Evaluation of traumatic spinal cord edema using evoked potentials recorded from the spinal epidural space: An experimental study in the rat

Spinal cord evoked potentials (SCEP) elicited by simultaneous distal tibial and sural nerve stimulation were continuously recorded from the epidural space at the T 9 and T 12 levels of urethane anaesthetized rats before and after a unilateral incision (about 3 mm deep and 5 mm long) in the right dorsal horn of the T 10–11 segments. The changes in SCEP were correlated with the increase in spinal cord water content measured 5 h after injury. In addition, the influence of serotonin (5-HT) in mediating such changes was explored using a pharmacological approach. The changes in SCEP immediately after injury correlated well with development of spinal cord edema measured 5 h after injury. Thus, the maximal negative peak (MNP) amplitude of SCEP decreased by an average of 64.0% immediately after injury and the water content of the spinal cord was increased from 71.6% (controls) to 77.6% 5 h after injury. Pretreatment with p-CPA (a serotonin synthesis inhibitor) prevented the initial decrease of the MNP amplitude and also the increase of water content (72.5%). On the other hand, pretreatment with cyproheptadine (a 5-HT 2 receptor antagonist) enhanced both the initial decrease of the MNP amplitude as well as the increase of water content (81.3%). The results show a good correlation between changes of SCEP immediately after injury and the magnitude of spinal cord edema ( r = 0.9) measured 5 h after injury. The findings reveal a major role of serotonin in mediating early changes of SCEP and later development of spinal cord edema and demonstrate a prognostic value of early SCEP recordings in predicting the final outcome of traumatic spinal cord injuries.