Influence of Previous Comorbidities and Common Complications on Motor Function after Early Surgical Treatment of Patients with Traumatic Spinal Cord Injury

2016 ◽  
Vol 33 (24) ◽  
pp. 2175-2180 ◽  
Author(s):  
Michael Kreinest ◽  
Lisa Ludes ◽  
Bahram Biglari ◽  
Maike Küffer ◽  
Ansgar Türk ◽  
...  
2019 ◽  
Vol 44 (2) ◽  
pp. 498-506 ◽  
Author(s):  
Belen G. Alvarado-Sanchez ◽  
Hermelinda Salgado-Ceballos ◽  
Sergio Torres-Castillo ◽  
Juan Rodriguez-Silverio ◽  
Monica E. Lopez-Hernandez ◽  
...  

2020 ◽  
Author(s):  
Daniel J. Modulevsky ◽  
Charles M. Cuerrier ◽  
Maxime Leblanc-Latour ◽  
Ryan J. Hickey ◽  
Ras-Jeevan K. Obhi ◽  
...  

ABSTRACTAs of yet, no standard of care incorporates the use of a biomaterial to treat traumatic spinal cord injury (SCI)1–5. However, intense development of biomaterials for treating SCI have focused on the fabrication of microscale channels to support the regrowth of axons while minimizing scar tissue formation6–10. We previously demonstrated that plant tissues can be decellularized and processed to form sterile, biocompatible and implantable biomaterials that support cell infiltration and vascularization in vivo11–13. Notably, the vascular bundles of plant tissues are also composed of microscale channels with geometries thought to be relevant for supporting neural tissue regeneration9,14. We hypothesized that decellularized vascular bundles would support neural regeneration and the recovery of motor function. Therefore, rats which received a complete T8-T9 spinal cord transection were implanted with plant-derived channeled scaffolds. Animals which received the scaffolds alone, with no therapeutic stem cells or other interventions, demonstrated a significant and stable improvement in motor function over six months compared to controls. Histological analysis reveals minimal scarring and axonal regrowth through the scaffolds, further confirmed with tracer studies. Taken together, our work defines a novel route for exploiting naturally occurring plant microarchitectures to support the repair of functional spinal cord tissue.


1999 ◽  
Vol 80 (4) ◽  
pp. 293-295
Author(s):  
I. N. Pleshchinsky ◽  
E. K. Valeev ◽  
G. G. Yafarova ◽  
N. L. Alekseeva

It is known that traumatic spinal cord injury leads to a number of structural and functional changes. As a result of trauma, the spinal cord is cut off, compressed and softened by central hemorrhagic necrosis, and local damage to the axons is determined within a few hours.


2021 ◽  
Vol 12 ◽  
Author(s):  
Alise Lattard ◽  
Gaëtan Poulen ◽  
Sylvain Bartolami ◽  
Yannick N. Gerber ◽  
Florence E. Perrin

In traumatic spinal cord injury, the initial trauma is followed by a cascade of impairments, including excitotoxicity and calcium overload, which ultimately induces secondary damages. The sigma-1 receptor is widely expressed in the central nervous system and is acknowledged to play a key role in calcium homeostasis. Treatments with agonists of the sigma-1 receptor induce beneficial effects in several animal models of neurological diseases. In traumatic injury the use of an antagonist of the sigma-1 receptor reversed several symptoms of central neuropathic pain. Here, we investigated whether sigma-1 receptor activation with PRE-084 is beneficial or detrimental following SCI in mice. First, we report that PRE-084 treatment after injury does not improve motor function recovery. Second, using ex vivo diffusion weighted magnetic resonance imaging completed by histological analysis, we highlight that σ1R agonist treatment after SCI does not limit lesion size. Finally, PRE-084 treatment following SCI decreases NeuN expression and increases astrocytic reactivity. Our findings suggest that activation of sigma-1 receptor after traumatic spinal cord injury is detrimental on tissue preservation and motor function recovery in mice.


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