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Many U.S. Gulf War-era veterans complained of poor cognition following the war. This study assessed neuropsychological functioning in veterans 10 years after the war through objective tests. 2189 Gulf War-era veterans (1061 deployed, 1128 non-deployed) were examined at 1 of 16 U.S. Veterans Affairs medical centers. Outcomes included neuropsychological domains derived from factor analysis and individual test scores. Deployed veterans performed significantly worse than non-deployed veterans on 2 of 8 factors (motor speed & sustained attention, analysis not corrected for multiple comparisons) and on 4 of 27 individual test variables (Trails A & B, California Verbal Learning Test – List B, and Continuous Performance Test sensitivity, with only Trails B surviving Bonferroni correction). Within deployed veterans, Khamisiyah exposure was negatively correlated with motor speed after controlling for emotional distress. Depressive symptoms and self-reported exposure to toxicants were independently and significantly associated with worse sustained attention. Other factors were also associated with self-reported exposures. The findings were not a result of differential effort across groups. Gulf War deployment is associated with subtle declines of motor speed and sustained attention, despite overall intact neuropsychological functioning. Evidence suggests that toxicant exposures influence both these functions, and depressive symptoms also influence attention. (JINS, 2009, 15, 717–729.)
Gulf War veterans reported multiple psychological symptoms immediately after the war; the temporal course of these symptoms remains unclear.
To assess the prevalence of war-era onset mental disorders in US veterans deployed to the Gulf War and in non-deployed veterans 10 years after the war.
Mental disorders were diagnosed using structured clinical interviews. Standard questionnaires assessed symptoms and quality of life.
Gulf War-era onset mental disorders were more prevalent in deployed veterans (18.1%, n=1061) compared with non-deployed veterans (8.9%, n=1128). The prevalence of depression and anxiety declined 10 years later in both groups, but remained higher in the deployed group, who also reported more symptoms and a lower quality of life than the non-deployed group. Remission of depression may be related to the presence of comorbid psychiatric disorders and level of education. Remission of anxiety was related to treatment with medication.
Gulf War deployment was associated with an increased prevalence of mental disorders, psychological symptoms and a lower quality of life beginning during the war and persisting at a lower rate 10 years later.
All organisms are exposed to stimuli construed as stressors and all organisms mount a characteristic physiologic response to stress to maintain homeostasis (Herman et al., 1996). Many physical illnesses can be linked to life stress, particularly in aged individuals (McEwen & Stellar, 1993; Clauw & Chrousos, 1997; Katz, 1996). Impairments in the physiological responses to stress have particularly been associated with immune, endocrine, neurological, and psychiatric disorders. Examples of neuropsychiatric disorders, which are associated with dysregulation of the stress response, include depression, post-traumatic stress disorder, and neurodegenerative disorders (Kathol et al., 1989; Charney et al., 1993; McEwen, 1992, Landfield & Eldridge, 1991; Sapolsky et al., 1986; Landfield et al., 1992).
Activation of physiologic stress responses involve the sympathetic nervous system and the hypothalamic–pituitary–adrenal (HPA) axis. The HPA axis is the best characterized component of the physiologic stress response. In aging, this stress component undergoes significant changes. As mentioned, changes are associated with neurologic and psychiatric disorders in late life, and it has been hypothesized that these changes are related to the pathogenesis of some of these disorders. The purpose of this chapter is to discuss the alterations in the HPA axis which occur with normal aging and also to relate these changes within the context of disorders of aging. We will initially discuss the physiology of the HPA axis. This discussion will be followed by a discussion of animal and human studies which have examined the HPA axis in normal aging and disease states in late life.
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