The rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion was studied in an epidural balloon compression model. Intracranial morphology and brain tissue water content were assessed with magnetic resonance imaging (MRI). Fast and slow components of the transverse relaxation time (T2) were used as indicators of brain oedema development. During balloon compression a progressive prolongation of both the fast and the slow T2 components took place. Following deflation of the balloon both components increased rapidly, particularly the slow-T2. The MR scans displayed progressive occlusion of the aqueduct, and obliteration of the ambient and pontine cisterns. The changes in morphology and in water content after decompression had largely the same time course as the development of the rebound of ICP. In contrast, no changes in morphology and tissue water content occurred after hydrostatic brain compression achieved by subarachnoid fluid infusion. The findings suggest that the intracranial pressure rebound is caused by cerebral oedema accumulated during and particularly in the recirculation phase after an ischaemic injury of adequate intensity and adequate duration.