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.
"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). "
"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). "
"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. "
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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.
Somatosensory & Motor Research 02/2014; 31(2). DOI:10.3109/08990220.2014.887562 · 0.64 Impact Factor
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