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Elevated brain volume in acute mountain sickness (AMS)
Author(s) -
Roach Robert,
Subudhi Andrew,
Browne Vaughn,
Sheen Paige,
Altobelli Steve,
Caprihan Arvind
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a874-a
Subject(s) - medicine , lightheadedness , placebo , anesthesia , nausea , brain edema , altitude sickness , dexamethasone , effects of high altitude on humans , pathology , alternative medicine , anatomy
The pathophysiology of AMS remains unexplained. In high altitude cerebral edema, considered a late‐form of AMS, there is marked vasogenic cerebral edema. However, whether the brain swells in AMS has not been thoroughly explored. Methods: To explore the role of brain swelling in AMS we exposed 25 healthy volunteers to simulated high altitude in a hypobaric chamber (Pb=430 mmHg) for 10 hrs in a placebo‐controlled, cross‐over, single blind trial. 15 of the 25 developed AMS (headache plus nausea, dizziness or lightheadedness) with a Lake Louise AMS score > 2. Volunteers completed high‐resolution 3‐T, T1‐SPGR MRI scans before and after hypobaric exposure. Volumetric analyses were completed using FSL SIENA. Results: Brain volume was greater in AMS+ (p<0.01). 15 AMS+ subjects were invited back for the 2nd arm of the trial in which they received 4mg dexamethasone (DEX) PO q 8h, starting the day before hypobaric exposure. One investigator was aware of the assigned medication (VB), but was not involved in symptom assessment, MRI imaging or data analysis. 10 subjects completed DEX prophylaxis. DEX completely blocked brain swelling and AMS symptoms. The mechanisms by which DEX blocks brain swelling in acute hypobaric hypoxia are unknown. Possibilities include prevention of blood‐brain barrier breakdown. We conclude that AMS may be initiated by brain swelling. Supported, in part, by NIH‐HL‐070362.