The cerebral etiology of high-altitude cerebral edema and acute mountain sickness

Hackett, Peter H.

doi:10.1580/1080-6032(1999)010[0097:tceoha]2.3.co;2

Cited by 81 publications

(57 citation statements)

References 46 publications

(57 reference statements)

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“…Lassen and coworkers 3,4 have suggested that in newcomers to higher altitude, the occurrence of high-altitude cerebral edema (HACE), a potentially lethal manifestation of acute mountain sickness (AMS), resulted from a disturbed CA, combined with an elevated pressure in the cerebral microcirculation. Other investigators [5][6][7] have repeatedly supported this hypothesis. On the contrary, it is commonly assumed that Sherpas, who are high-altitude natives of Tibetan ancestry, have an intact autoregulatory response to blood-pressure variations, as a hallmark of a healthy cerebral vasculature.…”

mentioning

confidence: 84%

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Jansen

Krins

Basnyat

et al. 2000

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Background and Purpose-Impaired cerebral autoregulation (CA) from high-altitude hypoxia may cause high-altitude cerebral edema in newcomers to a higher altitude. Furthermore, it is assumed that high-altitude natives have preserved CA. However, cerebral autoregulation has not been studied at altitude. Methods-We studied CA in 10 subjects at sea level and in 9 Sherpas and 10 newcomers at an altitude of 4243 m by evaluating the effect of an increase of mean arterial blood pressure (MABP) with phenylephrine infusion on the blood flow velocity in the middle cerebral artery (Vmca), using transcranial Doppler. Theoretically, no change of Vmca in response to an increase in MABP would imply perfect autoregulation. Complete loss of autoregulation is present if Vmca changes proportionally with changes of MABP. Results-In the sea-level group, at a relative MABP increase of 23Ϯ4% during phenylephrine infusion, relative Vmca did not change essentially from baseline Vmca (2Ϯ7%, Pϭ0.36), which indicated intact autoregulation. In the Sherpa group, at a relative MABP increase of 29Ϯ7%, there was a uniform and significant increase of Vmca of 24Ϯ9% (PϽ0.0001) from baseline Vmca, which indicated loss of autoregulation. The newcomers showed large variations of Vmca in response to a relative MABP increase of 21Ϯ6%. Five subjects showed increases of Vmca of 22% to 35%, and 2 subjects showed decreases of Vmca of 21% and 23%. Conclusions-All Sherpas and the majority of the newcomers showed impaired CA. It indicates that an intact autoregulatory response to changes in blood pressure is probably not a hallmark of the normal human cerebral vasculature at altitude and that impaired CA does not play a major role in the occurrence of cerebral edema in newcomers to the altitude.

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mentioning

confidence: 84%

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Jansen

Krins

Basnyat

et al. 2000

Stroke

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“…Therefore, the current finding is probably an amplification of a normal phenomenon, whose finalism could be the prevention of extreme vasodilation at higher levels of CO 2 and/or MCFV. It is well known that extreme cerebral vasodilation, due to hypercapnia or hypoxia (typically occurring at high altitude) can lead to severe headache and even predispose to cerebral oedema [23,24]. This may be relevant in COPD, as hypercapnia (and often hypoxia) is a common complication in this disease.…”

Section: Increased Resting Mcfv In Mild Copd Patientsmentioning

confidence: 99%

Autonomic and cerebrovascular abnormalities in mild COPD are worsened by chronic smoking

Bernardi¹,

Casucci²,

Haider³

et al. 2008

Eur Respir J

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Patients with chronic obstructive pulmonary disease (COPD) may develop hypercapnia and hypoxia, two main determinants of cerebral blood flow. The current authors tested whether cerebrovascular regulation was altered in mild COPD, modified by manoeuvres acutely improving autonomic cardiovascular modulation or influenced by smoking habit.In 15 eucapnic normoxic mild COPD patients (eight smokers) and 28 age-matched controls (14 smokers), midcerebral artery blood flow velocity (MCFV), end-tidal carbon dioxide tension (PET,CO 2 ), arterial oxygen saturation (Sa,O 2 ), ECG and blood pressure at rest were monitored during progressive hypercapnic hyperoxia, isocapnic hypoxia, slow breathing and oxygen administration. MCFV, arterial baroreflex and dynamic MCFV-blood pressure relationships were compared by phase analysis.COPD and control smokers showed higher MCFV (when corrected for PET,CO 2 ), lower cerebrovascular resistance index and lower sensitivity to hypercapnia than nonsmokers, with equal sensitivity to Sa,O 2 and similar phase analysis. Arterial baroreflex was depressed in all COPD patients. Slow breathing and oxygen administration improved baroreflex sensitivity and reduced MCFV in all COPD patients.Patients with mild chronic obstructive pulmonary disease show autonomic dysfunction. Chronic smoking induces cerebral vasodilation and impairs cerebrovascular control. All abnormalities can be partly corrected by improving the cardio-and cerebrovascular autonomic modulation, suggesting that functional autonomic abnormalities are already present at an early stage of disease.

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“…Global encephalopathy rather than focal findings, characterizes high -altitude cerebral edema [27]. Despite normal cerebral oxygenation and normal global cerebral metabolism, vasogenic edema develops in humans (and sheep) who become moderately ill with acute mountain sickness / high altitude cerebral edema during 24 hour or more of hypoxic exposure [28]. The exact cause of high altitude cerebral edema is not known.…”

Section: High Altitude Cerebral Edemamentioning

confidence: 99%

Cerebral Edema and its Management

Jha¹

2003

Medical Journal Armed Forces India

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The cerebral etiology of high-altitude cerebral edema and acute mountain sickness

Cited by 81 publications

References 46 publications

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Cerebral Autoregulation in Subjects Adapted and Not Adapted to High Altitude

Autonomic and cerebrovascular abnormalities in mild COPD are worsened by chronic smoking

Cerebral Edema and its Management

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