High Altitude Flight and MRI Brain Lesions

In the past ten years, there have been several studies showing a small but significant increase in white matter brain lesions in professional and other high frequency divers. At least one such study correlated the increase in lesions to the number of accents from depth at over 10 meters per minute. This may implicate nitrogen micro-bubbles due to rapid decompression as a scuba diver ascends quickly as the cause, rather than the more ordinary arteriosclerosis seen with aging in the brain.

This past month, a similar study was published (it had been also announced at the AAN meeting in March 2013). This one was done in Air Force pilots rather than divers. In particular, the study looked at brain MRI scans in U2 spy plane pilots, who use a partially pressurized cabin with supplemental oxygen in a very high altitude, almost space-like low pressure environment during their flights. Once again, an increase in white matter brain lesions not explainable by atherosclerosis was seen. Micro-bubbles forming during the plane's ascent? Probably. Additionally, though there were no discernible cognitive consequences in the diver studies, the affected pilots had a slight decrease in some tests of cognition.

Although there had been a theory that venous bubbles forming in the body outside the head were being shunted through an atrial defect in the heart on the way to the brain, such as via a patent ductus arteriosus, recent studies have not shown that patent ductus arteriosus or atrial septal defect correlated with these lesions in divers as much as those rapid ascents do.

So, whenever possible, always ascend slowly when coming up from a dive, folks.



White matter hyperintensities on MRI in high-altitude U-2 pilots

Authors: Stephen McGuire, MD, Paul Sherman, MD, Leonardo Profenna, MD, MPH, Patrick Grogan, MD, John Sladky, MD, Anthony Brown, MD, Andrew Robinson, MD, Laura Rowland, PhD, Elliot Hong, MD, Beenish Patel, BS, David Tate, PhD, Elaine S. Kawano, BA, Peter Fox, MD and Peter Kochunov, PhD

doi: 10.1212/WNL.0b013e3182a1ab12

Neurology August 20, 2013 vol. 81 no. 8 729-735

Objective: To demonstrate that U-2 pilot occupational exposure to hypobaria leads to increased incidence of white matter hyperintensities (WMH) with a more uniform distribution throughout the brain irrespective of clinical neurologic decompression sickness history.

Methods: We evaluated imaging findings in 102 U-2 pilots and 91 controls matched for age, health, and education levels. Three-dimensional, T2-weighted, high-resolution (1-mm isotropic) imaging data were collected using fluid-attenuated inversion recovery sequence on a 3-tesla MRI scanner. Whole-brain and regional WMH volume and number were compared between groups using a 2-tailed Wilcoxon rank sum test.

Results: U-2 pilots demonstrated an increase in volume (394%; p = 0.004) and number (295%; p < 0.001) of WMH. Analysis of regional distribution demonstrated WMH more uniformly distributed throughout the brain in U-2 pilots compared with mainly frontal distribution in controls.

Conclusion: Pilots with occupational exposure to hypobaria showed a significant increase in WMH lesion volume and number. Unlike the healthy controls with predominantly WMH in the frontal white matter, WMH in pilots were more uniformly distributed throughout the brain. This is consistent with our hypothesized pattern of damage produced by interaction between microemboli and cerebral tissue, leading to thrombosis, coagulation, inflammation, and/or activation of innate immune response, although further studies will be necessary to clarify the pathologic mechanisms responsible.

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