Abstract
After traumatic spinal cord injury, an acute phase triggered by trauma is followed by a subacute phase involving inflammatory processes. We previously demonstrated that peripheral serum cytokine expression changes depend on neurological outcome after spinal cord injury. In a subsequent intermediate phase, repair and remodeling takes place under the mediation of growth factors such as Insulin-like Growth Factor 1 (IGF-1). IGF-1 is a promising growth factor which is thought to act as a neuroprotective agent. Since previous findings were taken from animal studies, our aim was to investigate this hypothesis in humans based on peripheral blood serum. Forty-five patients after traumatic spinal cord injury were investigated over a period of three months after trauma. Blood samples were taken according to a fixed schema and IGF-1 levels were determined. Clinical data including AIS scores at admission to the hospital and at discharge were collected and compared with IGF-1 levels. In our study, we could observe distinct patterns in the expression of IGF-1 in peripheral blood serum after traumatic spinal cord injury regardless of the degree of plegia. All patients showed a marked increase of levels seven days after injury. IGF-1 serum levels were significantly different from initial measurements at four and nine hours and seven and 14 days after injury, as well as one, two and three months after injury. We did not detect a significant correlation between fracture and the IGF-1 serum level nor between the quantity of operations performed after trauma and the IGF-1 serum level. Patients with clinically documented neurological remission showed consistently higher IGF-1 levels than patients without neurological remission. This data could be the base for the establishment of animal models for further and much needed research in the field of spinal cord injury.
Highlights
Spinal cord injury continues to be one of the biggest challenges in modern medicine
After traumatic spinal cord injury, an acute phase triggered by trauma is followed by a subacute phase involving inflammatory processes
The body reacts most likely as a part of its repair mechanisms and thereby increased anabolic metabolism with an increased expression of Insulin-like Growth Factor 1 (IGF-1)[40, 50, 51].This process can be understood in our study by the significant increase of IGF-1 levels in serum seven days after injury
Summary
Spinal cord injury continues to be one of the biggest challenges in modern medicine. Even though promising approaches have been investigated recently[1,2,3], we have not yet succeeded in creating an adequate therapy concept that promises healing or at least partial remission by reintroducing integrity to lesioned nerve pathways and thereby restoring their function [4, 5].Injury to the spinal cord leads to loss of sensory, motor or autonomic nerve function and ranges from partial impairment of individual modalities in mild cases up to total loss of all function in cases of complete disruption of the spinal cord [4, 6,7,8,9]. After life-threatening injuries have been addressed in the hyper-acute phase, acute and subacute treatment is primarily used to prevent further progression of the primary injury and to reduce further loss of neurological function [5, 6]. The preservation of residual function in patients after spinal cord injury may mean the difference between total dependency and loss of quality of life, or possibly a reintegration in their professional as well as private activities and improved recovery after spinal cord injury [10, 11]. Stopping the progression of neurological damage with early relief operations and the best supportive care possible as well as physical therapy and exercise administered early in hospitalization to regain old skills is of great importance in the treatment of traumatic spinal cord injury. After the acute phase, which includes the trauma itself, the laceration or contusion of neurons and the surrounding glia, vessels and connective tissue, a second, subacute phase, in which the inflammatory process is set in motion, is further damaging to tissue and for introducing repair mechanisms [13]
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