scholarly journals Epidural stimulation of the spinal cord in spinal cord injury: current status and future challenges

2011 ◽  
Vol 11 (10) ◽  
pp. 1351-1353 ◽  
Author(s):  
Victor Reggie Edgerton ◽  
Susan Harkema
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Current Status ◽  
Epidural Stimulation ◽  
Cord Injury ◽  
Future Challenges ◽  
Stimulation Of

Stem Cell Transplantation: A Promising Therapy for Spinal Cord Injury

2020 ◽  
Vol 15 (4) ◽  
pp. 321-331 ◽  
Author(s):  
Zhe Gong ◽  
Kaishun Xia ◽  
Ankai Xu ◽  
Chao Yu ◽  
Chenggui Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Spinal Cord Injury ◽  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Therapeutic Potential ◽  
Embryonic Stem ◽  
Current Status ◽  
Cord Injury

Spinal Cord Injury (SCI) causes irreversible functional loss of the affected population. The incidence of SCI keeps increasing, resulting in huge burden on the society. The pathogenesis of SCI involves neuron death and exotic reaction, which could impede neuron regeneration. In clinic, the limited regenerative capacity of endogenous cells after SCI is a major problem. Recent studies have demonstrated that a variety of stem cells such as induced Pluripotent Stem Cells (iPSCs), Embryonic Stem Cells (ESCs), Mesenchymal Stem Cells (MSCs) and Neural Progenitor Cells (NPCs) /Neural Stem Cells (NSCs) have therapeutic potential for SCI. However, the efficacy and safety of these stem cellbased therapy for SCI remain controversial. In this review, we introduce the pathogenesis of SCI, summarize the current status of the application of these stem cells in SCI repair, and discuss possible mechanisms responsible for functional recovery of SCI after stem cell transplantation. Finally, we highlight several areas for further exploitation of stem cells as a promising regenerative therapy of SCI.

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

2005 ◽  
Vol 102 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Steven L. Jinks ◽  
Carmen L. Dominguez ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Minimum Alveolar Concentration ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Partial Recovery ◽  
Spinal Transection ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Stimulation Of

Background Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury. Methods The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra. Results A large decrease in MAC (to </= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by >/= 90%) in both chronic and acute cold-block spinal animals. Conclusions The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.

The effects of epidural stimulation on individuals living with spinal cord injury or disease: a scoping review

2021 ◽  
Vol 26 (5) ◽  
pp. 344-369
Author(s):  
Hope Jervis Rademeyer ◽  
Cindy Gauthier ◽  
Kei Masani ◽  
Maureen Pakosh ◽  
Kristin E. Musselman
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Scoping Review ◽  
Epidural Stimulation ◽  
Cord Injury

Epidural electrical stimulation to facilitate locomotor recovery after spinal cord injury

2021 ◽  
Author(s):  
Johannie Audet ◽  
Charly G. Lecomte
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Stimulation ◽  
Clinical Implementation ◽  
Preclinical Models ◽  
Lumbosacral Region ◽  
Locomotor Recovery ◽  
Promising Therapeutic Approach ◽  
Cord Injury ◽  
Stimulation Of

Tonic or phasic electrical epidural stimulation of the lumbosacral region of the spinal cord facilitates locomotion and standing in a variety of preclinical models with severe spinal cord injury. However, the mechanisms of epidural electrical stimulation that facilitate sensorimotor functions remain largely unknown. This review aims to address how epidural electrical stimulation interacts with spinal sensorimotor circuits and discusses the limitations that currently restrict the clinical implementation of this promising therapeutic approach.

Pancreatitis following spinal cord injury

1977 ◽  
Vol 47 (6) ◽  
pp. 917-922 ◽  
Author(s):  
Michael E. Carey ◽  
Francis C. Nance ◽  
Homer D. Kirgis ◽  
Harold F. Young ◽  
Lloyd C. Megison ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Parasympathetic Nervous System ◽  
Sphincter Of Oddi ◽  
Systemic Circulation ◽  
Content Type ◽  
Pancreatic Damage ◽  
Cord Injury ◽  
Tract Infections ◽  
Stimulation Of

✓ Six cases of pancreatitis following spinal cord injury are presented. No single, etiologically accepted mechanism already postulated to cause pancreatitis can account for all the cases reported. The authors hypothesize that spinal cord disruption may produce pancreatitis by sympathetic-parasympathetic nervous system imbalance resulting in over-stimulation of the sphincter of Oddi. This may lead to stasis of secretions with absorption of amylase into the systemic circulation, and structural pancreatic damage. Pancreatitis in those with cord injuries is easily overlooked because abdominal pain is usually absent and fever is usually attributed to more frequently occurring pulmonary or urinary tract infections. Recognition of this complication is important in order to decrease the morbidity and mortality that follows spinal cord damage.

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