Psychosomatic paradigms in psoriasis: Psoriasis, stress and mental health

Byline: T. Sathyanarayana Rao, K. Basavaraj, Keya. Das The human race is exposed to vagaries of life in terms of various hazards; or as the Greek would have it, "we are all but a heartbeat away from disaster. " Major cause for psychopathology has been attributed to stress. A catalyst or precipitator of psychiatric illness and a stimulant to substantial mental agony. The term "stress" was coined by Hans Selye (1907-1982) who laid the concept of the adrenocortical system being the vital responder to stress. [sup][1] The more rudimentary term psychosomatic disease mirrors those illnesses whose evolutions are channeled by psychological (thoughts, emotions and behavior) issues; in contrast somatopsychic diseases echoes those where the biologic aspect of the disease affects the psyche. [sup][2] Psychocutaneous medicine impacts on the interaction between the mind, the brain and the skin. The brain and the skin originate from same germ layer i.e., the embryonic ectoderm and are under the influence of the same hormones and neurotransmitters. Psychiatric expertise focuses on the "internal indiscernible disease" conversely dermatological expertise focuses on "external discernible disease. " Factors of a psychopathological nature tend to play an etiological role in the development of skin disorders, can exacerbate pre-existing skin disorder as well as patients suffering from dermatological disorders may bear the brunt of disfigurement. [sup][3] Psoriasis being a key disease in the cluster of psychocutaneous disorders, it has become a focus for exploration. Due to the intimate interplay between psychosocial factors and psoriasis, this disease confirms the said definitions. [sup][2] Psoriasis is a common, chronic, recurrent inflammatory disease of the skin, characterized by circumscribed, erythematous, dry, scaly plaques of varying sizes. [sup][2] The incidence of disease is 1-2% of the general population. [sup][4],[5] Stress acts as a catalyst for the onset as well as exacerbation of psoriasis. [sup][6],[7],[8] The neurogenic inflammation hypothesis of psoriasis put forth by Farber et al . states that neuropeptides like substance P (SP) and nerve growth factor (NGF) act as a crux in its pathogenesis. Unmyelinated terminals of sensory fibers in skin release SP and other NP's thereby resulting in generation of local neurogenic inflammation in those who are genetically primed. [sup][1] SP is synthesized in the dorsal root ganglion of nociceptor C fibers and transmitted peripherally in granules. Colocalization with other NP's including calcitonin gene related peptide and vasoactive intestinal peptide (VIP) in cutaneous sensory nerve endings are found via histochemical staining methods. [sup][9] Stressful life events are associated with higher levels of SP in the central and the peripheral nervous system of animal models. [sup][1] SP expressing neurons are in close and functional proximity of mast cells, which when activated release VIP. [sup][10] Autonomic pathways of the descending type via dorsal root ganglia in the spinal cord through SP containing neurons stimulate release of NP's, the neurons extend onto having connections to opioid interneurons in the dorsal horn. Increased release of adrenocorticotropic hormone, glucocorticoids and adrenalin during stress may be attributed to the stimulation of hypothalamic-pituitary-adrenal axis. Significantly increased expression of NGF in keratinocytes regulates skin innervations and up regulates NP's, this has found to be an early event in the pathogenesis of Psoriasis. NGF causes the proliferation of T lymphocytes and brings about mass cell degranulation resulting in production of a chemokine resulting in production of a chemokine RANTES,which is chemotactic for resting Cd4+ memory t cells and memory t cells. [sup][1] The severity of psoriasis is found to be ever fluctuating. Individuals are likely to cycle between differing levels of severity throughout their life time. …