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Hypoxia-induced acute mountain sickness is associated with intracellular cerebral edema: a 3 T magnetic resonance imaging study

Schoonman, Guus G ; Sandor, Peter S ; Nirkko, Arto C ; Lange, Thomas ; Jaermann, Thomas ; Dydak, Ulrike ; Kremer, Christine LU ; Ferrari, Michel D ; Boesiger, Peter and Baumgartner, Ralf W (2008) In Journal of Cerebral Blood Flow and Metabolism 28(1). p.198-206
Abstract
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 N(2) to obtain arterial O(2) 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... (More)
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 N(2) to obtain arterial O(2) 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. (Less)
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author
; ; ; ; ; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
subject
keywords
cerebral edema, high-altitude illness, hypoxia, MR imaging
in
Journal of Cerebral Blood Flow and Metabolism
volume
28
issue
1
pages
198 - 206
publisher
Nature Publishing Group
external identifiers
  • pmid:17519973
  • scopus:37549071518
  • pmid:17519973
ISSN
1559-7016
DOI
10.1038/sj.jcbfm.9600513
language
English
LU publication?
no
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neurology, Malmö (013027010)
id
aa27428e-b0e7-49c8-9a17-91146cda7524 (old id 1144246)
date added to LUP
2016-04-01 13:07:40
date last changed
2022-02-11 19:23:46
@article{aa27428e-b0e7-49c8-9a17-91146cda7524,
  abstract     = {{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 N(2) to obtain arterial O(2) 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&lt;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.}},
  author       = {{Schoonman, Guus G and Sandor, Peter S and Nirkko, Arto C and Lange, Thomas and Jaermann, Thomas and Dydak, Ulrike and Kremer, Christine and Ferrari, Michel D and Boesiger, Peter and Baumgartner, Ralf W}},
  issn         = {{1559-7016}},
  keywords     = {{cerebral edema; high-altitude illness; hypoxia; MR imaging}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{198--206}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Journal of Cerebral Blood Flow and Metabolism}},
  title        = {{Hypoxia-induced acute mountain sickness is associated with intracellular cerebral edema: a 3 T magnetic resonance imaging study}},
  url          = {{http://dx.doi.org/10.1038/sj.jcbfm.9600513}},
  doi          = {{10.1038/sj.jcbfm.9600513}},
  volume       = {{28}},
  year         = {{2008}},
}