In 1984, Churchland1 contended that the Cartesian mind-body dualism is refuted by the observation that damage to specific parts of the physical brain produces observable changes in specific mental processes. There can now be no doubt about this fact among behavioral scientists. However, the converse proposition (ie, that mental processes can produce brain damage) is less clear. There is no question that psychological events can change the brain. Neural plasticity is now understood to be the structural basis of learning. Stressful experiences mediated by release of glucocorticoid stress hormones have been shown to produce atrophy of the hippocampus in animals.2 However, the atrophic effect is not ubiquitous because stress and glucocorticoids also lead to hypertrophy of another brain area, the amygdala.3 It could be spurious to refer to a brain that has atrophied in some areas but hypertrophied in other areas (presumably as an adaptive response) as damaged.
"However, they were careful to point out that the observed association between PTSD and the subsequent development of dementia does not necessarily imply a causal relationship, in that it could also be due to common risk factors underlying both PTSD and dementia . One such common risk factor could be lower intelligence . A limitation was that dementia was not separated into its different subtypes, leaving a possible association between PTSD and any specific pathophysiological mechanism(s) potentially leading to the development of dementia unclear. "
[Show abstract][Hide abstract] ABSTRACT: The physiological consequences of acute and chronic stress on a range of organ systems have been well documented after the pioneering work of Hans Selye more than 70 years ago. More recently, an association between exposure to stressful life events and the development of later-life cognitive dysfunction has been proposed. Several plausible neurohormonal pathways and genetic mechanisms exist to support such an association. However, many logistical and methodological barriers must be overcome before a defined causal linkage can be firmly established. Here the authors review recent studies of the long-term cognitive consequences of exposures to cumulative ordinary life stressors as well as extraordinary traumatic events leading to posttraumatic stress disorder. Suggestive effects have been demonstrated for the role of life stress in general, and posttraumatic stress disorder in particular, on a range of negative cognitive outcomes, including worse than normal changes with aging, Alzheimer's disease, and vascular dementia. However, given the magnitude of the issue, well-controlled studies are relatively few in number, and the effects they have revealed are modest in size. Moreover, the effects have typically only been demonstrated on a selective subset of measures and outcomes. Potentially confounding factors abound and complicate causal relationships despite efforts to contain them. More well-controlled, carefully executed longitudinal studies are needed to confirm the apparent association between stress and dementia, clarify causal relationships, develop reliable antemortem markers, and delineate distinct patterns of risk in subsets of individuals.
Alzheimer's and Dementia 06/2014; 10(3):S155–S165. DOI:10.1016/j.jalz.2014.04.008 · 12.41 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Decreased hippocampal volume is described in posttraumatic stress disorder (PTSD) and depression. However, it is not known whether it is a risk factor for the development of PTSD or a consequence of PTSD. We sought to determine the effects of PTSD and depressive symptoms on hippocampal volume.
Clinical and magnetic resonance imaging data were collected in a cross sectional study of 244 Gulf War veterans. Measures included lifetime and current Clinician Administered PTSD Scale, Hamilton Depression Scale, Life Stressor Checklist, and Lifetime Drinking History. Magnetic resonance imaging data were acquired with a 1.5-T scanner and analyzed with automated and semiautomated image processing techniques.
Eighty-two veterans had lifetime PTSD, 44 had current PTSD, and 38 had current depression. In the linear regression analysis, current PTSD symptoms (standardized coefficient β = -.25, p = .03) but neither lifetime PTSD symptoms nor current depression were associated with smaller hippocampal volume. Gender, age, history of early life trauma, education, lifetime and current alcohol use, current marijuana use, and treatment with antidepressants did not have independent effects. Participants with chronic PTSD had, on average, a smaller hippocampus compared with those with remitted PTSD.
The finding that current but not lifetime PTSD symptom severity explains hippocampal size raises two possibilities: either a small hippocampus is a risk factor for lack of recovery from PTSD (trait) or PTSD effects on hippocampal volume are reversible once PTSD symptoms remit and the patient recovers (state).
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