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

Abstract

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; 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.ResultsWe 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).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.

CrossTalk proposal: Barometric pressure, independent of , is the forgotten parameter in altitude physiology and mountain medicine

“…) and the cerebral oxygenation/perfusion (DiPasquale et al . ) do seem unaffected by the differential P B . Overall, there are currently (November 2019) >50 peer reviewed scientific publications reporting different responses between HH vs .…”

Acute hypoxia diminishes the relationship between blood pressure and subarachnoid space width oscillations at the human cardiac frequency

“…As the left ventricle stroke volume remains unchanged, the net result is an increase in cardiac output [ 1 ]. Higher cardiac output and blood pressure (BP) lead to augmented cerebral blood flow (CBF), cerebral blood volume and subsequently to elevated intracranial pressure (ICP) [ 2 , 3 ]. Furthermore, hypoxia augments concentrations of hypoxia-inducible transcription factor, circulating pro-inflammatory cytokines and reactive oxygen species, with subsequent vascular leakage and enhanced blood-brain barrier permeability [ 4 , 5 ].…”

Acute and Chronic Effects of Hypobaric Exposure upon the Brain

“…A growing body of evidence suggests that is not only hypoxia, but hypobaria that contributes to the development of AMS [36][37][38][39][40]. The underlying pathophysiology of AMS remains poorly understood.…”