6%) in the early period. The average amount of blood used for patients was 2.91 U (min: 0, max: 13 U, SD: 2.66). This study has shown us that lateral compression injuries are more common, and that low hemoglobin levels, high inflammation parameters, previous abdominal surgery, accompanying fractures, and lung injury are the main characteristics of patients with earthquake-related pelvic injuries. It also demonstrates that for the optimal use of materials and implants, experience in different techniques is required, and shows the significant need for blood transfusions in the treatment of these injuries. Level IV, Therapeutic study.

Exogenous NT-3 Promotes Phenotype Switch of Resident Macrophages and Improves Sciatic Nerve Injury through AMPK/NF-κB Signaling Pathway.

Neurotrophin-3 (NT-3) is an important family of neurotrophic factors with extensive neurotrophic activity, which can maintain the survival and regeneration of nerve cells. However, the mechanism of NT-3 on macrophage phenotype transformation after sciatic nerve injury is not clear. In this study, we constructed a scientific nerve compression injury animal model and administered different doses of NT-3 treatment through osmotic minipump. 7 days after surgery, we collected sciatic nerve tissue and observed the distribution of macrophage phenotype through iNOS and CD206 immunofluorescence. During the experiment, regular postoperative observations were conducted on rats. After the experiment, sciatic nerve tissue was collected for HE staining, myelin staining, immunofluorescence staining, and Western blot analysis. To verify the role of the AMPK/NF-κB pathway, we applied the AMPK inhibitor Compound C and the NF-κB inhibitor BAY11-7082 to repeat the above experiment. Our experimental results reveal that NT-3 promotes sciatic nerve injury repair and polarization of M2 macrophage phenotype, promotes AMPK activation, and inhibits NF-κB activation. The repair effect of high concentration NT-3 on sciatic nerve injury is significantly enhanced compared to low concentration. Compound C administration can weaken the effect of NT-3, while BAY 11-7082 can enhance the effect of NT-3. In short, NT-3 significantly improves sciatic nerve injury in rats, promotes sciatic nerve function repair, accelerates M2 macrophage phenotype polarization, and improves neuroinflammatory response. The protective effects of NT-3 mentioned above are partially related to the AMPK/NF-κB signal axis.

Exploring the Therapeutic Potential of Mesenchymal Stem Cells-derived conditioned medium: An In-depth Analysis of Pain Alleviation, Spinal CCL2 Levels, and Oxidative Stress.

Neuropathic pain, a debilitating condition, remains a significant challenge due to the lack of effective therapeutic solutions. This study aimed to evaluate the potential of mesenchymal stromal cell (MSC)-derived conditioned medium in alleviating neuropathic pain induced by sciatic nerve compression injury in adult male rats. Forty Wistar rats were randomly assigned to four groups: control, nerve injury, nerve injury with intra-neural injection of conditioned medium, and nerve injury with intra-neural injection of culture medium. Following sciatic nerve compression, the respective groups received either 10 µl of conditioned medium from amniotic fluid-derived stem cells or an equal volume of control culture medium. Behavioral tests for cold allodynia, mechanical allodynia, and thermal hyperalgesia were conducted, and the spinal cord was analyzed using Western Blot and oxidative stress assays. The behavioral experiments showed a decrease in mechanical hyperalgesia and cold allodynia in the group receiving conditioned medium compared to the injury group and the control medium group. Western blot data revealed a decrease in the expression of the CCL2 protein and an increase in GAD65. Oxidative stress tests also showed increased levels of SOD and glutathione in conditioned media-treated animals compared to animals with nerve injury. The findings suggest that conditioned medium derived from amniotic fluid-derived stem cells can effectively reduce neuropathic pain, potentially through the provision of supportive factors that mitigate oxidative stress and inflammation in the spinal cord.

NeuroAiDTM-II (MLC901) Promoted Neurogenesis by Activating the PI3K/AKT/GSK-3β Signaling Pathway in Rat Spinal Cord Injury Models.

Traumatic damage to the spinal cord (SCI) frequently leads to irreversible neurological deficits, which may be related to apoptotic neurodegeneration in nerve tissue. The MLC901 treatment possesses neuroprotective and neuroregenerative activity. This study aimed to explore the regenerative potential of MLC901 and the molecular mechanisms promoting neurogenesis and functional recovery after SCI in rats. A calibrated forceps compression injury for 15 s was used to induce SCI in rats, followed by an examination of the impacts of MLC901 on functional recovery. The Basso, Beattie, and Bresnahan (BBB) scores were utilized to assess neuronal functional recovery; H&E and immunohistochemistry (IHC) staining were also used to observe pathological changes in the lesion area. Somatosensory Evoked Potentials (SEPs) were measured using the Nicolet® Viking Quest™ apparatus. Additionally, we employed the Western blot assay to identify PI3K/AKT/GSK-3β pathway-related proteins and to assess the levels of GAP-43 and GFAP through immunohistochemistry staining. The study findings revealed that MLC901 improved hind-limb motor function recovery, alleviating the pathological damage induced by SCI. Moreover, MLC901 significantly enhanced locomotor activity, SEPs waveform, latency, amplitude, and nerve conduction velocity. The treatment also promoted GAP-43 expression and reduced reactive astrocytes (GFAP). MLC901 treatment activated p-AKT reduced p-GSK-3β expression levels and showed a normalized ratio (fold changes) relative to β-tubulin. Specifically, p-AKT exhibited a 4-fold increase, while p-GSK-3β showed a 2-fold decrease in T rats compared to UT rats. In conclusion, these results suggest that the treatment mitigates pathological tissue damage and effectively improves neural functional recovery following SCI, primarily by alleviating apoptosis and promoting neurogenesis. The underlying molecular mechanism of this treatment mainly involves the activation of the PI3K/AKT/GSK-3β pathway.

Cortical spheroids show strain-dependent cell viability loss and neurite disruption following sustained compression injury.

Sustained compressive injury (SCI) in the brain is observed in numerous injury and pathological scenarios, including tumors, ischemic stroke, and traumatic brain injury-related tissue swelling. Sustained compressive injury is characterized by tissue loading over time, and currently, there are few in vitro models suitable to study neural cell responses to strain-dependent sustained compressive injury. Here, we present an in vitro model of sustained compressive neural injury via centrifugation. Spheroids were made from neonatal rat cortical cells seeded at 4000 cells/spheroid and cultured for 14 days in vitro. A subset of spheroids was centrifuged at 104, 209, 313 or 419 rads/s for 2 minutes. Modeling the physical deformation of the spheroids via finite element analyses, we found that spheroids centrifuged at the aforementioned angular velocities experienced pressures of 10, 38, 84 and 149 kPa, respectively, and compressive (resp. tensile) strains of 10% (5%), 18% (9%), 27% (14%) and 35% (18%), respectively. Quantification of LIVE-DEAD assay and Hoechst 33342 nuclear staining showed that centrifuged spheroids subjected to pressures above 10 kPa exhibited significantly higher DNA damage than control spheroids at 2, 8, and 24 hours post-injury. Immunohistochemistry of β3-tubulin networks at 2, 8, and 24 hours post-centrifugation injury showed increasing degradation of microtubules over time with increasing strain. Our findings show that cellular injuries occur as a result of specific levels and timings of sustained tissue strains. This experimental SCI model provides a high throughput in vitro platform to examine cellular injury, to gain insights into brain injury that could be targeted with therapeutic strategies.

Spinal cord injury in high-risk complex adult spinal deformity surgery: review of incidence and outcomes from the Scoli-RISK-1 study

Study designClinical case series.ObjectiveTo describe the cause, treatment and outcome of 6 cases of perioperative spinal cord injury (SCI) in high-risk adult deformity surgery.SettingAdult spinal deformity patients were enrolled in the multi-center Scoli-RISK-1 cohort study.MethodsA total of 272 patients who underwent complex adult deformity surgery were enrolled in the prospective, multi-center Scoli-RISK-1 cohort study. Clinical follow up data were available up to a maximum of 2 years after index surgery. Cases of perioperative SCI were identified and an extensive case review was performed.ResultsSix individuals with SCI were identified from the Scoli-RISK-1 database (2.2%). Two cases occurred intraoperatively and four cases occurred postoperatively. The first case was an incomplete SCI due to a direct intraoperative insult and was treated postoperatively with Riluzole. The second SCI case was caused by a compression injury due to overcorrection of the deformity. Three cases of incomplete SCI occurred; one case of postoperative hematoma, one case of proximal junctional kyphosis (PJK) and one case of adjacent segment disc herniation. All cases of post-operative incomplete SCI were managed with revision decompression and resulted in excellent clinical recovery. One case of incomplete SCI resulted from infection and PJK. The patient’s treatment was complicated by a delay in revision and the patient suffered persistent neurological deficits up to six weeks following the onset of SCI.ConclusionDespite the low incidence in high-risk adult deformity surgeries, perioperative SCI can result in devastating consequences. Thus, appropriate postoperative care, follow up and timely management of SCI are essential.

EVALUATION AND MANAGEMENT STRATEGIES FOR PATIENTS WITH BLUNT ABDOMINAL TRAUMA: A HOSPITAL-BASED STUDY

Introduction:Blunt trauma to the abdomen occurs due to forces that induce shearing, compression, or deceleration injuries, particularly affecting anatomical structures that are relatively immobile. The evaluation of abdominal injuries is challenging and often results in missed diagnoses due to the complexity of symptoms and the difficulty in identifying subtle signs of internal injury. Aims & Objectives:To study the clinical presentation, evaluation, diagnostic investigations, and management strategies for various intra-abdominal organ injuries resulting from blunt trauma to the abdomen. Methods: - Following initial resuscitation and attainment of hemodynamic stability, all blunt abdominal trauma patients underwent meticulous clinical history-taking and comprehensive physical examination. Subsequent management decisions, whether operative or non-operative, were determined based on the integrated findings of clinical assessments and radiological evaluations. Results:Between August 2022 and August 2023, fifty (50) patients with blunt trauma to the abdomen were admitted to Basaveshwara Teaching and General Hospital, Kalaburagi. In this study, males predominated in the 21 to 30-year age group, which represented the most frequent demographic for abdominal blunt trauma. Traffic collisions were identified as the leading cause of abdominal blunt trauma. The spleen emerged as the organ most frequently affected. Of the patients, 28 underwent conservative management, while 22 required surgical intervention. Conclusion:In cases of blunt trauma to the abdomen, the early hours following injury are critically significant and represent a crucial window, often referred to as the golden period of trauma, associated with higher survival rates. Timely intervention andappropriate management during this phase have been shown to significantly decrease morbidity and mortality rates associated with blunt trauma abdomenandappropriate management during this phase have been shown to significantly decrease morbidity and mortality rates associated with blunt trauma abdomen.

A novel minimally invasive and versatile kyphoplasty balloon-based model of porcine spinal cord injury.

Spinal cord injury (SCI) animal models often utilize an open surgical laminectomy, which results in animal morbidity and also leads to changes in spinal canal diameter, spinal cord perfusion, cerebrospinal fluid flow dynamics, and spinal stability which may confound SCI research. Moreover, the use of open surgical laminectomy for injury creation lacks realism when considering human SCI scenarios. We developed a novel, image-guided, minimally invasive, large animal model of SCI which utilizes a kyphoplasty balloon inserted into the epidural space via an interlaminar approach without the need for open surgery. The model was validated in 5 Yucatán pigs with imaging, neurofunctional, histologic, and electrophysiologic findings consistent with a mild compression injury. Few large animal models exist that have the potential to reproduce the mechanisms of spinal cord injury (SCI) commonly seen in humans, which in turn limits the relevance and applicability of SCI translational research. SCI research relies heavily on animal models, which typically involve an open surgical, dorsal laminectomy which is inherently invasive and may have untoward consequences on animal morbidity and spinal physiology that limit translational impact. We developed a minimally invasive, large animal model of spinal cord injury which utilizes a kyphoplasty balloon inserted percutaneously into the spinal epidural space. Balloon inflation results in a targeted, compressive spinal cord injury with histological and electrophysiological features directly relevant to human spinal cord injury cases without the need for invasive surgery. Balloon inflation pressure, length of time that balloon remains inflated, and speed of inflation may be modified to achieve variations in injury severity and subtype.

Purtscher Retinopathy Resulting from a Car Crash Accident-Multimodal Imaging Value.

Purtscher retinopathy is a rare but severe sight-threatening eye condition that mostly occurs in middle-aged men after chest compression or head injury. In cases such as acute pancreatitis, connective tissue disorders, kidney failure or COVID-19 infection with similar ocular findings but no history of trauma, a diagnosis of Purtscher-like retinopathy is made. We present a case of a 72-year-old female with typical symptoms of Purtscher retinopathy in both eyes after a car crash accident. Although the pathophysiology of the disease is not fully understood, the main cause of Purtscher retinopathy seems to be an embolic occlusion of the precapillary arterioles which supply the superficial peripapillary capillaries. Activation of the C5a component of the complement predisposes the leukocytes to aggregation, which obstructs blood flow. The main symptom of Purtscher retinopathy is sudden, painless deterioration of vision which occurs up to 48 h after the injury. In most patients, the changes observed in the fundus of the eye resolve within several months, and visual acuity slowly improves, sometimes even returning to the state from before the injury. However, risk factors such as older age, high hyperopia, and late treatment implementation can make the prognosis less favorable.

Posterior-only fixation in pelvic fractures: Is it sufficient in lateral compression injuries?

PurposeLateral compression (LC) injuries account for more than two-thirds of all pelvic fractures. The goal of surgical treatment is to provide adequate stability and early mobilization. The consensus on posterior fixation of such injuries is strong in the literature; however, the necessity of anterior ring fixation is not clear. Therefore, this study was formulated to determine the practicability of posterior-only fixation in LC injuries. MethodsBetween March 2015 and May 2020, all patients with LC type pelvic ring fractures who were admitted and operated upon in a single level 1 trauma center were included in this cross-sectional observational study. Demographic data, co-morbidities, treatment, types of surgical fixation, concomitant injuries and surgeries, surgical complications, length of hospital stay, injury to weight bearing duration, and follow-up period were documented. Functional outcome and quality of life were assessed using Majeed score and SF-36 questionnaire. Non-normally distributed data were presented as median (Q1, Q3) and normally distributed data were presented as mean ± SD. Spearman's rank correlation coefficient was used for correlation analysis. ResultsA total of 25 patients were included, with a mean age of 29.8 years. All patients were managed operatively with posterior-only fixation. The median Majeed score was 90 (76, 95). The median physical component summary score was 69.37 (38.75, 85.62). The median mental component summary score was 63.95 (39.25, 87.87). There was no significant difference compared to population norms of both physical component summary and mental component summary. Injury to weight bearing time correlated significantly (p = 0.002) with Majeed score as well as SF-36 score (p = 0.044). No other variable had a significant association with outcomes. ConclusionPosterior-only fixation is sufficient for fixing LC injuries with up to 80% of cases having good to excellent functional outcomes. However, comparative studies with larger sample sizes are needed for further validation.

Current Clinical Concepts: Rehabilitation of Thoracic Outlet Syndrome.

Thoracic outlet syndrome (TOS) involves inconsistent symptoms, presenting a challenge for medical providers to diagnose and treat. Thoracic outlet syndrome is defined as a compression injury to the brachial plexus, subclavian artery or vein, or axillary artery or vein occurring between the cervical spine and upper extremity. Three common subcategories are now used for clinical diagnosis: neurogenic, arterial, and venous. Postural position and repetitive motions such as throwing, weightlifting, and manual labor can lead to symptoms. Generally, TOS is considered a diagnosis of exclusion for athletes due to the poor accuracy of clinical testing, including sensitivity and specificity. Thus, determining a definitive diagnosis and reporting injury is difficult. Current literature suggests there is not a gold standard diagnostic test. Rehabilitation has been shown to be a vital component in the recovery process for neurogenic TOS and for arterial TOS and venous TOS in postoperative situations.

Mechanism of IRF5-regulated CXCL13/CXCR5 Signaling Axis in CCI-induced Neuropathic Pain in Rats.

Neuropathic pain is chronic and affects the patient's life. Studies have shown that IRF5 and CXCL13/CXCR5 are involved in neuropathic pain; however, their interactions are unknown. In this study, a rat neuropathic pain model was constructed by inducing chronic compression injury (CCI). IRF5 recombinant lentiviral vector and CXCL13 neutralizing antibody were administered to investigate their action mechanisms in neuropathic pain. Consequently, the new strategies for disease treatment could be evolved. The CCI rats were intrathecally injected with recombinant lentivirus plasmid LV-IRF5 (overexpression), LV-SH-IRF5 (silencing), and CXCL13 neutralizing antibody. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured. The tumor necrosis factor (TNF)-alpha, interleukin (IL)-1β, and IL-6 levels were recorded via the enzyme-linked immunosorbent assay (ELISA). The spinal cord was stained using hematoxylin-eosin (HE). The binding of IRF5 to CXCL13 was analyzed by chromatin immunoprecipitation (ChIP) and dual luciferase reporter assay. The IRF5, neuronal nuclei (NeuN), CXCL13, and CXCR5 expressions were detected through quantitative real-time polymerase chain reaction and Western blot. The MWT and TWL values in the CCI group were lower than in the Sham group. The expressions of CXCL13, CXCR5, and IRF5 in CCI rats were gradually increased with the modeling time. IRF5 silencing suppressed the expression of NeuN and lumbar enlargement in CCI rats and promoted MWT and TWL. Moreover, IRF5 silencing inhibited the expressions of CXCR5 and CXCL13 genes and down-regulated the expression levels of inflammatory factors. IRF5 was directly and specifically bound with the endogenous CXCL13 promoter and thus regulated it. IRF5 overexpression exacerbated the disease phenotype of CCI-induced neuropathic pain in rats. Administration of CXCL13 neutralizing antibodies reversed the IRF5 overexpression effects. The IRF5 silencing alleviated neuropathic pain in CCI rats by downregulating the pain threshold, inflammatory cytokine levels, and CXCL13/CXCR5 signaling. IRF5 overexpression exacerbated the disease parameters of CCI-induced neuropathic pain in rats; however, they were reversed by neutralizing antibodies against CXCL13.

Myelinated peripheral axons are more vulnerable to mechanical trauma in a model of enlarged axonal diameters.

The velocity of axonal impulse propagation is facilitated by myelination and axonal diameters. Both parameters are frequently impaired in peripheral nerve disorders, but it is not known if the diameters of myelinated axons affect the liability to injury or the efficiency of functional recovery. Mice lacking the adaxonal myelin protein chemokine-like factor-like MARVEL-transmembrane domain-containing family member-6 (CMTM6) specifically from Schwann cells (SCs) display appropriate myelination but increased diameters of peripheral axons. Here we subjected Cmtm6-cKo mice as a model of enlarged axonal diameters to a mild sciatic nerve compression injury that causes temporarily reduced axonal diameters but otherwise comparatively moderate pathology of the axon/myelin-unit. Notably, both of these pathological features were worsened in Cmtm6-cKo compared to genotype-control mice early post-injury. The increase of axonal diameters caused by CMTM6-deficiency thus does not override their injury-dependent decrease. Accordingly, we did not detect signs of improved regeneration or functional recovery after nerve compression in Cmtm6-cKo mice; depleting CMTM6 in SCs is thus not a promising strategy toward enhanced recovery after nerve injury. Conversely, the exacerbated axonal damage in Cmtm6-cKo nerves early post-injury coincided with both enhanced immune response including foamy macrophages and SCs and transiently reduced grip strength. Our observations support the concept that larger peripheral axons are particularly susceptible toward mechanical trauma.

Establishment of Facial Nerve Injury Rat Model for Idiopathic Facial Paralysis Research.

Idiopathic facial paralysis is the most common type of facial nerve injury, accounting for approximately 70% of peripheral facial paralysis cases. This disease can not only lead to a change in facial expression but also greatly impact the psychology of patients. In severe cases, it can affect the normal work and life of patients. Therefore, the research on facial nerve injury repair has important clinical significance. In order to study the mechanism of this disease, it is necessary to carry out relevant animal experiments, among which the most important task is to establish an animal model with the same pathogenesis as human disease. The compression of the facial nerve within the petrous bone, especially the nerve trunk at the junction of the distal end of the internal auditory canal and the labyrinthine segment, is the pathogenesis of idiopathic facial paralysis. In order to simulate this common disease, a compression injury model of the main extracranial segment of the facial nerve was established in this study. The neurological damage was evaluated by behavioral, neuroelectrophysiological, and histological examination. Finally, 50 g constant force and 90 s clamp injury were selected as the injury parameters to construct a stable idiopathic facial paralysis model.

Inosine Improves Functional Recovery and Cell Morphology Following Compressive Spinal Cord Injury in Mice.

Spinal cord injury (SCI) is one of the most serious conditions of the central nervous system, causing motor and sensory deficits that lead to a significant impairment in the quality of life. Previous studies have indicated that inosine can promote regeneration after SCI. Here we investigated the effects of inosine on the behavioral and morphological recovery after a compressive injury. Adult female C57BL/6 mice were subjected to laminectomy and spinal cord compression using a vascular clip. Inosine or saline injections were administered intraperitoneally, with the first dose performed 24 h after injury and daily for 7 days after injury. The mice were evaluated using Basso Mouse Scale (BMS), locomotor rating scale, and pinprick test for 8 weeks. At the end, the animals were anesthetized and euthanized, and the spinal cords were collected for morphological evaluation. Inosine-treated animals presented better results in the immunostaining for oligodendrocytes and in the number of myelinated fibers through semithin sections compared to saline-treated animals, showing that there was a greater preservation of the white matter. Analysis of the immunoreactivity of astrocytes and evaluation of the inflammatory profile with macrophage labeling revealed that the animals of the inosine group had a lower immunoreactivity when compared to control, which suggests a reduction of the glial scar and less inflammation, respectively, leading to a more favorable microenvironment for spinal cord regeneration. Indeed, inosine-treated animals scored higher on the BMS scale and presented better results on the pinprick test, indicating that the treatment contributed to motor and sensory recovery. After the animals were sacrificed, we obtained the electroneuromyography, where the inosine group showed a greater amplitude of the compound muscle action potential. These results indicate that inosine contributed to the regeneration process in the spinal cord of mice submitted to compressive injury and should be further investigated as a candidate for SCI therapy.

Galectin-3 absence alters lymphocytes populations dynamics behavior and promotes functional recovery after spinal cord injury in mice

Spinal cord injury (SCI) results from various mechanisms that damage the nervous tissue and the blood-brain barrier, leading to sensory and motor function loss below the injury site. Unfortunately, current therapeutic approaches for SCI have limited efficacy in improving patients outcomes. Galectin-3, a protein whose expression increases after SCI, influences the neuroinflammatory response by favoring pro-inflammatory M1 macrophages and microglia, while inhibiting pro-regenerative M2 macrophages and microglia, which are crucial for inflammation resolution and tissue regeneration. Previous studies with Galectin-3 knock-out mice demonstrated enhanced motor recovery after SCI. The M1/M2 balance is strongly influenced by the predominant lymphocytic profiles (Th1, Th2, T Reg, Th17) and cytokines and chemokines released at the lesion site. The present study aimed to investigate how the absence of galectin-3 impacts the adaptive immune system cell population dynamics in various lymphoid spaces following a low thoracic spinal cord compression injury (T9-T10) using a 30 g vascular clip for one minute. It also aimed to assess its influence on the functional outcome in wild-type (WT)and Galectin-3 knock-out (GALNEG) mice. Histological analysis with hematoxylin-eosin and Luxol Fast Blue staining revealed that WT and GALNEG animals exhibit similar spinal cord morphology. The absence of galectin-3 does not affect the common neuroanatomy shared between the groups prompting us to analyze outcomes between both groups. Following our crush model, both groups lost motor and sensory functions below the lesion level. During a 42-day period, GALNEG mice demonstrated superior locomotor recovery in the Basso Mouse Scale (BMS) gait analysis and enhanced motor coordination performance in the ladder rung walk test (LRW) compared to WT mice. GALNEG mice also exhibited better sensory recovery, and their electrophysiological parameters suggested a higher number of functional axons with faster nerve conduction. Seven days after injury, flow cytometry of thymus, spleen, and blood revealed an increased number of T Reg and Th2 cells, accompanied by a decrease in Th1 and Th17 cells in GALNEG mice. Immunohistochemistry conducted on the same day exhibited an increased number of Th2 and T Reg cells around the GALNEG's spinal cord lesion site. At 42-day dpi immunohistochemistry analyses displayed reduced astrogliosis and greater axon preservation in GALNEG's spinal cord seem as a reduction of GFAP immunostaining and an increase in NFH immunostaining, respectively. In conclusion, GALNEG mice exhibited better functional recovery attributed to the milder pro-inflammatory influence, compensated by a higher quantity of T Reg and Th2 cells. These findings suggest that galectin-3 plays a crucial role in the immune response after spinal cord injury and could be a potential target for clinical therapeutic interventions.

The Spine is the Tree of Life: A Systematic Review and Meta-Analysis of the Radiographic Findings Related to Spinal Injuries in Athletes.

This review article explores spinal injuriesin athletes participating in various sporting activities. It also highlights the various mechanisms of injuries that contribute to spinal injuries in each sport. Electronic databases such as PubMed, Cochrane Library, Web of Science, Embase, MEDLINE Ovid, and Google Scholar were searched for articles from 2000 to 2022 on spine injuries in sports and radiological studies discussing the various injury patterns among athletes. Studies werescoured in accordance with the inclusion criteria, and relevant data such as the number of participants, sporting activities, spine injuries, and outcomes were retrieved. Fifteen articles that met the inclusion criteria were included in the study. Cervical spine injuries are common in athletes who participate in contact sports such as football. Similarly, athletes in collision sports such as football, rugby, and hockey are likely to suffer stingers due to traction and compression injuries. Players engaged in such assoccer, baseball, and swimming, are likely to suffer from spondylolysis. Soccer players are more prone to multiple lesions compared toathletes in sports such as baseball because the sport involves training exercises such as jogging and running without kicking any ball. In swimmers, spondylolysis is common in breaststroke and butterfly styles since they involve repeated flexion and hyperextension of the lumbar spine. CT is essential for diagnosing spondylolysis as it demonstrates the lesions more accurately. Ice hockey is associated with a significant incidence of cervical spine injuries, mostly due to players being constantly checked/pushed from behind. Spine injuries are common in elite athletes across several sports. About 10% of spinal injuries in the United States result from sports activities. In diagnosing spine injuries, imaging modalities such as MRI, CT, or plain radiographs are essential. From a radiologist's perspective, these testshelp immensely in deciding which treatment is required for a particular athlete or how the injury can be optimally managed. Achieving recovery from a specific spine injury usually depends on the kind of injury and the rehabilitation process the athletes undergo before returning to play.

Stigmasterol alleviates neuropathic pain by reducing Schwann cell-macrophage cascade in DRG by modulating IL-34/CSF1R.

This study aimed to investigate the potential therapeutic applications of stigmasterol for treating neuropathic pain. Related mechanisms were investigated by DRG single-cell sequencing analysis and the use of specific inhibitors in cellular experiments. In animal experiments, 32 male Sprague-Dawley rats were randomly divided into the sham operation group, CCI group, ibuprofen group, and stigmasterol group. We performed behavioral tests, ELISA, H&E staining and immunohistochemistry, and western blotting. Cell communication analysis by single-cell sequencing reveals that after peripheral nerve injury, Schwann cells secrete IL-34 to act on CSF1R in macrophages. After peripheral nerve injury, the mRNA expression levels of CSF1R pathway and NLRP3 inflammasome in macrophages were increased in DRG. Invitro studies demonstrated that stigmasterol can reduce the secretion of IL-34 in LPS-induced RSC96 Schwann cells; stigmasterol treatment of LPS-induced Schwann cell-conditioned medium (L-S-CM) does not induce the proliferation and migration of RAW264.7 macrophages; L-S-CM reduces CSF1R signaling pathway (CSF1R, P38MAPK, and NFκB) activation, NLRP3 inflammasome activation, and ROS production. Invivo experiments have verified that stigmasterol can reduce thermal and cold hyperalgesia in rat chronic compressive nerve injury (CCI) model; stigmasterol can reduce IL-1β, IL-6, TNF-α, CCL2, SP, and PGE2 in serum of CCI rats; immunohistochemistry and western blot confirmed that stigmasterol can reduce the levels of IL-34/CSF1R signaling pathway and NLRP3 inflammasome in DRG of CCI rats. Stigmasterol alleviates neuropathic pain by reducing Schwann cell-macrophage cascade in DRG by modulating IL-34/CSF1R axis.

Pirfenidone's Potential for Motor Recovery following Spinal Cord Compression Injury

Objective: The aim of this research was to access the ability of pirfenidone in improving motor activity of hindlimbs in rats following compression injury to spinal cord. Study Design: Experimental lab-based study. Settings: Institute of Basic Medical Sciences, Khyber Medical University Peshawar, Pakistan. Duration: From March 2020 to April 2023. Methods: Injury induction at the T7 spinal cord level was carried out using a 70gm force aneurysm clip in rats. The rats were divided into three groups: Group A received a daily placebo, Group B received a daily dose of pirfenidone at 200 mg/kg/day, and Group C received a daily dose of pirfenidone at 500 mg/kg/day. Each group was further subdivided into two sub-groups, labeled as Groups 1 and 2, each consisting of 5 rats. The experiment lasted for 14 and 28 days. On the final day, all rats underwent BBB scoring to evaluate the motor activity in their hind limbs. Results: BBB scores showed statistically significant differences both between and within groups. Among the SCI groups, those treated with pirfenidone displayed higher BBB scores compared to those without pirfenidone treatment. Conclusion: Pirfenidone may improve motor function post-spinal cord injury by reducing fibrosis, preventing collagen buildup in the core of glial scars, and reducing reactive astrocytosis in the scar's outer region. This dual action could promote axonal regeneration and enhance synaptic connections, aiding in neurological recovery.