Brain abscess evolution was studied in an experimental model in the cat correlating the computed tomographic scan appearance with intracranial pressure, brain edema and histopathological findings. Brain inflammation was produced by direct inoculation of Staphylococcus aureus into the white matter. Abscesses developed in all animals. The ring enhancement around the necrotic focus seen at an early stage after contrast-medium injection cannot be equated with capsule formation as long as the abscess diameter increased. Parallel to the acute stage of abscess, the intraventricular pressure increased due to the rising mass effect and the spreading edma. The morphological investigations revealed on the seventh day an extreme enlargement of extracellular spaces with immense amount of edema fluid, rich in protein and fibrin. Some blood vessels in the close vicinity of the abscess showed gaps within the endothelial cell layer. When encapsulation developed, ring enhancement became more homogeneous and decreased in diameter. In spite of encapsulation, a circumscribed disturbance of the blood-brain barrier persisted which was responsible for a belated resolution of edema and a slow decrease of intracranial pressure. Only therapy with dexamethasone could effect a marked change in the course of the disease.