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A temporal framework for understanding the effects of stressful life events on inflammation in patients with multiple sclerosis.
Brain Behav Immun 2006; 20(1):27-36BB

Abstract

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.

Authors+Show Affiliations

Department of Psychiatry and Neurology, University of California, San Francisco, CA 94131, USA. dmohr@itsa.ucsf.eduNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15894458

Citation

Mohr, David C., and Daniel Pelletier. "A Temporal Framework for Understanding the Effects of Stressful Life Events On Inflammation in Patients With Multiple Sclerosis." Brain, Behavior, and Immunity, vol. 20, no. 1, 2006, pp. 27-36.
Mohr DC, Pelletier D. A temporal framework for understanding the effects of stressful life events on inflammation in patients with multiple sclerosis. Brain Behav Immun. 2006;20(1):27-36.
Mohr, D. C., & Pelletier, D. (2006). A temporal framework for understanding the effects of stressful life events on inflammation in patients with multiple sclerosis. Brain, Behavior, and Immunity, 20(1), pp. 27-36.
Mohr DC, Pelletier D. A Temporal Framework for Understanding the Effects of Stressful Life Events On Inflammation in Patients With Multiple Sclerosis. Brain Behav Immun. 2006;20(1):27-36. PubMed PMID: 15894458.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A temporal framework for understanding the effects of stressful life events on inflammation in patients with multiple sclerosis. AU - Mohr,David C, AU - Pelletier,Daniel, PY - 2005/01/04/received PY - 2005/03/13/revised PY - 2005/03/27/accepted PY - 2005/5/17/pubmed PY - 2006/3/10/medline PY - 2005/5/17/entrez SP - 27 EP - 36 JF - Brain, behavior, and immunity JO - Brain Behav. Immun. VL - 20 IS - 1 N2 - 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. SN - 0889-1591 UR - https://www.unboundmedicine.com/medline/citation/15894458/A_temporal_framework_for_understanding_the_effects_of_stressful_life_events_on_inflammation_in_patients_with_multiple_sclerosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0889-1591(05)00062-0 DB - PRIME DP - Unbound Medicine ER -