European journal of pain : EJP
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Chronic pain is often associated with comorbidities such as anxiety and depression, resulting in a low health-related quality of life. The mechanisms underlying this association are not clear, but a disturbance in the pain control systems from the brain stem has been suggested. Thirty neuropathic pain (NP) patients, 28 patients with fibromyalgia (FM), and 26 pain-free age- and gender-matched controls were included and examined with respect to mental distress (self-rated Symptom Checklist-92), depression (doctor-rated Hamilton Depression Scale and self-rated Major Depression Inventory), and anxiety (doctor-rated Hamilton Anxiety Scale and self-rated Anxiety Inventory). ⋯ However, these scores are low compared to other studies on mental distress in chronic pain patients. Only few chronic pain patients meet the diagnostic criteria for depression (NP 3.3%, FM 7.1%), and associations between pain and mental symptoms were only found in the FM group despite similar pain intensities. The findings suggest that different mechanisms are responsible for the development of mood disorders in the two patient groups.
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Diffusion Tensor Imaging (DTI) is a promising new imaging method allowing in vivo mapping of anatomical connections in the living human brain. We combined DTI with functional magnetic resonance imaging (fMRI) to investigate the anatomical relationships between areas involved in visceral sensations in humans. Non-painful and moderately painful rectal distensions were performed in 11 healthy women (38.4+/-3.1years). fMRI was used to analyse the changes in brain activity during both types of distension. ⋯ DTI revealed direct connections between insula, and the four areas more frequently activated in this study, i.e. ACC, thalamus, S1, S2 and PFC. The combined use of fMRI and DTI in healthy subjects during rectal distension revealed a neural network of visceral sensory perception involving the insula, thalamus, somatosensory cortices, ACC and PFC.
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Most forms of visceral pain generate intense referred hyperalgesia but the mechanisms of this enhanced visceral hypersensitivity are not known. The on-cells of the rostral ventromedial medulla (RVM) play an important role in descending nociceptive facilitation and can be sensitized to somatic mechanical stimulation following peripheral nerve injury or hindpaw inflammation. Here we have tested the hypothesis that visceral noxious stimulation sensitizes RVM ON-like cells, thus promoting an enhanced descending facilitation that can lead to referred visceral hyperalgesia. ⋯ Moreover, ON-like cells acquired a novel response to CRD and responded to heat stimulation in the innocuous range. OFF-like neurons responded to capsaicin administration with a brief (<5 min) inhibition of activity followed by an enhanced inhibition to noxious stimulation and a novel inhibition to innocuous stimulation (CRD and heat) at early time points (10 min post capsaicin). These results support the hypothesis that noxious visceral stimulation may cause referred hypersensitivity by promoting long-lasting sensitization of RVM ON-like cells.
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Animal models for mechanical pressure or heat nociception usually only measure the threshold response latency. In this study, the effect of typical sensitising treatments on the lasting nocifensive behaviour elicited after a supra-threshold heating stimulus - the hyperpathic component of hypernociception - was assessed. Male Wistar rats received either intra-plantar (i.pl.) injection of 350ng PGE(2) (50microL) or topical application (t.a.) of 100% dimethylsulfoxide (DMSO), and 10mM capsaicin. ⋯ Capsaicin neonatal treatment (CNT) (50mg/kg) reduced the sensitisation induced by DMSO and capsaicin (P<0.01), but not that induced by PGE(2). These data suggest that the heat-induced lasting nociception is probably conveyed by Aeth nociceptors, and PGE(2) seems to be more selective to induce this phenomenon than the thermal threshold lowering. In addition, this hyperpathic effect induced by DMSO and capsaicin seems to be indirectly mediated by PGE(2) and C-fibres.
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Mechanical hyperalgesia may develop following tissue inflammation or nerve injury. Basically, peripheral sensitization leads to primary hyperalgesia at the site of injury, whereas secondary hyperalgesia occurs in the surrounding tissue and results from central sensitization. The present study focuses on the cerebral processing of secondary mechanical hyperalgesia. ⋯ In contrast to PPC, we found a significant correlation between increases of magnetic field strengths within bilateral S2 with the increase of pain ratings during pin-prick hyperalgesia. We conclude that the S2 cortex may be involved for the processing of secondary mechanical hyperalgesia in the human brain. PPC activation may reflect higher attentional processing during mechanical hyperalgesia.