Evidence for cerebral edema, cerebral perfusion, and intracranial pressure elevations in acute mountain sickness.
We hypothesized that cerebral alterations in edema, perfusion, and/or intracranial pressure (ICP) are related to the development of acute mountain sickness (AMS).



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.



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).



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.
Psychiatry Department Massachusetts General Hospital Harvard Medical School Charlestown Massachusetts.
Dana M
DM
DiPasquale
Environmental Medicine and Military Performance Division U.S. Army Research Institute of Environmental Medicine Natick Massachusetts.
Stephen R
SR
Muza
Psychiatry Department Massachusetts General Hospital Harvard Medical School Charlestown Massachusetts.
Andrea M
AM
Gunn
Psychiatry Department Massachusetts General Hospital Harvard Medical School Charlestown Massachusetts.
Zhi
Z
Li
Psychiatry Department Massachusetts General Hospital Harvard Medical School Charlestown Massachusetts; Center for Space Medicine Baylor College of Medicine Houston Texas.
Quan
Q
Zhang
Department of Emergency Medicine Division of Wilderness Medicine Massachusetts General Hospital Harvard Medical School Boston Massachusetts.
N Stuart
NS
Harris
Psychiatry Department Massachusetts General Hospital Harvard Medical School Charlestown Massachusetts; Center for Space Medicine Baylor College of Medicine Houston Texas.
Gary E
GE
Strangman
D000208:Acute Disease; D000328:Adult; D000532:Altitude Sickness / Q000503:physiopathology*; D001274:Atmospheric Pressure; D001929:Brain Edema / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D015444:Exercise / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000150:complications; D019586:Intracranial Hypertension / Q000503:physiopathology; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D010100:Oxygen / Q000378:metabolism; D019265:Spectroscopy, Near-Infrared / Q000379:methods
D010100:Oxygen
Altitude; exercise; hemoglobin; hypobaria; hypoxia; illness; near‐infrared spectroscopy; normobaric; optic nerve sheath