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

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large enough, a voltage spike is produced and the signal is ultimately transmittedto the brain. When certain neurons fire too easily or too often hyperexcitablilitycan arise (Ratté et al. 2014).Injury-induced hyperexcitability is not limited to nociceptors. Hyperexcitabilityalso develops in myelinated afferents that normally convey innocuousinformation (e.g. normal movement and touch) and under neuropathicconditions, mechanical allodynia can occur (Campbell et al. 1988, Koltzenburget al. 1994, Devor 2009, King et al. 2011, Ratté et al. 2014).Hyperexcitability can make something perceived as painful feel even worse(hyperalgesia), or it can make things hurt that should not (allodynia). Accordingto Ratté et al. (2014), increasing the flow of ions through the cell membrane caneventually result in a ‘tipping point’ to be crossed, which triggers a change in thevoltage spiking pattern (i.e. lowering of threshold and increase in firing rate –see Fig. 4.11). However, as several different types of ion channels contribute tothe current, there are several different ways in which the tipping point can becrossed. This ability to produce the same result by multiple means is a commonfeature of complex systems. It makes systems more robust, as a given result canstill be achieved if one particular attempt to achieve this result fails. The work ofRatté and colleagues helps to explain why drugs that target just one type of ionchannel may fail to relieve neuropathic pain as maladaptive changes in any oneof several other ion channels may circumvent the therapeutic effect (Ratté et al.2014).Neuropathic pain is notoriously difficult to treat as it does not respond well tocommon painkillers. Ratté and colleagues suggest that a paradigm shift will beneeded to effectively treat neuropathic pain - recommending that treatmentsaimed at restoring normal regulation of excitability, rather than targeting ionchannels themselves, may present the best course of action (Ratté et al. 2014).TermAllodyniaFasciagenicPainDefinition, mechanism, characteristics and other important informationPain due to a stimulus that does not normally provoke pain – an unexpected pain response associatedwith different types of somatosensory stimuli applied to different tissues. A consequence of neuralhyperexcitationBecause fascia has been largely overlooked as a potential pain generator and because scarringimpacts fascia, specific consideration is given here. Fascia contains type C nociceptors and some ofthe free nerve endings in fascia are substance P-containing receptors, commonly assumed to benociceptive and rendering fascia a potential pain generator (Tesarz 2009). And, as previously noted,neurofascial coverings are innervated by nervi nervorum

Pathophysiological considerationElevated concentrations of biochemical substances associated with pain, inflammation and intercellular signaling arefound at active MTrP locations (e.g. inflammatory mediators, neuropeptides, catecholamines, pro-inflammatorycytokines, pain modulators). Increased levels of pain modulators, such as Substance P and bradykinins, are plausibleexplanations for the occurrence of pain associated with active MTrPs (Shah et al. 2005).

Pathophysiological consideration

Elevated concentrations of biochemical substances associated with pain, inflammation and intercellular signaling are

found at active MTrP locations (e.g. inflammatory mediators, neuropeptides, catecholamines, pro-inflammatory

cytokines, pain modulators). Increased levels of pain modulators, such as Substance P and bradykinins, are plausible

explanations for the occurrence of pain associated with active MTrPs (Shah et al. 2005).

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