Paulina Cewe, Victor E. Staartjes, Victor Gabriel El-Hajj, Ihab Ahmad Al-Rikabi, Basel Musmar, Joana M Roy, Dennis Troung, Mats Beckman, Marcus Ohlsson, Pascal Jabbour, Adrian Elmi-Terander, Erik Edström
Neurospine 2025;22(4):905-915. Published online December 31, 2025
Objective Traumatic vertebral artery injuries (tVAIs) are uncommon but potentially devastating if missed. While computed tomography angiography (CTA) is routinely used for diagnosis, data on the number needed to image (NNI) remain limited. We hence analyzed tVAI epidemiology and imaging practices at a major Scandinavian level 1 trauma center.
Methods A retrospective study (2013–2020) was performed based on a single-center trauma registry. Patients were grouped based on CTA imaging protocol used; selective screening (2013–2017) and universal screening (2018–2020). Imaging protocols, treatment strategies, and outcomes were analyzed.
Results Among 2,843 patients admitted with level 1 trauma and receiving CTA imaging, 62 had a tVAI (2.2%) yielding a NNI of 46 patients to diagnose 1 tVAI. Twenty-five of these patients (40.3%) were found to have a posterior circulation stroke, resulting in an incidence of 0.9%, and a NNI of 114 to diagnose 1 stroke on CTA. NNIs for both tVAI and stroke detection increased with adoption of universal screening (tVAI: 35→65; stroke: 90→149). However, the detection rate of tVAI during the universal screening period was not significantly higher than during the selective screening period (p=0.261).
Conclusion In our level 1 trauma cohort, the incidence of tVAI was 2.2% and stroke rate 0.9%. The NNI rose with universal screening, yet detection rates did not improve. These findings suggest that selective screening based on risk factors may be more efficient than a universal approach. Further research is needed to balance diagnostic accuracy with resource use in trauma care.
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Optimizing Diagnostic Yield: Evidence Against Universal Computed Tomography Angiography for Traumatic Vertebral Artery Injury Screening – A Commentary on “Epidemiology and Screening of Traumatic Vertebral Artery Injuries at a Large Scandinavian Level 1 Tr Jae Taek Hong Neurospine.2025; 22(4): 916. CrossRef
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Objective Unilateral biportal endoscopic (UBE) spine surgery is a minimally invasive technique that uses continuous irrigation to improve visualization and control bleeding. Effective water pressure management is crucial for patient safety, particularly at the cervical and thoracic levels where spinal cord injury risk is higher. However, real-time pressure monitoring remains underexplored. This study evaluates the impact of real-time water pressure monitoring on safety during UBE surgery.
Methods A prospective study was conducted involving 20 patients undergoing UBE lumbar spine surgery. Patients were divided into 2 groups based on the irrigation system: gravity-based or infusion pump. Real-time water pressure was monitored using a digital sensor throughout surgery. Each procedure was categorized into 3 phases: phase I, working space preparation; phase II, laminectomy; phase III, flavectomy, dura exposure, and discectomy. Data was analyzed according to the type of irrigation system and surgical phase.
Results The mean water pressure in the surgical field during UBE spine surgery was 17.98± 8.07 mmHg, with no significant differences between surgical phases. However, the infusion pump system maintained significantly lower mean pressure (12.10±3.51 mmHg) compared to the gravity-based system (23.86±6.97 mmHg, p=0.001). The infusion pump system consistently maintained a significantly lower mean water pressure compared to the gravity-based system.
Conclusion Real-time water pressure monitoring during UBE surgery enhances safety by enabling improved control of pressure within the surgical field. Both the gravity-based and infusion pump systems safely maintained working space pressure, with the pump system showing significantly lower pressure levels.
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Objective Regeneration of corticospinal tract (CST) axons after spinal cord injury (SCI) is a key element in rebuilding neuronal connections to restore voluntary motor function. However, it remains challenging owing to limited effective interventions. This study adopted a modified transcranial optogenetic technique to stimulate CST axon regeneration into the injury site of completely transected SCI and explore the underlying molecular mechanisms.
Methods A novel optogenetic light emitting diode (LED) device was used to stimulate the brain motor cortex in channelrhodopsin-2–yellow fluorescent protein (ChR2-YFP) transgenic mice to observe the regeneration of CST axons in the injury site of a complete SCI. The LED device was also used In vitro to stimulate the motor cortex slices of the transgenic mouse brain for observing the outgrowth of their neurites.
Results After transcranial optogenetic stimulation, the pyramidal neurons of bilateral cerebral motor cortices, in ChR2-YFP transgenic mice were activated, CST axons regenerated into the injury site of the spinal cord, and the motor function of the paralyzed hindlimbs improved. Proteomic analysis revealed that CST axon regeneration was associated with the activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway in the cerebral motor cortices. In vitro LED blue light illumination enhanced the outgrowth of neurites from the brain slices of transgenic mice. Treatment with a JAK2/STAT3 inhibitor led to a significant attenuation of neurite outgrowth.
Conclusion The modified transcranial optogenetic technique stimulated bilateral motor cortices, in the brains of ChR2-YFP transgenic mice. It increased the excitability of pyramidal neurons in the motor cortices, and promoted CST axon regeneration by activating the JAK2/STAT3 pathway, repairing complete SCI.
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Objective Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms.
Methods By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway.
Results In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway.
Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.
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Objective Spinal cord injury (SCI) leads to severe motor and sensory deficits, with limited treatment options. This study investigates how methylprednisolone-loaded nanoparticles (MP-NPs) modulate SCI repair by targeting solute carrier family 16 member 3 (SLC16A3) and reshaping the macrophage-inflammatory microenvironment.
Methods Transcriptome data were analyzed to identify differentially expressed genes (DEGs) associated with SCI. Immune infiltration and WGCNA (Weighted Gene Co-expression Network Analysis) identified genes linked to M2 macrophage polarization, pinpointing SLC16A3 as a key regulatory factor. MP-NPs were synthesized, characterized, and tested for their effects on macrophage polarization, neuronal protection, and SCI recovery in rats.
Results We identified 612 DEGs related to inflammation and immune response in SCI. SLC16A3, upregulated in SCI, was downregulated by MP-NPs. In vitro, MP-NPs promoted M2 macrophage polarization, enhanced neuronal survival, and supported neural stem cell differentiation. In vivo, MP-NPs significantly improved motor recovery, reduced inflammation, and facilitated neural repair in SCI rats.
Conclusion MP-NPs downregulate SLC16A3 and modulate the macrophage-inflammatory environment, promoting neural repair and functional recovery in SCI, offering a promising therapeutic strategy.
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Objective Spinal cord injury (SCI), one of the major disabilities concerning central nervous system injury, results in permanent tissue loss and neurological impairment. The existing therapeutic options for SCI are limited and predominantly consist of chemical compounds. In this study, we delved into the neuroprotective effects of myricetin, a natural flavonoid compound, and the underlying mechanisms, specifically in the context of SCI, utilizing an in vivo model. Previously, our investigations revealed an elevation in the phosphorylated form of Lin-11, Isl-1, and Mec-3 kinase1 (LIMK1) at chronic time points postinjury, coinciding with neuronal loss and scar formation. Our primary objective here was to assess the potential neuroprotective properties of myricetin in SCI and to ascertain if these effects were linked to LIMK inhibition, a hitherto unexamined pathway to date.
Methods Computational docking and molecular dynamics simulation studies were performed to assess myricetin’s potential to bind with LIMK. Then, using a rat contusion model, SCI was induced and different molecular techniques (Western blot, Evans Blue assay, quantitative reverse transcription polymerase chain reaction and immunohistochemistry) were performed to determine the effects of myricetin.
Results Remarkably, computational docking models identified myricetin as having a better interaction profile with LIMK than standard. Subsequent to myricetin treatment, a significant downregulation in phosphorylated LIMK expression was observed at chronic time points. This reduction correlated with a notable decrease in glial and fibrotic scar formation, and enhanced neuroprotection indicating a positive outcome in vivo.
Conclusion In summary, our findings underscore myricetin’s potential as a bioactive compound capable of attenuating SCI-induced injury cascades by targeting the LIMK pathway.
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Objective Oblique lumbar interbody fusion (OLIF), performed using a retroperitoneal approach, can lead to complications related to the approach, such as lumbar sympathetic chain injury (LSCI). Although LSCI is a common complication of OLIF, its reported incidence varies across studies due to an absence of specific diagnostic criteria. Moreover, research on the risk factors of postoperative sympathetic chain injuries after OLIF remains limited. Therefore, this study aimed to describe the incidence, and identify independent risk factors for LSCI, in patients with degenerative lumbar spinal diseases who underwent OLIF.
Methods Between October 2020 and August 2023, a retrospective review was conducted at our institute on 200 patients who underwent OLIF at 1 to 4 consecutive spinal levels (L1–5) for degenerative spinal diseases including spinal stenosis, spondylolisthesis, degenerative scoliosis. We excluded those with infections, trauma, tumors, and lower extremity edema/warmth due to other causes. The patients were categorized into 2 groups: those with and without LSCI symptoms. Demographic data, operative data, and pre- and postoperative parameters were evaluated for their association with LSCI using a univariate logistic regression model. Variables with a p-value <0.1 in the univariate analysis were included in a multivariate model to identify the independent risk factors.
Results Thirty-five of 200 patients (17.5%) developed LSCI symptoms after OLIF. Multivariate logistic regression analysis indicated that prolonged retraction time, particularly exceeding 31.5 miniutes, remained an independent risk factor (adjusted odds ratio, 12.59; p<0.001).
Conclusion This study demonstrated that prolonged retraction time was an independent risk factor for LSCI following OLIF, particularly when it exceeded 31.5 minutes. Protecting the lumbar sympathetic chain during surgery and minimizing retraction time are crucial to avoiding LSCI following OLIF.
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Objective The study aimed to investigate the role of N6-methyladenosine (m6A) modification in spinal cord injury (SCI) and its underlying mechanism, focusing on the interplay between m6A methyltransferase-like 3 (METTL3), miR-30c, and autophagy-related proteins.
Methods An SCI model was established in rats, and changes in autophagy-related proteins, m6A methylation levels, and miR-30c levels were analyzed. Hydrogen peroxide (H2O2)-stimulated spinal cord neuron cells (SCNCs) were used to assess the impact of METTL3 overexpression. The effects of STM2457, an antagonist of METTL3, were evaluated on cell viability, apoptosis, and autophagy markers in H2O2-stimulated SCNCs.
Results In the SCI model, decreased levels of autophagy markers and increased m6A methylation, miR-30c levels, and METTL3 were observed. Overexpression of METTL3 in SCNCs led to reduced cell viability, increased apoptosis, and suppressed autophagy. Conversely, co-overexpression of autophagy-related protein 5 (ATG5) or miR-30c inhibition reversed these effects. Knocking out METTL3 yielded opposite results. STM2457 treatment improved cell viability, reduced apoptosis, and upregulated autophagy markers in SCNCs, which also enhanced functional recovery in rats as measured by the Basso-Beattie-Bresnahan score and inclined plate test.
Conclusion STM2457 alleviated SCI by suppressing METTL3-mediated m6A modification of miR-30c, which in turn induces ATG5-mediated autophagy. This study provides insights into the role of m6A modification in SCI and suggests a potential therapeutic approach through targeting METTL3.
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This review aims to systematically evaluate the incidence, management strategies, and clinical outcomes of iatrogenic durotomy (ID) in endoscopic spine surgery and to propose a management flowchart based on the tear size and associated complications. A comprehensive literature search was conducted, focusing on studies involving endoscopic spinal procedures and incidental durotomy. The selected studies were analyzed for management techniques and outcomes, particularly in relation to the size of the dural tear and the presence of nerve root herniation. Based on these findings, a flowchart for intraoperative management was developed. A total of 14 studies were included, encompassing 68,546 patients. Varying incidences of ID, with management strategies largely dependent on the size of the dural tear, were found. Small tears (less than 5 mm) were often left untreated or managed with absorbable hemostatic agents, while medium (5–10 mm) and large tears (greater than 10 mm) required more complex approaches like endoscopic patch repair or open surgery. The presence of nerve root herniation necessitated immediate action, often influencing the decision to convert to open repair. Effective management of ID in endoscopic spine surgery requires a nuanced approach tailored to the size of the tear and specific intraoperative challenges, such as nerve root herniation. The proposed flowchart offers a structured approach to these complexities, potentially enhancing clinical outcomes and reducing complication rates. Future research with more rigorous methodologies is necessary to refine these management strategies further and broaden the applications of endoscopic spine surgery.
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Objective The therapeutic benefits of exosomes obtained from mesenchymal stem cells (MSCs) in acute spinal cord injury (SCI) have been demonstrated in recent years, but the precise mechanisms remain unknown. In this study, the efficacy and mechanisms of MSC-derived exosomes (MSC-Exo) in acute SCI were investigated.
Methods By utilizing a BV2 ferroptosis cellular model and an SCI rat model, we investigated the effects of MSC-Exo on iron death related indicators and NF-E2 related factor 2 (Nrf2)/GTP cyclolase I (GCH1)/5,6,7,8-tetrahydrobiopterin (BH4) signaling axis, as well as their therapeutic effects on SCI rats.
Results The results revealed that MSC-Exo effectively inhibited the production of ferrous iron, lipid peroxidation products malonaldehyde and reactive oxygen species, and ferroptosis-promoting factor prostaglandin-endoperoxide synthase 2. Concurrently, they upregulated ferroptosis suppressors FTH-1 (ferritin heavy chain 1), SLC7A11 (solute carrier family 7 member 11), FSP1 (ferroptosis suppressor protein 1), and GPX4 (glutathione peroxidase 4), contributing to enhanced neurological recovery in SCI rats. Further analysis showed the Nrf2/GTP/BH4 signaling pathway’s critical role in suppressing ferroptosis. Additionally, MSC-Exo was found to inhibit lipopolysaccharide-induced ferroptosis in BV2 cells and SCI rats by activating the Nrf2/GCH1/BH4 axis.
Conclusion In summary, the study demonstrates that MSC-Exo mitigates microglial cell ferroptosis via the Nrf2/GCH1/BH4 axis, showing potential for preserving and restoring neurological function post-SCI.
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Objective Surgical procedures for patients with posttraumatic syringomyelia (PTS) remain controversial. Until now, there have been no effective quantitative evaluation methods to assist in selecting appropriate surgical plans before surgery.
Methods We consecutively enrolled PTS patients (arachnoid lysis group, n = 42; shunting group, n = 14) from 2003 to 2023. Additionally, 19 intrathecal anesthesia patients were included in the control group. All patients with PTS underwent physical and neurological examinations and spinal magnetic resonance imaging preoperatively, 3–12 months postoperatively and during the last follow-up. Preoperative lumbar puncture was performed and blood-spinal cord barrier disruption was detected by quotient of albumin (Qalb, cerebrospinal fluid/serum).
Results The ages (p = 0.324) and sex (p = 0.065) of the PTS and control groups did not differ significantly. There were also no significant differences in age (p = 0.216), routine blood data and prognosis (p = 0.399) between the arachnoid lysis and shunting groups. But the QAlb level of PTS patients was significantly higher than that of the control group (p < 0.001), and the shunting group had a significantly higher QAlb (p < 0.001) than the arachnoid lysis group. A high preoperative QAlb (odds ratio, 1.091; 95% confidence interval, 1.004–1.187; p = 0.041) was identified as the predictive factor for the shunting procedure, with the receiver operating characteristic curve showing 100% specificity and 80.95% sensitivity for patients with a QAlb > 12.67.
Conclusion Preoperative QAlb is a significant predictive factor for the types of surgery. For PTS patients with a QAlb > 12.67, shunting represents the final recourse, necessitating the exploration and development of novel treatments for these patients.
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Objective Herein, we investigated whether mesenchymal stem cells (MSCs) transplantation combined with electroacupuncture (EA) treatment could decrease the proportion of proinflammatory microglia/macrophages and neurotoxic A1 reactive astrocytes and inhibit glial scar formation to enhance axonal regeneration after spinal cord injury (SCI).
Methods Adult rats were divided into 5 groups after complete transection of the spinal cord at the T10 level: a control group, a nonacupoint EA (NA-EA) group, an EA group, an MSC group, and an MSCs+EA group. Immunofluorescence labeling, quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blots were performed.
Results The results showed that MSCs+EA treatment reduced the proportion of proinflammatory M1 subtype microglia/macrophages, but increased the differentiation of anti-inflammatory M2 phenotype cells, thereby suppressing the mRNA and protein expression of proinflammatory cytokines (tumor necrosis factor-α and IL-1β) and increasing the expression of an anti-inflammatory cytokine (interleukin [IL]-10) on days 7 and 14 after SCI. The changes in expression correlated with the attenuated neurotoxic A1 reactive astrocytes and glial scar, which in turn facilitated the axonal regeneration of the injured spinal cord. In vitro, the proinflammatory cytokines increased the level of proliferation of astrocytes and increased the expression levels of C3, glial fibrillary acidic protein, and chondroitin sulfate proteoglycan. These effects were blocked by administering inhibitors of ErbB1 and signal transducer and activator of transcription 3 (STAT3) (AG1478 and AG490) and IL-10.
Conclusion These findings showed that MSCs+EA treatment synergistically regulated the microglia/macrophage subpopulation to reduce inflammation, the formation of neurotoxic A1 astrocytes, and glial scars. This was achieved by downregulating the ErbB1-STAT3 signal pathway, thereby providing a favorable microenvironment conducive to axonal regeneration after SCI.
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Objective Electroacupuncture (EA) has a definite effect on the treatment of spinal cord injuries (SCIs), but its underlying molecular mechanism remains unclear. Meanwhile, MiR106b-5p is an autophagy- and apoptosis-related microribonucleic acid, but whether it regulates the progression of autophagy and apoptosis in SCIs is yet undetermined. As such, this study aimed to elucidate the involvement of miR-106b-5p in the EA treatment of an SCI.
Methods The miR-106b-5p level was detected by quantitative real-time polymerase chain reaction. In vitro, SH-SY5Y cells were transfected with miR-106b-5p mimics or inhibitors to regulate the miR-106b-5p expression, while in vivo, SCI rats were treated with EA for 7 days at the bilateral Zusanli (ST36) and Jiaji (EX-B2) acupoints. The motor function was evaluated using the Basso-Beattie-Bresnahan (BBB) criteria. Further, autophagic vacuoles, pathological damage, and neuronal cell morphology were observed by transmission electron microscopy, as well as by hematoxylin and eosin and Nissl staining, respectively.
Results The miR-106b-5p level, which can interact directly with Beclin-1 by influencing its expression, as well as the expressions of P62, Caspase-3, and Bax, was upregulated after an SCI, but it decreased after EA. Moreover, the ratio of LC3-II to LC3-I was upregulated after EA. EA can enhance autophagy, reduce neuronal apoptosis, and minimize motor dysfunction and histopathological deficits after an SCI. More importantly, however, all the above effects induced by EA can be reversed after an injection of miR-106-5p agomir to produce an overexpression of miR-106b-5p.
Conclusion EA treatment could downregulate miR-106b-5p to alleviate SCI-mediated injuries by promoting autophagy and inhibiting apoptosis.
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Objective Spinal cord injury (SCI) is a severe type of neurological trauma. N6-methyladenosine (m6A) modification is one of the most common internal modifications of RNA. The role of METTL3, the predominant methylation enzyme of m6A modification, in SCI remains unclear. This study aimed to investigate the role of methyltransferase METTL3 in SCI.
Methods After establishing the oxygen-glucose deprivation (OGD) model of PC12 cells and rat spinal cord hemisection model, we found that the expression of METTL3 and the overall m6A modification level were significantly increased in neurons. The m6A modification was identified on B-cell lymphoma 2 (Bcl-2) messenger RNA (mRNA) by bioinformatics analysis, and m6A-RNA immunoprecipitation and RNA immunoprecipitation. In addition, METTL3 was blocked by the specific inhibitor STM2457 and gene knockdown, and then apoptosis levels were measured.
Results In different models, we found that the expression of METTL3 and the overall m6A modification level were significantly increased in neurons. After inducing OGD, inhibition of METTL3 activity or expression increased the mRNA and protein levels of Bcl-2, inhibited neuronal apoptosis, and improved neuronal viability in the spinal cord.
Conclusion Inhibition of METTL3 activity or expression can inhibit the apoptosis of spinal cord neurons after SCI through the m6A/Bcl-2 signaling pathway.
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