Page 84 - Journal of Special Operations Medicine - Spring 2016

EPO, whereas presence at 3,000m above sea level may could improve return-to-duty times and bolster perfor-
result in a sharp, almost twofold renal EPO production. mance. In addition, it will help establish new research
11
EPO has been shown to possess multiple neuroprotective directions in this area, such as those focusing on a bet-
properties. EPO was also shown to protect the astro- ter classification or a new treatment for PTH, PTSD, or
12
glial space by reducing the concentration of extracellular depression.
glutamate. In addition, EPO was shown to be an ef-
12
fective agent protecting and repairing many important Disclosures
processes in the nervous system. Furthermore, synthesis
of EPO in astrocytes could protect them against apopto- The authors have nothing to disclose.
genic chemicals or even low oxygen pressure. Overall,
12
EPO is currently viewed as a substance that can sustain References
antiapoptotic responses in many tissues where it can be
regarded as a general tissue- protective cytokine. 1. DeFraites RF. The armed forces health surveillance center: en-
hancing the military health system’s public health capabilities.
BMC Public Health. 2011;11(suppl 2):S1.
TBI is a complex process with several stages, the ini- 2. Theeler B, Lucas S, Riechers RG 2nd, et al. Post-traumatic
tial stage being the impact itself (i.e., blunt object or headaches in civilians and military personnel: a comparative,
blast) followed by several complex physiologic and clinical review. Headache. 2013;53:881–900.
biochemical reactions, such as accumulation of free 3. Armed Forces Health Surveillance Center. Incident diagnoses
of common symptoms (“sequelae”) following traumatic brain
radicals, direct trauma to cell membranes by free radi- injury, active component, U.S. Armed Forces, 2000–2012.
cals, and a cascade of inflammatory reactions follow- MSMR. 2013;20:9–13.
ing by cell apoptosis. 13–15 Cumulatively, these reactions 4. External causes of traumatic brain injury, 2000–2011. MSMR.
are likely to cause neurodegeneration and subsequent 2013;20:9–14.
PTH and potentially other adverse outcomes such as 5. Hoge CW, Clark JC, Castro CA. Commentary: women in
7
combat and the risk of post-traumatic stress disorder and de-
depression, PTSD, or sleeping disorders. An alteration pression. Int J Epidemiol. 2007;36:327–329.
or elimination of one or more of these posttrauma reac- 6. Chen YH, Kang JH, Lin HC. Patients with traumatic brain in-
tions is likely to result in fewer adverse outcomes as well jury: population-based study suggests increased risk of stroke.
as a better prognosis for TBI. If head trauma has oc- Stroke. 2011;42:2733–2739.
curred at high altitude, both profound cellular hypoxia 7. Mayer CL, Huber BR, Peskind E. Traumatic brain injury,
neuroinflammation, and post-traumatic headaches. Headache.
and higher EPO production by the kidneys are likely 2013;53:1523–1530.
to affect many complex physiologic and biochemical 8. Luks AM. Physiology in medicine: a physiologic approach
reactions following injury and, therefore, all post-TBI to prevention and treatment of acute high-altitude illnesses. J
outcomes. Thus, it is unclear whether high altitude is an Appl Physiol (1985). 2015;118:509–519.
additional risk factor for all negative outcomes associ- 9. Engelhardt S, Huang SF, Patkar S, et al. Differential responses
of blood-brain barrier associated cells to hypoxia and isch-
ated with TBI such as PTH, depression, or PTSD acutely emia: a comparative study. Fluids Barriers CNS. 2015;12:4.
or chronically post-TBI, and there is a need to conduct 10. Singh SB, Thakur L, Anand JP, et al. Effect of high altitude
further research in the area. It is likely that high altitude (ha) on event related brain potentials. Indian J Physiol Phar-
can trigger many negative post-TBI outcomes; however, macol. 2003;47:52–58.
some of them could be more affected than others due to 11. Eckardt KU, Boutellier U, Kurtz A, et al. Rate of erythro-
poietin formation in humans in response to acute hypobaric
the protective role of EPO. hypoxia. J Appl Physiol (1985). 1989;66:1785–1788.
12. Joyeux-Faure M. Cellular protection by erythropoietin: new
Knowledge that high altitude may trigger various post- therapeutic implications? J Pharmacol Exp Ther. 2007;323:
TBI outcomes may help justify additional screening, di- 759–762.
agnostic, preventive, and treatment procedures among 13. Morganti-Kossman MC, Lenzlinger PM, Hans V, et al. Produc-
tion of cytokines following brain injury: beneficial and deleteri-
Warfighters returning from military duties at high alti- ous for the damaged tissue. Mol Psychiatry. 1997;2:133–136.
tude. This is particularly important because, for example, 14. Raghupathi R, Graham DI, McIntosh TK. Apoptosis after
untreated headaches are known to cause various mental traumatic brain injury. J Neurotrauma. 2000;17:927–938.
issues, ranging from mental anguish and substance abuse 15. Farkas O, Povlishock JT. Cellular and subcellular change
to suicide. Moreover, PTSD and depression are the lead- evoked by diffuse traumatic brain injury: A complex web of
change extending far beyond focal damage. Prog Brain Res.
ing causes of medical visits and missed workdays among 2007;161:43–59.
Soldiers with TBI. Thus, proper diagnosis of post-TBI
outcomes among Soldiers returning from military duties
at high altitude would be essential and could include not Dr Ismailov is a medical doctor who earned his PhD in injury
only additional diagnostic procedures but also detailed and cardiovascular epidemiology from the University of Pitts-
evaluation for conditions such as PTSD, depression, burgh. Together with his collaborators from Pacific Institute
epilepsy, visual disturbance, cognitive functions, hearing for Research and Evaluation and University of Pittsburgh, he
loss, tinnitus, memory loss, anxiety, and insomnia. This conducted the first population-based studies that examined the

68 Journal of Special Operations Medicine Volume 16, Edition 1/Spring 2016