An Observational Cerebral Magnetic Resonance Imaging Study Following 7 Days at 4554 m

Abstract

Background: In human beings exposed to high altitude, cerebral magnetic resonance imaging (cMRI) revealed alterations ranging from subclinical cerebral edema formation to subtle brain abnormalities. Yet, brain structure after adaptation to high altitude and their recovery after return to lowlands have been rarely investigated. We, therefore, examined 10 healthy individuals by cMRI before, 12 hours after descent (R + 12h), and again 3.5 months (R + 3.5m) after a 7-day high altitude exposure at 4554 m. Results: After their 3-day lasting, stepwise ascent to 4554 m, all subjects suffered acute mountain sickness with a mean Lake Louise score of 5.8-1.7 after the first night at that altitude. Acute mountain sickness completely resolved after 4 days at 4554 m. While 12 hours after descent mean white and gray matter volumes were increased compared with before altitude exposure (p = 0.045 and p = 0.002), these volumes were normalized on R + 3.5m. Moreover, we observed significant focal volume alterations likely attributed to either vasogenic or cytotoxic edema formation. Two subjects presented new brain findings after altitude exposure. In one individual the number of preexisting white matter hyperintensities (WMHI) transiently increased, in the other individual a reversible splenial lesion syndrome (RESLES) emerged. Both findings had resolved 15 and 8 days after descent, respectively. None developed structural lesions like brain atrophy, cerebral infarcts, microbleeds, or highaltitude cerebral edema. Discussion: Three days after complete recovery from acute mountain sickness and after return to low altitude, subclinical vasogenic and cytotoxic edema, RESLES and WMHI are present in high-altitude acclimatized individuals. However, these cerebral alterations are reversible within months at lowland.

Brain structure and neurocognitive function in two professional mountaineers during 35 days of severe normobaric hypoxia

“…White matter seems particularly susceptible for hypoxic stress, which causes an increased serum filament level, a marker for neuro-axial injury, in healthy participants 44 h after ascending actively to 4454 m [15]. After 3 months of recovery, cerebrovascular alterations had regressed completely in our participants, which is in good agreement with the transient nature of hypobaric hypoxia induced cerebral responses [6].…”

“…It is speculated that her higher white matter hyperintensity burden at baseline may result from lower white matter integrity, which in turn could increase the susceptibility to hypoxia. However, a gender effect seemed unlikely because a similar phenomenon was also discovered in a male individual after 1 week at 4559 m [6]. White matter seems particularly susceptible for hypoxic stress, which causes an increased serum filament level, a marker for neuro‐axial injury, in healthy participants 44 h after ascending actively to 4454 m [15].…”

“…Sixteen hours of 12% normobaric hypoxia led to sodium accumulation in the cerebral extracellular space resulting in ionic edema [5]. Furthermore, cerebral magnetic resonance imaging (MRI) studies showed reversible local vasogenic and cytotoxic white matter edema in mountaineers returning from high altitude [6]. Irreversible damage to white and gray matter was seen after returning from extreme altitude [7].…”

Resting-State Neuronal Activity and Functional Connectivity Changes in the Visual Cortex after High Altitude Exposure: A Longitudinal Study

“…After 3 months of reoxygenation, the nerve cell activities of the visual cortex and motor cortex did not return to the baseline level, indicating that the proliferation of blood vessels caused by hypoxia could not be eliminated after 3 months of reoxygenation. Previous studies have found that 7 days of high altitude exposure can recover in 3.5 months after returning to the plains [ 20 ], therefore, we speculate that after 1 month of high altitude exposure, it would take more than 3 months to recover.…”

“…Another study showed that the occipital visual cortex thickened after 1 month of exposure to high altitude and recovered to the baseline level after participants returned to sea level for 2 months, but there were still abnormalities in the white matter [ 19 ]. A study found that cerebral alterations were reversible after an exposure of 7 day at a high altitude of 4554 m and then returning to sea level for 3.5 months [ 20 ]. These studies mainly focused on chronic high altitude exposure and relatively less work has been done based on acute high altitude exposure and to clarify whether these changes were reversible or not after returning to sea level through longitudinal studies.…”