Thread: Stress & MS
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Old 09-03-2014, 08:21 AM
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Snoopy Snoopy is offline
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Join Date: Sep 2006
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Snoopy Snoopy is offline
Magnate
Snoopy's Avatar
 
Join Date: Sep 2006
Posts: 2,280
15 yr Member
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Hi Rick and welcome to NeuroTalk.

Stress, anxiety, panic attacks and MS is a topic that I tend to be a little outspoken on

I do not believe stress impacts MS in regards to exacerbations (relapse, flare-up, attack). An increase in MS symptoms can be seen with stress and anxiety but even those without MS will experience neurological symptoms due to stress. Stress and anxiety can cause body wide symptoms for anyone.

Information on this topic:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002616/
Quote:
Stress is considered as some kind of change in an individual's life, requiring readjustments that surpass the ability of coping and leading to psychological or biological harm. Charcot already assumed that grief or anger might have a role in the occurrence of neurological diseases like MS [Charcot, 1877].

An association between stress and MS relapses seems theoretically unexpected on physiological grounds since stress stimulates the HPA axis resulting in increased levels of circulating endogenous cortisol, which controls inflammation and thus should biologically abort eventual relapses.

Hypothetically, acute stress (like major stressful life events) could induce higher cortisol levels than chronic stress (family and work stress) and have a major impact in reducing the risk of MS relapses.

Thus, stress may either have an immune-suppressive or increasing effect depending on its intensity and duration [Martinelli, 2000], mediated by a glucocorticoid resistance with downregulation of receptors on immune cells secondary to chronic stress.

Recently, consensus statements about the importance of stress regulation in MS were published, claiming the association between stressful life-events and MS relapses inconclusive, the cytokine response to psychological and physical stressors weakened, the HPA reactivity varied by disease subgroup and stage, and an autonomous nerve dysfunction correlated with inflammatory activity and disease progression [Heesen et al. 2007].
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