Cerebral haemodynamics were evaluated after a period of cerebral compression produced by subarachnoid fluid infusion or inflation of an epidural balloon. Release of the compression resulted in a marked cerebral hyperperfusion which was generalized in the case of hydrostatically raised pressure but restricted to supratentorial structures after balloon compression. A rebound of intracranial pressure (ICP) occurred only after balloon compression, indicating that loss of vasomotor tone per se was not the primary reason for the rebound of ICP. In the balloon compression experiments the hyperaemia passed into a stage of hypoperfusion attributable in part to a reduction in cerebral perfusion pressure due to the rebound of ICP and in part to an increase in flow resistance probably related to external compression of the vascular bed by the accumulation of brain oedema. The observed flow changes, i.e. delayed hypoperfusion preceded by hyperaemia, were similar to those after temporary ischaemia, indicating that the rebound response is a non-specific postischaemic phenomenon.