King CD, Wong F, Currie T, Mauderli AP, Fillingim RB, Riley JL 3rd. Deficiency in endogenous modulation of prolonged heat pain in patients with Irritable Bowel Syndrome and Temporomandibular Disorder
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. Pain
(Impact Factor: 5.21).
04/2009; 143(3):172-8. DOI: 10.1016/j.pain.2008.12.027
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 degrees 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 degrees C (control); and during noxious cold immersion in a (DNIC; 8.0-16.0 degrees 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.
Available from: Sylvia M Gustin
- "In conjunction with alterations in the ascending pathways, evidence suggests that the descending pain modulatory pathway in TMD (and other musculoskeletal/inflammatory pain conditions) is also affected (Bragdon et al., 2002; Kashima et al., 1999; King et al., 2009, Linnman et al., 2012). Interestingly, the most significant area of MD difference in TMD subjects was located in the PAG, a region shown to display anatomical changes in other chronic pain conditions (DaSilva et al., 2007; Rocca et al., 2006; Seminowicz et al., 2010). "
[Show abstract] [Hide abstract]
ABSTRACT: Accumulated evidence from experimental animal models suggests that neuroplastic changes at the dorsal horn are critical for the maintenance of various chronic musculoskeletal pain conditions. However, to date, no study has specifically investigated whether neuroplastic changes also occur at this level in humans. Using brain imaging techniques, we sought to determine whether anatomical changes were present in the medullary dorsal horn (spinal trigeminal nucleus caudalis) in subjects with the chronic musculoskeletal pain. In twenty-two subjects with painful temporomandibular disorders (TMDs) and forty pain-free controls voxel based morphometry of T1-weighted anatomical images and diffusion tensor images were used to assess regional grey matter volume and microstructural changes within the brainstem and, in addition, the integrity of ascending pain pathways. Voxel based morphometry revealed significant regional grey matter volume decreases in the medullary dorsal horn, in conjunction with alterations in diffusivity properties, namely an increase in mean diffusivity, in TMD subjects. Volumetric and mean diffusivity changes also occurred in TMD subjects in regions of the descending pain modulation system, including the midbrain periaqueductal grey matter and nucleus raphe magnus. Finally, tractography revealed altered diffusivity properties, namely decreased fractional anisotropy, in the root entry zone of the trigeminal nerve, the spinal trigeminal tract and the ventral trigeminothalamic tracts of TMD subjects. These data reveal that chronic musculoskeletal pain in humans is associated with discrete alterations in the anatomy of the medullary dorsal horn, as well as its afferent and efferent projections. These neural changes may be critical for the maintenance of pathological pain.
Copyright © 2015. Published by Elsevier Inc.
- "Animal and human studies have shown pain modulation following manual therapy may involve similar pathways (Skyba et al., 2003), however, multiple pain modulatory mechanisms may be involved in CPM and manual therapy-induced analgesia, involving spinal and supra-spinal networks (Bialosky et al., 2009; Yarnitsky, 2010; Knudsen et al., 2011). Of clinical significance, CPM may be sub-optimal, compared to healthy controls (HCs), in people with knee osteoarthritis (Kosek and Ordeberg, 2000; Arendt-Nielsen et al., 2010), fibromyalgia (Kosek and Hansson, 1997), irritable bowel syndrome, temporomandibular disorder (King et al., 2009), migraine and tension-type headaches (Sandrini et al., 2006). No inhibitory CPM is evoked in 70% of people with chronic pain (Lewis et al., 2012). "
[Show abstract] [Hide abstract]
ABSTRACT: People with chronic pain may exhibit pro-nociceptive phenotypes characterised partly by reduced conditioned pain modulation (CPM). Characterising variability in CPM in people with chronic low back pain (CLBP) may inform management.
To investigate pro/anti-nociceptive effects of a CPM protocol in age/sex-matched healthy controls (HCs) and people with CLBP.
Case-controlled trial (64 participants/group).
The CPM protocol involved: test stimulus (TS) (noxious pressure applied by algometer to lumbar region); conditioning stimulus (CS) (noxious heat applied by thermode to dorsal hand). CPM recruitment was measured by the change in pain intensity (rated on a numeric rating scale (NRS)) of the TS in the presence and absence of the CS.
Responses to this CPM protocol were variable for both groups with measures consistent with either inhibitory or facilitatory effects. A significantly greater proportion of facilitatory responses were seen in the CLBP cohort compared to HCs (73% versus 31%). In response to the CS, participants with CLBP demonstrated a mean increase in NRS scores (mean 1.3 points; p < 0.001), while HCs did not (mean -0.2 points; p = 0.35) and the between-group difference in change scores was significant (mean 1.4 points; p < 0.001; effect size (Hedges' g): 1.03).
In HCs and participants with CLBP this CPM protocol elicited responses consistent with varying pro/anti-nociceptive effects. The higher proportion of participants with CLBP demonstrating a facilitatory response suggests a pro-nociceptive phenotype may characterise this cohort.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Available from: Stefan Lautenbacher
- "A consensus group decided to use a different terminology for such tests in humans, by calling them CPM and thus, separating them from DNIC, which had been defined in pure physiological terms (Yarnitsky et al. 2010). The growing interest in CPM has been inspired by observations that a deficiency of CPM might be a risk factor for the development of chronic pain (Edwards 2005; Julien et al. 2005; de Souza et al. 2009; King et al. 2009; Yarnitsky et al. 2010; Lewis et al. 2012). Enthusiasm is dampened, however, by the fact that there is still no agreement on the ''ideal CPM protocol'', which leads to various combinations of different noxious stressors (e.g., electrical current, cold pressor pain, pressure pain) as conditioning and test stimuli. "
[Show abstract] [Hide abstract]
Abstract Background: Chemo-somatosensory evoked potentials (CSSEPs) elicited by chemical stimulation (CO₂ gas) of the nasal mucosa have been shown to be sensitive enough to pick up even weak analgesic effects. With the present study we wanted to investigate whether CSSEPs are also a sensitive tool to capture endogenous pain inhibitory mechanisms elicited by conditioned pain modulation (CPM; where a first conditioning stimulus reduces the sensitivity for a second test stimulus) with a conditioning stimulus of rather low noxious load.
Seventeen healthy participants were tested for CPM effects (conditioning stimulus: tonic heat pain with intensities around the pain threshold induced via a thermode; test stimulus: chemonasal stimulation (73% and 78% CO₂)) on CSSEPs and on self-report ratings.
We found significant CPM effects in the CSSEPS, with reduced amplitudes and prolonged latencies at several electroencephalogram (EEG) recording positions when using the lower CO₂ concentration (73% CO₂). In contrast to the visible inhibitory effects on the CSSEPs, subjective ratings of the test stimulus did not reflect CPM action.
The experimental pain model using CO₂ stimuli to elicit CSSEPs proved to be sensitive enough to capture weak CPM effects elicited by a conditioning stimulus of rather low noxious load. The usage of such mild noxious conditioning stimuli-in contrast to stimuli of higher noxious load (e.g., cold pressor test)-has the advantage that the activation of other types of pain inhibitory mechanisms in parallel (like attentional distraction, stress-induced analgesia) can be avoided.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.