Methylprednisolone inhibits early inflammatory processes but not ischemic cell death after experimental spinal cord lesion in the rat.

Experimental studies and clinical observations show that spinal cord lesions are greatly enlarged by a process called secondary cell death. A detailed understanding of the molecular and cellular processes underlying these events is still lacking. In clinical studies using methylprednisolone in spinal cord injured patients a mega-dose of methylprednisolone applied during the first few hours after injury was found to improve the neurological outcome. In the present study the possible neuroprotective mechanism of methylprednisolone was assessed by histologically studying its effect on the extent of secondary cell death and on early inflammatory reactions following partial transection of the spinal cord in the rat. Our results show that a single high dose of 30 or 60 mg/kg methylprednisolone affects neither the time course nor the extent of secondary cell death. In contrast, methylprednisolone markedly suppressed the invasion of the injured spinal cord tissue by polymorphonuclear granulocytes and macrophages. The role of these inflammatory cells in traumatic CNS lesions is very unclear at present. It is possible that they lead to further damage of the injured spinal cord tissue and that the beneficial effect of methylprednisolone is at least partially due to its anti-inflammatory effect, thereby inhibiting bystander damage of invading inflammatory cells.