Psychophysiological disorders are true dermatologic diseases that are exacerbated by emotional stressors. It is not to say that because someone is stressed emotionally or physically that they will develop a disease, but that a stressor that disrupts the homeostatic balance of the patient can exacerbate a chronic condition.
Atopic dermatitis, acne, rosacea, herpes simplex, psoriasis and hyperhidrosis are all examples of conditions that patients report worsen when they are under stress. When a patient presents with a flare, it is not uncommon that, when prompted, the patient will report some stressor in their everyday life.
The hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system are among the two major neural pathways that are activated by stressors. There is a multitude of chemical signals released in response to stress. For this article, I am going to give a basic version of these complex pathways to illustrate the take home point that the mind impacts the body.
The hypothalamus is triggered by neurosensory signals to release corticotropin-releasing hormone (CRH) and vasopressin. CRH then goes on to activate the HPA axis, which leads to the release of adrenocorticotropin hormone (ACTH), which then induces the adrenal cortex to secrete glucocorticoids along with catecholamines.
CRH also releases norepinephrine and epinephrine from the adrenal medulla. All of these mediators have dramatic effects on the immune system.1 New literature and novel treatments with off-label use of naltrexone, address the role of psychological stress and increased CNS levels of opioid neuropeptides, which not only cause pruritus but aggravate certain dermatological conditions with both psychosomatic and immunological components, such as psoriasis, chronic idiopatic urticaria and atopic dermatitis.2 (See Figure 1.)
Another piece to this complex puzzle is the role of neuropeptides, such as calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP) and substance P. These mediators are released from nerve terminals present in the cutaneous sensory nerves. The complex interplay between these mediators on the immune system, specifically the activation of mast cells and T- lymphocytes, exacerbate many inflammatory skin conditions.2
1. Harth, W., Gieler, U., Kusnir, D., Tausk, F.A.(2009). Clinical Management in Psychodermatology. New York City: Springer.
2. Koo, J., Lee, C.S. (Eds.) (2003). Psychocutaneous Medicine. New York: Marcel Dekker, Inc.