Brain edema (BE), defined as an increase in tissue water content leading to an increase in tissue volume, is a common histopathologic response associated with a number of acute and subacute brain lesions. In some cases BE is a result of an unbalance of physical forces, hydrostatic or osmotic gradients driving the water in the tissue (hypertensive encephalopathy, hydrocephaly, plasma hypoosmolarity). In most cases however BE is associated with complex brain tissue alterations. According to Klatzo (1967) two physiopathological types can be described: vasogenic edema follows a breakdown of blood brain barrier to proteins. Edema fluid enlarges the extra-cellular space and spreads within the white matter; cytotoxic edema is an intra-cellular retention of water due to various disorders of ionic balance across the plasmic cell membrane. In both cases the hydrostatic gradient between the vascular lumen and the tissue plays a major role in the amount and spread of the edema fluid. In both cases also, toxic substances produced by tissue destruction act as factors of secondary damage causing more blood brain barrier lesions and/or cellular membrane alterations and eventually enhance edema. In various pathological conditions vasogenic and cytotoxic edema are associated: edema around circumscribed lesions such as hematomas, traumatic contusions, tumors, abscesses is basically a vasogenic edema with a secondary cytotoxic component. Ischemic edema is initially a pure cytotoxic phenomenon with a secondary osmotic edema and lately a vasogenic component. The formation of BE leads to an increase in tissue pressure which may reduce local cerebral blood flow. If blood supply is already impaired this can lead to energy shortage and further tissue destruction. If the bulk of edema is large enough intracranial pressure rises up, brain shifts and herniations may occur. Hypertonic solutions and corticoids are the more widely used drugs against brain edema. Hypertonic solutions remove water from the normal brain and hence may reduce intracranial pressure rather than treat edema. Corticoids, through various discrete mechanisms interfere with some toxic substances, enhance energetic metabolism and allow tissue restitution with a rather limited effect on edema itself.