Traumatic Brain Injury and Effects of Altitude - Human Performance ...

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Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the Literaturewith AMS affecting more than four out of five individuals who fly directly to above 3800 meters (about12, 500 feet) (Basnyat & Murdoch, 2003).Individuals who develop symptoms of AMS should not ascend further, and should descend if theirsymptoms worsen or fail to improve. Immediate descent is critical if cerebral or pulmonary symptomsappear. Supplemental oxygen may help to relieve AMS symptoms.High-altitude cerebral edema (HACE) is relatively unusual, with prevalence estimated at between 0.5%and 4.0% of individuals who climb to altitudes above 2500 meters (8000 feet). However, because theprecise pathophysiology of neither syndrome is fully understood and because the incidence of HACE isdramatically less than that of AMS, it is not clear that the two syndromes reflect identical processes orvulnerabilities. Signs and symptoms of HACE may include dizziness, intense weakness, tingling, ataxia,altered consciousness, papilloedema (optic disc swelling), retinal hemorrhages and focal neurologicaldeficits. These symptoms can develop very quickly and are potentially fatal. As symptoms develop, thetime to loss of consciousness may be as little as 1-10 minutes (Clarke, 2006). Treatment requiresimmediate descent and oxygen supplementation. If HACE is not promptly managed and relieved, it canlead to brain herniation, coma, and death. Because HACE is usually preceded by AMS symptoms, it isoften regarded as the “end stage” of AMS.The precise pathophysiological bases of AMS and HACE are not known, and are difficult to ascertainpartly due to individual differences. When these syndromes occur, they appear to follow from a seriesof systemic and cerebral changes that may involve increased cerebral blood flow (due to hypoxia)and/or vasogenic edema, both of which can cause to brain swelling and raised ICP (see Figure 3, below).Vasogenic edema has been observed in cases of moderate to severe AMS and HACE, perhaps due todisruption of BBB permeability. These and related hypotheses are the focus of continuing research,analysis, and review (Basnyat & Murdoch, 2003; Hackett, 1999a, 1999b; Hackett & Roach, 2001; Roach& Hackett, 2001; West, 2004; Wilson et al., 2009).Treatment with dexamethasone (anti-inflammatory steroid) is sometimes recommended to treat HACE(Schoene, 2005). However, recent clinical research suggests that steroids have no clear beneficial effecton TBI and may even have deleterious effects; therefore, steroids are NOT recommended for reducingICP in individuals who have sustained traumatic brain injury (TBI) (Bullock & Povlishock, 2007). Otherpharmacotherapeutic options for the prevention and treatment of altitude-related illnesses in otherwisehealthy individuals are reviewed elsewhere (Wilson et al., 2009; Wright et al., 2008).A third altitude-related illness is known as high-altitude pulmonary edema (HAPE), which usuallypresents in the first 24-48 hours after arrival at altitudes higher than 2500 meters (approximately 8000feet). HAPE may or may not follow AMS, but often co-occurs with signs of HACE. HAPE is a cardiopulmonarysyndrome that usually appears first as dyspnea (shortness of breath) and reduced tolerance forexercise. This can lead to dry cough (which can later become productive), tachypnea (rapid breathing),tachycardia (rapid heart rate) and fever. Cold is a risk factor for HAPE. HAPE is more common in menthan in women, and in individuals with pre-existing cardiopulmonary circulation abnormalities. Again,descent and supplemental oxygen are the recommended treatments.September 14, 2010 10
Traumatic Brain Injury (TBI) and Effects of Altitude:An Analysis of the LiteratureFigure 3. Proposed pathogenesis of ACE and HACEFinally, exposure to high altitude may be associated with other focal neurological disturbances that canpresent separately from AMS or HACE; these include transient ischemic attacks, double vision,scotomas, 6 and cerebral venous thrombosis. While these neurological impairments may accompanyHACE and be related to hypoxia, they do not necessarily follow the same course (Basnyat et al., 2004).NEUROPSYCHOLOGICAL EFFECTS OF ALTITUDE EXPOSURENeuropsychological impairments have been observed in climbers exposed to extreme altitudes with andwithout the use of supplemental oxygen (Virues-Ortega et al., 2004). In particular, several investigatorshave found evidence for persistent cognitive functional impairment in climbers exposed to extremealtitudes without oxygen assistance. Regard et al. (1989) performed comprehensive neuropsychologicaltesting on eight mountaineers who had previously reached summits higher than 8500 meters (above 27,000 feet) on multiple occasions without supplementary oxygen. Five of the eight climbers showedpersisting mild cognitive impairments in their concentration, short-term memory, cognitive flexibilityand control of errors. Although the degree of impairment did not correlate with length of exposure to6 Areas of partial alteration in the visual field.September 14, 2010 11
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