Article

MRI Evidence: Acute Mountain Sickness Is Not Associated with Cerebral Edema Formation during Simulated High Altitude

Department of Sports Science, Medical Section, University of Innsbruck, Innsbruck, Austria.
PLoS ONE (Impact Factor: 3.23). 11/2012; 7(11):e50334. DOI: 10.1371/journal.pone.0050334
Source: PubMed

ABSTRACT

Acute mountain sickness (AMS) is a common condition among non-acclimatized individuals ascending to high altitude. However, the underlying mechanisms causing the symptoms of AMS are still unknown. It has been suggested that AMS is a mild form of high-altitude cerebral edema both sharing a common pathophysiological mechanism. We hypothesized that brain swelling and consequently AMS development is more pronounced when subjects exercise in hypoxia compared to resting conditions. Twenty males were studied before and after an eight hour passive (PHE) and active (plus exercise) hypoxic exposure (AHE) (F(i)O(2) = 11.0%, P(i)O(2)∼80 mmHg). Cerebral edema formation was investigated with a 1.5 Tesla magnetic resonance scanner and analyzed by voxel based morphometry (VBM), AMS was assessed using the Lake Louise Score. During PHE and AHE AMS was diagnosed in 50% and 70% of participants, respectively (p>0.05). While PHE slightly increased gray and white matter volume and the apparent diffusion coefficient, these changes were clearly more pronounced during AHE but were unrelated to AMS. In conclusion, our findings indicate that rest and especially exercise in normobaric hypoxia are associated with accumulation of water in the extracellular space, however independent of AMS development. Thus, it is suggested that AMS and HACE do not share a common pathophysiological mechanism.

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    • "During 40 min of normobaric hypoxia, Dubowitz et al. (2009) found decreased CSF volume, increased cerebral blood volume and brain swelling, but no differences between those suffering from AMS and those not. Another recent CMRI study reported slightly increased grey and white matter volumes and accumulation of water in the extracellular space in hypoxia, but no relationship with AMS (Mairer et al. 2012). "
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    ABSTRACT: Despite decades of research, the exact pathogenic mechanisms underlying acute mountain sickness (AMS) are still poorly understood. This fact frustrates the search for novel pharmacological prophylaxis for AMS. The prevailing view is that AMS results from an insufficient physiological response to hypoxia and that prophylaxis should aim at stimulating the response. Starting off from the opposite hypothesis that AMS may be caused by an initial excessive response to hypoxia we suggest that directly or indirectly blunting specific parts of the response might provide promising research alternatives. This reasoning is based on the observations that 1) humans, once acclimatized, can climb Mt Everest experiencing arterial partial oxygen pressures (PaO2 ) as low as 25 mmHg without AMS symptoms, 2) paradoxically AMS usually develops at much higher PaO2 levels, and 3) several biomarkers, suggesting initial activation of specific pathways at such PaO2 , are correlated with AMS. Apart from looking for substances that stimulate certain hypoxia triggered effects, such as the ventilatory response to hypoxia, we suggest to also investigate pharmacological means aiming at blunting certain other specific hypoxia activated pathways, or stimulating their agonists, in the quest for better pharmacological prophylaxis for AMS. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Mar 2015 · Acta Physiologica
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    ABSTRACT: Objective: Acute mountain sickness (AMS) is common at high altitude and may lead to high altitude cerebral edema (HACE) if not properly recognized. Previous studies have suggested that AMS is associated with increases in intracranial pressure (ICP). Increased ICP has been associated with increased intra-ocular pressure (IOP). This study was designed to determine the association between IOP and AMS. Methods: Subjects were recruited from a convenience sample of travelers in the Khumbu region of Nepal, elevation 14,410 ft (4392 m). Study participation involved completion of a questionnaire to assess for AMS by the Lake Louise Score (LLS), followed by three IOP measurements in each eye. Investigators were blinded to the LLS. Subjects with a history of ocular surgery were excluded. Three IOP measurements per eye were made using an applanation tonometer (Tono-Pen XL(®), Reichart Technologies) and averaged across both eyes. Multivariable logistic regression analysis was used to estimate the association between IOP and AMS while adjusting for age, ascent or descent, and use of acetazolamide. IOP and blood O2 saturation were compared using a Spearman correlation coefficient. Results: 161 subjects were enrolled with a median age of 36 (IQR: 29-45) years; 60% were male, 75% were ascending, and 64% were taking acetazolamide; additionally, 38%, (95% CI: 31%-47%) were diagnosed with AMS (LLS ≥3). The median IOP was 21 (IQR 18-24) mmHg. The logistic regression model demonstrated no association between IOP and AMS as measured by LLS (odds ratio [OR] 1.0, 95% CI: 0.9-1.1),age (OR 1.0, 95% CI: 0.9-1.0) or with use of acetazolamide (OR 1.4, 95% CI: 0.6-2.6). Ascent (OR 0.4, 95% CI: 0.2-0.9) was negatively associated with IOP but not significantly so. IOP and O2 saturation were not correlated (p=0.93). Conclusions: IOP measured at high altitude is not associated with the diagnosis of AMS. Other approaches to diagnose AMS easily and accurately are needed.
    No preview · Article · Dec 2013 · High altitude medicine & biology
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    ABSTRACT: Objectives: Ascent to high altitude may result in a hypobaric hypoxic brain injury. The development of acute mountain sickness (AMS) is considered a multifactorial process with hypoxia-induced blood-brain barrier (BBB) dysfunction and resultant vasogenic oedema cited as one potential mechanism. Peripheral S100B is considered a biomarker of BBB dysfunction. This study aims to investigate the S100B release profile secondary to hypoxic brain injury and comment on BBB disturbance and AMS. Methods: A prospective field study of 12 subjects who ascended Mt Fuji (3700 m) was undertaken. Results: The mean baseline plasma S100B level was 0·11 μg/l (95% CI 0·09-0·12), which increased to 0·22 μg/l (95% CI 0·17-0·27) at the average of three high altitude levels (2590, 3700, and 2590 m on descent) (P < 0·001). The mean level for the seven subjects who experienced AMS rose from 0·10 to 0·19 μg/l compared to 0·12 to 0·25 μg/l for the five subjects who did not develop AMS (P = 0·33). Conclusion: Ascending to 3700 m resulted in elevated plasma S100B levels but this was not associated with AMS.
    No preview · Article · Feb 2014 · Neurological Research
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