Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition. Pain

Département des Sciences de la Santé, Université du Québec en Abitibi-Témiscamingue, Rouyn-Noranda, Que., Canada.
Pain (Impact Factor: 5.21). 04/2005; 114(1-2):295-302. DOI: 10.1016/j.pain.2004.12.032
Source: PubMed

ABSTRACT A deficit of endogenous pain inhibitory systems has been suggested to contribute to some chronic pain conditions, one of them being fibromyalgia. The aim of the investigation was to test whether endogenous pain inhibitory systems were activated by a spatial summation procedure in 30 fibromyalgia, 30 chronic low back pain, and 30 healthy volunteers who participated in a cross-over trial (two sessions). Each session consisted of visual analog scale ratings of pain during the immersion of different surfaces of the arm in circulating noxious cold (12 degrees C) water. The arm was arbitrarily divided into eight segments from the fingertips to the shoulder. One session was ascending (from the fingertips to the shoulder) and the other was descending (from the shoulder to the fingertips); they included eight consecutive 2-min immersions separated by 5-min resting periods. For healthy and low back pain subjects, pain was perceived differently during the ascending and descending sessions (P=0.0001). The descending session resulted in lower pain intensity and unpleasantness. This lowering of the perception curve seems to be due to a full recruitment of inhibitory systems at the beginning of the descending session as opposed to a gradual recruitment during the ascending session. For fibromyalgia subjects, no significant differences were found between the increasing and decreasing sessions (P>0.05). These data support a deficit of endogenous pain inhibitory systems in fibromyalgia but not in chronic low back pain. The treatments proposed to fibromyalgia patients should aim at stimulating the activity of those endogenous systems.

Download full-text


Available from: Serge Marchand, Aug 11, 2015
1 Follower
38 Reads
  • Source
    • "However, the conditioned stimulus was a 12 °C water bath (Julien et al. 2005), as compared to 4 °C in the current study. Thus, differences could be related to the intensity of the conditioning stimulus, and in people with chronic low back pain, CPM may only be deficient at higher intensities (Julien et al. 2005). Alternatively, we examined PPT values during CPM over the painful area (lumbar), while prior studies measured PPT values outside area of pain (leg and upper trapezius) (Knudsen and Drummond 2009; Martel et al. 2013). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Quantitative sensory testing is widely used in human research to investigate the state of the peripheral and central nervous system contributions in pain processing. It is a valuable tool to help identify central sensitization and may be important in the treatment of low back pain. The aim of this study was to evaluate changes in local and segmental hypersensitivity and endogenous pain inhibition in people with chronic nonspecific low back pain. Thirty patients with chronic low back pain and thirty healthy subjects were studied. Pressure pain thresholds (PPTs) were measured from the lumbar region and over the tibialis anterior muscle (TA). A cold pressor test was used to assess the activation of conditioned pain modulation (CPM), and PPTs in the lumbar region were recorded 30 s after immersion of participant's foot in a bucket with cold water. People with chronic low back pain have significantly lower PPT than controls at both the lumbar region [89.5 kPa (mean difference) 95 % CI 40.9-131.1 kPa] and TA [59.45 kPa (mean difference) 95 % CI 13.49-105.42 kPa]. During CPM, people with chronic low back pain have significantly lower PPT than controls in lumbar region [118.6 kPa (mean difference) 95 % CI 77.9-159.2 kPa]. Women had significantly lower PPTs than men in both lumbar region [101.7 kPa (mean difference) 95 % CI 37.9-165.7 kPa] and over the TA [189.7 kPa (mean difference) 95 % CI 14.2-145.2 kPa]. There was no significant difference in PPTs in men between healthy controls and those with low back pain, suggesting the significant differences are mediated primarily by difference between women.
    Experimental Brain Research 05/2015; 233(8). DOI:10.1007/s00221-015-4309-6 · 2.04 Impact Factor
  • Source
    • "tterns that might predict treatment response in fi - bromyalgia to the selective 5 - HT and NE reuptake inhibitor MLN . Since preclinical studies have indicated that dual reuptake inhibitors are thought to have a favorable effect on endogenous pain inhibition which is believed to be dysfunctional in fibromyalgia ( Lautenbacher and Rollman , 1997 ; Julien et al . , 2005 ) , we specifically focused on rs - fc to brain regions involved in antinociception and pain modulation such as : the periaqueductal gray ( PAG ) , the rostral part of the ante - rior cingulate cortex ( ACC ) , the dorsolateral prefrontal cortex ( DLPFC ) and the amygdala ."
    [Show abstract] [Hide abstract]
    ABSTRACT: Fibromyalgia is a chronic pain syndrome characterized by widespread pain, fatigue, and memory and mood disturbances. Despite advances in our understanding of the underlying pathophysiology, treatment is often challenging. New research indicates that changes in functional connectivity between brain regions, as can be measured by magnetic resonance imaging (fcMRI) of the resting state, may underlie the pathogenesis of this and other chronic pain states. As such, this parameter may be able to be used to monitor changes in brain function associated with pharmacological treatment, and might also be able to predict treatment response. We performed a resting state fcMRI trial using a randomized, placebo-controlled, cross-over design to investigate mechanisms of action of milnacipran (MLN), a selective serotonin and norepinephrine reuptake inhibitor (SNRI), in fibromyalgia patients. Our aim was to identify functional connectivity patterns at baseline that would differentially predict treatment response to MLN as compared to placebo. Since preclinical studies of MLN suggest that this medication works by augmenting antinociceptive processes, we specifically investigated brain regions known to be involved in pain inhibition. 15 fibromyalgia patients completed the study, consisting of 6 weeks of drug and placebo intake (order counterbalanced) with an interspersed 2 week wash out period. As a main finding we report that reductions in clinical pain scores during MLN were associated with decreased functional connectivity between pro-nociceptive regions and antinociceptive pain regions at baseline, specifically between the rostral part of the anterior cingulate cortex (ACC) and the insular cortex (IC), as well as between the periaqueductal gray (PAG) and the IC: patients with lower preexisting functional connectivity had the greatest reduction in clinical pain. This pattern was not observed for the placebo period. However a more robust placebo response was associated with lower baseline functional connectivity between the ACC and the dorsolateral prefrontal cortex. This study indicates that ACC–IC connectivity might play a role in the mechanism of action of MLN, and perhaps more importantly fcMRI might be a useful tool to predict pharmacological treatment response.
    Clinical neuroimaging 12/2014; 6. DOI:10.1016/j.nicl.2014.09.007 · 2.53 Impact Factor
  • Source
    • "Fibromyalgia (FM) is a chronic pain syndrome characterized by widespread musculoskeletal pain, tenderness and a number of other cognitive, psychological and somatic symptoms (Wolfe et al., 1990). Although the origin of FM has not yet been determined, there is consistent evidence in favour of central nervous system involvement (Staud, 2004; Abeles et al., 2007; Dadabhoy et al., 2008), including both central sensitization and deficits in central inhibitory processes (Julien et al., 2005; Jensen et al., 2009, 2012; Petersel et al., 2011; Woolf, 2011). From this perspective, it has been proposed that a generalized sensory hypervigilance , understood as a central amplification of sensory inputs, including but not limited to painful ones, may be at the root of the disorder (Kosek et al., 1996; McDermid et al., 1996; Dohrenbusch et al., 1997). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background It has been suggested that fibromyalgia (FM) patients show increased sensory processing of nociceptive and non-nociceptive stimuli and also reduced habituation. Although this pattern of increased reactivity has been established for the somatosensory modality, its generalization to other sensory modalities remains controversial.Methods Auditory evoked potentials were obtained using a paired-stimuli paradigm from a sample of 52 FM female patients and 55 healthy women matched for age and socio-economic status. Sensory gating of the P50 component, as indicated by P50 suppression rates to the second identical stimuli, was analysed in relation to clinical indices of FM, including algometry of tender points and a number of self-reported questionnaires.ResultsSensory gating mechanisms in FM patients proved to be normal, robust and as efficient as those recorded in control subjects. There was no correlation between P50 suppression rates and indices of clinical or experimental (threshold or tolerance) pain. In addition, P50 sensory gating was not related to the other main symptoms of FM, including fatigue, sleep dysfunction or co-morbid depression, nor to hypersensitivity to noise or headache.Conclusions The results indicate that FM patients do not present significant deficits in early sensory gating when processing auditory stimuli, and therefore challenge the ‘generalized hypersensitivity’ hypothesis of FM.
    European journal of pain (London, England) 12/2014; 19(4). DOI:10.1002/ejp.627 · 2.93 Impact Factor
Show more