https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(03)13591-X.pdf

High-altitude illness

Cellular hypoxia is the common final pathway of brain injury that occurs not just after asphyxia, but also when cerebral perfusion is impaired directly (eg, embolic stroke) or indirectly (eg, raised intracranial pressure after head injury). We Review recent advances in the understanding of neurological clinical syndromes that occur on exposure to high altitudes, including high altitude headache (HAH), acute mountain sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mechanisms, and physiology that underpin them. We also present the vasogenic and cytotoxic bases for HACE and explore venous hypertension as a possible contributory factor. Although the factors that control susceptibility to HACE are poorly understood, the effects of exposure to altitude (and thus hypobaric hypoxia) might provide a reproducible model for the study of cerebral cellular hypoxia in healthy individuals. The effects of hypobaric hypoxia might also provide new insights into the understanding of hypoxia in the clinical setting.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(09)70014-6.pdf

The cerebral effects of ascent to high altitudes

Objective: To determine the incidence of acute mountain sickness in a general population of visitors to moderate elevations, the characteristics associated with it, and its effect on physical activ...

Acute Mountain Sickness in a General Tourist Population at Moderate Altitudes

At any point 1–5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

https://err.ersjournals.com/content/errev/26/143/160096.full.pdf

Acute high-altitude sickness

Acute mountain sickness: pathophysiology, prevention, and treatment.

Persons with acute altitude sickness hypoventilate at high altitude compared with persons without symptoms. We hypothesized that their hypoventilation was due to low initial hypoxic ventilatory res...

Low acute hypoxic ventilatory response and hypoxic depression in acute altitude sickness.

The cause of headache in persons going to high altitude is unknown. Relatively severe hypoxemia in susceptible subjects could induce large increases in cerebral blood flow that then could initiate ...

A. Tucker

Papers

Low acute hypoxic ventilatory response and hypoxic depression in acute altitude sickness.

Headache at high altitude is not related to internal carotid arterial blood velocity.