64 Aviation, Space, and Environmental Medicine x Vol. 81, No. 1 x January 2010
J ERSEY SL, B ARIL RT, M C C ARTY RD, M ILLHOUSE CM. Severe neuro-
logical decompression sickness in a U-2 pilot. Aviat Space Environ
Med 2010; 81:64 – 8.
Severe neurological decompression sickness (DCS) has been a rare
entity in the U.S. Air Force, including the U-2 community. In over 50 yr
of operation, few U-2 pilots reported severe neurological DCS in fl ight
despite the extreme altitudes at which they operate. This article describes
a near-fatal case of neurological DCS that occurred during a combat
mission. The injury left the pilot with permanent cognitive defi cits that
correlated with focal lesions present on magnetic resonance imaging of
his brain. To our knowledge, the images presented herein are the fi rst to
show radiological evidence of brain injury induced by altitude DCS.
Though only a single case, the objective and clinical fi ndings in the case
pilot are similar to results documented in divers suffering DCS with cen-
tral nervous system injury and victims of traumatic brain injury. DCS will
remain a potentially serious threat to current and future air and space
Keywords: U-2 , case report , altitude , decompression sickness , neu-
rological symptoms , traumatic brain injury , magnetic resonance
fl ight. DCS and its sequelae are recognized complica-
tions in persons exposed to changes in environmental
pressure commonly seen in high altitude aviation or
scuba diving. Symptoms vary widely, ranging from mild
joint pain, to serious neurological manifestations, and
even death. In contrast to diving-related DCS, death or
incapacitation from DCS are virtually unheard of in mod-
ern aviation. This is due partly to redundant systems
protecting aviators and the fact that descent from alti-
tude serves as compressive therapy ( 1 , 7 , 13 , 14 ).
U-2 pilots are at signifi cant risk of DCS due to frequent
long sorties at extreme altitudes. The U-2S is a high-
altitude surveillance aircraft fl own by a single pilot. Typical
missions involve fl ights over 70,000 ft (21,336 m ) for
greater than 9 h. The aircraft is pressurized with a dif-
ferential ratio to maintain a cabin pressure below 35,000 ft
(10,668 m), so pilots wear a full pressure suit in case of
unexpected cabin decompression. Aviators also undergo
denitrogenation ( “ pre-breathing ” ) by breathing 100% oxy-
gen for at least 1 h before fl ight. Pre-breathing establishes
an oxygen gradient to offl oad nitrogen from tissues to
the blood, thereby decreasing nitrogen stored in the body.
These measures have been effective at preventing aviation-
related DCS over time.
Despite increased risk, no deaths, incapacitation, or
lasting injuries due to DCS have been reported among
ECOMPRESSION sickness (DCS) remains a signifi -
cant concern for U-2 pilots during high-altitude
U-2 pilots in over fi ve decades. In a 1996 survey of ac-
tive/retired U-2 pilots, approximately 70% reported at
least one episode of DCS during their career. Of those,
12.7% were severe enough to cause the pilot to alter the
fl ight plan or abort the mission, but no lasting injuries
were reported ( 2 ). In this article, we present a case of
near-fatal DCS with neurological symptoms in a U-2S
pilot during fl ight with permanent sequelae.
During a high-altitude reconnaissance mission in sup-
port of combat operations in 2006, a 47-yr-old male U-2S
pilot experienced severe physical and cognitive manifes-
tations of neurological DCS. The pilot performed stan-
dard prefl ight procedures, including donning a full
pressure suit and pre-breathing for 1 h at rest. Approxi-
mately 2.5 h into fl ight [cabin altitude 28,000 ft (8534.4 m)],
the pilot complained of bilateral knee pain which dissi-
pated after he increased the internal pressure of his pres-
sure suit. Moments later, he noticed ankle pain. Thinking
it was caused by poor position, the pilot adjusted his
rudder pedals with no relief. Simultaneously, he sensed
the aircraft rolling, which he attributed to momentary
spatial disorientation caused by head movement. Over
the next 2 h, the pilot experienced gradually worsening
concentration, confusion, fatigue, and headache. Recog-
nizing his deteriorating condition, the pilot tried eating,
drinking, increasing oxygen supply, and increasing suit
pressure, with only minimal relief. The pilot rationalized
his symptoms as “ old man problems ” and did not alert
The pilot fi rst notifi ed ground controllers he was “ feel-
ing ill ” 4 h later, but elected to continue. Minutes later,
he reported severe weakness and diffi culty breathing.
As the pilot’s cognition worsened, controllers provided
step-by-step instructions for even the most basic cockpit
From the 99 th Reconnaissance Squadron, Beale Air Force Base, CA.
This manuscript was received for review in March 2008 . It was ac-
cepted for publication in October 2009 .
Address correspondence and reprint requests to: Sean L. Jersey,
M.D., 9 th AMDS/SGOAF, 15301 Warren Shingle Road, Beale AFB, CA
95903; email@example.com .
Reprint & Copyright © by the Aerospace Medical Association,
Severe Neurological Decompression Sickness in a
Sean L. Jersey , Robert T. Baril , Richmond D. McCarty ,
and Christina M. Millhouse
Aviation, Space, and Environmental Medicine x Vol. 81, No. 1 x January 2010
SEVERE DCS IN A U-2 PILOT — JERSEY ET AL.
operations. Suspecting DCS, controllers directed the pi-
lot to return to the deployed base from which his fl ight
originated. Hostile airspace prevented immediate de-
scent, which lengthened the pilot’s hypobaric exposure.
As the pilot’s mental status deteriorated, ground con-
trollers experienced increasingly longer episodes of ra-
dio silence before all voice communications eventually
ceased. Meanwhile, the pilot had to open his helmet
facemask to clear debris after an episode of spontaneous
emesis. This exposed him to an extremely hypoxic and
hypobaric environment for the remainder of the fl ight.
The pilot’s symptoms progressed to include color vision
loss, hemianopsia, visual disturbances, hearing loss, and
repeated emesis. The pilot was unaware of his surround-
ings throughout descent to the airfi eld. Other pilots ob-
served the U-2S descending in a stall before recovering
spontaneously. The pilot made multiple attempts to land
on the wrong runway, coming within 5 ft (1.5 m) of a
likely fatal ground impact at one point. Fortunately, dur-
ing one approach, the pilot regained enough situational
awareness just prior to ground impact to land the plane
Upon landing, rescue personnel found the pilot slumped
over the instrument panel with emesis contaminating
the cockpit. The fl ight surgeon controlling the scene was
a hyperbaric medicine specialist. His initial clinical as-
sessment was “ severe DCS with neurologic symptoms
and incipient cardiovascular collapse. ” Rescue person-
nel extracted the pilot and initiated intravenous hydra-
tion and 100% oxygen by aviator’s mask. Treatment
continued en route to a nearby host-nation hyperbaric
facility via helicopter. The helicopter restricted fl ight to
300 – 500 ft (91.4 – 152.4 m) above ground level to mini-
mize nitrogen bubble re-expansion.
Brief physical examination was accomplished on the
runway. Notable fi ndings included clinical signs and
symptoms of shock with pale clammy skin, thready pulse,
and lethargy. A bluish-purple, mottled rash consistent
with cutis marmarota was seen over his torso. Periph-
eral oxygen saturation was 89% (off oxygen). Respiratory
rate was slow and shallow while auscultation of the
lungs revealed diffuse rales and crackles. His carotid
pulse was thready and no radial pulses were palpable.
Neurologically, the pilot had a Glasgow Coma Scale of
14 (opened eyes to speech) and was diffi cult to arouse.
He had diffi culty with serial 7s and judgement. Deep
tendon refl exes were hyperactive with normal Babinski
response. He was unable to stand or walk and fi nger-to-
nose pointing was abnormal.
The pilot’s past medical history was signifi cant for two
reported prior episodes of DCS with joint and skin mani-
festations in 1999 that resolved with surface level oxygen.
During this deployment, the pilot denied any daily medi-
cations. His body mass index was 31. He denied prior to-
bacco use and alcohol ingestion during the day before
fl ight. There were no recent hypobaric or hyperbaric ex-
posures. The pilot had suffered from viral gastroenteritis
5 d prior to this incident. However, he was symptom free
2 d before the incident. He was a highly experienced pi-
lot, also serving temporarily as squadron commander.
The pilot underwent hyperbaric oxygen treatment
(HBOT) after arriving at the host nation medical facility.
He initially underwent U.S. Navy Treatment Table 6 (USN
TT6) with two extensions at 60 fsw. During the fi rst oxy-
genation break, he vomited and remained diffi cult to
arouse. By the third break, he reported improvement in
symptoms and tolerated oral fl uids. HBOT was halted
and the pilot remained hospitalized. His medical work-up
included transthoracic echocardiogram, various labora-
tory studies, electroencephalogram, and electrocardio-
gram. These tests were unremarkable. However, computed
tomography of the brain demonstrated areas of low at-
tenuation in the bifrontal and temporal regions. There-
fore, MRI was performed to determine the extent of injury.
The radiologist described multiple punctuate cortical and
sub-cortical lesions involving the bifrontal and parietal
lobes, likely due to microvascular ischemia ( Fig. 1 ). The
consulting neurologist and radiologist concluded the
fi ndings were consistent with high altitude DCS. Given
the pilot’s marked improvement after HBOT and these
MRI fi ndings, the fl ight surgeon deferred further tests.
The pilot showed persistent cognitive and fi ne motor
defi cits (e.g., he could not remember how to shave) 12 h
after initial treatment. Thus the fl ight surgeon initiated a
second USN TT6 HBOT without extensions. After treat-
ment, the pilot could recall details about the mishap and
his global condition improved (i.e., he performed daily
activities without assistance). Over the next 2 d, the pilot
Fig. 1. Initial FLAIR MRI images through frontal and parietal lobes
showing multiple cortical lesions involving the bifrontal areas, likely due
to microvascular ischemia (solid arrows).
66 Aviation, Space, and Environmental Medicine x Vol. 81, No. 1 x January 2010
SEVERE DCS IN A U-2 PILOT — JERSEY ET AL.
underwent two Treatment Table 9 sessions until his symp-
toms no longer improved with HBOT. A second MRI
showed marked improvement; all cerebral lesions had al-
most disappeared except a right frontal lesion, which was
smaller. He was discharged from the hospital 7 d after ad-
mission. The pilot remained with his squadron for another
8 d before returning home on an uneventful commercial
fl ight. Investigation of the aircraft showed all systems
functioned properly, including life support systems.
The pilot reported subjective resolution of his symp-
toms following HBOT. Accordingly, he was evaluated
by a neurologist on return to home station who docu-
mented a normal neurological examination. Another
MRI of the head was consistent with previous exams.
This MRI demonstrated a focal lesion in the right frontal
lobe ( Fig. 2 ). It also showed multiple areas of gliosis in-
volving cortical gray matter and subcortical white mat-
ter within the frontal lobes on T2 and FLAIR images.
The lesions were in proximity to watershed zones, con-
sistent with ischemic injury ( Fig. 3 ). Similar lesions oc-
curred in the right cerebellum ( Fig. 4 ). Given the patient’s
clinical history and earlier MRI reports, the neurologist
concluded these lesions represented sequelae of anoxic
injury during his DCS incident.
The fl ight surgeon returned the pilot to fl ying status
3 mo later, after completing the required aeromedical con-
sultations. The pilot continued to deny recurrent symp-
toms and stated his desire to return to fl ying. An altitude
chamber ride was not deemed necessary. To mitigate
risk, the pilot resumed fl ight in stages. Initially, he fl ew
four sorties with an instructor pilot in the unit’s compan-
ion jet trainer, the T-38. Next, he fl ew a two-seat training
U-2 with an instructor pilot on two low-altitude and two
high-altitude sorties. Only then did he return to fl ying
solo in the U-2S. The pilot’s initial fl ights took place with-
out incident. However, he experienced dizziness and
disorientation on his second solo. Symptoms resolved
after infl ating his pressure suit and the pilot landed
uneventfully. After discussion with hyperbaric medi-
Fig. 2. Subsequent FLAIR MRI image completed at home station
demonstrating a persistent lesion along the right frontal sulcus consistent
with microvascular ischemia secondary to DCS (solid arrow).
Fig. 3. FLAIR MRI image demonstrating punctate areas of hyperinten-
sity within the brain (straight arrows). Lesions are located predominately
along gray-white matter junctions of the inferior-lateral left frontal lobe.
A similar lesion is noted in the periventricular white matter along the left
atrium of the ventricle (curved arrow). Lesions do not enhance (images
not shown) and are most consistent with gliotic foci secondary to micro-
vascular ischemic changes.
Fig. 4. FLAIR MRI image depicting similar punctate lesions in the
right cerebellum (solid arrows).
Aviation, Space, and Environmental Medicine x Vol. 81, No. 1 x January 2010
SEVERE DCS IN A U-2 PILOT — JERSEY ET AL.
cine consultants, the pilot’s symptoms were felt to be
manifestations of anxiety. He was placed on duties not
including fl ying and released after 1.5 h of oxygen by
aviator’s mask. The pilot drove unassisted to his home, lo-
cated at 1800 ft (548.6 m) elevation difference from the
base. The pilot experienced a severe retro-orbital head-
ache 36 h later. Over the next 3 wk, he experienced short-
term memory loss, recurrent headaches, and “ feeling in
the fog. ” His symptoms partially improved with time,
but he did not seek acute treatment.
Due to potential recurrence of DCS symptoms, the pi-
lot underwent evaluation by the Aeromedical Consulta-
tion Service (ACS) to obtain a waiver for continued
fl ying. During interviews, the pilot admitted to multiple
unreported prior incidents of joint DCS. He also reported
being hospitalized in 1991 “ for dehydration ” which, in
retrospect, the pilot believed was actually neurological
DCS. His ACS evaluation included normal neurology
exam, transesophageal echocardiogram with bubble study,
and electroencephalogram. Repeat MRI showed stable
gliotic lesions. Signifi cantly, a neuro-psychology exam
showed cognitive defi cits with variable performance dec-
rements corresponding to the brain areas demonstrating
lesions on MRI. These fi ndings indicated the pilot would
have diffi culty managing complex problem-solving tasks
in novel fl ying situations. Any re-injury could cause fur-
ther defi cits and he had a higher risk of seizure (though
the absolute risk could not be quantifi ed). Overall, the
ACS concluded the pilot’s risk of incapacitation was
greater than 1% per year, which is the generally accepted
cut-off standard for acceptance of incapacitating risk
frequency. Consequently, the ACS recommended per-
manent disqualifi cation.
The pilot retired from the military and never returned
to fl ying. At the time of this publication, he reported
persistent headaches, degraded visual acuity, joint pain,
personality changes, short-term memory loss, and cog-
nitive defi cits. These defi cits prevent him from obtaining
a commercial pilot’s license or other comparable em-
ployment. The pilot also reported ongoing diffi culty ob-
taining clinical care and disability compensation from
the Department of Veteran Affairs. His diffi culty may be
due in part to the unique mechanism of injury and sub-
tle nature of his cognitive defi cits.
This case is unique considering the pilot suffered a se-
vere brain injury during fl ight that was nearly fatal and
left him with permanent cognitive disabilities. In avia-
tion, DCS with central nervous system involvement is
rare. In a prospective series of 447 altitude chamber sub-
jects at Armstrong Laboratory, only 0.5% exhibited frank
central nervous system involvement ( 11 ). Similarly, re-
sidual defi cits are rarely reported and are short-term in
nature. Deaths are virtually unknown after 1959 and the
institution of HBOT ( 1 , 11 , 13 , 14 ). In contrast, deaths and
permanent injury are more prevalent among divers af-
fl icted with central nervous system DCS. Also, the spi-
nal cord is most commonly affected in divers, whereas
the brain is usually affected in aviators ( 14 ).
This case was also unique to the U-2 community at the
time. Historically, DCS incidence has been diffi cult to
assess in the fl ying community due to reluctance among
pilots to report incidents for fear of being disqualifi ed
from fl ying. Bendrick et al. found the prevalence of DCS
among U-2 pilots is higher than previously reported, but
no instances of permanent disability or death ( 2 ). Our
search of historical records, published literature, and safety
records uncovered few cases of neurological DCS com-
parable in severity to the subject case. One occurred in
2002 when neurological symptoms manifested after land-
ing ( 9 ). At least three other in-fl ight cases occurred after
2006. Whether these cases refl ect an increase above ex-
pected incidence of neurological DCS or a natural conse-
quence of policy changes that promote reporting is a
matter of conjecture.
This is the fi rst case we are aware of documenting ra-
diological evidence on MRI of neurological DCS in a pi-
lot. Objective radiological evidence of neurological injury
is unusual in DCS. Diagnostic modalities evaluated thus
far (CT, MRI, SPECT, and PET imaging) have shown low
sensitivity in detecting pathological changes in the brain
with aviators or divers affl icted with neurological DCS.
Consequently, they have little use in acute diagnosis
( 5 , 8 ). Similar to results with soldiers suffering traumatic
brain injuries, the utility of imaging in documenting clini-
cal progress of neurological DCS patients has not been
proven. When present, MRI and CT lesions tend to cor-
relate with a higher degree of structural damage and
greater likelihood of residual defi cits ( 3 , 5 , 6 , 8 ). In this
case, there was direct correlation between the pilot’s physi-
cal exam and MRI fi ndings ( Fig. 3 and 4 ). Confusion,
temporary amnesia, and personality changes in this pi-
lot are indicative of a temporal-frontal lobe injury — the
clinical equivalent of stroke. He also displayed cerebel-
lar fi ndings, including ataxia and impaired equilibrium.
One could argue his lesions resulted from previous DCS
injuries or another undiagnosed condition. Gliotic le-
sions have been found in asymptomatic divers and
chamber attendants ( 4 , 5 ). While no studies have been
performed in aviators, routine altitude exposures of U-2
pilots could plausibly result in similar fi ndings. Unfor-
tunately, no earlier studies are available for comparison
in this case as neuroradiological studies are not routine
screening exams. However, standard three-sequence MRI
studies performed at the home station (diffusion, appar-
ent diffusion coeffi cient, and T-2 weighted sequences)
indicated this pilot’s lesions were acute. Clinically, the
pilot had no antecedent signs or symptoms on multiple
fl ying physical exams to suggest a pre-existing neuro-
logical condition. Additionally, improvements noted in
sequential MRI studies by the host nation correlated clini-
cally with the pilot’s neurological status as HBOT pro-
gressed. Most importantly, defi cits persisting in this pilot
today are consistent with his MRI lesions.
The degree to which one person is more susceptible to
DCS than another is a matter of debate. Generally ac-
cepted risk factors increasing susceptibility to aviation
DCS include higher altitude, longer exposure, greater
in-fl ight activity, and lack of pre-oxygenation. However,
68 Aviation, Space, and Environmental Medicine x Vol. 81, No. 1 x January 2010
SEVERE DCS IN A U-2 PILOT — JERSEY ET AL.
multiple individual factors, including age, obesity, hy-
dration status, physical condition, gender, and prior DCS
( 12 , 14 ), may increase susceptibility. Altogether, any of
these factors, or the combination, could have infl uenced
this pilot’s condition. Unfortunately, studies to date have
been unable to predict an individual’s specifi c risk of
DCS with certainty ( 10 , 12 , 14 ).
Ultimately, if prevention fails, pilots must recognize
DCS and seek treatment. Current protocol is to descend
immediately and initiate surface level oxygen via avia-
tor’s or tight-fi tting non-rebreather mask. HBOT must
be initiated immediately for severe symptoms. For mild
cases (i.e., joint pain), HBOT is indicated if symptoms do
not improve within 30-60 min of treatment, or if symp-
toms worsen. Hyperbaric medicine specialists should be
consulted for guidance ( 8 ).
Diagnosing and treating DCS can be diffi cult under
typical fl ying conditions. One is tempted to criticize the
case pilot for not landing sooner. In that sense, he recog-
nized a degree of complacency in his early decision mak-
ing. On the other hand, the pilot sustained a frontal lobe
lesion that likely impaired his judgment. More gener-
ally, aviators routinely make compromises for practical
reasons that can delay seeking treatment for DCS. For
one, pilots and astronauts place considerable pressure
on themselves to complete their missions. Combat espe-
cially may force military pilots to subjugate personal
safety to mission needs. Two, diagnosis of DCS is diffi -
cult, even for medical experts. For example, the pilot at-
tempted a logical sequence of actions to correct likely
physiological problems (i.e., cramped seating, hypogly-
cemia, hypoxia, etc.) before considering DCS. These were
reasonable actions fl ight surgeons perform when trou-
bleshooting in-fl ight problems. Finally, fl ights over oceans
or wilderness place pilots far from available HBOT. In
this case, controllers concluded the pilot would be safer
landing at an airfi eld known to him rather than closer,
but unfamiliar emergency fi elds. While this increased
the pilot’s exposure, on-scene medics endorsed the deci-
sion in order to provide lifesaving HBOT on landing.
We reported lessons learned from this near-fatal phys-
iological incident to improve fl ying safety. Despite the
stellar safety record in aviation-related DCS since 1960,
this case demonstrates that DCS remains a serious po-
tential threat to fl ight operations. The potential for DCS
will persist as advances in aerospace technology con-
tinue to push the limits of high altitude fl ight. For exam-
ple, the Air Force’s newest fi ghter, the F-22 Raptor, can
cruise at altitudes greater than 60,000 ft (18,288 m), while
commercial companies are developing spacefl ights for
tourists. Future aviators would benefi t from continued
research as our understanding of DCS pathophysiology
and treatment evolves.
The authors thank the dedicated U.S. and host nation profession-
als who treated this pilot. We also thank Doctors Bendrick, West, and
Nunneley, who provided expert review of this article, and Dr. Palka for
interpreting the MRI images. Most importantly, we thank the mishap
pilot for sharing his experience and continued service to the nation.
Views and opinions expressed in this article are solely those of the
authors and do not refl ect offi cial policy of the Department of the Air
Force, Department of Defense, or U.S. Government.
Authors and affi liations: Sean L. Jersey, M.S., M.D., and Christina M.
Millhouse, M.D., 99th Reconnaissance Squadron, Beale AFB, CA;
Robert T. Baril, D.O., USAF David Grant Medical Center Radiology
Residence Program, Travis AFB, CA; and Richmond D. McCarty,
D.O., North Mississippi Medical Center Family Medicine Residency
Program, Tupelo, MS.
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