Traumatic brain injury and stroke are both characterized by an ischemic core surrounded by a penumbra of low to hyperemic flows. The underperfused ischemic core is the focus of edema development, but the source of the edema fluid is not known. We hypothesized that flow of edema fluid into the tissue is derived from cerebral venous circulation pressure, which always exceeds intracranial pressure (ICP). As a first step toward testing this hypothesis, the aim of the current study was to determine whether cerebral venous pressure in the normal brain is always equal to or higher than ICP. In studies on 2 pigs, cerebral cortical venous, intracranial (subarachnoid), sagittal sinus, and central venous pressures were monitored with manipulation of ICP by raising and lowering a reservoir above and below the external auditory meatus zero point. The results show that cerebral venous pressure is always higher than or equal to ICP at pressures of up to 60 mmHg. On the basis of these observations, we hypothesize that increased cerebral venous pressure initiated after traumatic brain injury and stroke drives edema fluid into the tissue, which thereby increases ICP and a further increase in cerebral venous pressure in a vicious cycle of brain edema.