Introduction
Despite decades of research, the pathophysiology of acute mountain sickness (AMS) is unknown. The classic hypothesis is that persistent and/or transient elevations in intracranial pressure (ICP) cause AMS.
Objective
To make continuous, direct, invasive measurements of ICP alongside AMS (Lake Louise Questionnaire [LLQ]) in hypobaric hypoxia (4500 m).
Methods
To date, we have recruited three men who had previously been cured of a hematologic malignancy and as such had an Ommaya reservoir implanted. A needle was placed inside the Ommaya reservoir for direct measurement of intraventricular pressure.
Results
Participant 1: ICP at sea level was 13 mm Hg. After 9 hours at altitude, mean ICP remained normal (14 mm Hg), but large fluctuations in ICP (>20 mm Hg) were observed, alongside symptoms of AMS (LLQ, 6). Administration of 100% O2 stabilized ICP and symptoms resolved. With removal of 100% O2, ICP pressure waves began and symptoms returned. Participant 2: ICP decreased slightly at altitude (SL, 11 vs altitude, 6.6 mm Hg) and no pressure waves were observed over the first 9 hours. This subject reported only a very mild headache. During sleep, ICP fluctuated in opposition to oscillations in SaO2. The participant woke with mountain sickness (LLQ = 10), which declined by 24 hours (LLQ = 4), where ICP was below the sea level value (3 mm Hg). Participant 3: ICP at sea level was 16 mm Hg. After 9 hours at altitude, ICP was substantially elevated (26 mm Hg) with symptoms of AMS (LLQ = 5). ICP was persistently >20 mm Hg while asleep, and the participant woke with muscle paralysis and severe AMS. Adminitration of 100% O2 reduced ICP (11 mm Hg) and resolved symptoms. This study was ended because of the possibility of mild cerebral edema.
Conclusions
These preliminary observations suggest that persistent or transient elevations in ICP preceded the onset of AMS.
Funding
WMS Houston Grant (2013).