Evidence for cerebral edema, cerebral perfusion, and intracranial pressure elevations in acute mountain sickness

Abstract

Abstract Introduction: We hypothesized that cerebral alterations in edema, perfusion, and/or intracranial pressure (ICP) are related to the development of acute mountain sickness (AMS). Methods: To vary AMS, we manipulated ambient oxygen, barometric pressure, and exercise duration. Thirty‐six subjects were tested before, during and after 8 h exposures in (1) normobaric normoxia (NN; 300 m elevation equivalent); (2) normobaric hypoxia (NH; 4400 m equivalent); and (3) hypobaric hypoxia (HH; 4400 m equivalent). After a passive 15 min ascent, each subject participated in either 10 or 60 min of cycling exercise at 50% of heart rate reserve. We measured tissue absorption and scattering via radio‐frequency near‐infrared spectroscopy (NIRS), optic nerve sheath diameter (ONSD) via ultrasound, and AMS symptoms before, during, and after environmental exposures. Results: We observed significant increases in NIRS tissue scattering of 0.35 ± 0.11 cm−1 (P = 0.001) in subjects with AMS (i.e., AMS+), consistent with mildly increased cerebral edema. We also noted a small, but significant increase in total hemoglobin concentrations with AMS+, 3.2 ± 0.8 μmolL−1 (P < 0.0005), consistent with increased cerebral perfusion. No effect of exercise duration was found, nor did we detect differences between NH and HH. ONSD assays documented a small but significant increase in ONSD (0.11 ± 0.02 mm; P < 0.0005) with AMS+, suggesting mildly elevated ICP, as well as further increased ONSD with longer exercise duration (P = 0.005). Conclusion: In AMS+, we found evidence of cerebral edema, elevated cerebral perfusion, and elevated ICP. The observed changes were small but consistent with the reversible nature of AMS.