Klatzo's classification of brain edema into two types, vasogenic and c
ytotoxic, has been in general use since 1967. The former involves over
all brain swelling due to fluid entry from the vasculature because of
openings in the blood-brain barrier (BBB), whereas the latter refers t
o cell swelling without any loss of the normal impermeability of the B
BB. This review principally covers new work that identifies the intrac
ellular swelling of astrocytes as a major form of cytotoxic edema seen
in many different kinds of brain injury. The term edema should be ret
ained because of its familiarity; however, because such intracellular
swelling is usually not a response to toxins, it is suggested that the
term cellular edema is preferable to cytotoxic edema. The difficultie
s involved in measuring cellular edema clinically are discussed, and t
he belief that a ''pure'' form of either edema is unlikely to exist. I
t is emphasized that the mechanisms and direct consequences of vasogen
ic and cellular edema are so different that the connection is mainly s
emantic. Studies conducted in vitro have identified several potentiall
y damaging secondary consequences of astrocytic swelling. One of the m
ost important of these seems likely to be the increased release of exc
itatory amino acids from swollen astrocytes. Potential mechanisms for
inhibition of the increased release of amino acids have been identifie
d in vitro and could prove therapeutically useful.