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In this communication, we demonstrate the sequential expression of endogenous molecules, including immediate early genes (IEGs), cytokines, neurotrophins, and neurotrophin receptors in the injured spinal cord. In the acute phase, expression of IEGs and cytokines mRNAs were rapidly upregulated within 1 h in nonneuronal cells in the lesioned sites and the surrounding spinal white and gray matter. Maximal expression was observed at 1 h for c-fos and TNF-alpha mRNAs, at 3 h for c-jun and IL-6 mRNAs, and at 6 h for IL-1 beta mRNA, and these signals were virtually nondetectable after 6-12 h from the onset of the injury. Some of these genes products may promote the degeneration of damaged cells and tissues, while others may be involved in the subsequent repair processes. In the subacute phase, expression of NGF, BDNF, NT-3, p75LNGFR and Trk B mRNAs began to increase in the nonneuronal cells and neuronal cells from 6 h, and peaked at 24-72 h in the area where expression of mRNAs for IEGs and cytokines overlapped. Signals for IL-6 mRNA were also observed in motoneurons at 24-72 h after the injury, with the suggestion that these molecules may be involved in promoting axonal sprouting in the injured spinal cord. Of further interest was the finding that this upregulation of IL-1 beta, BDNF, and NT-3 mRNAs in injured spinal cord was attenuated by treatment with high dose glucocorticoids, with the suggestion that the downregulation of BDNF and NT-3 might be disadvantageous to survival and axonal sprouting of spinal neurons.

Spinal cord monitoring, based on spinal cord potentials recorded close to the conus medullaris and evoked by stimulating rostral spinal cord, has been extensively used clinically in Japan. To understand how such spinal cord evoked potentials (SCEP) reflect injurious effects on the spinal cord, we carried out the following animal experiments. The effects of spinal cord distraction, compression, and combined compression and hypotension or hypoxia were examined. We found that there is a critical point of compression or distraction of the spinal cord at which SCEP amplitude decreases significantly. Acute hypotension concomitant with moderate compression increases the risk of insult to the cord. Accordingly, we believe that repetitive monitoring and rapid feedback to the surgeon are indispensable to intraoperative spinal cord monitoring. Furthermore, hypotension should be carefully avoided whenever symptoms of spinal cord compression occur. A comparative study of SCEP and spinal SEP indicates that both potentials can substitute for each other, although the sensitivity of the SCEP for detecting hazardous effects is higher.