Spinal Cord Injury: Preventing Secondary Injury

1992 ◽  
Vol 3 (1) ◽  
pp. 44-54 ◽  
Author(s):  
S. Diane Coen

Spinal cord injury is devastating to the victim, as well as being costly in terms of medical expenses, lost wages, and lost independence. The initial damage to the spinal cord results from several mechanisms of injury—flexion, extension, compression, penetration, rotation, and the disease process. When the spinal cord is injured and there is necrosis of the nervous tissue, no regeneration of that tissue occurs. Unlike in the peripheral nervous system, where regeneration is possible, the spinal cord is part of the central nervous system, as is the brain. The spinal cord extends from the base of the skull to the L1 vertebrae: the cervical levels innervate the diaphragm and muscles of the arms; the thoracic levels innervate the muscles of the chest and abdomen; and the lumbar and sacral levels innervate the muscles of the legs. In addition, the sacral levels are responsible for bowel, bladder, and sexual function. The higher the level of injury, the more severe the loss of function because, not only is the level of injury affected, but also the levels below. Injury occurs by initial trauma to the surrounding ligaments, bones, and muscles, which then affect the spinal cord. There may be total loss of function with damage completely across the cord or partial loss of function with damage affecting only part of the cord. No current treatment can reverse this initial injury, which causes irreversible damage within minutes of injury. Secondary damage occurs as the injury spreads over several hours. Treatment can help prevent this secondary damage

1997 ◽  
Vol 36 (04/05) ◽  
pp. 372-375 ◽  
Author(s):  
J. R. Sutton ◽  
A. J. Thomas ◽  
G. M. Davis

Abstract:Electrical stimulation-induced leg muscle contractions provide a useful model for examining the role of leg muscle neural afferents during low-intensity exercise in persons with spinal cord-injury and their able-bodied cohorts. Eight persons with paraplegia (SCI) and 8 non-disabled subjects (CONTROL) performed passive knee flexion/extension (PAS), electrical stimulation-induced knee flexion/extension (ES) and voluntary knee flexion/extension (VOL) on an isokinetic dynamometer. In CONTROLS, exercise heart rate was significantly increased during ES (94 ± 6 bpm) and VOL (85 ± 4 bpm) over PAS (69 ± 4 bpm), but no changes were observed in SCI individuals. Stroke volume was significantly augmented in SCI during ES (59 ± 5 ml) compared to PAS (46 ± 4 ml). The results of this study suggest that, in able-bodied humans, Group III and IV leg muscle afferents contribute to increased cardiac output during exercise primarily via augmented heart rate. In contrast, SCI achieve raised cardiac output during ES leg exercise via increased venous return in the absence of any change in heart rate.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Sheng-Yu Cui ◽  
Wei Zhang ◽  
Zhi-Ming Cui ◽  
Hong Yi ◽  
Da-Wei Xu ◽  
...  

Abstract Background Spinal cord injury (SCI) is associated with health burden both at personal and societal levels. Recent assessments on the role of lncRNAs in SCI regulation have matured. Therefore, to comprehensively explore the function of lncRNA LEF1-AS1 in SCI, there is an urgent need to understand its occurrence and development. Methods Using in vitro experiments, we used lipopolysaccharide (LPS) to treat and establish the SCI model primarily on microglial cells. Gain- and loss of function assays of LEF1-AS1 and miR-222-5p were conducted. Cell viability and apoptosis of microglial cells were assessed via CCK8 assay and flow cytometry, respectively. Adult Sprague-Dawley (SD) rats were randomly divided into four groups: Control, SCI, sh-NC, and sh-LEF-AS1 groups. ELISA test was used to determine the expression of TNF-α and IL-6, whereas the protein level of apoptotic-related markers (Bcl-2, Bax, and cleaved caspase-3) was assessed using Western blot technique. Results We revealed that LncRNA LEF1-AS1 was distinctly upregulated, whereas miR-222-5p was significantly downregulated in LPS-treated SCI and microglial cells. However, LEF1-AS1 knockdown enhanced cell viability, inhibited apoptosis, as well as inflammation of LPS-mediated microglial cells. On the contrary, miR-222-5p upregulation decreased cell viability, promoted apoptosis, and inflammation of microglial cells. Mechanistically, LEF1-AS1 served as a competitive endogenous RNA (ceRNA) by sponging miR-222-5p, targeting RAMP3. RAMP3 overexpression attenuated LEF1-AS1-mediated protective effects on LPS-mediated microglial cells from apoptosis and inflammation. Conclusion In summary, these findings ascertain that knockdown of LEF1-AS1 impedes SCI progression via the miR-222-5p/RAMP3 axis.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Emma K. A. Schmidt ◽  
Pamela J. F. Raposo ◽  
Abel Torres-Espin ◽  
Keith K. Fenrich ◽  
Karim Fouad

Abstract Background Minocycline is a clinically available synthetic tetracycline derivative with anti-inflammatory and antibiotic properties. The majority of studies show that minocycline can reduce tissue damage and improve functional recovery following central nervous system injuries, mainly attributed to the drug’s direct anti-inflammatory, anti-oxidative, and neuroprotective properties. Surprisingly the consequences of minocycline’s antibiotic (i.e., antibacterial) effects on the gut microbiota and systemic immune response after spinal cord injury have largely been ignored despite their links to changes in mental health and immune suppression. Methods Here, we sought to determine minocycline’s effect on spinal cord injury-induced changes in the microbiota-immune axis using a cervical contusion injury in female Lewis rats. We investigated a group that received minocycline following spinal cord injury (immediately after injury for 7 days), an untreated spinal cord injury group, an untreated uninjured group, and an uninjured group that received minocycline. Plasma levels of cytokines/chemokines and fecal microbiota composition (using 16s rRNA sequencing) were monitored for 4 weeks following spinal cord injury as measures of the microbiota-immune axis. Additionally, motor recovery and anxiety-like behavior were assessed throughout the study, and microglial activation was analyzed immediately rostral to, caudal to, and at the lesion epicenter. Results We found that minocycline had a profound acute effect on the microbiota diversity and composition, which was paralleled by the subsequent normalization of spinal cord injury-induced suppression of cytokines/chemokines. Importantly, gut dysbiosis following spinal cord injury has been linked to the development of anxiety-like behavior, which was also decreased by minocycline. Furthermore, although minocycline attenuated spinal cord injury-induced microglial activation, it did not affect the lesion size or promote measurable motor recovery. Conclusion We show that minocycline’s microbiota effects precede its long-term effects on systemic cytokines and chemokines following spinal cord injury. These results provide an exciting new target of minocycline as a therapeutic for central nervous system diseases and injuries.


2009 ◽  
Vol 18 (3) ◽  
pp. 336-344 ◽  
Author(s):  
Adem Aslan ◽  
Mustafa Cemek ◽  
Olcay Eser ◽  
Korhan Altunbaş ◽  
Mehmet Emin Buyukokuroglu ◽  
...  

2021 ◽  
Vol 14 (8) ◽  
pp. 792
Author(s):  
Seong-Jun Kim ◽  
Wan-Kyu Ko ◽  
Gong-Ho Han ◽  
Daye Lee ◽  
Yuhan Lee ◽  
...  

Neuroinflammation forms a glial scar following a spinal cord injury (SCI). The injured axon cannot regenerate across the scar, suggesting permanent paraplegia. Molecular chirality can show an entirely different bio-function by means of chiral-specific interaction. In this study, we report that d-chiral glutathione (D-GSH) suppresses the inflammatory response after SCI and leads to axon regeneration of the injured spinal cord to a greater extent than l-chiral glutathione (L-GSH). After SCI, axon regrowth in D-GSH-treated rats was significantly increased compared with that in L-GSH-treated rats (*** p < 0.001). Secondary damage and motor function were significantly improved in D-GSH-treated rats compared with those outcomes in L-GSH-treated rats (** p < 0.01). Moreover, D-GSH significantly decreased pro-inflammatory cytokines and glial fibrillary acidic protein (GFAP) via inhibition of the mitogen-activated protein kinase (MAPK) signaling pathway compared with L-GSH (*** p < 0.001). In primary cultured macrophages, we found that D-GSH undergoes more intracellular interaction with activated macrophages than L-GSH (*** p < 0.001). These findings reveal a potential new regenerative function of chiral GSH in SCI and suggest that chiral GSH has therapeutic potential as a treatment of other diseases.


2001 ◽  
Vol 5 (1) ◽  
pp. 146-156
Author(s):  
Giuseppe Riva

The paper presents an overview of the ergonomic/design issues of a VR-enhanced orthopaedic appliance to be used in rehabilitation of patients with Spinal Cord Injury. First, some design considerations are described and an outline of aims which the tool should pursue are given. Finally, the design issues are described focusing both on the development of a test-bed rehabilitation device and on the description of a preliminary study detailing the use of the device with a long-term SCI patient. The basis for this approach is that physical therapy and motivation are crucial for maintaining flexibility and muscle strength and for reorganizing the nervous system after SCIs.


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