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

2016 ◽  
Vol 6 (3) ◽  
Author(s):  
Dana M. DiPasquale ◽  
Stephen R. Muza ◽  
Andrea M. Gunn ◽  
Zhi Li ◽  
Quan Zhang ◽  
...  
2018 ◽  
Vol 1 (1) ◽  
pp. 01-02
Author(s):  
Mao Tang ◽  
Lu Cixin

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


2007 ◽  
Vol 28 (1) ◽  
pp. 198-206 ◽  
Author(s):  
Guus G Schoonman ◽  
Peter S Sándor ◽  
Arto C Nirkko ◽  
Thomas Lange ◽  
Thomas Jaermann ◽  
...  

Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N2 to obtain arterial O2 saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80±0.09; 6 h hypoxia, 0.81 ± 0.09; P = 0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1 ±98.2; 6 h hypoxia, 450.7 ± 102.5; P < 0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients ( r = 0.83, P = 0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.


1995 ◽  
Vol 88 (s32) ◽  
pp. 26P-26P
Author(s):  
AD Wright ◽  
CHE Imray ◽  
MSC Morrissey ◽  
RJ Marchbanks ◽  
AR Bradwell

1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.


2006 ◽  
Vol 27 (5) ◽  
pp. 1064-1071 ◽  
Author(s):  
Kai Kallenberg ◽  
Damian M Bailey ◽  
Stefan Christ ◽  
Alexander Mohr ◽  
Robin Roukens ◽  
...  

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