Headaches, eye haemorrhages, and sleep disruption are just some of the effects on the brain caused by ascent to high altitude. These and other effects are discussed in a Review published in the February edition of The Lancet Neurology, Dr Mark Wilson, Centre for Altitude, Space and Extreme Environment Medicine, University College London, UK, and colleagues. The authors are part of the Caudwell Extreme Everest team, which visited Mount Everest in 2007 and are in the process of reporting data from a number of experiments from that expedition.
As air travel provides easier access to mountains, millions of people now travel to high altitudes each year for holidays, expeditions and work. Although oxygen concentration at altitude remains consistent at 21%, its partial pressure decreases as atmospheric pressure decreases. This “hypobaric hypoxia” can result in inadequate supply of oxygen to tissues, in particular to the highly oxygen-dependent brain.
High altitude illness has classically been thought of as a spectrum of disease from high altitude headache (HAH – occurring in up to 80% of travellers to high altitude and responding to simple analgesia such as paracetamol), through to acute mountain sickness (AMS – a more severe headache associated with gastrointestinal disturbance, lethargy or difficulty sleeping) to finally high altitude cerebral oedema (HACE – a condition that can progress from confusion and an unsteady gait to coma and death). In workers on the Qinghai-Tibetan Railway the incidence for AMS is 45-95% and 0.5% for HACE. Slow ascent can help prevent all the above conditions, but when symptoms develop, descent is a priority with the consideration of oxygen and dexamethasone for more severe cases.
This Review explains new concepts in the pathogenesis of these illnesses. An individual’s susceptibility to AMS may be more complex than the simple physiological (ability to maintain oxygen levels) and anatomical (the “tighter” brain – with less surrounding cerebrospinal fluid to buffer swelling causing increased susceptibility) theories might suggest. The role of genetic predisposition, factors such as hypoxia inducible factor and the venous system are discussed.
The neuropsychological effects of ascent to high altitude (with or without formal illness) also vary greatly on an individual level. Slowing of reflexes (such as pupil reaction) and motor skills and reduction in short term memory are all reported. Anxiety disorders and hallucinations (e.g. “third man” phenomenon where the presence of another imaginary climbing companion is convincing) are also noted especially at extreme altitude.
Investigations into high altitude illness predisposition include genetic work targeting specific genes, each thought to have a small but contributory role. The authors discuss investigation of the “tight-fit” hypothesis – the idea that people cope less well with the expansion of their brain at lower pressures. Measuring intracranial pressure has been attempted invasively and non-invasively. The invasive technique, which used a telemetric radio device, found that in three subjects the one who developed AMS also had a rise in intracranial pressure on minimal exertion (even head turning).
The authors conclude: “Investigation of the mechanisms that underlie differences in susceptibility to hypoxia-induced injury, whether they are physiological pathways, such as those that regulate compensatory oxygen delivery, pathophysiological pathways that affect oedema formation, or anatomical factors that affect cerebral or cranial compliance, might suggest novel prophylactic or therapeutic targets that are of broad clinical relevance.”
“The cerebral effects of ascent to high altitudes”
Mark H Wilson, Stanton Newman, Chris H Imray
Lancet Neurol 2009; 8: 175-91
The Lancet Neurology
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