Restructuring a New Cognitive Frame Work of the Neuropathogenesis of Atopic Dermatitis and Its Implications
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 6, Issue 1
Abstract
Chronic Atopic Dermatitis (AD) is inadequately managed in the primary health care and hospital settings [1,2]. Steroid phobia, emergence of methicillin resistant Staphylococcus aureus (MRSA), poor compliance to emollients therapy, inaccessibility to costly biologics and lack of effective preventive measures are all real problems to service providers taking care of children and adults suffering from this chronic distressing illness. Behavior disturbances, fear, anxiety, social isolation, stress and depression are negative emotional factors well reported associated with intractable pruritus of chronic AD [3]. The current treatments protocol focusing on the skin with its epidermal barrier and immunological aberrancy and hypersensitivity may not be sufficient to face up the present challenges. An escalating prevalence of chronic AD had been reported in most populated cities.In view of the aforesaid, the advent of non-invasive functional-MRI and related neuro-cognitive investigations, a new cognitive-mind-movement behaviour and skin inflammation neuro pathogenetic framework is suggested. This top down; cognitive - mind patient centered approach placed the objective of management of individual chronic AD sufferers to a more non-pharmacological, multi-disciplinary team approach procuring modern technologies with an aim to reconstruct the mind and cognition of patients, parents and the health care providers. Patients, parents, nurses, practitioners and the whole health care team are integrally educated on itch – scratch and itch – anxiety – scratch cognitive phenomenon of chronic AD. This new focus is very much different from the current disease - based approach practicing by front line practitioners, pediatricians and dermatologists treating solely the skin inflammation by immune-modulators, antibiotics and systemic antihistamines. The top down holistic approach is evidence based as researchers now have good evidences that a pruritogenic circuitry existed that linked up the central nervous system (CNS) to our outermost layer, the skin. Existence of A Pruritogenic Specific Neuron Signalling Pathway Pruritogenic Signal Transmission in The Skin Starting from the epidermis: keratinocytes; morphologically and functionally; is the outermost sensors of the peripheral nervous system (PNS) [4,5]. Epidermal keratinocytes possessed the widely distributed transient receptor potential (TRP); TRPV 1 receptors readily receiving environmental noxious stimuli including, heat, chemicals, pain and itch [5]. Depolarization signals through calcium (Ca++) cation influx. Free nerve endings belong to the small neuro C fibers are posited between individual keratinocytes, sending neuronal signals through its afferent neurons joined by its counterparts of neuronal receptors of the PNS in the skin dermis. Nerve free endings of the afferent neurons possess TRPV 1 receptors which are activated to secret Substance P(SP), nitric oxide (NO) locally and in the dorsal root ganglion (DRG) neurons. SP is known to be a potent pruritogenic neurotransmitter which triggers the glutamate pathway and by calcium influx through the NMDA; calcium channel propagated the sensation of pruritus. Calcitonin Gene Related Peptide (CGRP) and tachykinin are also produced.
Authors and Affiliations
Chan Kam Tim Michael
Keywords
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- EP ID EP592293
- DOI 10.26717/BJSTR.2018.06.001300
- Views 176
- Downloads 0
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