Diagnosis and prognosis of traumatic spinal cord injury.
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ABSTRACT:
SUBMITTER: van Middendorp JJ
PROVIDER: S-EPMC3864437 | biostudies-other | 2011 Dec
REPOSITORIES: biostudies-other
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Project description:PurposeThe long-term situation of children with spinal cord injury (SCI) was investigated, and suggestions for helping them better return to the society were provided.MethodsSCI patients less than 18 years old hospitalized in Beijing Boai Hospital from January 2011 to December 2020 were retrospectively analyzed. Information including motor function, complications, characteristic changes, self-care abilities, school attendance and social participation were collected by telephone interview and electronic questionnaire. All the answers were statistically analyzed.ResultsA total of 86 cases were enrolled, 77 girls and 9 boys, with a median injury age of 6 years and 2 months. The follow-up time was 3-130 months. The main cause of trauma in these children was sport injury (66.3%), the thoracic spinal cord was involved the most (91.9%), and complete SCIs accounted for the majority (76.7%). In terms of complications, children with complete SCIs were more likely to have urinary incontinence, constipation and characteristic changes (p < 0.05); whereas the incomplete SCIs often have spasticity (p < 0.05). As to the daily living abilities, children with incomplete lumbar SCIs were more capable to accomplish personal hygiene, transfer, and bathing independently than those with complete injuries, or cervical/thoracic SCIs, respectively (p < 0.05). Moreover, children older than 9 years care more able to dress and transfer independently than the youngers (p < 0.05). Wheelchair users accounted for 84.9% and more than half of them were able to propel wheelchair independently, and those who move passively in wheelchairs were mostly introverted kids (p < 0.05). Almost all (93.8%) children with incomplete injuries were able to walk independently. Most (79.1%) children continued to attending school, and 41.9% participated in interest classes. Unfortunately, 67.4% of the children spent less time playing with their peers than before the injury.ConclusionSCIs impair physical structures and function of children, affect their independence in daily living, and restrict school attendance and social interaction. Comprehensive rehabilitation after injury is a systematic work. Medical staff and caregivers should not only pay attention to neurological function, but also help them improve self-care abilities. It is also important to balance rehabilitation training and school work and social participation.
| S-EPMC9912184 | biostudies-literature
Project description:Traumatic spinal cord injury (SCI) results in impaired neurologic function that for many individuals is permanent and significantly impacts health, function, quality of life, and life expectancy. Many efforts have been taken to develop effective treatments for SCI; nevertheless, proven therapies targeting neurologic regeneration and functional recovery have been limited. Existing therapeutic approaches, including early surgery, strict blood pressure control, and consideration of treatment with steroids, remain debated and largely focus on mitigating secondary injury after the primary trauma has occurred. Today, there is more research being performed in SCI than ever before. Current clinical trials are exploring pharmacologic, cell-based, physiologic, and rehabilitation approaches to reduce secondary injury and also overcome barriers to neurorecovery. In the future, it is likely that tailored treatments combining many of these strategies will offer significant benefits for persons with SCI. This article aims to review key past, current and emerging neurologic and rehabilitation therapeutic approaches for adults with traumatic SCI.
| S-EPMC6095794 | biostudies-literature
Project description:Excessive inflammation post-traumatic spinal cord injury (SCI) induces microglial activation, which leads to prolonged neurological dysfunction. However, the mechanism underlying microglial activation-induced neuroinflammation remains poorly understood. Ruxolitinib (RUX), a selective inhibitor of JAK1/2, was recently reported to inhibit inflammatory storms caused by SARS-CoV-2 in the lung. However, its role in disrupting inflammation post-SCI has not been confirmed. In this study, microglia were treated with RUX for 24 hours and then activated with interferon-γ for 6 hours. The results showed that interferon-γ-induced phosphorylation of JAK and STAT in microglia was inhibited, and the mRNA expression levels of pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, interleukin-6, and cell proliferation marker Ki67 were reduced. In further in vivo experiments, a mouse model of spinal cord injury was treated intragastrically with RUX for 3 successive days, and the findings suggest that RUX can inhibit microglial proliferation by inhibiting the interferon-γ/JAK/STAT pathway. Moreover, microglia treated with RUX centripetally migrated toward injured foci, remaining limited and compacted within the glial scar, which resulted in axon preservation and less demyelination. Moreover, the protein expression levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 were reduced. The neuromotor function of SCI mice also recovered. These findings suggest that RUX can inhibit neuroinflammation through inhibiting the interferon-γ/JAK/STAT pathway, thereby reducing secondary injury after SCI and producing neuroprotective effects.
| S-EPMC8848590 | biostudies-literature
Project description:MicroRNAs (miRNAs) are a novel class of small non-coding RNAs that negatively regulate gene expression at the posttranscriptional level by binding to the 3' untranslated region of target mRNAs leading to their translational inhibition or sometimes degradation. We uncovered a previously unknown alteration in temporal expression of a large set of miRNAs following a contusive spinal cord injury (SCI) in adult rats using microarray analysis. These altered miRNAs can be classified into 3 categories: (1) up-regulation, (2) down-regulation and (3) an early up-regulation at 4 h followed by down-regulation at 1 and 7 days post-SCI. The bioinformatics analysis indicates that the potential targets for miRNAs altered after SCI include genes encoding components that are involved in the inflammation, oxidation, and apoptosis that are known to play important roles in the pathogenesis of SCI. These findings suggest that abnormal expression of miRNAs may contribute to the pathogenesis of SCI and are potential targets for therapeutic interventions following SCI.
| S-EPMC2810508 | biostudies-literature
Project description:Traumatic spinal cord injury (SCI) enhances the activity of S-nitrosoglutathione reductase (GSNOR) and inhibits the mitochondrial aldehyde dehydrogenase 2 (ALDH2) activity, resulting in prolonged and sustained pain and functional deficits. This study's objective was to test the hypotheses that GSNOR's specific inhibitor N6022 mitigates pain and improves functional recovery in a mouse model of SCI. Furthermore, the degree of recovery is enhanced and the rate of recovery is accelerated by an ALDH2 activator Alda-1. Using both wild-type and GSNOR-/- mice, the SCI model deployed for groups was contusion at the T9-T10 vertebral level. The enzymatic activity of GSNOR and ALDH2 was measured, and the expression of GSNOR and ALDH2 was determined by western blot analysis. Functional improvements in experimental animals were assessed with locomotor, sensorimotor, and pain-like behavior tests. Wild-type SCI animals had enhanced GSNOR activity and decreased ALDH2 activity, leading to neurovascular dysfunction, edema, and worsened functional outcomes, including locomotor deficits and pain. Compared to wild-type SCI mice, GSNOR-/- mice had better functional outcomes. Monotherapy with either GSNOR inhibition by N6022 or enhanced ALDH2 activity by Alda-1 correlated well with functional recovery and lessened pain. However, combination therapy provided synergistic pain-relieving effects and more significant functional recovery compared with monotherapy. Conclusively, dysregulations in GSNOR and ALDH2 are among the causative mechanisms of SCI injury. Either inhibiting GSNOR or activating ALDH2 ameliorates SCI. Combining the specific inhibitor of GSNOR (N6022) with the selective activator of ALDH2 (Alda-1) provides greater protection to the neurovascular unit and confers greater functional recovery. The study is novel, and the combination therapy (N6022 + Alda-1) possesses translational potential.
| S-EPMC7987823 | biostudies-literature
Project description:Activation of extracellular signal-regulated protein kinase 1/2 (ERK1/2) are implicated in the pathophysiology of spinal cord injury (SCI). However, the specific functions of individual ERK isoforms in neurodegeneration are largely unknown. We investigated the hypothesis that ERK2 activation may contribute to pathological and functional deficits following SCI and that ERK2 knockdown using RNA interference may provide a novel therapeutic strategy for SCI. Lentiviral ERK2 shRNA and siRNA were utilized to knockdown ERK2 expression in the spinal cord following SCI. Pre-injury intrathecal administration of ERK2 siRNA significantly reduced excitotoxic injury-induced activation of ERK2 (p < 0.001) and caspase 3 (p < 0.01) in spinal cord. Intraspinal administration of lentiviral ERK2 shRNA significantly reduced ERK2 expression in the spinal cord (p < 0.05), but did not alter ERK1 expression. Administration of the lentiviral ERK2 shRNA vector 1 week prior to severe spinal cord contusion injury resulted in a significant improvement in locomotor function (p < 0.05), total tissue sparing (p < 0.05), white matter sparing (p < 0.05), and gray matter sparing (p < 0.05) 6 weeks following severe contusive SCI. Our results suggest that ERK2 signaling is a novel target associated with the deleterious consequences of spinal injury.
| S-EPMC4048743 | biostudies-literature
Project description:Establishing the structure of a prospective spinal cord injury (SCI) patient registry.To develop a registry for patients with traumatic spinal cord injury (tSCI) in Austria as a base for addressing research questions, improving patient outcomes, and establishing a platform for future clinical trials.Coordinating institution: Paracelsus Medical University Salzburg, Austria; participating partners are located in nine states in Austria.The Austrian Spinal Cord Injury Study (ASCIS) collects longitudinal data on simple forms within a 7-stage follow-up examination timeline.The implementation of the ASCIS in 2012 created the first nationwide SCI patient registry in Austria. ASCIS is currently implemented in 17 trauma hospitals in 9 Austrian states, and over 150 individuals with acute tSCI have been registered to date. As in Austria, the structure of the health-care system does not involve a specialized SCI center covering the primary health care and the rehabilitation care, major challenges have to be overcome to involve all participating primary centers and rehabilitation centers, which perform tSCI patient care, for ASCIS. Through implementing ASCIS, a network of SCI clinicians and researchers, which is now beginning to support translational research and to initiate clinical trials for patients with tSCI, has formed.ASCIS is uniquely positioned in Austria to capture detailed information from the early acute to the chronic phases of tSCI, to provide this information also to bigger and translational settings, and to connect researchers and clinicians to facilitate clinical research on tSCI.
| S-EPMC5798911 | biostudies-literature
Project description:IntroductionNeuropathic pain is a common complication of spinal cord injury (SCI), and is notoriously difficult to adequately treat. Gunshot wounds (GSW) near the spinal cord may cause intractable chronic pain through spinal/nerve root transection, or reactive tissue formation resulting in nerve root compression from retained bullet fragments (RBF).Case presentationThis case report describes a 30-year-old man with a T12 AIS B incomplete spinal cord injury with paraplegia secondary to multiple GSW who presented with severe bilateral lower extremity dysesthesias and muscle spasms. Symptoms failed to improve with oral antispasmodic medications. After being diagnosed with Complex regional pain syndrome (CRPS) type I secondary to an SCI via GSW, he underwent a spinal cord stimulator (SCS) trial, which improved his symptoms by greater than 80%.DiscussionNeuropathic pain refractory to conservative treatment may benefit from SCS. Effects of therapy go beyond gate-theory in SCI patients, and may benefit patients at the cellular and molecular level. Our case demonstrates the effectiveness of SCS treatment in a patient who developed CRPS type 1 after GSW resulting in SCI.
| S-EPMC9478097 | biostudies-literature
Project description:Traumatic spinal cord injury (SCI) impedes signal transmission by disrupting both the local neurons and their surrounding synaptic connections. Although the majority of SCI patients retain spared neural tissue at the injury site, they predominantly suffer from complete autonomic and sensorimotor dysfunction. While there have been significant advances in the characterization of the spared neural tissue following SCI, the functional role of injury-induced interneuronal plasticity remains elusive. In healthy individuals, spinal interneurons are responsible for relaying signals to coordinate both sympathetic and parasympathetic functions. However, the spontaneous synaptic loss following injury alters these intricate interneuronal networks in the spinal cord. Here, we propose the synaptopathy hypothesis of SCI based on recent findings regarding the maladaptive role of synaptic changes amongst the interneurons. These maladaptive consequences include circuit inactivation, neuropathic pain, spasticity, and autonomic dysreflexia. Recent preclinical advances have uncovered the therapeutic potential of spinal interneurons in activating the dormant relay circuits to restore sensorimotor function. This review will survey the diverse role of spinal interneurons in SCI pathogenesis as well as treatment strategies to target spinal interneurons.
| S-EPMC7247430 | biostudies-literature
Project description:Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS). Traumatic brain injury (TBI) is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κ β, disruption of blood-brain barrier (BBB), and oxidative stress. Spinal cord injury (SCI) includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.
| S-EPMC4283270 | biostudies-other