Impairment of pain inhibition in chronic tension-type headache. Pain

Department of Physiological Psychology, University of Bamberg, Markusplatz 3, 96045 Bamberg, Germany.
Pain (Impact Factor: 5.21). 12/2005; 118(1-2):215-23. DOI: 10.1016/j.pain.2005.08.019
Source: PubMed


Evidence has been accumulated suggesting that a dysfunction in pain inhibitory systems, i.e. in 'diffuse noxious inhibitory controls' (DNIC)-like mechanisms, might be-amongst other factors-responsible for the development of anatomically generalized chronic pain like fibromyalgia. The aim of the present study was to look for similar impairments in chronic tension-type headache (CTTH) as a regionally specific pain syndrome. Twenty-nine CTTH patients and 25 age- and sex-matched healthy control subjects participated in the study. After baseline assessment of electrical detection and pain thresholds, tonic heat stimuli were concurrently applied by a thermode to the thigh to induce DNIC-like pain inhibition. Tonic heat stimuli were applied either slightly above ('pain' condition) or slightly below ('heat' condition) pain threshold. For determination of electrical detection and pain thresholds, electrocutaneous stimuli were administered either to the forearm (extra-cranial site) or to the temple (cranial site), using a multiple staircase procedure. The increase in the electrical detection and pain thresholds induced by concurrent tonic heat stimulation was significantly smaller in the CTTH patients than in the control subjects. This group difference was present during the 'pain' as well as the 'heat' condition. Furthermore, the electrical detection and pain thresholds were affected in this group-specific manner both at the forearm and at the temple. These findings suggest that patients with CTTH suffer from deficient DNIC-like pain inhibitory mechanisms in a similar manner, as do patients with anatomically generalized chronic pain like fibromyalgia.

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Available from: Stefan Lautenbacher, Dec 15, 2013
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    • "More controversial is the hypothesis that such individual difference characteristics confer risk of, or protection against, chronic pain. Cross-sectional studies indicate that people with chronic pain conditions differ from painfree controls in their responses to traditional psychophysical pain sensitivity tests with chronic pain patients showing greater pain sensitivity (Clauw et al. 1999; Giesecke et al. 2004; King et al. 2009) and less CPM (Lautenbacher and Rollman 1997; Banic et al. 2004; Herren-Gerber et al. 2004; Pielsticker et al. 2005; King et al. 2009; John 2011; Dailey et al. 2013). "
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    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.
    Full-text · Article · May 2015 · Experimental Brain Research
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    • "In humans, the conditioning stimulus modulating the response to the test stimulus can be painful or non-painful and CPM can inhibit or facilitate this response [11]. CPM can be associated with changes in neuronal activity at multiple sites from spinal cord dorsal horn, medullary nucleus reticularis dorsalis, periaqueductal gray matter [12] [13] [14] to prefrontal cortex [15] [16] Understanding the mechanisms involved in CPM is important because it is impaired in several hyperalgesic conditions (see for a review [17]: tension-type headache [18], migraine [19] [20], fibromyalgia [21] [22], irritable bowel syndrome [23], osteoarthritis [24] and chronic post-surgical pain [25]. Functional neuroimaging studies have shown that activations of primary somatosensory (SI), prefrontal (PFC) or anterior cingulate cortices (ACC) are associated with conditioned pain modulation [15] [16] [26]. "
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    ABSTRACT: The mechanisms underlying conditioned pain modulation (CPM) are multifaceted. We searched for a link between individual differences in prefrontal cortex activity during multi-trial heterotopic noxious cold conditioning and modulation of the cerebral response to phasic heat pain. In 24 healthy female subjects we conditioned laser heat stimuli to the left hand by applying alternatively ice-cold or lukewarm compresses to the right foot. We compared pain ratings with cerebral fMRI BOLD responses. We also analyzed the relation between CPM and BOLD changes produced by the heterotopic cold conditioning itself, as well as the impact of anxiety and habituation of cold-pain ratings. Specific cerebral activation was identified in precuneus and left posterior insula/SII respectively during early and sustained phases of cold application. During cold conditioning laser pain decreased (n=7), increased (n=10) or stayed unchanged (n=7). At the individual level, the psychophysical effect was directly proportional to the cold-induced modulation of the laser-induced BOLD response in left posterior insula/SII. The latter correlated with the BOLD response recorded 80sec earlier during the initial 10-sec phase of cold application in anterior cingulate, orbitofrontal and lateral prefrontal cortices. High anxiety and habituation of cold pain were associated with greater laser heat-induced pain during heterotopic cold stimulation. The habituation was also linked to the early cold-induced orbitofrontal responses. We conclude that individual differences in conditioned pain modulation are related to different levels of prefrontal cortical activation by the early part of the conditioning stimulus, possibly due to different levels in trait anxiety. Copyright © 2014. Published by Elsevier B.V.
    Full-text · Article · Nov 2014 · Behavioural Brain Research
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    • "We could demonstrate a dose-dependent CPM effect of the conditioning stimuli ('painful stimulation' > 'not painful stimulation' > 'no stimulation') on the electrical pain thresholds, which is in line with the results of Fujii et al. (2006) or Lautenbacher et al. (2008). However, other studies could not confirm this observation (Lautenbacher and Rollman, 1997; Pielsticker et al., 2005; Kunz et al., 2006). Thus, there are contradictory findings regarding the relationship between the strength of the conditioning stimulus and the extent of the CPM effects (for review, see Pud et al., 2009). "
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    ABSTRACT: Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.
    Full-text · Article · Aug 2014 · European journal of pain (London, England)
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