[libribook.com] Traumatic Scar Tissue Management 1st Edition
Wound HealingThe NS plays an important role in mediating normal wound healing via theinvolvement of various neuropeptides and growth factors. Noxious stimulicauses nerves to release neuropeptides such as substance P and CGRP andcertain growth factors (e.g. NGF). And, along with healthy scar formation, inorder to re-establish normal functioning post-injury, innervation of the injuredtissue must also be re-established.Wounds initially display hyperinnervation, similar to hypervascularization seenin early wound healing. With normal wound healing, nerve density willnormalize with scar maturation. Although densities may return to normal,normal responsiveness is not always re-established, as nerve end organs cannotregenerate and therefore sensory deficit or aberrancies may occur. In spite of theclinical significance of abnormal innervation in scars, the NS has been largelyignored in the pathophysiology of scars.The role of the NS in wound healing, normal and abnormal, is covered in greaterdetail in Chapter 5.Impact of Trauma and Pathophysiological Scars onthe NSAs nerves traverse throughout the body they track between and pass throughvarious tissues and structures. The greater proportion of our larger nerves trackin the superficial fascia and smaller nerves in the clefts created betweenperimysial bundles.Irritation or compression at any point along the complex network of the NS canevoke changes not only locally but also in distant regions and can elicitautonomic disturbances.Excessive scarring in the layers of tissue a nerve is travelling through canimpede all manner of NS functioning (e.g. nerve and electromagneticconduction, local and systemic responsiveness, sensitization, intraneural bloodand nerve supply).Additionally, injured or distressed somatic tissues adjacent to nerve structures
release inflammatory substances that can chemically irritate neural elements.This suggests that a nerve does not have to be entrapped in scar tissue, it can alsobe impacted by scarring in neighboring tissue.Pressure and compression constitute the most common forms of nerve injury ascomplete severance is rare. While nerve injury grading classification systems,such as Seddon (1943) and Sunderland (1952), describe the severity of neuralinjury (neuropraxia, axonotmesis, neurotmesis) and consider negativesymptomology (e.g. numbness and weakness), they do not includeconsiderations for positive symptomology like neuropathic pain.
- Page 362 and 363: Pathophysiological ConsiderationA n
- Page 364 and 365: Clinical ConsiderationThere is an e
- Page 366 and 367: Clinical ConsiderationDiane Jacobs
- Page 368 and 369: Clinical ConsiderationIt appears th
- Page 370 and 371: Clinical ConsiderationAlthough musc
- Page 372 and 373: Clinical ConsiderationThe form of s
- Page 374 and 375: Example 2Ruffini stimulation result
- Page 376 and 377: Table 4.1Summary of receptor typolo
- Page 378 and 379: • Therapeutic outcome include enh
- Page 380 and 381: NS FunctionThe primary functions of
- Page 382 and 383: Clinical ConsiderationMechanorecept
- Page 384 and 385: Clinical ConsiderationIn addition t
- Page 386 and 387: Clinical ConsiderationManual techni
- Page 388 and 389: large enough, a voltage spike is pr
- Page 390 and 391: PathophysiologicalconsiderationUnde
- Page 392 and 393: Table 4.2Important pain terms. Vari
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- Page 396 and 397: disorders (diabetes mellitus), drug
- Page 398 and 399: forms of negative plasticity includ
- Page 400 and 401: Central and peripheral sensitizatio
- Page 402 and 403: Clinical ConsiderationFollowing per
- Page 404 and 405: ExampleHypersensitive nerves (assoc
- Page 406 and 407: Example 1Hypersensitized nerve fibe
- Page 408 and 409: Clinical ConsiderationIt is suggest
- Page 410 and 411: Clinical ConsiderationNeuropathic p
- Page 414 and 415: Clinical ConsiderationNeural and ci
- Page 416 and 417: Compression SyndromesAlthough perip
- Page 418 and 419: Pathophysiological ConsiderationIf
- Page 420 and 421: Pathophysiological ConsiderationUni
- Page 422 and 423: Clinical ConsiderationAs is the cas
- Page 424 and 425: Pathophysiological ConsiderationFas
- Page 426 and 427: Damasio AR, Grabowski TJ, Bechara A
- Page 428 and 429: Magee DJ (2008) Orthopedic physical
- Page 430 and 431: Stecco C, Porzionato A, Macchi V et
- Page 432 and 433: CHAPTER 5Wound healing and scarsNev
- Page 434 and 435: Wound HealingWound healing, a compl
- Page 436 and 437: Table 5.1Stages of wound healing
- Page 438: Clinical ConsiderationBecause thera
- Page 441 and 442: fibroblast growth factor (FGF), epi
- Page 443 and 444: Clinical ConsiderationDuring wound
- Page 445 and 446: Clinical ConsiderationAlthough the
- Page 447 and 448: Pathophysiological ScarsPathophysio
- Page 450 and 451: Figure 5.3Adapted from Huang et al.
- Page 452 and 453: Pathophysiological considerationFib
- Page 454 and 455: Table 5.2Important pathophysiologic
- Page 456 and 457: According to Klingler (2012):… pa
- Page 458 and 459: Table 5.3Scar types and related ter
- Page 460 and 461: unyielding or pliable and mobile. R
Wound Healing
The NS plays an important role in mediating normal wound healing via the
involvement of various neuropeptides and growth factors. Noxious stimuli
causes nerves to release neuropeptides such as substance P and CGRP and
certain growth factors (e.g. NGF). And, along with healthy scar formation, in
order to re-establish normal functioning post-injury, innervation of the injured
tissue must also be re-established.
Wounds initially display hyperinnervation, similar to hypervascularization seen
in early wound healing. With normal wound healing, nerve density will
normalize with scar maturation. Although densities may return to normal,
normal responsiveness is not always re-established, as nerve end organs cannot
regenerate and therefore sensory deficit or aberrancies may occur. In spite of the
clinical significance of abnormal innervation in scars, the NS has been largely
ignored in the pathophysiology of scars.
The role of the NS in wound healing, normal and abnormal, is covered in greater
detail in Chapter 5.
Impact of Trauma and Pathophysiological Scars on
the NS
As nerves traverse throughout the body they track between and pass through
various tissues and structures. The greater proportion of our larger nerves track
in the superficial fascia and smaller nerves in the clefts created between
perimysial bundles.
Irritation or compression at any point along the complex network of the NS can
evoke changes not only locally but also in distant regions and can elicit
autonomic disturbances.
Excessive scarring in the layers of tissue a nerve is travelling through can
impede all manner of NS functioning (e.g. nerve and electromagnetic
conduction, local and systemic responsiveness, sensitization, intraneural blood
and nerve supply).
Additionally, injured or distressed somatic tissues adjacent to nerve structures