The Effects of Glucosteroids upon Experimental Brain Edema

Summary

Brain edema has been produced in rabbits, cats, dogs, and monkeys by the intracranial implantation of hydrophillic materials, stab wounds, implantation of viable brain tumors, inflation of extradural or subdural balloons, and cortical or spinal cord freezing injury. The temporal course of the evolution and resolution of brain edema in each of these models has been studied by gross photography, the extravasation of fluorescent protein tracers, wet weight/dry weight determinations, light microscopy, histochemistry, and electron microscopy. In a similar series of animals, the effects of glucosteroids given in several ways have been evaluated. Dexamethasone, cortisone, prednisone, and prednisolone have been utilized in dosages varying from 0.25 to 2.5 mg/kg/24 h. Animals have been pre-treated with steroids for 24 and 48 h prior to lesion production, and steroids have then been begun at the time of lesion production and at regular intervals up to 72 h after lesion production. The effects of the administration of glucosteroids upon the same parameters of edema estimation have been assessed. The cold injury model provides the best quantitative data. The administration of glucosteroids to animals in which a cold or spinal cord freezing injury has been inflicted results in a gross reduction in brain edema with reduced extravasation of dye protein complexes. Wet weight/dry weight determinations demonstrate significant retardations in the development of brain edema. At 24 and 48 h there is an approximate 50% reduction in edema, and at 72 h, a reduction of almost 30% persists. Light microscopic and histochemical differences were not striking. Electron microscopic studies revealed definite reduction in astrocytic volume and in white matter extracellular space in treated animals. The resolution of edema appeared to be accelerated. In addition, there was a marked reduction in postedema astrogliosis in animals receiving glucosteroids.