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manuelletherapie 2009; 13(4): 167-172
DOI: 10.1055/s-0028-1109756
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© Georg Thieme Verlag KG Stuttgart · New York

Übersicht über Schmerzmechanismen: Implikationen für Diagnose und physiotherapeutische Behandlung „problematischer” Schmerzpatienten

Overview of Pain Mechanisms: Implications for the Diagnosis and Management of ”Problem” Pain Patients with Physical TherapyM. Zusman1
  • 1School of Physiotherapy, Curtin University of Technology, Perth, Australien
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Publication History

Manuskript eingetroffen: 2.2.2009

Manuskript akzeptiert: 8.05.2009

Publication Date:
22 September 2009 (online)

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Zusammenfassung

Das häufigste auftretende und zu behandelnde Problem in der klinischen Praxis von Physiotherapeuten ist Schmerz. Dies betrifft oft bestimmte Arten von besonders „schwierigen” Schmerzsyndromen ohne zugrundeliegende organische Ursachen sowie wiederkehrende anhaltende Schmerzstörungen.

Die vorliegende Arbeit liefert einen Überblick über periphere und zentralnervöse Mechanismen bei entzündlichen und neuropathischen Schmerzen.

Abstract

The most common problem physiotherapists encounter in clinical practice and are required to treat is pain. This often involves certain types of particularly ”difficult” pain syndromes without underlying organic causes as well as prolonged relapsing pain disorder.

This article gives an overview of peripheral and central nervous system mechanisms for inflammatory and neuropathic pain.

Schlüsselwörter

periphere Schmerzmechanismen - zentralnervöse Schmerzmechanismen - Diagnose - Behandlung - Physiotherapie

Key words

peripheral pain mechanisms - central nervous pain mechanisms - diagnosis - treatment - physiotherapy

Literatur

  • 1 Amir R, Argoff C, Bennett G. et al . The role of sodium channels in chronic inflammatory and neuropathic pain.  The Journal of Pain. 2006;  7 S1-S29
    Search in Google Scholar
  • 2 Barad M. Fear extinction in rodents: basic insight to clinical promise.  Current Opinion in Neurobiology. 2005;  15 710-715
    Search in Google Scholar
  • 3 Bennett G. Can we distinguish between inflammatory and neuropathic pain?.  Pain Research and Management. 2006;  11 11A-15A
    Search in Google Scholar
  • 4 Bouton M E. Context, ambiguity and unlearning: sources of relapse after behavioural extinction.  Biological Psychiatry. 2002;  52 976-986
    Search in Google Scholar
  • 5 Campbell J, Meyer R. Mechanisms of neuropathic pain.  Neuron. 2006;  52 77-92
    Search in Google Scholar
  • 6 Clauw D J, Crofford L J. Chronic widespread pain and fibromyalgia: what we know, and what we need to know.  Best Practice & Research Clinical Rheumatology. 2003;  17 685-701
    Search in Google Scholar
  • 7 Costigan M, Wollf C J. Pain: molecular mechanisms.  The Journal of Pain. 2000;  1 35-44
    Search in Google Scholar
  • 8 Devor M. Sodiun channels and mechanisms of neuropathic pain.  The Journal of Pain. 2006;  7 S3-S12
    Search in Google Scholar
  • 9 Dray A. Pharmacology of inflammatory pain. Merskey H, Loeser JD, Dubner R The Paths of Pain 1975 – 2005 Seattle; IASP 2005
    Search in Google Scholar
  • 10 Gold M S. Molecular basis of receptors. Merskey H, Loeser JD, Dubner R The Paths of Pain 1975 – 2005 Seattle; IASP 2005
    Search in Google Scholar
  • 11 Ji R R, Kohno T, Moore K A. et al . Central sensitisation and LTP: do pain and memory share similar mechanisms?.  Trends in Neurosciences. 2003;  26 696-706
    Search in Google Scholar
  • 12 Kawasaki Y, Kohno T, Zhang Z Y. et al . Ionotropic and metabotropic receptors, protein kinase A, protein kinase C, and src contribute to C-fiber-induced ERK activation and camp response element binding protein phosphorylation in dorsal horn neurons, leading to central sensitisation.  The Journal of Neuroscience. 2004;  24 8310-8321
    Search in Google Scholar
  • 13 Maren S. Synaptic mechanisms of associative memory in the amygdala.  Neuron. 2005;  47 783-786
    Search in Google Scholar
  • 14 Neugebauer V. Subcortical processing of nociceptive information: basal ganglia and amygdala. Cervero F, Jensen TS Handbook of Clinical Neurology Amsterdam; Elsevier 2006
    Search in Google Scholar
  • 15 Senapati A K, Huntington P J, Peng Y B. Spinal dorsal horn neuron response to mechanical stimuli is decreased by electrical stimulation of the primary motor cortex.  Brain Research. 2005;  1036 173-179
    Search in Google Scholar
  • 16 Treede R D, Klein T, Magerl W. Pain memory and central sensitisation in humans. Flor H, Kalso E, Dostrovsky JO Proceedings of the 11th World Congress on Pain Seattle; IASP 2006
    Search in Google Scholar
  • 17 Turk D. Understanding pain sufferers: the role of cognitive processes.  The Spine Journal. 2004;  4 1-7
    Search in Google Scholar
  • 18 Wall P D. Interview: Ready for action (McCrone J).  New Scientist. 1999;  5 48-51
    Search in Google Scholar
  • 19 Woolf C J. Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy.  Life Sciences. 2004;  74 2605-2610
    Search in Google Scholar
  • 20 Woolf C J. Pain: moving from symptom control toward mechanism-specific pharmacologic management.  Annals of Internal Medicine. 2004;  104 441-451
    Search in Google Scholar
  • 21 Zusman M. Associative memory for movement-evoked chronic back pain and its extinction with musculoskeletal physiotherapy.  Physical Therapy Reviews. 2008;  13 57-68
    Search in Google Scholar
  • 22 Zusman M. Mechanisms of peripheral neuropathic pain: implications for musculoskeletal physiotherapy.  Physical Therapy Reviews. 2008;  13 313-323
    Search in Google Scholar

Max Zusman,

DipPT (WAust) GradDipHlthSc (WAIT) MAppSc(Curtin), School of Physiotherapy, Curtin University of Technology

Perth WA 6845

Australia

Email: M.Zusman@curtin.edu.au