Aarhus University Seal / Aarhus Universitets segl

Asbjørn Mohr Drewes

Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Standard

Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis. / Olesen, Søren Schou; Brock, Christina; Krarup, Anne Lund; Funch-Jensen, Peter; Arendt-Nielsen, Lars; Wilder-Smith, Oliver H; Drewes, Asbjørn Mohr.

I: Clinical Gastroenterology and Hepatology, Bind 8, Nr. 8, 2010, s. 724-30.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Olesen, SS, Brock, C, Krarup, AL, Funch-Jensen, P, Arendt-Nielsen, L, Wilder-Smith, OH & Drewes, AM 2010, 'Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis', Clinical Gastroenterology and Hepatology, bind 8, nr. 8, s. 724-30. https://doi.org/10.1016/j.cgh.2010.03.005

APA

Olesen, S. S., Brock, C., Krarup, A. L., Funch-Jensen, P., Arendt-Nielsen, L., Wilder-Smith, O. H., & Drewes, A. M. (2010). Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis. Clinical Gastroenterology and Hepatology, 8(8), 724-30. https://doi.org/10.1016/j.cgh.2010.03.005

CBE

Olesen SS, Brock C, Krarup AL, Funch-Jensen P, Arendt-Nielsen L, Wilder-Smith OH, Drewes AM. 2010. Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis. Clinical Gastroenterology and Hepatology. 8(8):724-30. https://doi.org/10.1016/j.cgh.2010.03.005

MLA

Olesen, Søren Schou o.a.. "Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis". Clinical Gastroenterology and Hepatology. 2010, 8(8). 724-30. https://doi.org/10.1016/j.cgh.2010.03.005

Vancouver

Olesen SS, Brock C, Krarup AL, Funch-Jensen P, Arendt-Nielsen L, Wilder-Smith OH o.a. Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis. Clinical Gastroenterology and Hepatology. 2010;8(8):724-30. https://doi.org/10.1016/j.cgh.2010.03.005

Author

Olesen, Søren Schou ; Brock, Christina ; Krarup, Anne Lund ; Funch-Jensen, Peter ; Arendt-Nielsen, Lars ; Wilder-Smith, Oliver H ; Drewes, Asbjørn Mohr. / Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis. I: Clinical Gastroenterology and Hepatology. 2010 ; Bind 8, Nr. 8. s. 724-30.

Bibtex

@article{25b006c0367911df9806000ea68e967b,
title = "Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis",
abstract = "BACKGROUND & AIMS:: Pain is a prominent symptom in chronic pancreatitis (CP), but the underling mechanisms are incompletely understood. We investigated the role of descending pain modulation from supraspinal structures as well as central nervous system sensitization in patients with pain from CP. METHODS:: Twenty-five patients with CP and 15 healthy volunteers were included. Descending pain modulation was investigated by diffuse noxious inhibitory control (DNIC; a descending inhibitory response following conditioning stimulation). Central pain processing was investigated as the perceptual responses to multimodal (electrical, thermal, and mechanical) stimulations of the rectosigmoid and evoked brain potentials following electrical stimulation of the rectosigmoid. RESULTS:: Compared with healthy volunteers, the efficacy of DNIC was reduced in patients with CP (13%+/-21% vs. 39%+/-22%, respectively; F=3.8, P=.01); central sensitization was indicated by remote hyperalgesia in the rectosigmoid to electrical (21+/-15mA vs. 27+/-15mA; F = 6.2, P = .02) and heat stimulation (51+/-5C vs. 53+/-4C; F = 5.9, P= .02). Compared with controls, patients with CP had increased latency of the early P1 peak to rectosigmoid stimulation (85+/-21 ms vs. 108+/-28 ms, respectively; P=.02), possibly reflecting reorganization of central pain pathways. CONCLUSIONS:: Patients with CP have impairments in inhibitory pain modulation and evidence of central sensitization. Treatment of their pain should therefore focus not only on the pancreas, but also on descending pain modulation from supraspinal structures and central nervous system sensitization.",
author = "Olesen, {S{\o}ren Schou} and Christina Brock and Krarup, {Anne Lund} and Peter Funch-Jensen and Lars Arendt-Nielsen and Wilder-Smith, {Oliver H} and Drewes, {Asbj{\o}rn Mohr}",
note = "Copyright {\textcopyright} 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.",
year = "2010",
doi = "10.1016/j.cgh.2010.03.005",
language = "English",
volume = "8",
pages = "724--30",
journal = "Clinical Gastroenterology and Hepatology",
issn = "1542-3565",
publisher = "W.B. Saunders Co.",
number = "8",

}

RIS

TY - JOUR

T1 - Descending Inhibitory Pain Modulation is Impaired in Patients with Chronic Pancreatitis

AU - Olesen, Søren Schou

AU - Brock, Christina

AU - Krarup, Anne Lund

AU - Funch-Jensen, Peter

AU - Arendt-Nielsen, Lars

AU - Wilder-Smith, Oliver H

AU - Drewes, Asbjørn Mohr

N1 - Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.

PY - 2010

Y1 - 2010

N2 - BACKGROUND & AIMS:: Pain is a prominent symptom in chronic pancreatitis (CP), but the underling mechanisms are incompletely understood. We investigated the role of descending pain modulation from supraspinal structures as well as central nervous system sensitization in patients with pain from CP. METHODS:: Twenty-five patients with CP and 15 healthy volunteers were included. Descending pain modulation was investigated by diffuse noxious inhibitory control (DNIC; a descending inhibitory response following conditioning stimulation). Central pain processing was investigated as the perceptual responses to multimodal (electrical, thermal, and mechanical) stimulations of the rectosigmoid and evoked brain potentials following electrical stimulation of the rectosigmoid. RESULTS:: Compared with healthy volunteers, the efficacy of DNIC was reduced in patients with CP (13%+/-21% vs. 39%+/-22%, respectively; F=3.8, P=.01); central sensitization was indicated by remote hyperalgesia in the rectosigmoid to electrical (21+/-15mA vs. 27+/-15mA; F = 6.2, P = .02) and heat stimulation (51+/-5C vs. 53+/-4C; F = 5.9, P= .02). Compared with controls, patients with CP had increased latency of the early P1 peak to rectosigmoid stimulation (85+/-21 ms vs. 108+/-28 ms, respectively; P=.02), possibly reflecting reorganization of central pain pathways. CONCLUSIONS:: Patients with CP have impairments in inhibitory pain modulation and evidence of central sensitization. Treatment of their pain should therefore focus not only on the pancreas, but also on descending pain modulation from supraspinal structures and central nervous system sensitization.

AB - BACKGROUND & AIMS:: Pain is a prominent symptom in chronic pancreatitis (CP), but the underling mechanisms are incompletely understood. We investigated the role of descending pain modulation from supraspinal structures as well as central nervous system sensitization in patients with pain from CP. METHODS:: Twenty-five patients with CP and 15 healthy volunteers were included. Descending pain modulation was investigated by diffuse noxious inhibitory control (DNIC; a descending inhibitory response following conditioning stimulation). Central pain processing was investigated as the perceptual responses to multimodal (electrical, thermal, and mechanical) stimulations of the rectosigmoid and evoked brain potentials following electrical stimulation of the rectosigmoid. RESULTS:: Compared with healthy volunteers, the efficacy of DNIC was reduced in patients with CP (13%+/-21% vs. 39%+/-22%, respectively; F=3.8, P=.01); central sensitization was indicated by remote hyperalgesia in the rectosigmoid to electrical (21+/-15mA vs. 27+/-15mA; F = 6.2, P = .02) and heat stimulation (51+/-5C vs. 53+/-4C; F = 5.9, P= .02). Compared with controls, patients with CP had increased latency of the early P1 peak to rectosigmoid stimulation (85+/-21 ms vs. 108+/-28 ms, respectively; P=.02), possibly reflecting reorganization of central pain pathways. CONCLUSIONS:: Patients with CP have impairments in inhibitory pain modulation and evidence of central sensitization. Treatment of their pain should therefore focus not only on the pancreas, but also on descending pain modulation from supraspinal structures and central nervous system sensitization.

U2 - 10.1016/j.cgh.2010.03.005

DO - 10.1016/j.cgh.2010.03.005

M3 - Journal article

C2 - 20304100

VL - 8

SP - 724

EP - 730

JO - Clinical Gastroenterology and Hepatology

JF - Clinical Gastroenterology and Hepatology

SN - 1542-3565

IS - 8

ER -