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Brain magnetic resonance imaging (MRI) and neurological changes after a single high altitude climb


Medicine & Science in Sports & Exercise: July 1999 - Volume 31 - Issue 7 - p 969-972
Clinical Sciences: Clinically Relevant

Brain magnetic resonance imaging (MRI) and neurological changes after a single high altitude climb. Med. Sci. Sports Exerc., Vol. 31, No. 7, pp. 969-972, 1999.

Purpose: Neurological impairment, mental dysfunction, and brain imaging changes caused by severe hypoxia have been described by several authors. However, the occurrence of transitory, long lasting, or permanent brain damage has been debated. Although climbing to 8000 m is reserved to a small number of climbers, there are hundreds of lowlanders spending relatively short holidays climbing peaks up to 6000 m in the Andes or in the Himalayas. They are usually not well acclimated and often suffer from acute mountain sickness (AMS). The aim of this study was to examine the effect of a single high altitude exposure on the changes in brain MRI and neuropsychological testing in climbers.

Methods: Brain MRI, medical history, and a battery of neuropsychological tests were obtained in eight male climbers between 31 and 48 yr of age a few days before and between 5 and 10 d after returning to sea level following ascent to altitudes of over 6000 m without oxygen.

Results: The mean AMS symptom score recorded at 5500 m was three in all climbers, headache being the predominant symptom.

Conclusion: We did not observe the changes in brain imaging and in neuropsychological testing observed by other authors. The residual central nervous system impairment following return from high altitude was not observed in our study, and the good results in neuropsychological testing were well correlated with the unchanged brain MRI imaging.

Departments of Radiology and Anesthesiology, Hôpital des Enfants Reine Fabiola and Hôpital Brugmann, Brussels, BELGIUM; and Departments of Radiology and Anesthesiology, Hôpital Cantonal de Genève, SWITZERLAND

Submitted for publication September 1998.

Accepted for publication October 1998.

Address for correspondence: Mehrak Anooshiravani, Department of Radiology, Geneva University Hospital, Rue Micheli du Crest, 24, CH-1211 Geneva 14, Switzerland. E-mail:

Brain integrity and function are dependent on the oxygen supply. A decrease in brain oxygen delivery, whatever the cause, may result in transitory or permanent neurological deficits (13). Recently, the highest peaks of the world have been attracting more and more climbers. Neurological impairment, mental dysfunction, and brain imaging changes occurring after high altitude climbs (above 8000 m) have been described by several authors (3,5,6,8,9,14). During the ascent the main clinical manifestations of hypoxia are acute mountain sickness (AMS), high altitude cerebral edema, or high altitude pulmonary edema. Brain magnetic resonance imaging (MRI) and neuropsychological testing abnormalities have been described in up to 50% of the published series of climbers after extreme high altitude climbs (6,7).

Although climbing to 8000 m is reserved to a small number of professional climbers, every year thousands of lowlanders climb more accessible peaks up to 6000 m (Aconcagua, Kilimanjaro, etc.). They are usually not well acclimated and often suffer AMS. Since AMS is a manifestation of brain hypoxia, one may ask whether climbing to 6000 m leads to permanent brain impairment? If brain damage occurred during recreational climbing, it could have dramatic professional and social consequences.

We tried to answer the following question: does a single high altitude exposure at 6000 m lead to changes in brain MRI and neuropsychological testing in nonprofessional climbers?

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After the study protocol was approved by the ethics committee of our institution, eight nonprofessional climbers gave written informed consent and were entered into the study. Any climber with drug addiction or chronic alcohol intake was excluded.

They participated in three different expeditions: to the Ojos del Salado (6869 m) in Chile, to the Tocclaraju (6034 m) and Alpamayo (5947 m) in Peru, and to the Korzenskaia (7100 m) in Tadjikistan. These three expeditions represented the typical high altitude exposure trips. The first one was a combination of tourism and trekking ending with the easy climb of the highest peak of Chile (6859 m). The second was a trekking trip with the climb of two high peaks in Peru. The last trip was organized by the Belgian Federation of Mountaineering with the climbers spending 30 d in the surroundings of the Korzenskaia for acclimatization before climbing.

The medical history and clinical examination were unremarkable in all subjects. Three climbers had previously climbed over 4000 m, four had ascended over 6000 m, and one had never been above 2000 m. This study did not impose any restrictions concerning the acclimatization program, the medical follow-up, or the diet during the expedition. The AMS symptom score (AMSss) was recorded every day during the ascent.

The variables used as criteria of exposure to altitudes were the number of nights spent over 4500 m, nights over 5500 m, and highest altitudes reached.

The neuropsychological tests were performed by the same physician a few days before and within 10 d after return to sea level. These tests are commonly used in the Belgian population. They included:

  1. Concentration (D2 test): Subjects had to find from a list and cross out with a pen as many given symbols as possible during 12 periods of 20 s.
  2. Number to symbol association (Code test): Subjects had to match as many symbols as possible to given numbers in 90 s.
  3. Logic association (Matrix test): Subjects had to complete a logic series of six drawings choosing the one missing from another series of six randomly associated. Subjects had to complete as many series as possible during 20 min.
  4. Association memory: A list of 10 pairs of words was presented to the subject; then the examiner immediately repeated the first word of the pair and the subject had to provide the second.
  5. Pure memory: A list of 15 words was presented; then the subject was invited to perform simple mathematical calculations for 30 s and then asked to report as many words as possible for 60 s.

The brain MRI studies were performed shortly before and within 10 d after return to sea level using a 0.5 T magnet (Gyroscan, Philips, The Netherlands). The following scans were obtained: T1 (TE = 25, TR = 344), Proton density (TE = 23, TR = 3441), and T2 (TE = 120, TR = 3441). Proton density and T2 imaging were done in the axial and coronal planes while T1 weighted imaging was done in the axial plane. Two radiologists studied the MRI independently.

The medical follow-up during the expedition consisted of the daily observation of the Lake Louise Acute Mountain Sickness symptoms score (AMSss). All participants took acetazolamide for AMS prevention. Aspirin was the only medication taken for the treatment of AMS.

After the expedition, each climber filled out a short questionnaire concerning general well-being during the climb.

The statistical analysis for the neuropsychological tests was by paired Wilcoxon ranked test. A P < 0.05 was considered statistically significant.

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The climbers were male subjects between 31 and 48 yr of age with a mean of 37 yr. The first group of three climbers spent eight nights over 4500 m, two over 5500 m, and reached the altitude of 6200 m. The second group of three climbers spent 12 nights over 4500 m, six over 5500 m, and reached 7100 m. The last group of two climbers spent eight nights up to 4500 m, three over 5500 m, and reached 6800 m.

The mean AMSss recorded at 5500 m was 3 ± 1 (range 2-4) in all climbers, headache being the predominant symptom. The other symptoms were mainly sleep disturbance, anorexia, nausea, and periorbital edema. No subject suffered from ataxia. All subjects admitted to have taken acetazolamide, aspirin, and paracetamol when they felt the need. The MRI studies showed no changes in the brain imaging after the climbs (Fig. 1A and B). We incidentally noticed the interval development of sinus disease in two subjects and aggravation of preexisting sinusitis in four subjects. There were no significant changes in the neuropsychological tests while two subjects complained of euphoria and two others of memory disturbances after return to sea level. All subjects returned to their professional occupations normally after the expedition. There was an improvement in two tests and no changes in the others (Table 1).

Figure 1-A

Figure 1-A



During the ascent between 5000 m and the summit, all subjects suffered from neurological symptoms such as lightheadedness, headache, insomnia, and decision-making difficulties. There was no correlation between the AMSss and the results of brain MRI and neuropsychological testing.

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The neurological symptoms characteristic of brain hypoxia observed in our climbers during the ascent did not lead to MRI or neuropsychological changes. Contrary to many other observations (3,5,6,8,9,14), organic cerebral injury and changes in brain function did not occur in our climbers despite neurological symptoms after a hypoxic exposure of around 6000-7000 m. All subjects improved their test scores, but this was probably a result of the practice effect.

Evidence suggests that the imaging and functional changes described previously are caused by hypoxic brain injury (14). At the altitude of 6000 m, the oxygen partial pressure is about 74 mm Hg, and the arterial oxygen partial pressure is lower (15). It is therefore not surprising that brain cells may suffer in these conditions and particularly in the most sensitive areas such as the globus pallidus and the limbic zone (10). Although the cause of brain impairment is hypoxia, this may or may not lead to permanent brain damage. This situation is comparable to injuries resulting from cerebral hypoperfusion or carbon monoxide intoxication when there is incomplete ischemia with a reversible decrease in cerebral function (2). The altitude threshold of brain injury is unfortunately impossible to determine and depends on many interacting variables. Not only the characteristics of the altitude (oxygen partial pressure, speed of ascent, time spent at high altitude) but also personal characteristics of climbers (age, sex, individual susceptibility, acclimatization, ventilatory response to hypoxia, exercise, prophylaxis) may define this threshold.

Brain imaging abnormalities have been reported after extreme and nonextreme high altitude expeditions. Findings include subacute (cerebral edema and venous thrombosis) or chronic lesions (atrophy and infarcts) (6,7,11,12).

Garrido et al. (7) described cortical atrophy and high signal areas of the white matter on T2-weighted MRI scans, a finding commonly observed in healthy elderly patients consistent with myelin pallor of vascular origin (4). In another study comparing pre- and post-ascent MRI studies, Garrido et al. (7) observed new high intensity white matter abnormalities in two of nine climbers, also correlating with the severity of the neurological symptoms (7).

We did not see any of the MRI abnormalities described by Garrido et al. (7) before or after the expeditions in climbers exposed to high altitude hypoxia. We must keep in mind that high signal intensity foci are common incidental findings on MR images, and their quantification is subject to observer variability (1,16). The effect of altitude hypoxia on brain MRI should therefore be determined through comparative longitudinal studies.

The discrepancies concerning the effect of altitude on the brain among different studies (3,5-10,14), including ours, may be explained by whether climbers in each series had reached their threshold of altitude-induced brain injury.

In our study we may assume that this threshold was not reached, probably because of the favorable combination of the aforementioned factors (moderate altitude between 5500 m and 7000 m, good acclimatization, prophylactic treatment by acetazolamide, and mild AMSss).

Few studies have dealt with the use of brain imaging techniques in the evaluation of AMS (6,7). We believe that more well designed prospective imaging studies are needed to determine the incidence and the nature of detectable brain MRI lesions to clarify the potential risk of permanent brain injury at different altitudes.

In conclusion, we suggest that a single, short exposure to high altitude hypoxia, with no significant medical problems and a mild AMS during the climb, may not be sufficient to cause subacute detectable anatomical (MRI) or neuropsychological changes. We, however, strongly recommend the usual precaution of smooth acclimatization.

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1. Awad, I. A., R. F. Spetzker, J. A. Hodak, A. Catherine, R. N. Awad, and F. Williams, Jr. Incidental lesions noted on MRI of the brain: prevalence and clinical significance in various aged groups. Neurosurgery 20:222-227, 1987.
2. Branston, N. M., A. J. Strong, and L. Synon. Extacellular potassium activity, evoked potential and tissue blood flow: relationship during progressive ischemia in baboon cerebral cortex. J. Neurol. Sci. 32:305-310, 1977.
3. Cavaletti, G. and G. Tredici. Long lasting neuropsychological changes after a single high altitude climb. Acta Neurol. Scand. 87:103-105, 1993.
4. Chimowitz, M. I., M. L. Estes, A. J. Furlan, and I. A. Awad. Further observations on the pathology of subcortical lesions identified on MRI. Arch. Neurol. 49:747-752, 1992.
5. Clark, C. F., R. K. Heaton, and A. N. Wiens. Neuropsychological functioning after prolonged high altitude exposure in mountaineering. Aviat. Space Environ. Med. 54:202-207, 1983.
6. Garrido, E., A. Castello, J. L. Ventura, A. Capdevila, and F. A. Rodriguez. Cortical atrophy and other brain MRI changes after extremely high-altitude climbs without oxygen. Int. J. Sports Med. 14:232-234, 1993.
7. Garrido, E., R. Segura, A. Capdevilla, et al. New evidence from MRI of brain changes after climbs at extreme altitude. Eur. J. Appl. Physiol. 70:477-481, 1995.
8. Hornbein, T. F. Long term effects of high altitude on brain function. Int. J. Sports Med. 13:S43-S45, 1992.
9. Hornbein, T. F., B. D. Townes, R. B. Schoene, J. R. Sutton, and C. S. Houston. The cost to central nervous system of climbing to extremely high altitude. N. Engl. J. Med. 321:1714-1729, 1989.
10. Regard, M., O. Oelz, P. Brugger, and T. Landis. Persistent cognitive impairment in climbers after repeated exposure to extreme altitude. Neurology 39:210-213, 1989.
11. Shiota, J., K. Sugita, O. Isono, and S. Araki. A case of acute mountain sickness with bilateral lesion of pallidum. Rinsho Shinkeigaku 30:630-634, 1990.
12. Song, S. Y., T. Asaji, Y. Taizaki, et al. Cerebral thrombosis at altitude: its pathogenesis and problems of prevention and treatment. Aviat. Space Environ. Med. 57:71-6, 1986.
13. Ward, M. P., J. S. Milledge, and J. B. West. Central nervous system. In: High Altitude Medicine and Physiology, M. P. Ward, J. S. Milledge, J. B. West (Eds.). London: Chapmann & Hall, 1989, pp. 311-325.
14. West, J. B. Do climbs to extreme altitude cause brain damage? Lancet 16:387-388, 1986.
15. West, J. B. Physiological response to hypoxia. In: High Altitude Medicine and Physiology, M. P. Ward, J. S. Milledge, J. B. West (Eds.). London: Chapmann & Hall, 1989, pp. 67-79.
16. Yetkin, F. Z., V. M. Haughton, M. E. Fisher, et al. High signal foci on MR images of the brain: observer variability in their quantification. Am. J. Radiol. 159:185-188, 1992.


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