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Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)

BACKGROUND: Sensory abnormalities are a key feature of Complex Regional Pain Syndrome (CRPS). In order to characterise these changes in patients suffering from acute or chronic CRPS I, we used Quantitative Sensory Testing (QST) in comparison to an age and gender matched control group. METHODS: 61 pa...

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Autores principales: Huge, Volker, Lauchart, Meike, Förderreuther, Stefanie, Kaufhold, Wibke, Valet, Michael, Azad, Shahnaz Christina, Beyer, Antje, Magerl, Walter
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453233/
https://www.ncbi.nlm.nih.gov/pubmed/18648647
http://dx.doi.org/10.1371/journal.pone.0002742
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author Huge, Volker
Lauchart, Meike
Förderreuther, Stefanie
Kaufhold, Wibke
Valet, Michael
Azad, Shahnaz Christina
Beyer, Antje
Magerl, Walter
author_facet Huge, Volker
Lauchart, Meike
Förderreuther, Stefanie
Kaufhold, Wibke
Valet, Michael
Azad, Shahnaz Christina
Beyer, Antje
Magerl, Walter
author_sort Huge, Volker
collection PubMed
description BACKGROUND: Sensory abnormalities are a key feature of Complex Regional Pain Syndrome (CRPS). In order to characterise these changes in patients suffering from acute or chronic CRPS I, we used Quantitative Sensory Testing (QST) in comparison to an age and gender matched control group. METHODS: 61 patients presenting with CRPS I of the upper extremity and 56 healthy subjects were prospectively assessed using QST. The patients' warm and cold detection thresholds (WDT; CDT), the heat and cold pain thresholds (HPT; CPT) and the occurrence of paradoxical heat sensation (PHS) were observed. RESULTS: In acute CRPS I, patients showed warm and cold hyperalgesia, indicated by significant changes in HPT and CPT. WDT and CDT were significantly increased as well, indicating warm and cold hypoaesthesia. In chronic CRPS, thermal hyperalgesia declined, but CDT as well as WDT further deteriorated. Solely patients with acute CRPS displayed PHS. To a minor degree, all QST changes were also present on the contralateral limb. CONCLUSIONS: We propose three pathomechanisms of CRPS I, which follow a distinct time course: Thermal hyperalgesia, observed in acute CRPS, indicates an ongoing aseptic peripheral inflammation. Thermal hypoaesthesia, as detected in acute and chronic CRPS, signals a degeneration of A-delta and C-fibres, which further deteriorates in chronic CRPS. PHS in acute CRPS I indicates that both inflammation and degeneration are present, whilst in chronic CRPS I, the pathomechanism of degeneration dominates, signalled by the absence of PHS. The contralateral changes observed strongly suggest the involvement of the central nervous system.
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spelling pubmed-24532332008-07-23 Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I) Huge, Volker Lauchart, Meike Förderreuther, Stefanie Kaufhold, Wibke Valet, Michael Azad, Shahnaz Christina Beyer, Antje Magerl, Walter PLoS One Research Article BACKGROUND: Sensory abnormalities are a key feature of Complex Regional Pain Syndrome (CRPS). In order to characterise these changes in patients suffering from acute or chronic CRPS I, we used Quantitative Sensory Testing (QST) in comparison to an age and gender matched control group. METHODS: 61 patients presenting with CRPS I of the upper extremity and 56 healthy subjects were prospectively assessed using QST. The patients' warm and cold detection thresholds (WDT; CDT), the heat and cold pain thresholds (HPT; CPT) and the occurrence of paradoxical heat sensation (PHS) were observed. RESULTS: In acute CRPS I, patients showed warm and cold hyperalgesia, indicated by significant changes in HPT and CPT. WDT and CDT were significantly increased as well, indicating warm and cold hypoaesthesia. In chronic CRPS, thermal hyperalgesia declined, but CDT as well as WDT further deteriorated. Solely patients with acute CRPS displayed PHS. To a minor degree, all QST changes were also present on the contralateral limb. CONCLUSIONS: We propose three pathomechanisms of CRPS I, which follow a distinct time course: Thermal hyperalgesia, observed in acute CRPS, indicates an ongoing aseptic peripheral inflammation. Thermal hypoaesthesia, as detected in acute and chronic CRPS, signals a degeneration of A-delta and C-fibres, which further deteriorates in chronic CRPS. PHS in acute CRPS I indicates that both inflammation and degeneration are present, whilst in chronic CRPS I, the pathomechanism of degeneration dominates, signalled by the absence of PHS. The contralateral changes observed strongly suggest the involvement of the central nervous system. Public Library of Science 2008-07-23 /pmc/articles/PMC2453233/ /pubmed/18648647 http://dx.doi.org/10.1371/journal.pone.0002742 Text en Huge et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Huge, Volker
Lauchart, Meike
Förderreuther, Stefanie
Kaufhold, Wibke
Valet, Michael
Azad, Shahnaz Christina
Beyer, Antje
Magerl, Walter
Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)
title Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)
title_full Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)
title_fullStr Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)
title_full_unstemmed Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)
title_short Interaction of Hyperalgesia and Sensory Loss in Complex Regional Pain Syndrome Type I (CRPS I)
title_sort interaction of hyperalgesia and sensory loss in complex regional pain syndrome type i (crps i)
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453233/
https://www.ncbi.nlm.nih.gov/pubmed/18648647
http://dx.doi.org/10.1371/journal.pone.0002742
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