Rapid ascent to altitude can result in high altitude headache, acute mountain sickness and on occasion high altitude cerebral and pulmonary oedema. The exact mechanisms by which these clinical syndromes develop have yet to be fully determined. The brain is particularly sensitive to a lack of oxygen and several adaptive mechanisms are thought to maintain adequate oxygen delivery. It is thought that the underlying mechanism behind the development of the high altitude cerebral syndromes relates to an increase in intracranial pressure (ICP). Cytotoxic (intracellular) and vasogenic (extracellular water accumulation due to increased permeability of the blood-brain barrier) oedema have been postulated as the mechanisms that underlie HACE. However, the rise in parenchymal volume or decrease in CSF volume could also be due to a rise in the cerebral blood flow and/or efferent restriction of cerebral venous outflow, thus increasing the ICP. Headache burden has been shown to be related to the retinal vein distension and individuals with relatively narrow transverse sinuses were more prone to hypoxia induced headaches. Preliminary evidence to supporting a unification hypothesis combining raised arterial inflow (with cytotoxic and vasogenic oedema) and restricted venous outflow theories will be discussed.