European journal of pain : EJP
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The middle cingulate cortex (MCC) has been implicated in pain processing by studies of cingulotomy for chronic pain and imaging studies documenting increased MCC blood flow in response to acute pain. The only previous report of quantitative sensory testing following cingulotomy described increased intensity and unpleasantness ratings of painful hot and cold stimuli in a single patient with psychiatric disease. We now report a case in which perception of pain and temperature was assessed before and after cingulotomy for obsessive-compulsive disorder (OCD). ⋯ Postoperative pain-evoked activation was demonstrated in the right (ipsilateral) parasylvian cortex but not of the MCC/SMA. Prior studies of forebrain lesions, and of cortical synchrony during the application of painful stimuli suggest the presence of functional connectivity between components of the MCC/SMA and the fronto-parietal opercula. Therefore present results suggest that cingulate lesions disinhibit ipsilateral parasylvian cortex and so are independent evidence of functional connectivity between these cortical areas, the defining characteristic of modules in a pain network.
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Temporal summation of "second pain" (TSSP) is the result of C-fiber-evoked responses of dorsal-horn neurons, termed "windup". This phenomenon is dependent on stimulus frequency (0.33 Hz) and relevant for central sensitization as well as chronic pain. Whereas, our previous functional magnetic resonance imaging (fMRI) study characterized neural correlates of TSSP in 11 healthy volunteers, the present study was designed to compare brain responses associated with TSSP across these healthy participants and 13 fibromyalgia (FM) patients. ⋯ Subsequently, the fMRI-data of both groups were combined to increase the power of our statistical comparisons. fMRI-statistical maps identified several brain regions with stimulus and frequency dependent activation consistent with TSSP, including ipsilateral and contralateral thalamus, medial thalamus, S1, bilateral S2, mid- and posterior insula, rostral and mid-anterior cingulate cortex. However, the stimulus temperatures necessary to evoke equivalent levels of TSSP and corresponding brain activity were less in FM patients. These results suggest that enhanced neural mechanisms of TSSP in FM are reflected at all pain related brain areas, including posterior thalamus, and are not the result of selective enhancement at cortical levels.
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In adults, evidence is accumulating that migraine is associated with altered central processing of pain stimuli and, possibly, changes in the allocation of attentional resources to such stimuli. In pediatric migraine, however, little is known about altered pain processing. We examined 15 children with migraine and 15 controls (age 10-15) in an oddball standards task. ⋯ Habituation across trials was similar in both groups. Hence, children with migraine may display an automatic attentional bias towards painful and potentially painful somatosensory stimuli. Consistent with the psychobiological perspective of chronic pain, such an attentional bias could constitute an important mechanism for migraine becoming a chronic problem.
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Interruption of a continuous noxious heat by a relatively greater noxious heat evokes reductions in pain experience when the original noxious heat returns. The reduction is greater than that evoked by continuous delivery of noxious heat. This disproportionate reduction in pain experience, known as offset analgesia, is presumably mediated by a mechanism different to adaptation or habituation. ⋯ There was no attenuation effect for the unchanging stimuli delivered across the 3 days of testing but attenuation effects enhanced the offset analgesia resulting in a larger offset analgesia effect on days 2 and 3. It is possible that offset analgesia and attenuation are mediated by inter-related mechanisms. Further studies might investigate whether offset analgesia involves inhibitory structures such as the PAG-RVM.
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Carriers of a particular haplotype of the GTP cyclohydrolase gene (GCH1) had less pain after surgery for chronic lumbar radiculopathy and a decreased sensitivity to some experimental mechanical pain stimuli. Ex-vivo, GCH1 upregulation and BH4 production after forskolin stimulation were reduced, while baseline BH4 concentrations were not affected. This suggested that the haplotype may mainly exert its modulating function when the GCH1 system is provoked. The present study aimed at (i) testing this hypothesis and (ii) independently reproducing the pain-decreasing effects of a particular GCH1 haplotype having been previously associated with pain protection. ⋯ This study verifies previous results that decreased GCH1 function or inducibility as a result of genetic polymorphisms protects against pain. This study extents previous results by showing that this pain protection is mainly conferred under conditions of hyperalgesia resulting from sensitization, supporting specific functions of BH4 in relation to particular aspects of pain.