Document Detail

The cerebral effects of ascent to high altitudes.
MedLine Citation:
PMID:  19161909     Owner:  NLM     Status:  MEDLINE    
Cellular hypoxia is the common final pathway of brain injury that occurs not just after asphyxia, but also when cerebral perfusion is impaired directly (eg, embolic stroke) or indirectly (eg, raised intracranial pressure after head injury). We Review recent advances in the understanding of neurological clinical syndromes that occur on exposure to high altitudes, including high altitude headache (HAH), acute mountain sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mechanisms, and physiology that underpin them. We also present the vasogenic and cytotoxic bases for HACE and explore venous hypertension as a possible contributory factor. Although the factors that control susceptibility to HACE are poorly understood, the effects of exposure to altitude (and thus hypobaric hypoxia) might provide a reproducible model for the study of cerebral cellular hypoxia in healthy individuals. The effects of hypobaric hypoxia might also provide new insights into the understanding of hypoxia in the clinical setting.
Mark H Wilson; Stanton Newman; Chris H Imray
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The Lancet. Neurology     Volume:  8     ISSN:  1474-4422     ISO Abbreviation:  Lancet Neurol     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-01-23     Completed Date:  2009-03-13     Revised Date:  2014-08-15    
Medline Journal Info:
Nlm Unique ID:  101139309     Medline TA:  Lancet Neurol     Country:  England    
Other Details:
Languages:  eng     Pagination:  175-91     Citation Subset:  IM    
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MeSH Terms
Air Pressure
Altitude Sickness / drug therapy,  genetics,  physiopathology*,  psychology
Anoxia / physiopathology
Brain Edema / etiology,  physiopathology
Cerebrovascular Circulation / physiology*
Chronic Disease
Headache / etiology,  physiopathology
Psychomotor Performance / physiology
Comment In:
Lancet Neurol. 2009 Jul;8(7):604; author reply 605   [PMID:  19539231 ]
Lancet Neurol. 2009 Jul;8(7):604-5; author reply 605   [PMID:  19539232 ]

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