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.