Memory for pain.

A growing literature reports that stressful life events are associated with exacerbation and the subsequent development of brain lesions in patients with multiple sclerosis (MS). The evolution an MS exacerbation occurs over a period of many months and involves many different biological processes that change over time. Likewise, the experience of stress also occurs over time, with an onset, a shift from acute to chronic in some cases, and resolution. Each of these phases is associated with unique biological features. Thus, the impact of stress on MS exacerbation may depend on the temporal trajectories of stress and MS exacerbation, and when the intersection between these two trajectories occurs. This paper presents a temporal model, along with three different temporal relationships and associated mechanisms by which stress may impact MS exacerbation. These include the onset of a stressor, which may be mediated by mast cell activation, the point that a stressor begins to become chronic, which may be mediated by glucocorticoid resistance in immune cells, and the resolution of the stressor, which may be mediated by a drop in cortisol. These three hypotheses are not necessarily mutually exclusive. Data on psychosocial mediators and moderators are also briefly reviewed and future research directions are discussed.

Acute Disease↗

PubMed2006

Delayed response and lack of habituation in plasma interleukin-6 to acute mental stress in men.

Acute mental stress induces a significant increase in plasma interleukin (IL)-6 levels as a possible mechanism for how psychological stress might contribute to atherosclerosis. We investigated whether the IL-6 response would habituate in response to a repetitively applied mental stressor and whether cortisol reactivity would show a relationship with IL-6 reactivity. Study participants were 21 reasonably healthy men (mean age 46+/-7 years) who underwent the Trier Social Stress Test (combination of a 3-min preparation, 5-min speech, and 5-min mental arithmetic) three times with an interval of 1 week. Plasma IL-6 and free salivary cortisol were measured immediately before and after stress, and at 45 and 105 min of recovery from stress. Cortisol samples were also obtained 15 and 30 min after stress. Compared to non-stressed controls, IL-6 significantly increased between rest and 45 min post-stress (p=.022) and between rest and 105 min post-stress (p=.001). Peak cortisol (p=.034) and systolic blood pressure (p=.009) responses to stress both habituated between weeks one and three. No adaptation occurred in diastolic blood pressure, heart rate, and IL-6 responses to stress. The areas under the curve integrating the stress-induced changes in cortisol and IL-6 reactivity were negatively correlated at visit three (r=-.54, p=.011), but not at visit one. The IL-6 response to acute mental stress occurs delayed and shows no adaptation to repeated moderate mental stress. The hypothalamus-pituitary-adrenal axis may attenuate stress reactivity of IL-6. The lack of habituation in IL-6 responses to daily stress could subject at-risk individuals to higher atherosclerotic morbidity and mortality.

Acute Disease↗