Page 83 - Journal of Special Operations Medicine - Spring 2016

81st Regional Support Command on 1 November 2011 where responsible for all aspects of the USASOC Science and Tech-
he served until his retirement on 17 May 2014. In his civil- nology Program. E-mail: gothardw@soc.mil.
ian capacity, Mr Gothard has served the US Army Special
Operations Command (USASOC) as a G8 Combat Develop- Keywords: US Army Special Operations Command Science
ments Officer, Chief of the G8 Advanced Technology Branch, and Technology Division; USASOC S&T; science and tech-
and the G9 Science and Technology Manager. He currently nology; special warfare; surgical strike operations
serves as the G9 Chief of the Science and Technology Division

and harmful. TBI induces a myriad other responses, in-
Traumatic Brain Injury cluding involvement of the peripheral immune system
and influx of potentially cytotoxic bloodborne proteins
and pathogens. This causes neuronal damage and glial
Its Outcomes and High Altitude
activation that can further contribute to BBB permeabil-
by Rovshan M. Ismailov, MD, PhD; Judith M. Lytle, PhD ity. Leukocytes, cytokines, and other inflammatory me-
diators cross the BBB after TBI, contributing to chronic
pathology. Many of these sequelae persist for days,
raumatic brain injury (TBI) has been frequently months, or years.
called a hallmark of military conflicts in Iraq
Tand Afghanistan. In addition, the Armed Forces Severity and duration of postconcussion syndrome (in-
Health Surveillance Center reports an increasing rate of cluding PTH) are not related to the severity of TBI. There
TBI in US Armed Forces that is greatest in the US Army. must be other factors at play. Wartime theaters of op-
The Congressional Research Service reports a total of eration have occurred in various parts of the world and
253,300 TBI cases between 1 January 2000 and 20 Au- very often much above the sea level. Altitude was a fac-
gust 2012, with the Army averaging about 20,000 TBIs tor in recent military operations in Iraq (Operation Iraqi
per year from 2007 to 2011. 1 Freedom and Operation New Dawn) and Afghanistan
(Operation Enduring Freedom). Iraq has an upper eleva-
Posttraumatic headache (PTH) remains the most frequent tion of approximately 12,000 ft (3,600m), and Afghan-
symptom after TBI and will continue to be a problem in istan has an upper elevation of approximately 24,000
the military healthcare system. One study showed that ft (7,200m). High altitude (4,900–11,500 ft) brings the
19% of Soldiers returning from combat duty in 2005 onset of physiological effects of diminished oxygen pres-
had symptoms consistent with migraine and that, for sure. At very high altitude (11,500–18,000 ft), maximum
migraine-like PTH, individuals who had the most severe arterial oxygen saturation falls below 90%. 8
2
headache pain had the highest headache frequencies.
However, TBI can also lead to a number of other nega- On one hand, cellular hypoxia is caused by decreased
tive outcomes, such as stroke, depression, various cogni- barometric pressure, predisposing to various negative
tive dysfunctions, posttraumatic stress disorder (PTSD), post-TBI outcomes. Hypoxic injuries are closely associ-
anxiety disorder, sleep disorders, epilepsy, visual distur- ated with disturbed BBB function, allowing substances
9
bance, hearing loss, tinnitus, and memory loss. For to cross the BBB. In addition, high elevation results in
3,4
example, injured active-duty Operation Iraqi Freedom lowered partial pressure of oxygen and the human brain
personnel presented with a substantially higher preva- responds to it by changing the responsiveness of cerebral
lence of PTSD than did uninjured personnel (32% versus circulation. Exposure to hypoxia has been also shown
10
14%). Population-based research evidence suggests that to result in multiple changes to the central nervous
5
TBI may increase risk of stroke by 10-fold, even after system, such as verbal working and short-term memory
adjusting for the most important confounders. 6 impairment, hippocampal atrophy, and neurodegenera-
tion, as well as a significant difference in the middle,
Among other sequelae, TBI triggers neuroinflammation posterior cerebral, and basilar artery flow velocity. 10
and activates microglia. While inflammation is repara-
tive acutely, chronic persistence may lead to secondary On the other hand, hypoxia can also trigger some po-
injuries, causing neurological symptoms such as head- tentially beneficial physiological reactions to protect the
7
ache. Further, mechanical trauma from TBI and resulting human body from damage. One potentially beneficial re-
neuroinflammation can alter blood–brain barrier (BBB) action is the higher production of erythropoietin (EPO)
function, allowing entry of substances from circulating by human kidneys. Previous research evidence suggests
blood into the brain’s interstitial space, both protective that subtle hypoxia can result in moderate production of

Editorials 67