Acute mountain sickness is not related to cerebral blood flow: a decompression chamber study

1999 ◽  
Vol 86 (5) ◽  
pp. 1578-1582 ◽  
Author(s):  
Ralf W. Baumgartner ◽  
Ioakim Spyridopoulos ◽  
Peter Bärtsch ◽  
Marco Maggiorini ◽  
Oswald Oelz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Transcranial Doppler Sonography ◽  
Simulated Altitude ◽  
Chamber Study ◽  
Mountain Sickness ◽  
Low Altitude ◽  
Artery Flow

To evaluate the pathogenetic role of cerebral blood flow (CBF) changes occurring before and during the development of acute mountain sickness (AMS), peak mean middle cerebral artery flow velocities ([Formula: see text]) were assessed by transcranial Doppler sonography in 10 subjects at 490-m altitude, and during three 12-min periods immediately (SA1), 3 (SA2), and 6 (SA3) h after decompression to a simulated altitude of 4,559 m. AMS cerebral scores increased from 0.16 ± 0.14 at baseline to 0.44 ± 0.31 at SA1, 1.11 ± 0.88 at SA2( P < 0.05), and 1.43 ± 1.03 at SA3( P < 0.01); correspondingly, three, seven, and eight subjects had AMS. Absolute and relative[Formula: see text] at simulated altitude, expressed as percentages of low-altitude values (%[Formula: see text]), did not correlate with AMS cerebral scores. Average %[Formula: see text] remained unchanged, because %[Formula: see text]increased in three and remained unchanged or decreased in seven subjects at SA2 and SA3. These results suggest that CBF is not important in the pathogenesis of AMS and shows substantial interindividual differences during the first hours at simulated altitude.

Relationship of cerebral blood flow regulation to acute mountain sickness.

1989 ◽  
Vol 8 (3) ◽  
pp. 143-148 ◽  
Author(s):  
S M Otis ◽  
M E Rossman ◽  
P A Schneider ◽  
M P Rush ◽  
E B Ringelstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Flow Regulation ◽  
Blood Flow Regulation ◽  
Mountain Sickness ◽  
Relationship Of

Cerebral Blood Flow in Acute Mountain Sickness and Treatment with Acetazolamide

1988 ◽  
Vol 74 (s18) ◽  
pp. 1P-1P ◽  
Author(s):  
AD Wright ◽  
AR Bradwell ◽  
J Jensen ◽  
N Lassen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

scholarly journals Regional cerebral blood flow during acute hypoxia in individuals susceptible to acute mountain sickness

2008 ◽  
Vol 160 (3) ◽  
pp. 267-276 ◽  
Author(s):  
Edward A.W. Dyer ◽  
Susan R. Hopkins ◽  
Joanna E. Perthen ◽  
Richard B. Buxton ◽  
David J. Dubowitz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Regional Cerebral Blood ◽  
Mountain Sickness

Autonomic cardiovascular regulation in subjects with acute mountain sickness

2005 ◽  
Vol 289 (6) ◽  
pp. H2364-H2372 ◽  
Author(s):  
Paola A. Lanfranchi ◽  
Roberto Colombo ◽  
George Cremona ◽  
Paolo Baderna ◽  
Liliana Spagnolatti ◽  
...  
Keyword(s):  
High Altitude ◽  
Potential Role ◽  
Acute Mountain Sickness ◽  
Low Frequency ◽  
Short Term ◽  
Mountain Sickness ◽  
Low Altitude ◽  
Normalized Units ◽  
Hypoxic Gas Mixture

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.

scholarly journals Regional Differences in the Cerebral Blood Flow Velocity Response to Hypobaric Hypoxia at High Altitudes

2015 ◽  
Vol 35 (11) ◽  
pp. 1846-1851 ◽  
Author(s):  
Berend Feddersen ◽  
Pritam Neupane ◽  
Florian Thanbichler ◽  
Irmgard Hadolt ◽  
Vera Sattelmeyer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Hypobaric Hypoxia ◽  
Cerebral Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Acute Mountain Sickness ◽  
Transcranial Doppler Sonography ◽  
Beta Activity

Symptoms of acute mountain sickness (AMS) may appear above 2,500 m altitude, if the time allowed for acclimatization is insufficient. As the mechanisms underlying brain adaptation to the hypobaric hypoxic environment are not fully understood, a prospective study was performed investigating neurophysiological changes by means of near infrared spectroscopy, electroencephalograpy (EEG), and transcranial doppler sonography at 100, 3,440 and 5,050 m above sea level in the Khumbu Himal, Nepal. Fourteen of the 26 mountaineers reaching 5,050 m altitude developed symptoms of AMS between 3,440 and 5,050 m altitude (Lake-Louise Score ≥ 3). Their EEG frontal beta activity and occipital alpha activity increased between 100 and 3,440 m altitude, i.e., before symptoms appeared. Cerebral blood flow velocity (CBFV) in the anterior and middle cerebral arteries (MCAs) increased in all mountaineers between 100 and 3,440 m altitude. During further ascent to 5,050 m altitude, mountaineers with AMS developed a further increase in CBFV in the MCA, whereas in all mountaineers CBFV decreased continuously with increasing altitude in the posterior cerebral arteries. These results indicate that hypobaric hypoxia causes different regional changes in CBFV despite similar electrophysiological changes.

Effect of magnesium, high altitude and acute mountain sickness on blood flow velocity in the middle cerebral artery

2004 ◽  
Vol 106 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Christopher LYSAKOWSKI ◽  
Erik VON ELM ◽  
Lionel DUMONT ◽  
Jean-Daniel JUNOD ◽  
Edömer TASSONYI ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
High Altitude ◽  
Blood Flow Velocity ◽  
Rescue Medication ◽  
Acute Mountain Sickness ◽  
Median Score ◽  
Magnesium Supplementation ◽  
Mountain Sickness

Cerebral blood flow is thought to increase at high altitude and in subjects suffering from acute mountain sickness (AMS); however, data from the literature are contentious. Blood flow velocity in the middle cerebral artery (MCAv) may be used as a proxy measure of cerebral blood flow. Using transcranial Doppler sonography, MCAv was measured during normo- and hyper-ventilation in subjects who participated in a trial that tested the effect of magnesium supplementation on the prevention of AMS. First, MCAv was recorded at 353 m (baseline). Subjects were then randomized to receive oral magnesium citrate and matching placebo. A second measurement was taken after a 24±2 h ascent from 1130 m to 4559 m (altitude I), and a third after a 20–24 h stay at 4559 m (altitude II). Using multivariate linear regression, an association was sought between MCAv and magnesium supplementation, subjects′ age and gender, altitude itself, a temporary stay at altitude, and the presence of AMS (Lake Louise Score >6 with ataxia, nausea and/or headache). Subjects with AMS had additional Doppler recordings immediately before and after rescue medication (oxygen, dexamethasone and acetazolamide). Forty-seven subjects had measurements at baseline, 39 (21 receiving magnesium and 18 placebo) at altitude I and 26 (13 receiving magnesium and 13 placebo) at altitude II. During hyperventilation, MCAv decreased consistently (for each measurement, P<0.001). Magnesium significantly increased MCAv by 8.4 cm·s-1 (95% confidence interval, 1.8–15), but did not prevent AMS. No other factors were associated with MCAv. Eleven subjects had severe AMS [median score (range), 11 (8–16)] and, after rescue medication, the median score decreased to 3 (range, 0–5; P=0.001), but MCAv remained unchanged (65±18 cm·s-1 before compared with 67±16 cm·s-1 after rescue medication; P=0.79). MCAv was increased in subjects who received magnesium, but was not affected by exposure to high altitude or by severe AMS.

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