Intracranial Pressure, High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 88 (s32) ◽  
pp. 26P-26P
Author(s):  
AD Wright ◽  
CHE Imray ◽  
MSC Morrissey ◽  
RJ Marchbanks ◽  
AR Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Intracranial Pressure at High Altitude and Acute Mountain Sickness

1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Raised Intracranial Pressure ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Pressure Changes ◽  
Serial Measurements

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.

scholarly journals The cerebral venous system and hypoxia

2016 ◽  
Vol 120 (2) ◽  
pp. 244-250 ◽  
Author(s):  
Mark H. Wilson ◽  
Christopher H. E. Imray
Keyword(s):  
Intracranial Pressure ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Venous Outflow ◽  
Edema Formation ◽  
Care Environment ◽  
Fluid Production ◽  
High Altitude Cerebral Edema ◽  
Blood Inflow ◽  
Mountain Sickness

Most hypobaric hypoxia studies have focused on oxygen delivery and therefore cerebral blood inflow. Few have studied venous outflow. However, the volume of blood entering and leaving the skull (∼700 ml/min) is considerably greater than cerebrospinal fluid production (0.35 ml/min) or edema formation rates and slight imbalances of in- and outflow have considerable effects on intracranial pressure. This dynamic phenomenon is not necessarily appreciated in the currently taught static “Monro-Kellie” doctrine, which forms the basis of the “Tight-Fit” hypothesis thought to underlie high altitude headache, acute mountain sickness, and high altitude cerebral edema. Investigating both sides of the cerebral circulation was an integral part of the 2007 Xtreme Everest Expedition. The results of the relevant studies performed as part of and subsequent to this expedition are reviewed here. The evidence from recent studies suggests a relative venous outflow insufficiency is an early step in the pathogenesis of high altitude headache. Translation of knowledge gained from high altitude studies is important. Many patients in a critical care environment develop hypoxemia akin to that of high altitude exposure. An inability to drain the hypoxemic induced increase in cerebral blood flow could be an underappreciated regulatory mechanism of intracranial pressure.

Cerebral spinal fluid dynamics: effect of hypoxia and implications for high-altitude illness

2016 ◽  
Vol 120 (2) ◽  
pp. 251-262 ◽  
Author(s):  
Justin S. Lawley ◽  
Benjamin D. Levine ◽  
Michael A. Williams ◽  
Jon Malm ◽  
Anders Eklund ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
High Altitude ◽  
Cerebral Spinal Fluid ◽  
Acute Mountain Sickness ◽  
Spinal Fluid ◽  
Brain Swelling ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
Brain Water

The pathophysiology of acute mountain sickness and high-altitude cerebral edema, the cerebral forms of high-altitude illness, remain uncertain and controversial. Persistently elevated or pathological fluctuations in intracranial pressure are thought to cause symptoms similar to those reported by individuals suffering cerebral forms of high-altitude illness. This review first focuses on the basic physiology of the craniospinal system, including a detailed discussion of the long-term and dynamic regulation of intracranial pressure. Thereafter, we critically examine the available literature, based primarily on invasive pressure monitoring, that suggests intracranial pressure is acutely elevated at altitude due to brain swelling and/or elevated sagittal sinus pressure, but normalizes over time. We hypothesize that fluctuations in intracranial pressure occur around a slightly elevated or normal mean intracranial pressure, in conjunction with oscillations in arterial Po2 and arterial blood pressure. Then these modest fluctuations in intracranial pressure, in concert with direct vascular stretch due to dilatation and/or increased blood pressure transmission, activate the trigeminal vascular system and cause symptoms of acute mountain sickness. Elevated brain water (vasogenic edema) may be due to breakdown of the blood-brain barrier. However, new information suggests cerebral spinal fluid flux into the brain may be an important factor. Regardless of the source (or mechanisms responsible) for the excess brain water, brain swelling occurs, and a “tight fit” brain would be a major risk factor to produce symptoms; activities that produce large changes in brain volume and cause fluctuations in blood pressure are likely contributing factors.

Optic nerve sheath diameter changes at high altitude and in acute mountain sickness: meta-regression analyses

2020 ◽  
pp. bjophthalmol-2020-317717
Author(s):  
Tou-Yuan Tsai ◽  
George Gozari ◽  
Yung-Cheng Su ◽  
Yi-Kung Lee ◽  
Yu-Kang Tu
Keyword(s):  
Optic Nerve ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Optic Nerve Sheath Diameter ◽  
Optic Nerve Sheath ◽  
Cochrane Library ◽  
Regression Analyses ◽  
Spline Regression ◽  
Nerve Sheath ◽  
Mountain Sickness

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.

scholarly journals A Prospective Epidemiological Study of Acute Mountain Sickness in Nepalese Pilgrims Ascending to High Altitude (4380 m)

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75644 ◽  
Author(s):  
Martin J. MacInnis ◽  
Eric A. Carter ◽  
Michael G. Freeman ◽  
Bidur Prasad Pandit ◽  
Ashmita Siwakoti ◽  
...  
Keyword(s):  
High Altitude ◽  
Epidemiological Study ◽  
Acute Mountain Sickness ◽  
Prospective Epidemiological Study ◽  
Mountain Sickness

Abstract 14359: Single Nucleotide Polymorphisms in Genes Involved in L-arginine / Dimethylarginine Metabolism Predispose for Pulmonary Hypertension and Acute Mountain Sickness at High Altitude

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Juliane Hannemann ◽  
Julia Zummack ◽  
PATRICIA SIQUES ◽  
JULIO BRITO ◽  
Rainer Boeger
Keyword(s):  
Pulmonary Hypertension ◽  
Relative Risk ◽  
Genetic Variability ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Minor Allele ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Mountain Sickness ◽  
Study Participants

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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