Abstract
Objective: Hypoxic exposure in healthy subjects can induce acute mountain sickness including headache, lethargy, cerebral dysfunction, and substantial cerebral structural alterations which, in worst case, can lead to potentially fatal high altitude cerebral edema. Within this context, the relationships between high altitude-induced cerebral edema, changes in cerebral perfusion, increased brain parenchyma volume, increased intracranial pressure, and symptoms remain unclear.Methods: In 11 subjects before and after 6 days at 4350 m, we performed multiparametric magnetic resonance investigations including anatomical, apparent diffusion coefficient and arterial spin labeling sequences.Results: After the altitude stay, while subjects were asymptomatic, white matter volume (+0.7 ± 0.4%, p = 0.005), diffusion (+1.7 ± 1.4%, p = 0.002), and cerebral blood flow (+28 ± 38%; p = 0.036) were significantly increased while cerebrospinal fluid volume was reduced (−1.4 ± 1.1%, p = 0.009). Optic nerve sheath diameter (used as an index of increased intracranial pressure) was unchanged from before (5.84 ± 0.53 mm) to after (5.92 ± 0.60 mm, p = 0.390) altitude exposure. Correlations were observed between increases in white matter volume and diffusion (rho = 0.81, p = 0.016) and between changes in CSF volume and changes in ONSD s (rho = −0.92, p = 0.006) and symptoms during the altitude stay (rho = −0.67, p = 0.031).Conclusions: These data demonstrate white matter alterations after several days at high altitude when subjects are asymptomatic that may represent the normal brain response to prolonged high altitude exposure.
Highlights
These authors suggested that the development of cerebral subedema with increased brain parenchyma volumes as well as venous outflow restriction may induce an increase in intracranial pressure probably responsible for symptoms Lawley et al (2014) explored the relationship between changes in brain volume, magnetic resonance imaging-derived intracranial pressure, and acute mountain sickness (AMS) symptoms in 13 subjects exposed to FiO2 = 0.12 for 10 h
We hypothesized that WM volume would be increased together with increased apparent diffusion coefficient (ADC) and reduced fractional anisotropy but unchanged Optic nerve sheath diameter (ONSD), which would characterize the normal brain response to prolonged hypobaric hypoxic exposure
Lake Louise score and perceived headache increased during the first days at high altitude with individual maximum scores reached within the first 3 days (mean maximal Lake Louise score 6 ± 3 pts, mean maximal perceived headache 57 ± 16 mm; all p < 0.05 compared to sea level) while on the last day at high altitude (Day 6) scores were not significantly different anymore compared to sea level (Lake Louise score 1 ± 1 pts, headache 13 ± 15 mm; all p > 0.05)
Summary
Hypoxic exposure in healthy subjects can induce acute mountain sickness including headache, lethargy, cerebral dysfunction, and substantial cerebral structural alterations which, in worst case, can lead to potentially fatal high altitude cerebral edema. The relationships between high altitude-induced cerebral edema, changes in cerebral perfusion, increased brain parenchyma volume, increased intracranial pressure, and symptoms remain unclear
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