Reverse Association Between High-Altitude Headache and Nasal Congestion

Cephalalgia ◽  
2007 ◽  
Vol 27 (8) ◽  
pp. 899-903 ◽  
Author(s):  
S Jafarian ◽  
F Gorouhi ◽  
J Lotfi

No evidence is available to show that nasal congestion is a manifestation of exposing an individual to high altitude and hypoxia. Since both nasal congestion and high-altitude headache are vasogenic, we explored whether there is a coincidence between these two symptoms. A prospective observational study was carried out on a cohort of 118 adults (>18 years old) in a mountain clinic at 3450 m. After 24 h of ascent, an interview was held to ask if each individual experienced acute mountain sickness symptoms (headache, etc.) and nasal congestion. Sixty-six (55.9%) individuals mentioned headache within 24 h after ascent and nasal congestion was reported by 34 (28.8%) individuals. There was a reverse association between headache and nasal congestion ( P < 0.001). In conclusion, there is a reverse association between altitude headache and nasal congestion, probably as result of contradictory autoregulation effects or exaggerated sympathetic activity.

2010 ◽  
Vol 11 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Shih-Hao Wang ◽  
Yu-Cheng Chen ◽  
Wei-Fong Kao ◽  
Yu-Jr Lin ◽  
Jih-Chang Chen ◽  
...  

2020 ◽  
pp. bjophthalmol-2020-317717
Author(s):  
Tou-Yuan Tsai ◽  
George Gozari ◽  
Yung-Cheng Su ◽  
Yi-Kung Lee ◽  
Yu-Kang Tu

Background/aimsTo assess changes in optic nerve sheath diameter (ONSD) at high altitude and in acute mountain sickness (AMS).MethodsCochrane Library, EMBASE, Google Scholar and PubMed were searched for articles published from their inception to 31st of July 2020. Outcome measures were mean changes of ONSD at high altitude and difference in ONSD change between subjects with and without AMS. Meta-regressions were conducted to investigate the relation of ONSD change to altitude and time spent at that altitude.ResultsEight studies with 248 participants comparing ONSD from sea level to high altitude, and five studies with 454 participants comparing subjects with or without AMS, were included. ONSD increased by 0.14 mm per 1000 m after adjustment for time (95% CI: 0.10 to 0.18; p<0.01). Restricted cubic spline regression revealed an almost linear relation between ONSD change and time within 2 days. ONSD was greater in subjects with AMS (mean difference=0.47; 95% CI: 0.14 to 0.80; p=0.01; I2=89.4%).ConclusionOur analysis shows that ONSD changes correlate with altitude and tend to increase in subjects with AMS. Small study number and high heterogeneity are the limitations of our study. Further large prospective studies are required to verify our findings.


PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75644 ◽  
Author(s):  
Martin J. MacInnis ◽  
Eric A. Carter ◽  
Michael G. Freeman ◽  
Bidur Prasad Pandit ◽  
Ashmita Siwakoti ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Juliane Hannemann ◽  
Julia Zummack ◽  
PATRICIA SIQUES ◽  
JULIO BRITO ◽  
Rainer Boeger

Introduction: Chronic (CH) and chronic-intermittent (CIH) exposure to hypoxia at high altitude causes acute or chronic mountain sickness and elevation of mean pulmonary arterial pressure (mPAP). This is paralleled by increased plasma levels of ADMA, an endogenous inhibitor of NO synthesis. ADMA is cleaved by dimethylarginine dimethylaminohydrolase (DDAH1 and DDAH2), whilst symmetric dimethylarginine (SDMA) is cleaved by AGXT2. Arginase (ARG1 and ARG2) competes with endothelial NO synthase (NOS3) for L-arginine as substrate. We have shown previously that baseline ADMA (at sea level) determines mPAP after six months of CIH; cut-off values of 25 mm Hg and 30 mm Hg are being used to diagnose high altitude pulmonary hypertension. Hypothesis: We hypothesized that genetic variability in genes coding for core enzymes of ADMA, SDMA, and L-arginine metabolism may predispose individuals for high altitude disease and pulmonary hypertension. Methods: We genotyped 16 common single nucleotide polymorphisms in the NOS3, DDAH1, DDAH2, AGXT2, ARG1 and ARG2 genes of 69 healthy male Chilean subjects. Study participants adhered to a CIH regimen (5d at 3,550m, 2d at sea level) for six months. Metabolites were measured by LC-MS/MS; mPAP was estimated by echocardiography at six months, and altitude acclimatization was assessed by Lake Louise Score and arterial oxygen saturation. Results: Carriers of the minor allele of DDAH1 rs233112 had a higher mean baseline ADMA level (0.76±0.03 vs. 0.67±0.02 μmol/l; p<0.05), whilst the major allele of DDAH2 rs805304 was linked to an exacerbated increase of ADMA in hypoxia (0.10±0.03 vs. 0.04±0.04 μmol/l; p<0.02). Study participants carrying the minor allele of ARG1 rs2781667 had a relative risk of elevated mPAP (>25 mm Hg) of 1.70 (1.56-1.85; p<0.0001), and carriers of the minor allele of NOS3 rs2070744 had a relative risk of elevated mPAP (>30 mm Hg) of 1.58 (1.47-1.69; p<0.0001). The NOS3 and DDAH2 genes were associated with the incidence of acute mountain sickness. Conclusions: We conclude that genetic variability in the L-arginine / ADMA / NO pathway is an important determinant of high altitude pulmonary hypertension and acute mountain sickness. DDAH1 is linked to baseline ADMA, whilst DDAH2 determines the response of ADMA to hypoxia.


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