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Volume 143, Issue 3, Pages 172-178 (June 2009)


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Deficiency in endogenous modulation of prolonged heat pain in patients with Irritable Bowel Syndrome and Temporomandibular Disorder

Christopher D. KingacCorresponding Author Informationemail addressemail address, Fong Wongb, Tom Currieb, Andre P. Mauderlibc, Roger B. Fillingimac, Joseph L. Riley 3rdac

Received 5 August 2008; received in revised form 28 October 2008; accepted 1 December 2008. published online 12 March 2009.

Refers to article:
Diffuse Noxious Inhibitory Control (DNIC) as a tool for exploring dysfunction of endogenous pain modulatory systems , 01 April 2009
Luis Villanueva
PAIN®
June 2009 (Vol. 143, Issue 3, Pages 161-162)
Full Text | Full-Text PDF (77 KB)

Abstract 

Females with Irritable Bowel Syndrome (IBS) and Temporomandibular Disorder (TMD) are characterized by enhanced sensitivity to experimental pain. One possible explanation for this observation is deficiencies in pain modulation systems such as Diffuse Noxious Inhibitory Control (DNIC). In a few studies that used brief stimuli, chronic pain patients demonstrate reduced DNIC. The purpose of this study was to compare sensitivity to prolonged heat pain and the efficacy of DNIC in controls to IBS and TMD patients. Heat pain (experimental stimulus; 44.0–49.0°C), which was applied to left palm, was continuously rated during three 30-s trials across three separate testing sessions under the following conditions: without a conditioning stimulus; during concurrent immersion of the right foot in a 23.0°C (control); and during noxious cold immersion in a (DNIC; 8.0–16.0°C) water bath. Compared to controls, IBS and TMD patients reported an increased sensitivity to heat pain and failed to demonstrate pain inhibition due to DNIC. Controls showed a significant reduction in pain during the DNIC session. These findings support the idea that chronic pain patients are not only more pain sensitive but also demonstrate reduced pain inhibition by pain, possibly because of dysfunction of endogenous pain inhibition systems.

a Department of Community Dentistry & Behavioral Science, University of Florida College of Dentistry, 1329 SW 16th Street, Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA

b Department of Prosthodontics, University of Florida College of Dentistry, 1329 SW 16th St., Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA

c Comprehensive Center for Pain Research, University of Florida College of Dentistry, 1329 SW 16th St., Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA

Corresponding Author InformationCorresponding author. Address: Department of Community Dentistry & Behavioral Science, University of Florida College of Dentistry, 1329 SW 16th St., Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA. Tel.: +1 352 273 5971; fax: +1 352 273 5985.

PII: S0304-3959(08)00765-3

doi:10.1016/j.pain.2008.12.027


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