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

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PathophysiologicalconsiderationUnder normal circumstances an axonis not mechanically sensitive –otherwise every time we moved wewould collapse in pain. However,inflammation of a neurofascialenvelope can render the associatednociceptors mechanicallyhypersensitive (Bove 2008).HyperalgesiaNeuropathic painNeuropathyNociceptionNociceptive painRadicular or radiating pain/sensationHeightened pain sensation from a stimulus that normally provokes pain, aconsequence of hyperexcitation involving peripheral or centralsensitization or both• Primary hyperalgesia: occurs at the site of injury, associated withincreased sensitivity of peripheral receptors (e.g. local nocis activatedby substances released as a result of injured tissue)• Secondary hyperalgesia: occurs in tissue outside the site of injury,associated with central sensitization (e.g. changes in spinal cord glialand satellite cells and voltage spiking pattern changes)• Opioid-induced hyperalgesia: sensitization associated with long-termuse of exogenous opioids (e.g. heroine, oxycodone)Pain that arises as a consequence of injury or disease affecting thesomatosensory NS (Treede et al. 2008, Correa-Illanes et al. 2010).Neuropathic pain may occur as a manifestation of various conditions thatcause nerve damage, such as viral infections (postherpetic neuralgia),metabolic disorders (diabetes mellitus), drug-induced toxicity,inflammation, cancer, trauma, and postsurgical complications.Hyperalgesia to light touch that can occur with neuropathic pain iscomparable to secondary hyperalgesia and thought to be associated withcentral sensitization. Treede (2008) suggests that neuropathic pain beviewed as a clinical description not a diagnosis.Disturbance of function or pathological change in a nerveDetection of (noxious) stimuli that are capable of producing tissue injury.Consequences of encoding may be autonomic (e.g. elevation of bloodpressure) or behavioral (e.g. withdrawal reflex)Pain that arises from actual or threatened damage to non-neural tissueUsually perceived as lancinating, sharp, shooting pain or paresthesia feltin a dermatome, myotome or sclerotome because of direct involvement ofa spinal nerve or nerve root. It is distinguished from nociception as theaxons are stimulated along their course rather than at the terminal-endreceptors. Stimulation may occur as a result of mechanical deformation ofa dorsal root ganglion, mechanical stimulation of previously damagednerve roots, inflammation of a dorsal root ganglion and, possibly, byischemic damage to dorsal root ganglia (Howe et al. 1977, Murphy 1977,Howe 1979). Radicular pain differs from referred pain in several respects.While pain can also be perceived deeply, radicular pain displays acutaneous quality (perceived in the skin as well as deeply) whereasreferred pain lacks any cutaneous quality (IASP 2014)

Referred painSensitizationPain perceived at a location other than the site of the painfulstimulus/origin (e.g. referred pain associated with MTrPs). Referred painmay thus occur in a region that is either remote from or directlycontiguous with the source of pain, but the two locations aredistinguishable on the basis of their different nerve supply. Pain can bereferred into the corresponding myotome, dermatome or sclerotome fromany somatic or visceral tissue innervated by a nerve root, but, confusingly,sometimes it is not referred according to the commonly known pattern.Referred pain is a common occurrence in problems associated with themusculoskeletal system. Pain quality is usually described as deep andaching and although its central locus is recognizable and constant, itsmargins are hard to define (Kellgren 1938, 1939, Feinstein et al. 1954,Magee 2008, IASP 2014)Changes in the PNS or CNS (adaptive or pathologic) that lead toheightened nociceptive responses and/or lower thresholds, i.e. a lowerintensity stimuli results in increased responsiveness. Clinically,sensitization may only be inferred indirectly from presenting phenomenasuch as hyperalgesia or allodynia, and may include dysfunction ofendogenous pain control systems:• Central sensitization: increased responsiveness of nociceptive neurons inthe CNS• Peripheral sensitization: increased responsiveness of nociceptiveneurons in the periphery

Pathophysiological

consideration

Under normal circumstances an axon

is not mechanically sensitive –

otherwise every time we moved we

would collapse in pain. However,

inflammation of a neurofascial

envelope can render the associated

nociceptors mechanically

hypersensitive (Bove 2008).

Hyperalgesia

Neuropathic pain

Neuropathy

Nociception

Nociceptive pain

Radicular or radiating pain/sensation

Heightened pain sensation from a stimulus that normally provokes pain, a

consequence of hyperexcitation involving peripheral or central

sensitization or both

• Primary hyperalgesia: occurs at the site of injury, associated with

increased sensitivity of peripheral receptors (e.g. local nocis activated

by substances released as a result of injured tissue)

• Secondary hyperalgesia: occurs in tissue outside the site of injury,

associated with central sensitization (e.g. changes in spinal cord glial

and satellite cells and voltage spiking pattern changes)

• Opioid-induced hyperalgesia: sensitization associated with long-term

use of exogenous opioids (e.g. heroine, oxycodone)

Pain that arises as a consequence of injury or disease affecting the

somatosensory NS (Treede et al. 2008, Correa-Illanes et al. 2010).

Neuropathic pain may occur as a manifestation of various conditions that

cause nerve damage, such as viral infections (postherpetic neuralgia),

metabolic disorders (diabetes mellitus), drug-induced toxicity,

inflammation, cancer, trauma, and postsurgical complications.

Hyperalgesia to light touch that can occur with neuropathic pain is

comparable to secondary hyperalgesia and thought to be associated with

central sensitization. Treede (2008) suggests that neuropathic pain be

viewed as a clinical description not a diagnosis.

Disturbance of function or pathological change in a nerve

Detection of (noxious) stimuli that are capable of producing tissue injury.

Consequences of encoding may be autonomic (e.g. elevation of blood

pressure) or behavioral (e.g. withdrawal reflex)

Pain that arises from actual or threatened damage to non-neural tissue

Usually perceived as lancinating, sharp, shooting pain or paresthesia felt

in a dermatome, myotome or sclerotome because of direct involvement of

a spinal nerve or nerve root. It is distinguished from nociception as the

axons are stimulated along their course rather than at the terminal-end

receptors. Stimulation may occur as a result of mechanical deformation of

a dorsal root ganglion, mechanical stimulation of previously damaged

nerve roots, inflammation of a dorsal root ganglion and, possibly, by

ischemic damage to dorsal root ganglia (Howe et al. 1977, Murphy 1977,

Howe 1979). Radicular pain differs from referred pain in several respects.

While pain can also be perceived deeply, radicular pain displays a

cutaneous quality (perceived in the skin as well as deeply) whereas

referred pain lacks any cutaneous quality (IASP 2014)

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