A variety of central nervous system (CNS) insults may be complicated by the acute development of pulmonary edema. This occurrence has been termed neurogenic pulmonary edema (NPE), and experimental models have clearly shown that CNS insults may cause pulmonary edema. Unfortunately, the pathophysiologic aspects of this response are not clearly understood. Basing an approach to the development of pulmonary edema on Starling's equation leads to the conclusion that NPE is caused by changes in pulmonary endothelial permeability and/or microvascular pressures. It was previously suggested (the "blast theory") that CNS insults caused acute systemic arterial and pulmonary venous spasm and increased venous return, which would result in a severe pulmonary vascular hydrostatic insult and a secondary permeability defect. Although such hydrostatic derangements may explain certain cases of NPE, recent clinical and experimental studies have indicated that CNS disorders may cause a permeability defect without a vascular insult. The mediating factor for a permeability defect is not clear. The implications of these findings are that NPE may be caused by either permeability abnormalities or hydrostatic insults, may present clinically in a variety of ways, and may require different approaches to treatment. Our understanding of the CNS sites that might mediate NPE is not sophisticated enough, at present, to define the neural mechanisms involved in the pathogenesis of NPE.