Pain
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Comparative Study
Dot-probe evaluation of selective attentional processing of pain cues in patients with chronic headaches.
Evidence supporting the notion that patients with chronic pain are characterized by attentional biases for sensory and affect pain words, and that such biases are mediated by fear of pain, is mixed. The present investigation was an attempt to replicate and extend initial findings obtained with the dot-probe task. Thirty patients with chronic headache and 19 healthy controls were tested using a dot-probe task including affect pain, sensory pain, and neutral words. ⋯ These results do not provide convincing evidence that patients with chronic headache selectively attend to affect or sensory pain cues when compared to healthy controls. The significant cross-groups associations between anxiety sensitivity and current pain description and indices of selective attention are consistent with the notion that attentional biases may be influenced by fear propensity and current concerns. Implications of the findings and future research directions are discussed.
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The aim of this study was to investigate the relationship between psychosocial work characteristics and neck and upper limb symptoms and to examine to what extent this relationship could be explained by other risk factors. Data were used from a prospective cohort study in a working population, with a follow-up period of 3 years. ⋯ Partly, but not exclusively, these relationships were intermediated by an increased exposure to physical risk factors and increased stress symptoms. Personal characteristics did not considerably influence the main effects of the identified risk factors.
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Comparative Study
Brain processing during mechanical hyperalgesia in complex regional pain syndrome: a functional MRI study.
Complex Regional Pain Syndromes (CRPS) are characterized by a triad of sensory, motor and autonomic dysfunctions of still unknown origin. Pain and mechanical hyperalgesia are hallmarks of CRPS. There are several lines of evidence that central nervous system (CNS) changes are crucial for the development and maintenance of mechanical hyperalgesia. ⋯ The stimulation of the affected limb was painful (mechanical hyperalgesia) and led to a significantly increased activation of the S1 cortex (contralateral), S2 (bilateral), insula (bilateral), associative-somatosensory cortices (contralateral), frontal cortices and parts of the anterior cingulate cortex. The results of our study indicate a complex cortical network activated during pin-prick hyperalgesia in CRPS. The underlying neuronal matrix comprises areas not only involved in nociceptive, but also in cognitive and motor processing.
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Comparative Study
Sensory and motor effects of experimental muscle pain in patients with lateral epicondylalgia and controls with delayed onset muscle soreness.
This study compares the effect of experimental muscle pain on deep tissue sensitivity and force attenuation in the wrist extensors of patients with lateral epicondylalgia (n=20), and healthy controls (n=20) with experimentally induced sensori-motor characteristics simulating lateral epicondylalgia. Delayed onset muscle soreness (DOMS) in wrist extensors of healthy controls was induced by eccentric exercise in one arm 24h prior to injection (Day 0). Saline-induced pain intensity (visual analogue scale, VAS), distribution, and quality were assessed quantitatively in both arms for both groups. ⋯ Patients demonstrated significant bilateral hyperalgesia at extensor carpi radialis brevis during and post saline-induced pain compared to pre-injection and healthy controls (P<0.04). The sore arm in patients and the DOMS arms in healthy subjects showed significantly reduced maximal force (P<0.0001), at all Day 1 times compared with the control arms. In patients, the bilateral increase in deep tissue sensitivity and enlarged referred pain areas during saline-induced pain might suggest involvement of central sensitisation.
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Activation of extracellular signal-regulated kinase (ERK), a mitogen activated-protein kinase (MAPK), in dorsal horn neurons contributes to inflammatory pain by transcription-dependent and -independent means. We have now investigated if ERK is activated in the spinal cord after a spinal nerve ligation (SNL) and if this contributes to the neuropathic pain-like behavior generated in this model. An L5 SNL induces an immediate (<10 min) but transient (<6 h) induction of phosphoERK (pERK) restricted to neurons in the superficial dorsal horn. ⋯ Intrathecal injection of the MEK (ERK kinase) inhibitor PD98059 on Day 2, 10 or 21 reduces SNL-induced mechanical allodynia. Our results suggest that ERK activation in the dorsal horn, as well as in the DRG, mediates pain through different mechanisms operating in different cells at different times. The sequential activation of ERK in dorsal horn microglia and then in astrocytes might reflect distinct roles for these two subtypes of glia in the temporal evolution of neuropathic pain.