Corticosteroids in ischemic stroke.

IN THE PATIENT with completed stroke there are few specific management options. Once damage has been sustained, objectives are limited: patient survival, reduction of neurological deficit to a minimum, effective rehabilitation to realize the potential of brain compensatory mechanisms, and secondary prophylaxis in hopes of avoiding a further ictus. The physician's concern must be to minimize the extent of tissue damage incurred as a direct or indirect result of the original vascular process. The record of the many medical interventions which have been advocated with that objective in mind — carbon dioxide inhalation, vasodilating agents, hyperventilation, induced hypertension, and stellate ganglion blockade, to name but a few employed in ischemic infarction — has not been inspiring, and such measures are rarely used today. One intervention, corticosteroid administration, first reported in the late 1950's, however, continues to be routine in many centers. The purpose of our discussion will be to examine, once again, the rationale for the use of corticosteroids in stroke and to assess the evidence that they do, in fact, accomplish the ends for which they are prescribed. Since corticosteroids have been thought to ameliorate the pathological processes in various brain lesions by reducing associated brain edema, we will also consider the nature of ischemic cerebral edema and the evidence that edema contributes to tissue injury.