Cerebral spinal fluid dynamics: effect of hypoxia and implications for high-altitude illness.
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.
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas; UT Southwestern Medical Center, Dallas, Texas; justinlawley@texashealth.org.
Justin S
http://orcid.org/0000-0003-2166-7966
JS
Lawley
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas; UT Southwestern Medical Center, Dallas, Texas;
Benjamin D
BD
Levine
Sandra and Malcolm Berman Brain & Spine Institute, Dept. of Neurology, Sinai Hospital, Baltimore, Maryland;
Michael A
MA
Williams
Department of Clinical Neuroscience, Umeå University, Umeå, Sweden;
Jon
J
Malm
Department of Radiation Sciences, Umeå University, Umeå, Sweden;
Anders
A
Eklund
Departments of Anesthesiology and Pediatrics, University of Colorado School of Medicine and Children's Hospital Colorado, Aurora, Colorado;
David M
DM
Polaner
Department of Biology, University of Colorado, Colorado Springs, Colorado; Altitude Research Center, Department of Emergency Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado; and.
Andrew W
AW
Subudhi
Institute for Altitude Medicine, Telluride, Colorado.
Peter H
PH
Hackett
Altitude Research Center, Department of Emergency Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado; and.
Robert C
RC
Roach
D000531:Altitude; D000532:Altitude Sickness / Q000503:physiopathology*; D000818:Animals; D001921:Brain / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D007427:Intracranial Pressure / Q000502:physiology
acute mountain sickness; headache and intracranial pressure; high-altitude cerebral edema