Abstract
A variety of physiologic, neurochemical, and morphologic sequelae have been either shown or postulated to result from spinal cord injury, yet the actual pathophysiologic substrate that leads to the loss of neurologic function remains uncertain.
Several treatment modalities have been investigated in spinal cord injury, but little consensus exists regarding their efficacy. Steroids in particular have been studied extensively with little agreement about their effects and possible mechanism of action. Recently naloxone has been found to improve neurologic function following spinal cord injury, and its effectiveness has not been challenged to date.
In the past most attempts at therapy in cases of brain injury were directed at control of edema, and, consequently, clinically beneficial effects were usually ascribed to control of the edematous process. This was particularly so in the case of steroids. Currently, emphasis has shifted to the study of various neurochemical systems (eicosanoids, serotonin, catecholamines) that, independently from edema may underlie functional disturbances resulting from trauma. Much of the pertinent information derives from the use of drugs in freezing lesion models of brain injury.
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