Pathophysiology of Traumatic Spinal Cord Injury

Couillard‐Després, Sébastien; Bieler, Lara; Vogl, Michael

doi:10.1007/978-3-319-46293-6_19

Cited by 35 publications

(58 citation statements)

References 198 publications

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“…The main determinants for SCI severity are the extent of initial destruction and duration of spinal cord compression. A cascade of events associated with secondary injury is activated by the onset of biochemical, mechanical and physiological changes within neural tissues [ 6 ]. Although clinical manifestation suggests complete functional loss, few segments remain connected by some axons during primary SCI phase, thus reflecting incomplete and partial injury state [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…Endothelial injury and inflammation subsequently increase the pore size and thus allow large plasma-derived molecules to pass through the cell membrane, resulting in vasogenic oedema [ 12 ]. This acute secondary injury phase continues from 2 h to 48 h. Continuous haemorrhage, oedema and inflammatory stage lead to substantial necrosis indicated by the increased concentration of specific inflammatory and the presence of structural biomarkers, e.g., glial fibrillary acidic protein (GFAP) or IL-6 in cerebrospinal fluid (CSF) [ 6 ]. These processes provoke free radical formation, glutamate-mediated excitotoxicity and neurotoxicity [ 12 ] ( Figure 1 c).…”

Section: Introductionmentioning

confidence: 99%

“…The Wallerian degeneration is manifested by the formation of retraction bulbs, a microtubule network that inhibits axonal regeneration [ 28 ]. The anterograde degenerative mechanism is termed as Wallerian degeneration; however, retrograde degeneration of axons is termed as axonal dieback [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

Anjum

Yazid

Daud

et al. 2020

IJMS

692

419

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Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. Many therapeutic strategies have been proposed to overcome neurodegenerative events and reduce secondary neuronal damage. Efforts have also been devoted in developing neuroprotective and neuro-regenerative therapies that promote neuronal recovery and outcome. Although varying degrees of success have been achieved, curative accomplishment is still elusive probably due to the complex healing and protective mechanisms involved. Thus, current understanding in this area must be assessed to formulate appropriate treatment modalities to improve SCI recovery. This review aims to promote the understanding of SCI pathophysiology, interrelated or interlinked multimolecular interactions and various methods of neuronal recovery i.e., neuroprotective, immunomodulatory and neuro-regenerative pathways and relevant approaches.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

Anjum

Yazid

Daud

et al. 2020

IJMS

692

419

View full text Add to dashboard Cite

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“…A number of studies have highlighted the potential benefits of multivariate techniques in the context of preclinical trials [2] and more specifically animal neurotrauma models [3][4][5][6][7]. Traumatic or ischemic events to the central nervous system such as stroke, spinal cord or traumatic brain injury are followed by a multi-faceted pathophysiology which manifests on molecular, histological and functional levels [8][9][10][11]. Individual biological mechanisms that are disrupted by or result from the neurotrauma such as apoptosis [12,13], neuroinflammation [14][15][16][17][18], oxidative stress [18][19][20] and plasticity alterations [21,22] have provided therapeutic targets in animal models.…”

Section: Introductionmentioning

confidence: 99%

Applying univariate vs. multivariate statistics to investigate therapeutic efficacy in (pre)clinical trials: A Monte Carlo simulation study on the example of a controlled preclinical neurotrauma trial

2020

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Background Small sample sizes combined with multiple correlated endpoints pose a major challenge in the statistical analysis of preclinical neurotrauma studies. The standard approach of applying univariate tests on individual response variables has the advantage of simplicity of interpretation, but it fails to account for the covariance/correlation in the data. In contrast, multivariate statistical techniques might more adequately capture the multi-dimensional pathophysiological pattern of neurotrauma and therefore provide increased sensitivity to detect treatment effects. Results We systematically evaluated the performance of univariate ANOVA, Welch's ANOVA and linear mixed effects models versus the multivariate techniques, ANOVA on principal component scores and MANOVA tests by manipulating factors such as sample and effect size, normality and homogeneity of variance in computer simulations. Linear mixed effects models demonstrated the highest power when variance between groups was equal or variance ratio was 1:2. In contrast, Welch's ANOVA outperformed the remaining methods with extreme variance heterogeneity. However, power only reached acceptable levels of 80% in the case of large simulated effect sizes and at least 20 measurements per group or moderate effects with at least 40 replicates per group. In addition, we evaluated the capacity of the ordination techniques, principal component analysis (PCA), redundancy analysis (RDA), linear discriminant analysis (LDA), and partial least squares discriminant analysis (PLS-DA) to capture patterns of treatment effects without formal hypothesis testing. While LDA suffered from a high false positive rate due to multicollinearity, PCA, RDA, and PLS-DA were robust and PLS-DA outperformed PCA and RDA in capturing a true treatment effect pattern.

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“…Severe urinary dysfunction is a phenomenon that occurs after SCI . The consequences of SCI on the lower urinary tract depended on the level, intensity and the time of injury …”

Section: Introductionmentioning

confidence: 99%

Effect of cerebrolysin on bladder function after spinal cord injury in female Wistar rats

et al. 2019

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Abbreviations & Acronyms ANOVA = analysis of variance BBB = Basso-Beattie-Bresnahan BDNF = brain-derived neurotrophic factor CL = cerebrolysin CNS = central nervous system DSD = detrusor sphincter dyssynergia GABA = gammaaminobutyric acid GDNF = glial cell linederived neurotrophic factor IGF-I = insulin-like growth factor i.p. = intraperitoneal MVP = maximum voiding pressure NDO = neurogenic detrusor overactivity NGB = neurogenic bladder NGF = nerve growth factor NT = neurotrophin SCI = spinal cord injury Correspondence: SakinehObjectives: To study the effect of cerebrolysin on bladder function after spinal cord injury using functional measurements in rats. Methods: A total of 60 female rats were enrolled in this study. After induction of complete transection at T9-T10 spinal vertebrae, cerebrolysin was injected intraperitoneally, and daily in three dosages until 7 days (1 week) and continued until 28 days (4 weeks) in three groups to show the impact of that on the bladder function. Urodynamic parameters were measured in the different groups. Results: Cerebrolysin injection in a dose of 1 mL/kg for 1 week showed a slight improvement in urodynamic parameters. However, infusion of 2.5 and 5 mL/kg cerebrolysin for 1 week caused an elevation in contractions and a decrease in compliance. In long-term 2.5 mL/kg cerebrolysin injection, an improvement in compliance was observed, despite relative contractions. Furthermore, the bladder pressure pattern in the 2.5 mL/kg infused rats for 4 weeks was similar to the control group, but in the group receiving 5 mL/kg cerebrolysin for 4 weeks, reduced bladder contractions and function were observed. Conclusions: Our findings suggest that cerebrolysin might be able to inhibit the emergence of neurogenic detrusor overactivity in spinal cord injured female rats.

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Pathophysiology of Traumatic Spinal Cord Injury

Cited by 35 publications

References 198 publications

Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

Applying univariate vs. multivariate statistics to investigate therapeutic efficacy in (pre)clinical trials: A Monte Carlo simulation study on the example of a controlled preclinical neurotrauma trial

Effect of cerebrolysin on bladder function after spinal cord injury in female Wistar rats

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