At- and Below-Level Pain in Spinal Cord Injury: Mechanisms and Diagnosis

2001 ◽  
Vol 7 (2) ◽  
pp. 30-40 ◽  
Author(s):  
Diana Cardenas ◽  
Jeffrey Rosenbluth
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Injury Mechanisms ◽  
Cord Injury

Physiologic Modulators of Neural Injury After Brain and Spinal Cord Injury

2017 ◽  
Author(s):  
W. Dalton Dietrich
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuronal Cell ◽  
Acute Injury ◽  
Secondary Injury ◽  
Edema Formation ◽  
Blood Brain Barrier Disruption ◽  
Injury Mechanisms ◽  
Cord Injury ◽  
Brain And Spinal Cord

Brain and spinal cord injury are leading causes of death and long-term disability, producing diverse burdens for the affected individuals, their families, and society. Such injuries, including traumatic brain injury, stroke, subarachnoid hemorrhage, and spinal cord injury, have common patterns of neuronal cell vulnerability that are associated with a complex cascade of pathologic processes that trigger the propagation of tissue damage beyond the acute injury. Secondary injury mechanisms, including oxidative stress, edema formation, changes in cerebral blood flow and vessel reactivity, metabolic and blood–brain barrier disruption, and neuroinflammation, are therefore important therapeutic targets. Several key physiological parameters require monitoring and intensive management during various phases of treatment to ameliorate secondary injury mechanisms and potentially protect against further neuronal injury. This chapter reviews the core physiological targets in the management of brain and spinal cord injury and relates them to secondary injury mechanisms and outcomes.

Why Do We Not Have a Drug to Treat Acute Spinal Cord Injury?

Neurotrauma ◽  
2018 ◽  
pp. 411-422
Author(s):  
James W. Geddes
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Acute Spinal Cord Injury ◽  
Secondary Injury ◽  
Functional Deficits ◽  
Injury Mechanisms ◽  
Cord Injury ◽  
Contusion Injury ◽  
Weight Drop ◽  
Intraspinal Hemorrhage

More than 100 years ago, Alfred Reginald Allen developed the weight-drop model of graded, reproducible contusion injury to the dorsal spinal cord. Allen also introduced the concept of secondary injury mechanisms, hypothesizing that hemorrhage and elevated intraspinal pressure contribute to the destruction of the spinal cord and functional deficits. Our understanding of the secondary injury cascade has advanced tremendously over the past 100 years, with numerous therapeutic targets identified. Yet we lack an effective drug treatment for acute spinal cord injury. Reasons for the failure to translate promising preclinical findings to successful clinical trials include concerns regarding the quality of preclinical studies, including possible bias and inappropriate statistical analysis; questions regarding the suitability of animal models; and the complexity of secondary mechanisms following spinal cord injury. Perhaps, however, we have overlooked the targets identified by Allen, namely the intraspinal hemorrhage and elevations in intraspinal pressure.

scholarly journals Concise Review: Bone Marrow for the Treatment of Spinal Cord Injury: Mechanisms and Clinical Applications

Stem Cells ◽  
2011 ◽  
Vol 29 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Karina T. Wright ◽  
Wagih El Masri ◽  
Aheed Osman ◽  
Joy Chowdhury ◽  
William E. B. Johnson
Keyword(s):  
Spinal Cord ◽  
Bone Marrow ◽  
Spinal Cord Injury ◽  
Clinical Applications ◽  
Concise Review ◽  
Injury Mechanisms ◽  
Cord Injury

scholarly journals Vascular mechanisms in the pathophysiology of human spinal cord injury

1997 ◽  
Vol 2 (1) ◽  
pp. E2
Author(s):  
Charles H. Tator ◽  
Izumi Koyanagi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
White Matter Lesions ◽  
Arterial System ◽  
Secondary Injury ◽  
Human Spinal Cord ◽  
Injury Mechanisms ◽  
Cord Injury

Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3-5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3-9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

Recovery of Function after Spinal Cord Injury: Mechanisms Underlying Transplant-Mediated Recovery of Function Differ after Spinal Cord Injury in Newborn and Adult Rats

1993 ◽  
Vol 123 (1) ◽  
pp. 3-16 ◽  
Author(s):  
Barbara S. Bregman ◽  
Ellen Kunkel-Bagden ◽  
Paul J. Reier ◽  
Hai Ning Dai ◽  
Marietta McAtee ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Recovery Of Function ◽  
Adult Rats ◽  
Injury Mechanisms ◽  
Cord Injury

scholarly journals Ketogenesis controls mitochondrial gene expression and rescues mitochondrial bioenergetics after cervical spinal cord injury in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Oscar Seira ◽  
Kathleen Kolehmainen ◽  
Jie Liu ◽  
Femke Streijger ◽  
Anne Haegert ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Alternative Fuels ◽  
Cervical Spinal Cord ◽  
Mitochondrial Gene ◽  
Injury Mechanisms ◽  
Cord Injury ◽  
Neuroprotective Strategies ◽  
Atp Generation ◽  
Specific Receptors

AbstractA better understanding of the secondary injury mechanisms that occur after traumatic spinal cord injury (SCI) is essential for the development of novel neuroprotective strategies linked to the restoration of metabolic deficits. We and others have shown that Ketogenic diet (KD), a high fat, moderate in proteins and low in carbohydrates is neuroprotective and improves behavioural outcomes in rats with acute SCI. Ketones are alternative fuels for mitochondrial ATP generation, and can modulate signaling pathways via targeting specific receptors. Here, we demonstrate that ad libitum administration of KD for 7 days after SCI rescued mitochondrial respiratory capacity, increased parameters of mitochondrial biogenesis, affected the regulation of mitochondrial-related genes, and activated the NRF2-dependent antioxidant pathway. This study demonstrates that KD improves post-SCI metabolism by rescuing mitochondrial function and supports the potential of KD for treatment of acute SCI in humans.

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