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

IntroductionWe hypothesized that cerebral alterations in edema, perfusion, and/or intracranial pressure (ICP) are related to the development of acute mountain sickness (AMS). MethodsTo 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; 300m elevation equivalent); (2) normobaric hypoxia (NH; 4400m equivalent); and (3) hypobaric hypoxia (HH; 4400m equivalent). After a passive 15 min ascent, each subject participated in either 10 or 60min 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. ResultsWe observed significant increases in NIRS tissue scattering of 0.350.11cm(-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 +/- 0.8molL(-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 +/- 0.02mm; P<0.0005) with AMS+, suggesting mildly elevated ICP, as well as further increased ONSD with longer exercise duration (P=0.005). ConclusionIn 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.