The pathogenesis of nervous system-induced pulmonary edema remains incompletely understood. There are two major causes: elevated intravascular pressure and pulmonary capillary leak. Thus, both hemodynamic (cardiogenic) or nonhemodynamic (noncardiogenic) components exist. These components often occur together in settings such as pulmonary edema following epileptic convulsions or intracranial pressure elevation. The hemodynamic component is relatively brief and may unmask a "pure" noncardiogenic pulmonary edema such as that seen in experimental seizures (see Fig. 6). Whether the hemodynamic changes produce a pulmonary capillary leak through pressure-induced mechanical injury to the pulmonary capillaries or whether some direct nervous system control over pulmonary capillary permeability exists remains uncertain. The neuroeffector site for nervous system-induced pulmonary edema appears relatively well established in regions about the caudal medulla, where nuclei regulating systemic arterial pressure and afferent and efferent pathways to and from the lungs are located.