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American Journal of Epidemiology Advance Access originally published online on August 30, 2006
American Journal of Epidemiology 2006 164(7):708-709; doi:10.1093/aje/kwj297
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American Journal of Epidemiology Copyright © 2006 by the Johns Hopkins Bloomberg School of Public Health All rights reserved; printed in U.S.A.

Letter to the Editor

RE: "CHRONIC MULTISYMPTOM ILLNESS COMPLEX IN GULF WAR I VETERANS 10 YEARS LATER"

Stephen C. Hunt, Mathew Jakupcak, Miles McFall, Mack Orsborn, Bradford Felker, Stephanie Larson and Michele Klevens

Deployment Health Clinic, VA Puget Sound Health Care System, University of Washington, Seattle, WA 98108

(e-mail: stephen.hunt{at}med.va.gov)

The high prevalence (28.9 percent) of chronic multisymptom illness (CMI) in combat veterans from the first Gulf War, noted in a recent Veterans Affairs study (1Go), corroborates the findings of earlier studies (2Go, 3Go) and is consistent with evidence of nonspecific physical symptoms associated with military combat dating back to the Civil War (4Go). The authors report an apparently indistinguishable CMI syndrome in non-deployed Gulf-era service personnel (15.8 percent), suggesting that war exposure increases the rate of what appears to be an identical syndrome that is not uncommon in the general population.

In the Veterans Affairs study (1Go), veterans with CMI, when compared with noncases, had higher rates of combat exposure. Relations between CMI and psychological trauma/post-traumatic stress disorder (PTSD) have been reported (5Go, 6Go); but what about the excess number of Gulf War veterans who did not have classical combat stressors but did develop CMI? Residual effects of toxic exposures have been proposed and reported (7Go–11Go); but why do we see an identical syndrome in nondeployed veterans and in the population at large? And to what extent can we anticipate, as the authors of the above paper projected, that CMI "is likely to be a common, persistent problem among veterans returning from the current Gulf War" (1Go, p. 66)?

Since 1994, we have assessed and treated over 600 veterans from the first Gulf War and over 450 from the current conflicts in Iraq and Afghanistan. Both clinical impressions and preliminary empirical evidence suggest that these two groups differ in a number of significant ways. The combat veterans currently returning from Iraq and Afghanistan seem to be reporting fewer medically unexplained symptoms, fewer concerns about toxic chemical exposures, fewer attributions of symptoms to such exposures, and more classical combat stressors, while exhibiting more classical combat-related PTSD. To us, the Iraq/Afghanistan group more resembles combat veterans from the Vietnam War than veterans from the first Gulf War. The Vietnam War, like the current conflict, was a war in which prolonged and continuous exposure to ambush was not uncommon and combatants routinely intermingled with civilians.

Numerous focus groups and publications and our inventories of our own clinical population suggest that the threat of toxic exposures was the primary stressor for many veterans deployed in the first Gulf War; in the current conflict, on the other hand, stressors commonly reported by the veterans include exposure to improvised explosive devices (IEDs), indirect fire (rocket-propelled grenades and mortars randomly striking bases), and ambushes.

For persons serving in Iraq and Afghanistan, the cues for threat include such things as benign-appearing vehicles, irregularities in the road surface, and suspicious persons or parcels—any of which may potentially harbor explosive devices. These veterans' symptoms (vigilance, hyperreactivity, reexperiencing) are often triggered by and result in scanning for external cues ("Is that car carrying explosives?... Is that person a suicide bomber?... Is that irregularity in the road an IED?"). During the first Gulf War, the cues for threat (hearing chemical alarms, repeatedly donning protective gear in the face of potentially toxic exposure) were accompanied by scanning for somatosensory cues ("Am I feeling anything unusual in my body, my arms, my legs, my breathing, my head?"). It appears to us that their symptoms (vigilance, hyperreactivity, reexperiencing) are oriented towards internal cues (somatosensory stimuli) and that what we are seeing in this group is a more "somatic" form of PTSD arising from exposure to this unique psychological trauma.

It may be that different wars involve different psychological traumas resulting in different manifestations of post-traumatic disturbances in sensory processing, with some syndromes being more internally focused and others more externally focused. Further research conducted with this in mind may assist us in better understanding and more effectively treating the health concerns of this most deserving group—our combat veterans.

ACKNOWLEDGMENTS

Conflict of interest: none declared.

References

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  2. Steele L. Prevalence and patterns of Gulf War illness in Kansas veterans: association of symptoms with characteristics of person, place, and time of military service. Am J Epidemiol 2000;152:992–1002.[Abstract/Free Full Text]
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  7. Asa PB, Cao Y, Garry RF. Antibodies to squalene in Gulf War syndrome. Exp Mol Pathol 2000;68:55–64.[CrossRef][Web of Science][Medline]
  8. Hollander DH. Beef allergy and the Persian Gulf syndrome. Med Hypotheses 1995;45:221–2.[CrossRef][Web of Science][Medline]
  9. Nicolson GL, Nicolson NL. Diagnosis and treatment of mycoplasmal infections in Persian Gulf War illness-CFIDS patients. Int J Occup Med Immunol Toxicol 1996;5:69–78.
  10. Abou-Donia MB, Wilmarth KR, Abdel-Ralman AA, et al. Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos. Fundam Appl Toxicol 1996;34:201–22.[CrossRef][Web of Science][Medline]
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This Article
Right arrow Extract Freely available
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kwj297v1
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