Mountain neurology

2019 ◽  
Vol 19 (5) ◽  
pp. 404-411 ◽  
Author(s):  
Marieke Cornelia Johanna Dekker ◽  
Mark H Wilson ◽  
William Patrick Howlett

Mountain climbers may develop specific illnesses that largely depend on the altitude reached and the rate of ascent. The popularity of travel to high altitude destinations, extreme tourist activities and mountain climbing means that neurologists in low-altitude countries are increasingly likely to encounter neurological problems and disorders in people exposed to high altitude. Additionally, they may have to advise patients with pre-existing neurological conditions on the risks of ascent to altitude. This article focuses on neurological-related high-altitude illnesses: acute mountain sickness and high-altitude cerebral oedema, as well as high-altitude retinopathy and other neurological disorders. This overview combines current understood pathogenesis with the experience of managing altitude-related illness at the foot of Mount Kilimanjaro in northern Tanzania, the tallest free-standing mountain in the world.

1991 ◽  
Vol 71 (3) ◽  
pp. 934-938 ◽  
Author(s):  
W. H. Reinhart ◽  
B. Kayser ◽  
A. Singh ◽  
U. Waber ◽  
O. Oelz ◽  
...  

The role of blood rheology in the pathogenesis of acute mountain sickness and high-altitude pulmonary edema was investigated. Twenty-three volunteers, 12 with a history of high-altitude pulmonary edema, were studied at low altitude (490 m) and at 2 h and 18 h after arrival at 4,559 m. Eight subjects remained healthy, seven developed acute mountain sickness, and eight developed high-altitude pulmonary edema. Hematocrit, whole blood viscosity, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability (filtration) were measured. Plasma viscosity and erythrocyte deformability remained unaffected. The hematocrit level was lower 2 h after the arrival at high altitude and higher after 18 h compared with low altitude. The whole blood viscosity changed accordingly. The erythrocyte aggregation was about doubled 18 h after the arrival compared with low-altitude values, which reflects the acute phase reaction. There were, however, no significant differences in any rheological parameters between healthy individuals and subjects with acute mountain sickness or high-altitude pulmonary edema, either before or during the illness. We conclude that rheological abnormalities can be excluded as an initiating event in the development of acute mountain sickness and high-altitude pulmonary edema.


2005 ◽  
Vol 98 (5) ◽  
pp. 1626-1629 ◽  
Author(s):  
Martha C. Tissot van Patot ◽  
Guy Leadbetter ◽  
Linda E. Keyes ◽  
Jamie Bendrick-Peart ◽  
Virginia E. Beckey ◽  
...  

Vascular endothelial growth factor (VEGF) is a hypoxia-induced protein that produces vascular permeability, and limited evidence suggests a possible role for VEGF in the pathophysiology of acute mountain sickness (AMS) and/or high-altitude cerebral edema (HACE). Previous studies demonstrated that plasma VEGF alone does not correlate with AMS; however, soluble VEGF receptor (sFlt-1), not accounted for in previous studies, can bind VEGF in the circulation, reducing VEGF activity. In the present study, we hypothesized that free VEGF is greater and sFlt-1 less in subjects with AMS compared with well individuals at high altitude. Subjects were exposed to 4,300 m for 19–20 h (baseline 1,600 m). The incidence of AMS was determined by using a modified Lake Louise symptom score and the Environmental Symptoms Questionnaire for cerebral effects. Plasma was collected at low altitude and after 24 h at high altitude, or at time of illness, and then analyzed by ELISA for VEGF and for soluble VEGF receptor, sFlt-1. AMS subjects had lower sFlt-1 at both low and high altitude compared with well subjects and a significant rise in free plasma VEGF on ascent to altitude compared with well subjects. We conclude that increased free plasma VEGF on ascent to altitude is associated with AMS and may play a role in pathophysiology of AMS.


2005 ◽  
Vol 289 (6) ◽  
pp. H2364-H2372 ◽  
Author(s):  
Paola A. Lanfranchi ◽  
Roberto Colombo ◽  
George Cremona ◽  
Paolo Baderna ◽  
Liliana Spagnolatti ◽  
...  

The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS ( P < 0.01). At high altitude, the low-frequency (LF) component of systolic BP variability (LFSBP) was higher ( P = 0.02) and the LF component of R-R variability in normalized units (LFRRNU) was lower ( P = 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LFRRNU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude ( P < 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LFSBP increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP ( P < 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.


1971 ◽  
Vol 33 (3) ◽  
pp. 735-742 ◽  
Author(s):  
David A. Stamper ◽  
Ray T. Sterner ◽  
Robert A. Kinsman

Additional information regarding the development of symptomatology subscales for the measurement of Acute Mountain Sickness (AMS) is presented. High item intercorrelations and strong factor loadings of items comprising symptom clusters (i.e., Arousal Level, Somatic Discomfort, Tired, and Mood) support the previously reported breakdown of the General High Altitude Questionnaire (GHAQ) into subscales. Rapid transition from low to high altitude resulted in an increase of these symptomatology subscale scores. Several subscale differences were also noted between Phenformin and Placebo Ss at low altitude. Such subscale measures could provide improved estimates of symptomatology, useful in assessing the effectiveness of various treatments intended to ameliorate AMS.


1989 ◽  
Vol 66 (5) ◽  
pp. 2136-2144 ◽  
Author(s):  
P. Bartsch ◽  
A. Haeberli ◽  
M. Franciolli ◽  
E. K. Kruithof ◽  
P. W. Straub

To examine whether intravascular coagulation and/or decreased fibrinolysis precedes high-altitude pulmonary edema (HAPE) we examined 25 male mountaineers (median age 40 yr) at low altitude (550 m) and after 6, 18, and 42 h at an altitude of 4,559 m, which was climbed in 24 h. In 14 subjects, 2 of whom showed radiological evidence of HAPE after 42 h, symptoms of acute mountain sickness (AMS) were mild or absent. Eleven subjects suffered from AMS, six of whom developed radiologically documented HAPE after 18 or 42 h. In the absence of AMS there were no significant changes at high altitude, with the exception of a decrease in bleeding time from 246 +/- 18 to 212 +/- 13 (SE) (P less than 0.05). In AMS, partial thromboplastine time decreased from 34.2 +/- 0.8 to 31.1 +/- 0.5 s (P less than 0.001) and factor VIII procoagulant activity and von Willebrand factor antigen were increased by 57 +/- 12 and 70 +/- 13%, respectively (P less than 0.001), whereas there were no significant changes in beta-thromboglobulin (BTG), fibrinopeptide A (FPA), and fibrin fragment B beta 15–42. In subjects with HAPE, BTG, FPA, and B beta 15–42 were normal before and in beginning HAPE. Preceding HAPE, euglobulin clot lysis time declined at high compared with low altitude from 289 +/- 48 to 201 +/- 42 min without venous occlusion (VO) and from 107 +/- 36 to 86 +/- 31 min after VO (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


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 ◽  
...  

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