When they first arrive at a high altitude, many individuals develop transient "mountain sickness." This syndrome devel- ops 8 to 24 h after arrival at altitude and lasts 4 to 8 d. It is characterized by headache, irritability, insomnia, breathlessness, and nausea and vomiting. Its cause is unsettled, but it appears to be associated with cerebral edema. The low PO2 at high altitude causes aeriolar dilation, and if cerebral autoregulation does not compensate, there is an increase in capillary pressure that ors increased transudation of fluid into brain tissue. Individuals who do not develop mountain sickness have a diuresis at high altitude, and urine volume is decreased in individuals who develop the condition. High-altitude illness includes not only mountain sickness but also two more serious syndromes that complicate it: high-altitude cerebral edema and high-altitude pulmonary edema. In high-altitude cerebral edema, the capillary leakage in mountain sickness progresses to frank brain swelling, with ataxia, disorientation, and in some cases coma and death due to herniation of the brain through the tentorium. High-altitude pulmonary edema is a patchy edema of the lungs that is related to the marked pulmonary hypeension that develops at high altitude. It has been argued that it occurs because not all pulmonary aeries have enough smooth muscle to constrict in response to hypoxia, and in the capillaries supplied by those aeries, the general rise in pulmonary aerial pressure causes a capillary pressure increase that disrupts their walls (stress failure).Ref: Ganong review of medical physiology 23rd edition Page no: 619