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RESEARCH AND PRACTICE |
The authors are with the University of Texas Southwestern Medical Center, Dallas. Robert W. Haley is with the Epidemiology Division, Department of Internal Medicine, and Ann Matt Maddrey and Howard K. Gershenfeld are with the Department of Psychiatry.
Correspondence: Requests for reprints should be sent to Robert W. Haley, MD, Epidemiology Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8874 (e-mail: robert.haley{at}utsouthwestern.edu).
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INTRODUCTION |
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 TOP INTRODUCTION References |
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In 1997, Haley et al. described a case definition of Gulf War syndrome composed of 3 primary symptom complexes (syndromes) beginning during or shortly after the war.2–4 This case definition, identified by a factor analysis of symptoms in 249 members of a battalion that served in the war, was found to be strongly associated (relative risks of 4 to 8) with self-reported wartime exposures to low-level chemical nerve agents and other cholinesterase-inhibiting chemicals,4 genetic susceptibility to chemical nerve agents and other organophosphates,5,6 abnormal audiovestibular tests indicating brainstem dysfunction,3,7 evidence of basal ganglia and brain stem neuronal loss as measured by magnetic resonance spectroscopy,8,9 and abnormal brain dopamine production.10 Results were recently replicated in an independent sample of Gulf War veterans.11
In 1998, we conducted a nested case–control study at the University of Texas Southwestern Medical Center involving individuals from a naval reserve battalion; 22 subjects with the highest scores on one of the 3 Haley syndrome factor scales were selected as case patients.2,3 This criterion allowed selection of subjects with symptoms most typical of the case definition irrespective of symptom severity (not measured) and total number of symptoms, and thus there was no bias for or against severity of illness. Sixteen healthy veterans matched with case patients in regard to age, sex, and education level were selected from the same battalion to serve as controls.3
We administered the Medical Outcomes Study 36-Item Short Form (MOS SF-36) self-report questionnaire, a validated, widely accepted measure of general health, functional status, and well-being, to assess the functional status and well-being of the case patients and controls.12 Because of the existence of population-based, noninstitutionalized norms, this questionnaire serves as the "gold standard" for comparisons among illnesses. Hundreds of published studies have applied the instrument in such comparisons.12
We found that the level of impairment of ill Gulf War veterans meeting the Haley case definition was generally far worse than that of patients with common illnesses known to have a substantial negative impact, including congestive heart failure, type 2 diabetes, recent acute myocardial infarction, chronic obstructive pulmonary disease, and clinical depression (Figure 1
).12 Moreover, a repeated measures analysis of variance (F1,20 = 18, P < .001) showed that the impact of Haley's "confusion–ataxia" syndrome was substantially worse than that of his "impaired cognition" and "central pain" syndromes, confirming earlier published observations.2–5,7,8,10 In other settings, low MOS SF-36 scores such as those revealed in this study have been shown to be highly predictive of inability to work at a paying job.12
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Acknowledgments |
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The study protocol was approved by the institutional review board of the University of Texas Southwestern Medical Center, and all subjects gave written informed consent before participating.
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Footnotes |
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Accepted for publication May 1, 2001.
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References |
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TOPINTRODUCTIONReferences |
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2. Haley RW, Kurt TM, Hom J. Is there a Gulf War syndrome? Searching for syndromes by factor analysis of symptoms. JAMA.1997;277:215–222.[Abstract]
3. Haley RW, Hom J, Roland PS, et al. Evaluation of neurologic function in Gulf War veterans: a blinded case–control study. JAMA. 1997;277:223–230.[Abstract]
4. Haley RW, Kurt TL. Self-reported exposure to neurotoxic chemical combinations in the Gulf War: a cross-sectional epidemiologic study. JAMA. 1997;277:231–237.[Abstract]
5. Haley RW, Billecke S, La Du BN. Association of low PON1 type Q (type A) arylesterase activity with neurologic symptom complexes in Gulf War veterans. Toxicol Appl Pharmacol.1999;157:227–233.[Medline]
6. Mackness B, Durrington PN, Mackness MI. Low paraoxonase in Persian Gulf War veterans self-reporting Gulf War syndrome. Biochem Biophys Res Commun.2000;276:729–732.[Medline]
7. Roland PS, Haley RW, Yellin W, Owens K. Vestibular dysfunction in Gulf War syndrome. Otolaryngol Head Neck Surg.2000;122:319–329.[Medline]
8.
Haley RW, Marshall WW, McDonald GG, Daugherty M, Petty F, Fleckenstein JL. Brain abnormalities in Gulf War syndrome: evaluation by 1H magnetic resonance spectroscopy. Radiology.2000;215:807–817.
9. Meyerhoff DJ, Lindgren J, Hardin D, Griffis JM, Weiner MW. Metabolic abnormalities in the brain of subjects with Gulf War illness. Proc Intl Soc Mag Reson Med.2001;994.
10.
Haley RW, Fleckenstein JL, Marshall WW, McDonald GG, Kramer GL, Petty F. Effect of basal ganglia injury on central dopamine activity in Gulf War syndrome: correlation of proton magnetic resonance spectroscopy and plasma homovanillic acid. Arch Neurol.2000;57:1280–1285.
11. Haley RW, Luk GD, Petty F. Use of structural equation modeling to test the construct validity of a case definition of Gulf War syndrome: invariance over developmental and validation samples, service branches and publicity. Psychiatry Res.2001;102:175–200.[Medline]
12. Ware JE, Snow KK, Kosinski M, Gandek B. SF-36 Health Survey Manual and Interpretation Guide. Boston, Mass: Health Institute; 1997.
13. Iowa Persian Gulf Study Group. Self-reported illness and health status among Gulf War veterans: a population-based study. JAMA. 1997;277:238–245.[Abstract]
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