Acute Mountain Sickness: Controversies and Advances

Abstract

This review discusses the impact of recent publications on pathophysiologic concepts and on practical aspects of acute mountain sickness (AMS). Magnetic resonance imaging studies do not provide evidence of total brain volume increase nor edema within the first 6 to 10 h of exposure to hypoxia despite symptoms of AMS. After 16 to 32 h at about 4500 m, brain volume increases by 0.8% to 2.7%, but morphological changes do not clearly correlate with symptoms of AMS, and lumbar cerebrospinal fluid pressure was unchanged from normoxic values in individuals with AMS. These data do not support the prevailing hypothesis that AMS is caused by cerebral edema and increased intracranial pressure. Direct measurement of increased oxygen radicals in hypoxia and a first study reducing AMS when lowering oxygen radicals by antioxidants suggest that oxidative stress is involved in the pathophysiology of AMS. Placebo-controlled trials demonstrate that theophylline significantly attenuates periodic breathing without improving arterial oxygen saturation during sleep. Its effects on AMS are marginal and clearly inferior to acetazolamide. A most recent large trial with Ginkgo biloba clearly showed that this drug does not prevent AMS in a low-risk setting in which acetazolamide in a low dose of 2 x 125 mg was effective. Therefore, acetazolamide remains the drug of choice for prevention and the recommended dose remains 2 x 250 mg daily until a lower dose has been tested in a high-risk setting and larger clinical trials with antioxidants have been performed.

SNPs, Linkage Disequilibrium and Transcriptional Factor Binding Sites Associated with Acute Mountain Sickness among Han Chinese at the Qinghai-Tibetan Plateau

“…Acute mountain sickness (AMS) is very common among some individuals who ascend to altitudes greater than 2600 m. The illness is characterized by headache, lightheadedness, breathlessness, fatigue, insomnia, anorexia, and nausea [1,2]. The symptoms of the illness begin 2-3 hours after ascent to the higher altitude.…”

Circulating miRNAs from Dried Blood Spots are Associated with High Altitude Sickness

“…Acute mountain sickness (AMS) is very common in lowlanders who ascend from sea level to altitudes greater than 2600 meters and is characterized by headache, lightheadedness, breathlessness, fatigue, insomnia, anorexia, and nausea [9,10]. Symptoms begin two to three hours after ascent.…”

Acute mountain sickness in disability and adaptive sports: Preliminary data

“…Known risk factors for HAI in individuals without disabilities include no exposure to HA in the preceding 2 months and ascent in ≤3 days [5,[7][8] as well as the altitude reached, the altitude at which the individual generally sleeps, and physical exertion at altitude [1]. However, independent risk factors for those with disabilities are still unknown.…”

“…Bartsch et al presented a comprehensive summary on the pathophysiology of AMS and state of the science [7]. AMS may be due to damage to the blood-brain barrier and cerebral vasculature from free radicals.…”

“…AMS may be due to damage to the blood-brain barrier and cerebral vasculature from free radicals. Little evidence has been found to suggest that cerebral edema or increased intracranial pressure is responsible for AMS, since these processes also occur in those individuals without symptoms [7,9]. However, some authors have suggested that individuals with less cerebrospinal fluid volume and thus less ability to accommodate for increased brain volume may be those who develop AMS [9].…”