Chronic stress

The musculoskeletal system consists of the muscles, bones, joints, tendons, and ligaments. Disorders related to the musculoskeletal system often are classified by etiology. Acute soft-tissue injuries include strains and sprains of muscles and ligaments. Repeated movements in sports, exercise, work, or activities of daily living may lead to repetitive strain injury, where cumulative damage occurs to the muscles, ligaments, or tendons.1-3 While tendonitis and bursitis can arise from acute injury, more commonly these conditions occur as a result of chronic stress.3,4 Other forms of chronic musculoskeletal pain, such as pain from rheumatoid arthritis (see Chap. 54) or osteoarthritis (see Chap. 55), are discussed elsewhere in this text. 

This suggestion receives support from the observation that chronic stress or glucocorticoid administration has been demonstrated to produce atrophy and death of vulnerable hippocampal neurons in rodents and primates. Furthermore, MRI studies have revealed reduced hippocampal volumes in patients with Cushing s disease... 

Kiecolt-Glaser, J.K. et al., Chronic stress alters the immune response to influenza virus vaccine in older adults, Proc. Natl. Acad. Sci. U.S.A., 93, 3043, 1996. 

A glucocorticoid-resistance model has been proposed to provide an explanation for how stress might influence diseases in which excessive inflammation is observed (e.g., allergies, autoimmune diseases, rheumatoid arthritis, and cardiovascular disease). In these cases, chronic stress diminishes the immune system s sensitivity to glucocorticoids that normally terminate the inflammatory response. For example, in a study of a group of 50 parents caring for a child undergoing treatment for pediatric cancer, whole blood of parents of cancer patients exhibited a lesser dexamethasone-dependent suppression of IL-6 production in vitro compared to parents of medically healthy children.94... 

Dhabhar, F.S. and McEwen, B.S., Acute stress enhances while chronic stress suppresses cell-mediated immunity in vivo A potential role for leukocyte trafficking, Brain Behav. Immun., 11, 286, 1997. 

Glaser, R. et al., Evidence for a shift in the Th-1 to Th-2 cytokine response associated with chronic stress and aging, J. Gerontol. Series A, Biol. Sci. Med. Sci., 56, M477, 2001. 

Glaser, R. and Kiecolt-Glaser, L, Chronic stress modulates the virus-specific immune response to latent herpes simplex virus type 1, Ann. Behav. Med., 78, 1997. 

Vedhara, K. et al., Chronic stress in elderly carers of dementia patients and antibody response to influenza vaccination, Lancet, 353, 627, 1999. 

Glaser, R. et al., Chronic stress modulates the immune response to a pneumococcal pneumonia vaccine, Psychosomat. Med., 804, 2000. 

Prolonged or chronic stress in combination with unhealthy lifestyle, a common phenomenon in today s societies, is potentially involved in the development of several different diseases in the following interrelated systems of our organism ... 

Little is known about the molecular mechanisms and complexity converting psychosocial stress into cellular dysfunction in the brain, endocrine, and immune systems. How ordinary and sustained maladapted psychosocial stressors, chronic stress, and an unhealthy lifestyle activate and exert an influence on the biochemistry of the neuro-endocrine-immune axes with implications for future health or disease, is an upcoming innovative research field due to the new and emerging fields of proteomics, metabonomics, and biochip technologies. 

The response of the brain to both acute and chronic stress can be discussed in terms of its capacity to demonstrate its dynamic plasticity. The term plasticity describes almost any change in the brain, from the chemical level to the formation of new neurons and synapses. Prolonged or chronic stress has specific effects on the structure and function of the synapses in different brain regions. The neurons in different regions may show signs of atrophy, cell death, as a result of chronic psychosocial stress, as well as after... 

In relatively recent years, it has become clear that under-nntrition of mother leads to low birth weight of the baby and this can increase the risk of development of degenerative disease in later life, e.g. hypertension, obesity, type 2 diabetes. One hypothesis is that the foetus adapts meta-bolically to deficiencies by increasing the number of cells in organs that perform specific functions that can overcome the deficiency, e.g. an increase in the number of liver cells that carry out gluconeogenesis, an increase in cells in the adrenal cortex to produce more of the chronic stress hormone, cortisol. These changes are carried over into adnlthood which can lead to an inadequate response of the liver to insulin so that insulin resistance develops. So far, however, it is unclear whether deficiencies in specific nntrients or undemutrition per se are responsible for snch changes (Chapter 15). 

Conrad CD, Galea LAM, Kuroda Y, McEwen B (1996) Chronic stress impairs rat spatial memory on the y maze, and this effect is blocked by tianeptine pretreatment. Behav Neurosci 110 1321-1334... 

Nalepa I, Kreiner G, Kowalska M, Sanak M, Zelek-Molik A, Vetulani J (2002) Repeated imipramine electroconvulsive shock increase alpha(lA)-adrenoceptor mRNA level in rat prefrontal cortex. Eur J Clin Pharmacol 444 151-159 Nesse RM, Ciu-tis GC, Thyer BA, McCann DS, Huber-Smith MJ, Knopf RF (1985) Endocrine and cardiovascular responses during phobic anxiety. Psychosom Med 47 320-332 Nisenbaiun LK, Zigmund MJ, Sved AF, Abercrombie ED (1991) Prior exposure to chronic stress results in enhanced synthesis and release of hippocampal norepinephrine in response to a novel stressor. J Neurosci 11 1473-1484 Nutt DJ (1989) Altered alpha2-adrenoceptor sensitivity in panic disorder. Arch Gen Psychiatry 46 165-169... 

Vyas A, Mitra R, Shankaranarayana Rao BS, Chattarji S (2002) Chronic stress induces contrasting patterns of dendritic remodeling in hippocampal and amygdaloid neurons. J Neurosci 22 6810-6818... 

The first report on cortisol levels in PTSD was that of Mason et al. who found that the mean 24-h urinary excretion of cortisol was significantly lower in combat Vietnam veterans with PTSD compared to psychiatric patients in four other diagnostic groups (Mason et al. 1986). The authors noted surprise at the fact that cortisol levels were low, since certain clinical features such as depression and anxiety [in PTSD] might have been expected to be associated with increased activity of the pituitary-adrenal cortical system. Since this initial observation, the majority of the evidence supports the conclusion that cortisol alterations in PTSD are different from those observed in acute and chronic stress, and major depression, but more importantly, that the HPA axis appears to be regulated differently. 

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