European journal of pain : EJP
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One of the most prominent features of secondary hyperalgesia is touch-evoked pain, i.e., pain evoked by dynamic tactile stimuli applied to areas adjacent or remote from the originating injury. It is generally accepted that the neurobiological mechanism of this sensory alteration involves the central nervous system (CNS) so that incoming impulses in low-threshold mechanoreceptors from the area of secondary hyperalgesia can evoke painful sensations instead of touch. ⋯ Here we review the evidence gathered in support of this model in the intervening years with special reference to experimental studies of antidromic activity (Dorsal Root Reflexes--DRRs) in nociceptive afferents and on the acquisition of low-threshold inputs by nociceptor-specific neurons in the spinal dorsal horn. We also discuss and identify potential molecular mechanisms that may underlie the presynaptic interaction model and therefore that could be responsible for the development of secondary hyperalgesia.
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Attentional bias in patients with chronic pain was investigated using the emotional Stroop task with personalized pain words. A group of 20 chronic pain patients with 20 matched controls participated in the experiment. Before administration of the emotional Stroop patients were asked to select the five best descriptors of their pain from a list of 19 sensory pain descriptors. ⋯ Results showed a weak Stroop interference effect with slower reaction times to pain words in the patient group, but they did not differ significantly from the controls. Both groups were slower on the threat words and displayed the classical Stroop interference effect for color words. The overall pattern of results are in line with previous Stroop studies on pain patients showing weak support for the attentional bias hypothesis.
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Awareness that SCI pain is common emerged during the past decade. However, there are a number of unresolved issues. There is a need for variety of experimental models to reflect diversity of SCI pains. ⋯ More attention should be given to a condition of the spinal cord below and above the SCI lesion. A consensus for what is an optimal SCI functional assessment for patients with sensory complaints and pain should be developed. Further extensive SCI pain research is needed prior to spinal cord regeneration trials in order to be able to cope with a potential for newly developed pains that may appear during incomplete spinal cord regenerative attempts.
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Aim of this study was to analyse the incidence CRPS-I after a fracture of the distal radius and to analyse risk factors. Patients who visited the Emergency Unit of the University Hospital, with a fracture of distal radius were asked to participate. As risk factors for CRPS-I, number of repositions (with or without local anaesthesia), additional cast changes and pain during the cast period, were assessed. ⋯ One female (1%, 95% CI: 0.2 to 6%), age 69 years with the following characteristics developed CRPS-I: one set of local anaesthetics, one repositioning attempt, no additional cast changes, average pain scores, no life events and her total score on the SCL-90 of 117, was slightly above average. Based on the results of this study it is concluded that the incidence of CRPS-I may be low (1%, 95% CI: 0.2 to 6%) after fractures of the distal radius. Further the risk factors described in literature play a minor role in the development of CRPS-I.
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The innervation of the temporomandibular joint (TMJ) has attracted particular interest because of the close association with complex mandibular movement. Although the pathological changes of disk innervation may have a crucial role in the development of TMJ pain, the innervation of the TMJ disk by experimentally induced arthritis has rarely been examined in detail. Arthritic rats were induced by injection with 0.1ml solution of Complete Freund's adjuvant (CFA). ⋯ In addition, the ratio of trkA- and p75-positive small- and medium-sized cells increased in trigeminal ganglia. It is assumed that increasing innervation of the TMJ disk may be important for the pathophysiology of TMJ pain. NGF and its receptors are likely involved in pathological changes of the TMJ disk.