Functional biomaterials for modulating the dysfunctional pathological microenvironment of spinal cord injury

Spinal cord injury(SCI)often results in irreversible loss of sensory and motor functions,and most SCIs are incurable with current medical practice.One of the hardest challenges in treating SCI is the development of a dysfunctional pathological microenvironment,which mainly comprises excessive inflammation,deposition of inhibitory molecules,neurotrophic factor deprivation,glial scar formation,and imbalance of vascular function.To overcome this challenge,implantation of functional biomaterials at the injury site has been regarded as a potential treatment for modulating the dysfunctional microenvironment to support axon regeneration,remyelination at injury site,and functional recovery after SCI.This review summarizes characteristics of dysfunctional pathological microenvironment and recent advances in biomaterials as well as the technologies used to modulate inflammatory microenvironment,regulate inhibitory microenvironment,and reshape revascularization microenvironment.Moreover,technological limitations,challenges,and future prospects of functional biomaterials to promote efficient repair of SCI are also discussed.This review will aid further understanding and development of functional biomaterials to regulate pathological SCI microenvironment.

Association between brain N-acetylaspartate levels and sensory and motor dysfunction in patients who have spinal cord injury with spasticity:an observational case-control study

Spinal cord injury is a severe and devastating disease,and spasticity is a common and severe complication that is notoriously refractory to treatment.However,the pathophysiological mechanisms underlying spasticity and its development remain largely unknown.The goal of the present study was to find differences,if any,in metabolites of the left precentral gyrus and basal ganglia of patients who have spinal cord injury with or without spasticity,and to explore the relationship between the brain metabolite concentrations and clinical status.Thirty-six participants were recruited for magnetic resonance spectroscopic examination:23 with spinal cord injury(12 with spasticity and 11 without spasticity)and 13 healthy controls.We acquired localized proton spectra from the precentral gyrus and basal ganglia via 10 mm^(3) voxels.Notably,univariate linear regression analysis demonstrated that the lower that the N-acetylaspartate concentration(a marker for neuronal loss)was in the precentral gyrus of the patients,the lower their ASIA(American Spinal Injury Association)light-touch scores,pinprick scores,and motor scores.Additionally,longer durations of injury were associated with higher N-acetylaspartate levels in the precentral gyrus.Compared with the healthy participants and patients without spasticity,N-acetylaspartate levels in the patients with spasticity were significantly lower in both the precentral gyrus and basal ganglia.Lower N-acetylaspartate levels also correlated with greater sensory and motor dysfunction in the patients who had spinal cord injury with spasticity.

A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities

Spinal cord injury(SCI)is a devastating and disabling medical condition generally caused by a traumatic event(primary injury).This initial trauma is accompanied by a set of biological mechanisms directed to ameliorate neural damage but also exacerbate initial damage(secondary injury).The alterations that occur in the spinal cord have not only local but also systemic consequences and virtually all organs and tissues of the body incur important changes after SCI,explaining the progression and detrimental consequences related to this condition.Psychoneuroimmunoendocrinology(PNIE)is a growing area of research aiming to integrate and explore the interactions among the different systems that compose the human organism,considering the mind and the body as a whole.The initial traumatic event and the consequent neurological disruption trigger immune,endocrine,and multisystem dysfunction,which in turn affect the patient's psyche and well-being.In the present review,we will explore the most important local and systemic consequences of SCI from a PNIE perspective,defining the changes occurring in each system and how all these mechanisms are interconnected.Finally,potential clinical approaches derived from this knowledge will also be collectively presented with the aim to develop integrative therapies to maximize the clinical management of these patients.

Mitochondrial dysfunction as a target in spinal cord injury:intimate correlation between pathological processes and therapeutic approaches

Traumatic spinal cord injuries interrupt the connection of all axonal projections with their neuronal targets below and above the lesion site. This interruption results in either temporary or permanent alterations in the locomotor, sensory, and autonomic functions. Damage in the spinal tissue prevents the re-growth of severed axons across the lesion and their reconnection with neuronal targets. Therefore, the absence of spontaneous repair leads to sustained impairment in voluntary control of movement below the injury. For decades, axonal regeneration and reconnection have been considered the opitome of spinal cord injury repair with the goal being the repair of the damaged long motor and sensory tracts in a complex process that involves:(1) resealing injured axons;(2) reconstructing the cytoskeletal structure inside axons;(3) re-establishing healthy growth cones;and(4) assembling axonal cargos. These biological processes require an efficient production of adenosine triphosphate, which is affected by mitochondrial dysfunction after spinal cord injury. From a pathological standpoint, during the secondary stage of spinal cord injury, mitochondrial homeostasis is disrupted, mainly in the distal segments of severed axons. This result in a reduction of adenosine triphosphate levels and subsequent inactivation of adenosine triphosphate-dependent ion pumps required for the regulation of ion concentrations and reuptake of neurotransmitters, such as glutamate. The consequences are calcium overload, reactive oxygen species formation, and excitotoxicity. These events are intimately related to the activation of necrotic and apoptotic cell death programs, and further exacerbate the secondary stage of the injury, being a hallmark of spinal cord injury. This is why restoring mitochondrial function during the early stage of secondary injury could represent a potentially effective therapeutic intervention to overcome the motor and sensory failure produced by spinal cord injury. This review discusses the most recent evidence linking mitochondrial dysfunction with axonal regeneration failure in the context of spinal cord injury. It also covers the future of mitochondria-targeted therapeutical approaches, such as antioxidant molecules, removing mitochondrial anchor proteins, and increasing energetic metabolism through creatine treatment. These approaches are intended to enhance functional recovery by promoting axonal regenerationreconnection after spinal cord injury.

Anatomical changes in the somatosensory system after large sensory loss predict strategies to promote functional recovery after spinal cord injury

Among cases of spinal cord injury are injuries involving the dorsal column in the cervical spinal cord that interrupt the major cutaneous afferents from the hand to the cuneate nucleus（Cu）in the brainstem.Deprivation of touch and proprioceptive inputs consequently impair skilled hand use.

Role of axon resealing in retrograde neuronal death and regeneration after spinal cord injury

Spinal cord injury leads to persistent behavioral deficits because mammalian central nervous system axons fail to regenerate. A neuron's response to axon injury results from a complex interplay of neuron-intrinsic and environmental factors. The contribution of axotomy to the death of neurons in spinal cord injury is controversial because very remote axotomy is unlikely to result in neuronal death, whereas death of neurons near an injury may reflect environmental factors such as ischemia and inflammation. In lampreys, axotomy due to spinal cord injury results in delayed apoptosis of spinal-projecting neurons in the brain, beyond the extent of these environmental factors. This retrograde apoptosis correlates with delayed resealing of the axon, and can be reversed by inducing rapid membrane resealing with polyethylene glycol. Studies in mammals also suggest that polyethylene glycol may be neuroprotective, although the mechanism(s) remain unclear. This review examines the early, mechanical, responses to axon injury in both mammals and lampreys, and the potential of polyethylene glycol to reduce injury-induced pathology. Identifying the mechanisms underlying a neuron's response to axotomy will potentially reveal new therapeutic targets to enhance regeneration and functional recovery in humans with spinal cord injury.

Tanshinone ⅡA improves functional recovery in spinal cord injury-induced lower urinary tract dysfunction

Tanshinone ⅡA, extracted from Salvia miltiorrhiza Bunge, exerts neuroprotective effects through its anti-inflammatory, anti-oxidative and anti-apoptotic properties. This study intravenously injected tanshinone ⅡA 20 mg/kg into rat models of spinal cord injury for 7 consecutive days. Results showed that tanshinone ⅡA could reduce the inflammation, edema as well as compensatory thickening of the bladder tissue, improve urodynamic parameters, attenuate secondary injury, and promote spinal cord regeneration. The number of hypertrophic and apoptotic dorsal root ganglion（L6–S1） cells was less after treatment with tanshinone ⅡA. The effects of tanshinone ⅡA were similar to intravenous injection of 30 mg/kg methylprednisolone. These findings suggested that tanshinone ⅡA improved functional recovery after spinal cord injury-induced lower urinary tract dysfunction by remodeling the spinal pathway involved in lower urinary tract control.

Early methylprednisolone impact treatment for sensory and motor function recovery in patients with acute spinal cord injury A self-control study

BACKGROUND： For the treatment of spinal cord injury, any pathological changes of the injured tissue should be primarily corrected or reversed. Any remaining fibrous function and neurons with intact structure should be retained, and the toxic substances caused by ischemia-hypoxia following spinal cord injury, should be eliminated to create a favorable environment that would promote neural functional recovery. OBJECTIVE： This study was designed to investigate the effects of the impact of early methylprednisolone-treatment on the sensory and motor function recovery in patients with acute spinal cord injury. DESIGN： A self-control observation. SETTING： Department of Spine Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China. PARTICIPANTS： Forty-three patients with acute spinal cord injury were admitted to the Department of Spine Surgery, First Affiliated Hospital of Nanjing Medical University, between October 2005 and September 2007. These patients were recruited for the present study. The patients comprised 33 males and 10 females, and all met with the inclusive criteria namely, the time between suffering from acute spinal cord injury and receiving treatment was less than or equal to eight hours. METHODS： According to the protocol determined by the State Second Conference of Acute Spinal Cord Injury of USA, all patients received the drop-wise administration of a 30-mg/kg dose of methylprednisolone （H200040339, 500 mg/bottle, Pharmacia N.V/S.A, Belgium） for 15 minutes within 8 hours post injury. After a 45-minute interval, methylprednisolone was administered at 5.4 mg/kg/h for 23 hours. MAIN OUTCOME MEASURES： Prior to and post treatment, acupuncture sense and light touch scoring were performed at 28 dermatomic area key points, including occipital tuberosity and supraclavicular fossa. At the same time, motor scoring of key muscles among 10 pairs of sarcomeres was also performed. RESULTS： All 43 patients participated in the final analysis. There was no significant difference of sensory and motor scores in patients with complete acute spinal cord injury between prior to and post methylprednisolone impact treatment （P 〉 0.05）. The motor score was significantly decreased in patients with incomplete acute spinal cord injury post methylprednisolone impact treatment （P 〈 0.01 ）. CONCLUSION： Early methylprednisolone impact may improve the motor function of patients with incomplete acute spinal cord injury. However, it has no influences on patients with complete acute spinal cord injury.

Transplantation of placenta-derived mesenchymal stem cell-induced neural stem cells to treat spinal cord injury

Because of their strong proliferative capacity and multi-potency, placenta-derived mesenchymal stem cells have gained interest as a cell source in the field of nerve damage repair. In the present study, human placenta-derived mesenchymal stem ceils were induced to differentiate into neural stem cells, which were then transplanted into the spinal cord after local spinal cord injury in rats. The motor functional recovery and pathological changes in the injured spinal cord were observed for 3 successive weeks. The results showed that human placenta-derived mesenchymal stem cells can differentiate into neuron-like cells and that induced neural stem cells contribute to the restoration of injured spinal cord without causing transplant rejection. Thus, these cells promote the recovery of motor and sensory functions in a rat model of spinal cord injury. Therefore, human placenta-derived mesenchymal stem cells may be useful as seed cells during the repair of spinal cord injury.

Spinal cord injury-induced cognitive impairment: a narrative review

Spinal cord injury is a serious damage to the spinal cord that can lead to life-long disability.Based on its etiology,spinal cord injury can be classified as traumatic or non-traumatic spinal cord injury.Furthermore,the pathology of spinal cord injury can be divided into two phases,a primary injury phase,and a secondary injury phase.The primary spinal cord injury phase involves the initial mechanical injury in which the physical force of impact is directly imparted to the spinal cord,disrupting blood vessels,axons,and neural cell membranes.After the primary injury,a cascade of secondary events begins,expanding the zone of neural tissue damage,and exacerbating neurological deficits.Secondary injury is a progressive condition characterized by pro-inflammatory cytokines,reactive oxygen species,oxidative damage,excitatory amino acids such as glutamate,loss of ionic homeostasis,mitochondrial dysfunction,and cell death.This secondary phase lasts for several weeks or months and can be further subdivided into acute,subacute,and chronic.One of the most frequent and devastating complications developed among the spinal cord injury population is cognitive impairment.The risk of cognitive decline after spinal cord injury has been reported to be 13 times higher than in healthy individuals.The exact etiology of this neurological complication remains unclear,however,many factors have been proposed as potential contributors to the development of this disorder,such as concomitant traumatic brain injury,hypoxia,anoxia,autonomic dysfunction,sleep disorders such as obstructive sleep apnea,body temperature dysregulation,alcohol abuse,and certain drugs.This review focuses on a deep understanding of the pathophysiology of spinal cord injury and its relationship to cognitive impairment.We highlight the main mechanisms that lead to the development of this neurological complication in patients with spinal cord injury.

Survey of spinal cord injury-induced neurogenic bladder studies using the Web of Science

OBJECTIVE：To identify global trends in research on spinal cord injury-induced neurogenic bladder, through a bibliometric analysis using the Web of Science. DATA RETRIEVAL：We performed a bibliometric analysis of studies on spinal cord injury-induced neurogenic bladder using the Web of Science.Data retrieval was performed using key words＂spinal cord injury＂,＂spinal injury＂,＂neurogenic bladder＂,＂neuropathic bladder＂,＂neurogenic lower urinary tract dysfunction＂,＂neurogenic voiding dysfunction＂,＂neurogenic urination disorder＂and ＂neurogenic vesicourethral dysfunction＂. SELECTION CRITERIA：Inclusion criteria：（a）published peer-reviewed articles on spinal cord injury-induced neurogenic bladder indexed in the Web of Science;（b）type of articles：original research articles and reviews;（c）year of publication：no limitation.Exclusion criteria：（a）articles that required manual searching or telephone access;（b）Corrected papers and book chapters. MAIN OUTCOME MEASURES：（1）Annual publication output;（2）distribution according to journals; （3）distribution according to subject areas;（4）distribution according to country;（5）distribution according to institution;and（6）top cited publications. RESULTS：There were 646 research articles addressing spinal cord injury-induced neurogenic bladder in the Web of Science.Research on spinal cord injury-induced neurogenic bladder was found in the Science Citation Index-Expanded as of 1946.The United States,Ireland and Switzerland were the three major countries contributing to studies in spinal cord injury-induced neurogenic bladder in the 1970s.However,in the 1990s,the United States,the United Kingdom,the Netherlands,Germany and Japan published more papers on spinal cord injury-induced neurogenic bladder than Switzerland,and Ireland fell off the top ten countries list.In this century,the United States ranks first in spinal cord injury-induced neurogenic bladder studies,followed by France,the United Kingdom,Germany,Switzerland and Japan.Subject categories including urology, nephrology and clinical neurology,as well as rehabilitation,are represented in spinal cord injury-induced neurogenic bladder studies. CONCLUSION：From our analysis of the literature and research trends,we conclude that spinal cord injury-induced neurogenic bladder is a hot topic that will continue to generate considerable research interest in the future.

A progressive compression model of thoracic spinal cord injury in mice： function assessment and pathological changes in spinal cord

Non-traumatic injury accounts for approximately half of clinical spinal cord injury, including chronic spinal cord compression. However, previous rodent spinal cord compression models are mainly designed for rats, few are available for mice. Our aim is to develop a thoracic progressive compression mice model of spinal cord injury. In this study, adult wild-type C57BL/6 mice were divided into two groups： in the surgery group, a screw was inserted at T9 lamina to compress the spinal cord, and the compression was increased by turning it further into the canal（0.2 mm） post-surgery every 2 weeks up to 8 weeks. In the control group, a hole was drilled into the lamina without inserting a screw. The results showed that Basso Mouse Scale scores were lower and gait worsened. In addition, the degree of hindlimb dysfunction in mice was consistent with the degree of spinal cord compression. The number of motor neurons in the anterior horn of the spinal cord was reduced in all groups of mice, whereas astrocytes and microglia were gradually activated and proliferated. In conclusion, this progressive compression of thoracic spinal cord injury in mice is a preferable model for chronic progressive spinal cord compression injury.

Dynamic changes in the systemic immune responses of spinal cord injury model mice

Intraspinal inflammatory and immune responses are considered to play central roles in the pathological development of spinal cord injury.This study aimed to decipher the dynamics of systemic immune responses,initiated by spinal cord injury.The spinal cord in mice was completely transected at T8.Changes in the in vivo inflammatory response,between the acute and subacute stages,were observed.A rapid decrease in C-reactive protein levels,circulating leukocytes and lymphocytes,spleen-derived CD4~+interferon-γ+T-helper cells,and inflammatory cytokines,and a marked increase in neutrophils,monocytes,and CD4~+CD25~+FOXP3~+regulatory T-cells were observed during the acute phase.These systemic immune alterations were gradually restored to basal levels during the sub-acute phase.During the acute phase of spinal cord injury,systemic immune cells and factors showed significant inhibition;however,this inhibition was transient,and the indicators of these serious disorders gradually returned to baseline levels during the subacute phase.All experiments were performed in accordance with the institutional animal care guidelines,approved by the Institutional Animal Care and Use Committee of Experimental Animal Center of Drum Tower Hospital,China(approval No.2019 AE01040)on June 25,2019.

Penile erectile dysfunction after brachial plexus root avulsion injury in rats

Our previous studies have demonstrated that some male patients suffering from brachial plexus injury, particularly brachial plexus root avulsion, show erectile dysfunction to varying degrees. However, the underlying mechanism remains poorly understood. In this study, we evaluated the erectile function after establishing brachial plexus root avulsion models with or without spinal cord injury in rats. After these models were established, we administered apomorphine （via a sub- cutaneous injection in the neck） to observe changes in erectile function. Rats subjected to simple brachial plexus root avulsion or those subjected to brachial plexus root avulsion combined with spinal cord injury had significantly fewer erections than those subjected to the sham operation. Expression of neuronal nitric oxide synthase did not change in brachial plexus root avulsion rats. However, neuronal nitric oxide synthase expression was significantly decreased in brachial plexus root avulsion ＋ spinal cord injury rats. These findings suggest that a decrease in neuronal nitric oxide synthase expression in the penis may play a role in erectile dysfunction caused by the combi- nation of brachial plexus root avulsion and spinal cord injury.

Repair mechanism of astrocytes and non-astrocytes in spinal cord injury

BACKGROUND Spinal cord injury(SCI)is a destructive disease that incurs huge personal and social costs,and there is no effective treatment.Although the pathogenesis and treatment mechanism of SCI has always been a strong scientific focus,the pathogenesis of SCI is still under investigation.AIM To determine the key genes based on the modularization of in-depth analysis,in order to identify the repair mechanism of astrocytes and non-astrocytes in SCI.METHODS Firstly,the differences between injured and non-injured spinal cord of astrocyte(HA),injured and non-injured spinal cord of non-astrocyte(FLOW),injured spinal cord of non-injured astrocyte(HA)and non-injured spinal cord of nonastrocyte(FLOW),and non-injured spinal cord of astrocyte(HA)and nonastrocyte(FLOW)were analyzed.The total number of differentially expressed genes was obtained by merging the four groups of differential results.Secondly,the genes were co-expressed and clustered.Then,the enrichment of GO function and KEGG pathway of module genes was analyzed.Finally,non-coding RNA,transcription factors and drugs that regulate module genes were predicted using hypergeometric tests.RESULTS In summary,we obtained 19 expression modules involving 5216 differentially expressed genes.Among them,miR-494,XIST and other genes were differentially expressed in SCI patients,and played an active regulatory role in dysfunction module,and these genes were recognized as the driving genes of SCI.Enrichment results showed that module genes were significantly involved in the biological processes of inflammation,oxidation and apoptosis.Signal pathways such as NF-kappa B/A20,AMPK and MAPK were significantly regulated.In addition,non-coding RNA pivot(including miR-136-5p and let-7d-5p,etc.)and transcription factor pivot(including NFKB1,MYC,etc.)were identified as significant regulatory dysfunction modules.CONCLUSION Overall,this study uncovered a co-expression network of key genes involved in astrocyte and non-astrocyte regulation in SCI.These findings helped to reveal the core dysfunction modules,potential regulatory factors and driving genes of the disease,and to improve our understanding of its pathogenesis.

Role of melatonin in spinal cord injury

Spinal cord injury (SCI) impairs the au-tonomic nervous system and is associated with dysfunc-tion or failure of multiple organs. Rehabilitation after SCI is a complicated process that involves improvement of motor and sensory function and amelioration of com-plications. Accumulating evidence has demonstrated that melatonin treatment could protect the neural tissues of the spinal cord from secondary injury after SCI. Melatonin is an indoleamine naturally produced by the pineal gland and other tissues. It can easily cross the blood-brain bar-rier and has been shown to have neuroprotective proper-ties in animal models with neurological injury, such as traumatic brain injury and SCI. We reviewed the potential mechanisms of melatonin treatment reducing SCI-relat-ed complications such as disruption of microcirculation, neurogenic bowel dysfunction, and circadian disorders.

Establishment and Functional Evaluation of a Rat Model of Spinal Cord Injury

Objective:To explore the modified Allen impactor method in establishing a rat model of spinal cord injury,and to preliminarily evaluate the motor function of the forelimbs and hindlimbs of rats.Methods:Thirty female SD rats with a body weight of 255±21g were randomly divided into two groups,namely the sham-operated group and the operated group,with 15 rats in each group.The spinal cord injury SD rat model was established by exposing but not injuring the spinal cord in the sham-operated group,while the SD rat model was established by the modified Allen impactor method in the operated group.The Basso-Beattie-Bresnahan(BBB)rating scale was used to assess the rats’hindlimb motor neurobehavior.A rat model of spinal cord injury was established by the modified Allen impactor method.After the cells were transplanted,the BBB score was used to evaluate the motor function;the changes in the motor function of rats with spinal cord injury were detected.Results:The motor function and sensory function of the forelimbs and hindlimbs of the rats showed significant changes after five days.The motor function of the forelimbs and hindlimbs of the rats in the sham-operated group were essentially normal after three days(about 20 points);the sensory function of the rats in the operated group decreased significantly after five days;however,in the sham-operated group,it decreased to 0.The motor function scores of the rats in the operated group at each point of time were significantly lower than those in the sham-operated group(p<0.05),while the forelimb motor function scores were significantly higher than those in the sham-operated group(p<0.05).Conclusion:The modified Allen impactor method that was used to establish a rat model of spinal cord injury in this study can significantly reduce the motor function of rats.

Governor vessel-unblocking and mind-regulating acupuncture therapy for sensory and motor dysfunction after spinal cord injury

Objective： To observe the difference in clinical efficacy between governor vessel-unblocking and mind- regulating acupuncture therapy combined with conventional rehabilitation therapy and simply conventional rehabilitation therapy for sensory and motor dysfunction of patients with spinal cord injury. Methods： Forty patients with spinal cord injury （SCI） were randomly assigned into rehabilitation combined with acupuncture group （group A） and rehabilitation group （group B）, with 20 patients in each group. In group A, governor vessel-unblocking and mind-regulating acupuncture therapy combined with conventional rehabilitation therapy was adopted, and Baihui（百会 GV 20）, Fengffu （风府GV 16）, Dazhui （大椎GV 14）, Zhiyang （至阳GV 9）, Mingmen （命门 GV 4） and Yfioyangguan （腰阳关 GV 3） were adopted as the main acupoints. Conventional rehabilitation therapy was also applied, including the rehabilitation training of joint, motion, respiration, urinary bladder and intestinal tract. In group B, conventional rehabilitation therapy was adopted as same as the group A. Treatment in the two groups was conducted for once a day, 6 times a week, and 12 weeks in total. ASIA motor score （MS）, ASIA sensory score （SS） and activity of daily living （ADL） score of patients in the two groups were observed before and after the treatment. Results： Before treatment, the differences in MS, SS and ADL score of patients in the two groups were not statistically significant （all P 〉 0.05）, and the results were comparable. After treatment, MS, SS and ADL score of patients in the two groups were all higher than that before the treatment （all P 〈 0.05）, and MS, SS and ADL score of the patients in group A were all higher than that in group B （all P 〈 0.05）. Conclusion： The curative effect of governor vessel-unblocking and mind-regulating acupuncture therapy combined with conventional rehabilitation therapy was superior to that of simply conventional rehabilitation therapy in the treatment of sensory and motor dysfunction of the patients with SCI.

Surgical reconstruction of spinal cord circuit provides functional return in humans

This mini review describes the current surgical strategy for restoring function after traumatic spinal nerve root avulsion in brachial or lumbosacral plexus injury in man. As this lesion is a spinal cord or central nervous injury functional return depends on spinal cord nerve cell growth within the central nervous system. Basic science, clinical research and human application has demonstrated good and useful motor function after ventral root avulsion followed by spinal cord reimplantation. Recently, sensory return could be demonstrated following spinal cord surgery bypassing the injured primary sensory neuron. Experimental data showed that most of the recovery depended on new growth reinnervating peripheral receptors. Restored sensory function and the return of spinal reflex was demonstrated by electrophysiology and functional magnetic resonance imaging of human cortex. This spinal cord surgery is a unique treatment of central nervous system injury resulting in useful functional return. Further improvements will not depend on surgical improvements. Adjuvant therapy aiming at ameliorating the activity in retinoic acid elements in dorsal root ganglion neurons could be a new therapeutic avenue in restoring spinal cord circuits after nerve root avulsion injury.

脊髓损伤病人膀胱功能障碍风险预测模型及其应用

目的:构建脊髓损伤病人膀胱功能障碍风险预测模型,并进行效果检验。方法:采用便利抽样法将2021年1月—2022年12月110例脊髓损伤病人纳为研究对象,按照是否发生膀胱功能障碍分为障碍组和正常组,采用单因素、多因素Logistic回归分析筛选脊髓损伤病人膀胱功能障碍的独立危险因素,据此拟合风险预测模型的回归方程,检验模型预测效果。结果:共29例(26.36%)脊髓损伤病人发生膀胱功能障碍;多因素分析结果显示,病程、损伤部位、排尿方式、泌尿系统感染、膀胱顺应性、逼尿肌括约肌失调为脊髓损伤病人膀胱功能障碍的独立影响因素(P<0.05);预测模型Hosmer-Lemeshow卡方检验结果显示,χ^(2)=8.203,P=0.336;C-index为0.818;AUC为0.794[95%CI(0.750,0.837)],约登指数为0.690,最佳截断值0.122,敏感度为94.4%,特异性为74.6%;模型预测准确率为81.81%。结论:本研究在脊髓损伤病人膀胱功能障碍的危险因素基础上,建立的风险预测模型具有良好拟合程度和区分能力,且准确度较高,能为临床早期预防、早期筛选、早期治疗和管理脊髓损伤病人膀胱功能障碍提供一定依据。