Abstract
Although the primary lesion caused by traumatic injury to the spinal cord is considered intractable, the secondary lesions and consequent clinical manifestations can be diminished considerably with early administration of steroids or by surgical decompression of the injured segment, removal of bony fragments and stabilization (1-3). The extent of the neurologic deficits caused by the lesion is determined by two main factors: the primary mechanical insult and the secondary insult caused by inflammation, compression and ischemia (4-6). The primary lesion is caused by the trauma itself and involves cellular death and tissue necrosis, independently of biological factors. The mechanisms underlying secondary lesions involve activation of inflammation, tissue ischemia, reperfusion deficits, edema, lipidic peroxidation, calcium influx, and particularly apoptosis. The secondary lesions constitute the main target for the development of novel therapeutic approaches (7-9). Among these novel strategies, new anti-apoptotic agents are being developed, in the hope that their administration might limit tissue damage and increase the potential for clinical recovery (10).
Highlights
Spinal cord injury is a devastating clinical condition that often causes permanent incapacity, especially in the younger population
The acute phase after spinal cord injury is of utmost relevance since numerous pathological processes take place during this period, in which cell death is the hallmark feature
It is assumed that cell death after trauma is caused by both necrosis and apoptosis, i.e., two distinct pathophysiological processes
Summary
Spinal cord injury is a devastating clinical condition that often causes permanent incapacity, especially in the younger population. The extent of the neurologic deficits caused by the lesion is determined by two main factors: the primary mechanical insult and the secondary insult caused by inflammation, compression and ischemia [4,5,6]. The mechanisms underlying secondary lesions involve activation of inflammation, tissue ischemia, reperfusion deficits, edema, lipidic peroxidation, calcium influx, and apoptosis. The secondary lesions constitute the main target for the development of novel therapeutic approaches [7,8,9]. Among these novel strategies, new anti-apoptotic agents are being developed, in the hope that their administration might limit tissue damage and increase the potential for clinical recovery [10]
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