[libribook.com] Traumatic Scar Tissue Management 1st Edition

Central and peripheral sensitization
Chronic pain is associated with significant functional, structural and chemical
changes in the brain – often termed sensitization, super or hypersensitization
(Siddall & Cousins 2004, Tracey & Bushnell 2009). The process of sensitization
involves noxious stimuli that results in prolonged pain or misinterpretation of
non-noxious stimuli (secondary hyperalgesia and allodynia). These changes
occur at the level of the brain cortex, peripheral nerves and/or receptors (Puretić
& Demarin 2012). Sensitization explains how pain can exist in the absence of
acute trauma or observable irritation of neuronal structures (Chaitow & DeLany
2008, Woolf 2011).
Neuropeptides, released from the nerve itself during the inflammatory response
following tissue injury (e.g. surgical and nonsurgical wounds), include substance
P and calcitonin gene-related peptide (CGRP). The influence of these
vasodilators eventually leads to edema and subsequent sensitizing effects on
nociceptors. The consequent decrease in the excitatory threshold to mechanical
stimuli allows the nerve to become increasingly sensitive to stimuli that
normally are classified as non-noxious (Mense 1993, 2003, 2009, Cady et al.
2011, Waters-Banker et al. 2014).
Prolonged activation of nociceptors and nociceptive input eventually can lead to
neuroplastic changes in the peripheral and CNS and the development of various
chronic pain syndromes (Krenz et al. 1999, Graven-Nielsen & Mense 2001,
Mense 2003, Waters-Banker et al. 2014).
The unrestricted production of neurotrophic growth factors after the sensitization
of afferent fibers eventually can lead to collateral sprouting of the afferents in the
periphery and fibers within the lamina of the spinal cord. Sprouting of afferents
amplifies their input to various pathways within the spinal cord. A potent
neurotrophic growth factor, nerve growth factor (NGF), is a known neuronal
sensitizing agent. NGF is released during injury and, when uncontrolled, can
lead to debilitating chronic pain syndromes (Carew et al. 1979, Krenz et al.
1999, Krenz & Weaver 1998, Mense 2009, Waters-Banker et al. 2014).
In the presence of pain and via the support of various neuropeptides – afferent
receptor sensitivity can change in such a way that normal physiological pressure