Spinal Nerve Injury Research Articles

Nerve injury augments Cacna2d1 transcription via CK2-mediated phosphorylation of the histone deacetylase HDAC2 in dorsal root ganglia

Development of chronic neuropathic pain involves complex synaptic and epigenetic mechanisms. Nerve injury causes sustained upregulation of α2δ-1 (encoded by the Cacna2d1 gene) in the dorsal root ganglion (DRG), contributing to pain hypersensitivity by directly interacting with and augmenting presynaptic NMDA receptor activity in the spinal dorsal horn. Under normal conditions, histone deacetylase 2 (HDAC2) is highly enriched at the Cacna2d1 gene promoter in the DRG, which constitutively suppresses Cacna2d1 transcription. However, nerve injury leads to HDAC2 dissociation from the Cacna2d1 promoter, promoting the enrichment of active histone marks and Cacna2d1 transcription in primary sensory neurons. In this study, we determined the mechanism by which nerve injury diminishes HDAC2 occupancy at the Cacna2d1 promoter in the DRG. Spinal nerve injury in rats increased serine-394 phosphorylation of HDAC2 in the DRG. Coimmunoprecipitation showed that nerve injury enhanced the physical interaction between HDAC2 and casein kinase II (CK2) in the DRG. Furthermore, repeated intrathecal treatment with CX-4945, a potent and specific CK2 inhibitor, markedly reversed nerve injury–induced pain hypersensitivity, HDAC2 phosphorylation, and α2δ-1 expression levels in the DRG. In addition, treatment with CX-4945 largely restored HDAC2 enrichment at the Cacna2d1 promoter and reduced the elevated levels of acetylated H3 and H4 histones, particularly H3K9ac and H4K5ac, at the Cacna2d1 promoter in the injured DRG. These findings suggest that nerve injury increases CK2 activity and CK2-HDAC2 interactions, which enhance HDAC2 phosphorylation in the DRG. This, in turn, diminishes HDAC2 enrichment at the Cacna2d1 promoter, thereby promoting Cacna2d1 transcription.

Spinal endoscopic technique in the surgical treatment of thoracic ossification of the ligamentum flavum

Thoracic ossification of the ligamentum flavum (TOLF) is a pathological heterotopic ossification disease in which the fibrous tissue of the ligamentum flavum of the thoracic spine converts into bony tissue, often leading to thoracic spinal stenosis and compression of the thoracic spinal cord nerve. When TOLF patients present with symptoms of spinal cord nerve compression, surgical treatment is usually required, and traditional open surgery is more invasive and carries a higher risk of spinal cord nerve injury. In recent years, domestic and foreign researchers have tried to apply spinal endoscopic techniques such as microendoscopy, percutaneous foraminoscopy, and unilateral biportal endoscopy for the treatment of TOLF, which can maximize the preservation of normal bone while achieving adequate decompression of the spinal cord nerve, with less damage to spinal stability, and have the advantages of less surgical trauma, less bleeding, and faster postoperative recovery. Due to the special anatomical structure of the thoracic vertebra, spinal endoscopic techniques should focus on safety and it is recommended that they are performed in experienced centers, and surgical indications should be strictly controlled.

Chronic shoulder pain due to spinal accessory nerve palsies present opportunities for improved care integration.

Aim: Chronic shoulder pain due to iatrogenic spinal accessory nerve (SAN) injury continues to be under-recognized, resulting in delayed time-to-diagnosis and poorer outcomes. Solutions are needed to improve the management of this condition, which can be challenging as care needs to be coordinated across pain management, neurophysiology, rehabilitationand reconstructive surgery.Cases: We present a series of sixpatients with shoulder pain refractory to conservative pain treatments to highlight how SAN injuries continued to be missed and treatment delayed, even at advanced care centers. The time to diagnosis of SAN palsy took an average of 21months and treatment was inconsistent for all patients.Discussion: None of the sixcases had initial suspicion of SAN palsy and only onepatient received targeted SAN injury care. SAN treatment should be started as early as possible so that patients can be referred for prompt surgical evaluation if they fail conservative management. Integrated care pathways may be a solution for formalizing multidisciplinary team involvement and improving SAN injury outcomes.Conclusion: Systemic processes, such as integrated care pathways, are needed to optimize early recognition and targeted treatment of SAN injury and may be beneficial for other underdiagnosed and undertreated neuropathic pain conditions.

Percutaneous Kyphoplasty via Transverse Process-Rib-Pedicle Approach for Upper and Middle Thoracic Osteoporosis Fracture with Pedicle Stenosis

ObjectiveTo explore the clinical effect of percutaneous kyphoplasty via Process-Rib-Pedicle approach for upper and middle thoracic osteoporosis fracture with Pedicle Stenosis. MethodsThis study is a retrospective observational study. In this study, we retrospectively analyzed the data of 62 patients with upper thoracic vertebral bone loss compression fracture (OVCF) treated via the Process-Rib-Pedicle pathway PKP at the First Affiliated Hospital of Soochow University from January 2020 to December 2022. The patients were divided into group A(Unilateral PKP, 38 cases) and group B(Bilateral PKP, 24 cases) . The aspects of surgical safety, clinical efficacy and radio-logical outcome were investigated. ResultsAll 62 patients successfully completed the surgery without any spinal cord, nerve, or vascular injury, and there were no complications such as infection and vascular embolism. The differences in VAS scores（P<0.05）, ODI functional index（P<0.05）, and Cobb angle（P<0.05） were significant when comparing preoperative and postoperative periods, and the differences were not significant when comparing the postoperative periods (P>0.05); There were no statistically significant differences in days of hospital stay(P=0.653), and the rate of bone cement leakage (P=0.537 )between the two groups. ConclusionFor upper middle osteoporotic thoracic vertebral fractures with pedicle stenosis, puncture via the Process-Rib-Pedicle path is a safe and reliable puncture route, and more than 2.5 ml of cement can achieve good clinical outcomes, regardless of bilateral or unilateral PKP.

The development of posterior reduction forceps for atlantoaxial dislocation and its preliminary application in irreducible atlantoaxial dislocation

ObjectiveTo develop posterior reduction forceps for atlantoaxial dislocation and evaluate the preliminary clinical application of this forceps in assisting simple posterior screw-rod system reduction and fixation in the treatment of irreducible atlantoaxial dislocation.MethodsBased on the posterior atlantoaxial screw-rod system, posterior reduction forceps was developed to assist simple posterior screw-rod system for the treatment of irreducible atlantoaxial dislocation. From January 2021 to October 2022, 10 cases with irreducible atlantoaxial dislocation were treated with this technique. The Japanese Orthopaedic Association (JOA) score was applied before and after surgery to evaluate the neurological status of the patient, and the Atlanto-dental interval (ADI) was measured before and after surgery to evaluate the atlantoaxial reduction. X-ray and CT were performed to evaluate internal fixation, atlantoaxial sequence and bone graft fusion during regular follow-up. MRI was performed to evaluate the status of atlantoaxial reduction and spinal cord compression after surgery.ResultsAll 10 patients were successfully operated, and there were no complications such as spinal nerve and vascular injury. Postoperative clinical symptoms were significantly relieved in all patients, and postoperative JOA score and ADI were significantly improved compared with those before surgery (P < 0.05).ConclusionsThe developed posterior reduction forceps for atlantoaxial dislocation can assist the simple posterior screw-rod system in the treatment of irreducible atlantoaxial dislocation to avoid the release in anterior or posterior approach and reduce the difficulty of surgery. The preliminary results of this technique are satisfactory and it has a good application prospect.

Alpha 2-adrenoceptor participates in anti-hyperalgesia by regulating metabolic demand.

The α2-adrenoceptor agonist dexmedetomidine is a commonly used drug for sedatives in clinics and has analgesic effects; however, its mechanism of analgesia in the spine remains unclear. In this study, we systematically used behavioural and transcriptomic sequencing, pharmacological intervention, electrophysiological recording and ultrasound imaging to explore the analgesic effects of the α2-adrenoceptor and its molecular mechanism. Firstly, we found that spinal nerve injury changed the spinal transcriptome expression, and the differential genes were mainly related to calcium signalling and tissue metabolic pathways. In addition, α2-adrenoceptor mRNA expression was significantly upregulated, and α2-adrenoceptor was significantly colocalised with markers, particularly neuronal markers. Intrathecal dexmedetomidine suppressed neuropathic pain and acute inflammatory pain in a dose-dependent manner. The transcriptome results demonstrated that the analgesic effect of dexmedetomidine may be related to the modulation of neuronal metabolism. Weighted gene correlation network analysis indicated that turquoise, brown, yellow and grey modules were the most correlated with dexmedetomidine-induced analgesic effects. Bioinformatics also annotated the involvement of metabolic processes and neural plasticity. A cardiovascular-mitochondrial interaction was found, and ultrasound imaging revealed that injection of dexmedetomidine significantly enhanced spinal cord perfusion in rats with neuropathic pain, which might be regulated by pyruvate dehydrogenase kinase 4 (pdk4), cholesterol 25-hydroxylase (ch25h) and GTP cyclohydrolase 1 (gch1). Increasing the perfusion doses of dexmedetomidine significantly suppressed the frequency and amplitude of spinal nerve ligation-induced miniature excitatory postsynaptic currents. Overall, dexmedetomidine exerts analgesic effects by restoring neuronal metabolic processes through agonism of the α2-adrenoceptor and subsequently inhibiting changes in synaptic plasticity.

Treatment Efficacy of CT-Guided Percutaneous Kyphoplasty Combined with Three-Dimensional Coordinate Guidance System on Osteoporotic Vertebral Compression Fracture

Purpose: To investigate the clinical effect of percutaneous kyphoplasty (PKP) guided by computed tomography (CT) combined with the three-dimensional coordinate guidance system on the treatment of osteoporotic vertebral compression fracture (OVCF). Methods: 32 cases of OVCF in the elderly admitted to our hospital from October 2019 to March 2021 underwent CT-guided PKP combined with the three-dimensional coordinate guidance system, and 36 vertebrae were treated. The patients’ VAS pain scores (visual analog scale) and ODI (Oswestry disability index) were observed after surgery, and the paired t-test was used to compare these indexes. Results: The 36 vertebrae that were treated with CT-guided PKP combined with the three-dimensional coordinate guidance system underwent unilateral pedicle puncture according to the path planned by CT images. With the ideal position of the puncture needle and a high success rate of puncture, the puncture time was 1.2–2.6 minutes, with an average of about 1.5 minutes; the injected bone cement ranged from 3 to 5.5 mL, with an average of 4.2 mL, and there were no spinal nerve injuries or leakage of the cement in the canal. VAS score decreased from 7.65 ± 0.60 before the operation to 2.59 ± 0.28 one day after the operation (P &lt; 0.01); ODI decreased from 62.3 ± 2.18 before the operation to 27.91 ± 1.32 after the operation (P &lt; 0.01). Conclusion: The application of CT-guided PKP combined with the three-dimensional coordinate guidance system has the advantages of accurate puncture, short operation time, less intraoperative bleeding, and low complications. This treatment is safe, reliable, and satisfactory for patients, and is worthy of clinical promotion.

α4 nicotinic receptors on GABAergic neurons mediate a cholinergic analgesic circuit in the substantia nigra pars reticulata.

Nicotinic acetylcholine receptors (nAChRs) regulate pain pathways with various outcomes depending on receptor subtypes, neuron types, and locations. But it remains unknown whether α4β2 nAChRs abundantly expressed in the substantia nigra pars reticulata (SNr) have potential to mitigate hyperalgesia in pain states. We observed that injection of nAChR antagonists into the SNr reduced pain thresholds in naïve mice, whereas injection of nAChR agonists into the SNr relieved hyperalgesia in mice, subjected to capsaicin injection into the lower hind leg, spinal nerve injury, chronic constriction injury, or chronic nicotine exposure. The analgesic effects of nAChR agonists were mimicked by optogenetic stimulation of cholinergic inputs from the pedunculopontine nucleus (PPN) to the SNr, but attenuated upon downregulation of α4 nAChRs on SNr GABAergic neurons and injection of dihydro-β-erythroidine into the SNr. Chronic nicotine-induced hyperalgesia depended on α4 nAChRs in SNr GABAergic neurons and was associated with the reduction of ACh release in the SNr. Either activation of α4 nAChRs in the SNr or optogenetic stimulation of the PPN-SNr cholinergic projection mitigated chronic nicotine-induced hyperalgesia. Interestingly, mechanical stimulation-induced ACh release was significantly attenuated in mice subjected to either capsaicin injection into the lower hind leg or SNI. These results suggest that α4 nAChRs on GABAergic neurons mediate a cholinergic analgesic circuit in the SNr, and these receptors may be effective therapeutic targets to relieve hyperalgesia in acute and chronic pain, and chronic nicotine exposure.

Traumatic spinal cord and peripheral nerve injuries: correlation of trauma type with subsequent disability

BackgroundTraumatic spinal cord and peripheral nerve injuries may lead to neurological deficits and fatal consequences. This study aimed to evaluate the characteristics of traumatic spinal cord and peripheral nerve injuries, examine the relationship between the type of injury and the affected nerves, and discuss appropriate prevention measures.ResultsOf these, 236 were males and 63 were females, and the mean age was 35.56 ± 15.10 years. Traffic accidents (56.9%) were the most common etiological factor. This study included 288 peripheral nerve injuries and 82 spinal cord injuries. The fibular nerve (n = 49) and cervical spinal cord (n = 35) were the most frequently injured areas. Permanent functional and sensorial losses associated with traumatic nerve injuries were observed in 239 (79.9%) cases, of which 171 exhibited loss of muscle strength, 114 presented with neuro-sensorial symptoms, 37 had urinary/faecal incontinence, and 1 demonstrated erectile dysfunction. And, the incidence of permanent loss of function was significantly higher following traffic accidents (χ\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\chi$$\\end{document}2 = 50.095, Adj. p < 0.001).ConclusionsPeripheral and spinal nerve injuries play a crucial role in forensic investigations, providing valuable insights into the circumstances surrounding a crime or injury. Their significance extends to both criminal and civil proceedings, influencing legal strategies, determinations of liability, and the quantification of damages. In this study, especially traffic accidents were significantly associated with nerve injuries leading to permanent loss of function, and the type of trauma was associated with the nerves injured. Therefore, this study will contribute to criminal and civil proceedings.

Long noncoding RNA small nucleolar RNA host gene 5 facilitates neuropathic pain in spinal nerve injury by promoting SCN9A expression via CDK9.

This study aims to explore the functions and mechanisms of long noncoding RNA small nucleolar RNA host gene 5 (SNHG5) in chronic constriction injury (CCI)-induced neuropathic pain (NP). An NP rat model was established using the CCI method and the NP severity was evaluated by paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). The expression of SNHG5, CDK9, and SCN9A was quantified in rat dorsal root ganglion, in addition to the detections of apoptosis, pathological changes, neuron number, and the co-localization of Nav1.7 and cleaved caspase-3 with NeuN. In ND7/23 cells, the apoptosis and lactate dehydrogenase concentration were assessed, as well as the relationship between SNHG5, CDK9, and SCN9A. In the dorsal root ganglion of CCI-treated rats, SNHG5 and SCN9A were upregulated and downregulation of SNHG5 suppressed SCN9A expression, increased the PWT and PWL, blocked neuroinflammation and neuronal apoptosis, and alleviated NP. Mechanistically, SNHG5 recruited CDK9 to enhance SCN9A-encoded Nav1.7 expression and promoted peripheral neuronal apoptosis and injury. In addition, SCN9A overexpression nullified the alleviative effects of SNHG5 deficiency on NP and neuron loss in CCI rats. In conclusion, SNHG5 promotes SCN9A-encoded Nav1.7 expression by recruiting CDK9, thereby facilitating neuron loss and NP after spinal nerve injury, which may offer a promising target for the management of NP.

Hyperbaric Lidocaine Aggravates Diabetic Neuropathic Pain by Targeting p38 MAPK/ERK and PINK1/Parkin-Mediated Mitophagy Signaling Pathway.

Diabetic neuropathic pain (DNP) is a complication of diabetes mellitus (DM). Hyperbaric lidocaine (HL), a local anesthetics drug, has neurotoxicity. The present study aims to study the effect and molecular mechanisms of HL on spinal nerve injury in DNP. The DNP rat model was established through a high-fat-glucose diet in combination with Streptozotocin (STZ) administration. SB203580 and PD98059 were utilized to inhibit p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated kinase (ERK). The mechanical paw withdrawal threshold (PWT) and the thermal paw withdrawal latency (PWL) were tested to evaluate rats' mechanical allodynia and thermal hyperalgesia. Hematoxylin-eosin (H&E) and terminal deoxynucleotidyltransferase-mediated dUTP nick-end Labeling (TUNEL) staining were performed to evaluate the pathological changes and neuron apoptosis in spinal cord tissues of L4-5. Western blotting analysis and reverse transcription-polymerase chain reaction (RT-qPCR) assay were used to measure the levels of proteins and mRNAs, respectively. PWT and PWL were decreased in DNP rats with serious spinal nerve injury. HL administration downregulated the PWT and PWL and aggravated spinal nerve injury in DNP rats, but isobaric lidocaine had no effects on these changes. Meanwhile, p38 MAPK/ERK signaling and PTEN-induced kinase 1 (PINK1)-mediated mitophagy were activated in DNP, which was enhanced by HL but not isobaric lidocaine. Blocking p38 MAPK/ERK signaling could effectively attenuate HL-induced spinal nerve injury and inhibit mitophagy. In summary, HL can aggravate spinal cord tissue damage in DNP rats by inducing PINK1-mediated mitophagy via activating p38 MAPK/ERK signaling. Our data provide a novel insight that supports the potential role of p38 MAPK/ERK signaling in acting as a therapeutic target for HL-induced neurotoxicity.

Spying on specific splicing in spinal nerve injury

Spying on specific splicing in spinal nerve injury

Modeling and Control of Two Degree of Freedom Bionic Foot

Many people are affected by conditions like stroke, spinal cord diseases, cerebral palsy, and nerve injuries, leading to impaired leg function. Bionic foot assist in maintaining stability and posture, offering vital aid to those with mobility issues for improved quality of life and rehabilitation. Consequently, the use of bionic foot has increased. Bionic foot comprising electrical and mechanical components, provide comfort and support for individuals with mobility problems. An encouraging solution is to introduce bionic foot robots to help patients having mobility problems during their recovery journey. Designed to mimic the human skeletal system, these robots offer valuable assistance in restoring the natural gait cycle of patients having mobility problems. The proposed approach introduces a bionic foot designed to support movement of human ankle joint, marking a significant advancement in rehabilitation technology. Although human ankle joint actually exhibits 3 DOF motion, we consider 2 DOF motion of human ankle joint i.e., plantarflexion and dorsiflexion and, inversion and eversion as they are dominant during normal motion of human body. We designed two systems to control the motion of human ankle joint. Firstly, we have used two actuators, one for each degree of freedom to control the motion of ankle joint. Secondly, we have used an actuator to control the plantarflexion and dorsiflexion motion and Spring-Damper system to control the inversion and eversion motion of the human ankle joint. For both systems, we derive the mathematical model and then we design the PD controller using MATLAB/Simulink. For plantarflexion and dorsiflexion motion, we give standard pattern of human ankle gait as input and for inversion and eversion motion, we provide pulsating signal as our input for both the systems. After implementation, the response of the human ankle motion was precise, accurate and smooth. The torque applied by the actuators was also in the acceptable range.

Review on Spina Bifida

Spinal bifida is a congenital defect in the spinal cord of the fetus. The most serious forms of infection lead to spinal cord and spinal cord nerve injury, which has a significant negative impact on the life of newborns. Currently, prenatal procedures require abdominal laparoscopic surgery and uterine hysterectomy, which may have serious consequences and risks for mothers. Renal injury and renal failure are among the most serious complications of spinal cord cord injury. Over the past few decades, a comprehensive treatment strategy has been implemented to minimize renal injuries. Furthermore, most patients dry their urine after primary school.

Targeted transcriptional upregulation of SENP1 by CRISPR activation enhances deSUMOylation pathways to elicit antinociception in the spinal nerve ligation model of neuropathic pain.

The voltage-gated sodium channel Na V 1.7 is an essential component of human pain signaling. Changes in Na V 1.7 trafficking are considered critical in the development of neuropathic pain. SUMOylation of collapsin response mediator protein 2 (CRMP2) regulates the membrane trafficking and function of Na V 1.7. Enhanced CRMP2 SUMOylation in neuropathic pain correlates with increased Na V 1.7 activity. Pharmacological and genetic interventions that interfere with CRMP2 SUMOylation in rodents with neuropathic pain have been shown to reverse mechanical allodynia. Sentrin or SUMO-specific proteases (SENPs) are vital for balancing SUMOylation and deSUMOylation of substrates. Overexpression of SENP1 and/or SENP2 in CRMP2-expressing cells results in increased deSUMOylation and decreased membrane expression and currents of Na V 1.7. Although SENP1 is present in the spinal cord and dorsal root ganglia, its role in regulating Na V 1.7 function and pain is not known. We hypothesized that favoring SENP1 expression can enhance CRMP2 deSUMOylation to modulate Na V 1.7 channels. In this study, we used a clustered regularly interspaced short palindromic repeats activation (CRISPRa) SENP1 lentivirus to overexpress SENP1 in dorsal root ganglia neurons. We found that SENP1 lentivirus reduced CRMP2 SUMOylation, Na V 1.7-CRMP2 interaction, and Na V 1.7 membrane expression. SENP1 overexpression decreased Na V 1.7 currents through clathrin-mediated endocytosis, directly linked to CRMP2 deSUMOylation. Moreover, enhancing SENP1 expression did not affect the activity of TRPV1 channels or voltage-gated calcium and potassium channels. Intrathecal injection of CRISPRa SENP1 lentivirus reversed mechanical allodynia in male and female rats with spinal nerve injury. These results provide evidence that the pain-regulating effects of SENP1 overexpression involve, in part, the modulation of Na V 1.7 channels through the indirect mechanism of CRMP2 deSUMOylation.

Effect of spirocyclopiperazinium salt compound LXM-15 on spinal nerve injury in rats.

Currently available therapies for neuropathic pain show limited efficacy. This study aimed to investigate the anti-nociceptive effect of the spirocyclopiperazinium salt compound LXM-15 in spinal nerve ligation (SNL) rats and to explore the potential mechanisms. Mechanical allodynia and thermal hyperalgesia tests were used to evaluate the effects of LXM-15 in SNL rats. The expression of CaMKIIα, CREB, JAK2, STAT3, c-fos and TNF-α was detected by western blotting, ELISA or qRT-PCR analysis. Receptor blocking test was performed to explore possible target. Administration of LXM-15 (1, 0.5, 0.25 mg/kg, i.g.) dose-dependently attenuated mechanical allodynia and thermal hyperalgesia in rats subjected to SNL (p < 0.01, p < 0.05), and the effects were completely blocked by peripheral α7 nicotinic or M4 muscarinic receptor antagonist (p > 0.05). LXM-15 significantly decreased the overexpression of phosphorylated CaMKIIα, CREB, JAK2 and STAT3 proteins and the mRNA levels of TNF-α and c-fos (p < 0.01, p < 05). All of the effects could be blocked by α7 or M4 receptor antagonist. Furthermore, LXM-15 reduced the protein expression of TNF-α and c-fos (p < 0.01, p < 0.05). No significant acute toxicity or abnormal hepatorenal function was observed. This is the first study to report that LXM-15 exerts significant anti-nociceptive effect on SNL rats. This effect may occur by activating peripheral α7 nicotinic and M4 muscarinic receptors, further inhibiting the CaMKIIα/CREB and JAK2/STAT3 signalling pathways, and finally inhibiting the expression of TNF-α and c-fos. Existing treatments for neuropathic pain show limited efficacy with severe adverse reactions. This paper is the first to report that LXM-15, a new spirocyclopiperazinium salt compound, exerts a significant anti-nociception in SNL rats without obvious toxicity. The underlying mechanisms include activating peripheral α7 nicotinic and M4 muscarinic receptors, then inhibiting the signalling pathways of CaMKIIα/CREB and JAK2/STAT3 and the expressions of TNF-α and c-fos. This study sheds new light on the development of novel analgesic drugs with fewer side effects.

Assessment of level IIB lymph nodes in oral cancer - Should we spare or care?

Objectives The extent of neck dissection over the years has evolved from a radical neck dissection to a super-selective neck dissection with an attempt to achieve a balance between oncological safety and acceptable morbidity. There is an ongoing debate concerning dissection of level IIB in both node negative and positive patients, primarily due to the low incidence of metastasis in this region and possible spinal accessory nerve injury. In this study, we intended to find the rate of metastasis to level IIB nodes in patients who were treated with neck dissection for oral cancers. Material and Methods Patients with squamous cell carcinoma of the oral cavity who underwent neck dissection were analyzed. Patients with clinically node negative (cN0) disease underwent selective neck dissection (SND), whereas patients with clinically node positive (cN+) disease underwent modified radical neck dissection (MRND). Results Out of the total 34 patients, 12 patients underwent MRND and 22 patients underwent SND. In the MRND group, three patients (25%) had positive level IIB nodes. The median number of IIB nodes removed was two and the median number of positive IIB nodes was one. In the SND group, the median number of IIB nodes removed was three and none of the patients had positive level IIB node. Conclusion In oral cancer with cN+, routine dissection of level IIB nodes has both therapeutic and prognostic values. Whereas, in patients with cN0, routine dissection of level IIB nodes can be omitted. Further large volume studies are needed on cN0 disease.

Does Age Affect the Rate of Spinal Nerve Injury after Selective Neck Dissection? Age as a Prognostic Factor of Spinal Nerve Injury after Selective Neck Dissection.

The objective of this study is to investigate whether age is a significant risk factor for spinal nerve injury following selective neck dissection (SND) in patients with head and neck cancer. A retrospective cohort study was conducted on patients who had undergone SND for head and neck cancer at a tertiary hospital between 2020 and 2022. The primary outcome was the incidence of spinal nerve injury after SND. The secondary outcomes included the types and severity of spinal nerve injury and the impact of age on these outcomes. A total of 78 patients were included in the study and subdivided into two groups. Two shoulder-specific questionnaires (the Shoulder Pain and Disability Index (SPADI) and the Shoulder Disability Questionnaire (SDQ)) were administered to assess shoulder morbidity postoperatively. Twelve patients showed shoulder impairment following surgery. We divided the sample into two age-based groups; the older group showed a higher rate of SAN injury and the younger group showed a lower rate of improvement over time. This study suggests that age is a significant risk factor for spinal nerve injury following SND in patients with head and neck cancer. Older patients are more likely to experience spinal nerve injury after SND than younger patients. The findings of this study may help in the development of strategies to prevent spinal nerve injury in older patients undergoing SND for head and neck cancer.

A novel technology named as selective fenestration and axial decompression for the surgical management of lumbar degenerative diseases

Study DesignA retrospective study. PurposeTo firstly introduce a new surgical techniquenamed asselectivefenestrationand axial decompression (SFAD) to improvethe surgical treatment effectsof lumbar degenerative diseases. Overview of literaturePosterior lumbar laminectomy and interbody fusion (LIF)is a standard surgical method for the treatment of lumbar degenerative diseases. However, its application has some limitations, and the incidence of spinal cord nerve injury is relatively high. MethodsThisretrospectiveclinicalstudy was conducted fromJanuary 2018 to February2020. A total of 101 eligible patients including 62 men and 39 women withlumbar disc herniation (LDH) or lumbar spinal stenosis (LSS)underwentLIF or SFADwere enrolled in this study.The average postoperative follow-up periodof the LIF and SFAD groups were 20.1 ± 3.7 months and 19.7 ± 4.1 months, respectively.The clinical effects,imaging manifestation,and postoperative complicationsin LIF and SFAD groups were analyzed. ResultsThe operative time, blood loss and hospital stay in SFAD group were significantly lower than those in LIF group (P < 0.05). Significant clinical improvements in VAS and ODIwere achieved in bothLIF and SFAD groupsafter surgery, respectively (P < 0.05).There was no statistical difference in improvements of VAS and ODI betweentheLIFandSFADgroups (P > 0.05).Similarly, improvementsofcobb angle ofoperated segment, intervertebral space height (ISH), intervertebral space foramen (IFH)andlumbar lordosis (LL)showed no statistical differencebetween thetwogroups (P > 0.05).Finally, theprevalence of complicationratesinLIF group were significantlyhigher than theSFADgroup during the follow-up period(P < 0.05) ConclusionsThe application ofSFADto the surgical treatment of lumbar degenerative diseases can realize the three-dimensional and precise decompression of spinal cord nerve, whichis one of the ideal alternatives to traditional LIF.

The spinal accessory nerve and its entry point into the posterior triangle of the neck.

The course of the spinal accessory nerve in the neck is long and superficial rendering it at high risk of injury during procedures performed in the posterior triangle. The majority of spinal accessory nerve injuries are iatrogenic in nature. This is associated with significant morbidity including reduction in shoulder movements, drooping of the shoulder, winging of the scapula and neuropathic pain. Knowledge of the nerve anatomy reduces the risk of intra-operative nerve injury. Traditional teaching describes the point of entry into the posterior triangle as the intersection between the upper and middle third of the posterior border of sternocleidomastoid. The aim of this study was to determine whether this is in fact the case and if so, whether this landmark can reliably be used to identify the spinal accessory nerve in order to improve patient outcomes. The spinal accessory nerve was identified unilaterally in 26 cadavers. The total length of sternocleidomastoid was measured as well as the length along the posterior border from the inferior aspect of the mastoid process to the point at which the accessory nerve enters the posterior triangle of the neck. These measurements were used to calculate the ratio of the entry point of the nerve into the posterior triangle along the length of the posterior border of sternocleidomastoid from its superior insertion point. The mean ratio was 0.35 with 95% confidence intervals of 0.33 to 0.36. Our findings confirm the traditional description of the entry point of the spinal accessory nerve into the posterior triangle of the neck. We describe a so-called 'safe zone' inferior to the midpoint of the posterior border of sternocleidomastoid within which the spinal accessory nerve is unlikely to be found, thereby reducing the risk of iatrogenic injury.