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Brain edema was produced by a standard cortical freezing lesion. The temporal course of the evolution and resolution of this edema has been reported elsewhere in detail. The effects of many types of therapy, both standard and investigational, upon this model of brain edema have been employed. Osmotic diuretics were found to have no effect upon the edema itself, but a reduction in the bulk of normal brain was evident. Maintenance of hypotension after lesion production essentially eliminated brain edema whereas prolonged hypertension increased brain edema dramatically. Focal excision of the cold injury itself immediately after lesion production prevented the development of brain edema. A beneficial effect on brain edema by focal excision was evident up to 24 h after injury at all time points from 6 h on. The addition of glucosteroids to focal excision reduced edema even further. Treatment of animals with dibenzyline, dimethyl sulfoxide, and diphenyl-p-phenylenediamine also had a beneficial effect upon the development of edema. Combination of steroids and osmotic diuretics was not of value. Focal excision with acetazolamide was extremely effective in reducing brain edema. A combination of DMSO and dexamethasone was more effective than either drug alone. Detailed studies to elucidate the effects of hypotension or hypertension in each of these therapeutic regimens were carried out.

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