Notice at the very last part of this article that damage has also has been observed in chamber techs - the guys that rode to altitude with us at Tyndall altitude chamber. It would be interesting to note how many more flights they took than aircrew did. As you can see below, this will be reported out eventually.

High-altitude pilots in the Air Force have brain lesion three times as often and four times as large as those seen in the brains of other military personnel according to a study of U2 pilots reported in Neurology, a scientific journal.

The lesions appeared on brain scans of a group of U-2 high altitude reconnaissance aircraft pilots.

"Normal young healthy adult brains have few (lesions), as we have demonstrated in our control group," said lead author Dr. Stephen McGuire of the University of Texas in San Antonio and the U.S. Air Force School of Aerospace Medicine at the Wright-Patterson Air Force Base in Ohio.

The pilots in the study had lesions called white matter hyperintensities, which appear as bright spots on brain scans and may be caused by reduced blood flow, similar to those seen with head trauma, McGuire said, though none had experienced such injuries.

The reconnaissance planes regularly fly at 64,000 feet and can go higher than 70,000 feet, where pilots can see the curvature of the Earth and the dividing line between night and day, while commercial flights typically cruise at about 40,000 feet. At high altitude, the spy planes maintain cabin pressure of 28,000 to 30,000 feet, compared to the average of 8,000 feet in a commercial flight.

High-altitude pilots are at increased risk of decompression sickness, or "the bends," in which decreasing pressure allows bubbles of gas to form in the blood and can lead to temporary slowed mental processing or permanent cognitive decline.

With heavier use of the U-2 planes between 2006 and 2010, the number of incidents of pilots experiencing decompression sickness rose somewhat, McGuire's team writes in the journal Neurology.

But the new study found an increased number of brain lesions even when the pilots had not experienced decompression sickness, indicating that some other aspect of a low-pressure environment might explain the results.

McGuire and his coauthors compared the brain scans of pilots with those of 91 other active duty military personnel of similar age, general health and education level. All the men were between the ages of 26 and 50 years old.

The pilots had more lesions and they were larger than in the comparison group.

Pilots had an average of 9.7 lesions versus 3.3 in the comparison group, and the lesions averaged .16 cubic centimeters in size for pilots compared to .04 cubic centimeters for non-pilots.

Brain lesions in the comparison group were concentrated in the frontal lobe, which is typical of the lesions seen with normal aging, but lesions were found equally distributed throughout the brain in the pilot group.

A higher number of brain lesions have been reported in mountain climbers and deep-sea divers as well, the authors note. In those instances, the lesions are thought to represent tissue damaged by gas bubbles or tiny clots in blood vessels.

"Being spots of cellular damage, white matter hyperintensities can be caused by many things - inflammation, infection, disease, trauma, vascular problems like small strokes, low oxygen, low glucose, or low air pressure," said R. Douglas Fields, a neuroscientist at National Institutes of Health and a mountain climber. "This is why they are seen in the normal population with increasing with age," Fields told Reuters Health by email.

Since they are tiny, many of the spots may be harmless, said Fields, who was not involved in the new study. But they do represent damage to white matter, which is where the communication trunk lines in the brain are buried deep below the gray matter on the brain's surface where all the synapses do their computational work.

"The effects of white matter injury can be very diverse and quite widespread, or only affect a local region," Fields said. "It all depends on what connections get damaged."

"More research needs to be performed before we can say for certain that these lesions are dangerous," said Dr. Sean Jersey, a lieutenant colonel in the Air Force and radiologist at David Grant Medical Center at Travis Air Force Base in California.

In the past, doctors saw the spots on brain scans as a normal indication of aging, he said, but over time they have also been linked to specific diseases, like heart disease, migraine headaches, diabetes, high blood pressure and infections. "In the case of our U-2 pilots or divers, they are probably the result of an occupational exposure which was previously unrecognized," he said by email according to a Reuters article.

A 2010 review of studies on the lesions seen in aging brains linked the spots to an increased risk of stroke, dementia and death.

The current study, however, found no impairment of mental processing among the pilots.

"The study was unable to identify any clinical deficits (i.e., observable neurologic defects, such as memory or motor difficulties) in any of the U-2 pilots studied, and all of them are still performing the extremely complex tasks associated with flying the U-2," according to Lieutenant Colonel Edward T. Sholtis, deputy director of public affairs for the Air Force.

"What we do not know is the long-term implication of these findings, which is why we are instituting a long-term monitoring program," Sholtis told Reuters Health by email.

Air Force flight operations guidelines are under review to potentially increase pilot downtime between high-altitude flights longer than nine hours, and limiting the length of deployments, he said.

"Any person exposed to extreme altitudes is at risk," including extreme high altitude mountain climbers and deep-sea divers, McGuire said.

SOURCE: Neurology, online August 20, 2013

Abstract

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.


Addenda:

pilot control group

Julian Hellmann-Regen
Julian Hellmann-Regen, Kim Hinkelmann, Francesca Regen

Sect. Clinical Neurobiology, Dept. of Psychiatry, Charite Campus Benjamin Franklin

McGuire et al. presented interesting data on the prevalence and location of white matter hyperintensities (WMH) in MRI scans of high-altitude pilots. [1] The authors demonstrated that WMHs differ between the pilot group and a matched group of healthy controls. They concluded that these differences may be the result of hypobaria in the pilot group.
While their findings add to aviation and altitude-related risks, military pilots are also exposed to other, potentially confounding factors including exposure to high Gz stress, radiation, or use of stimulant drugs, which may contribute to unspecific brain lesions. [2-4] With the inclusion of a "regular pilot" control group matched for these aviation-related factors, the suggested causal link between hypobaria and WMH development would be strengthened. In addition, previous reports indicating a trend of increased unspecific brain lesions in pilots could be further confirmed. [5]


1. McGuire S, Sherman P, Profenna L, et al. White matter hyperintensities on MRI in high-altitude U-2 pilots. Neurology 2013;81:729 -735.

2. Guillaume AI, Osmont D, Gaffie D, Sarron JC, Quandieu P. Physiological implications of mechanical effects of +Gz accelerations on brain structures. Aviat Space Environ Med 2002;73:171-177; discussion 178.

3. Greene-Schloesser D, Robbins ME, Peiffer AM, Shaw EG, Wheeler KT, Chan MD. Radiation-induced brain injury: A review. Front Oncol 2012;2:73.

4. Lyoo IK, Streeter CC, Ahn KH, et al. White matter hyperintensities in subjects with cocaine and opiate dependence and healthy comparison subjects. Psychiatry Res 2004;131:135-145.

5. Lim D, Park J, Choi WH, Bang DH, Jung OM, Kang S. Asymptomatic brain lesions in pilots: a comparative study with non-flying personnel using brain MRI. Aviat Space Environ Med 2012;83:865-871.

For disclosures, contact the editorial office at Neurology Journal.
Published September 24, 2013
Pilot control group

Stephen A McGuire, Principal Investigator

USAFSAM

Dr. Hellmann-Regen et al. make a relevant point: it would be ideal to compare our findings to those in another pilot group not exposed to high altitude. Even though this study has not yet been authorized, our unpublished results on 83 altitude-chamber technicians whose exposure occurred during their official duties as monitors for altitude chamber exposure has demonstrated the same findings. They have not been exposed to the stresses mentioned by Dr. Hellmann-Regen et al. We are in the process of preparing this study for publication.
For disclosures, please contact the editorial office at Neurology Journal.
Published September 24, 2013