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Psychoneuroendocrinology. 2007 Jul;32(6):604-18. Epub 2007 Jun 29.

Stress and hypothalamic-pituitary-adrenal axis function in experimental autoimmune encephalomyelitis and multiple sclerosis - a review.

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1
Institute of Neuroimmunology and Clinical MS Research (INiMS), University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. heesen@uke.uni-hamburg.de

Abstract

Multiple sclerosis (MS) is an inflammatory and degenerative disease of the CNS with an assumed autoimmune-mediated pathogenesis. Stressful life events have been hypothesized as potential triggers of disease exacerbation. Animal studies using experimental autoimmune encephalomyelitis (EAE), as a model for MS, suggest that decreased hypothalamic-pituitary-adrenal (HPA) function may play a role in the increased susceptibility and severity of the disease. Histopathological studies of the hypothalamus point to disturbances in corticotropin-releasing hormone (CRH) regulation as a result of MS lesions in this area. Functional endocrine tests (e.g., the combined Dexamethasone-CRH test) showed a disturbed negative feedback after steroid application in MS patients. Hyper- and hypoactivity of the HPA axis, have been described to be associated with more severe courses. This paper presents an overview of the evidence for a role of HPA dysfunction in EAE and MS based on stress-experimental studies.

PMID:
17602841
DOI:
10.1016/j.psyneuen.2007.05.002
[Indexed for MEDLINE]
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