The journal of pain : official journal of the American Pain Society
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Activity patterns are believed to play an important role in the development and perpetuation of chronic pain. So far, 3 important activity patterns have been studied: avoidance behavior, persistence behavior, and pacing behavior. Yet, empirical evidence is limited and inconclusive about the relationships between these activity patterns and important outcomes. Therefore, the present study was aimed at identifying activity patterns by means of factor analyses and determining their relationship with disability and depressive symptomatology in participants with chronic pain (N = 132). Items across different measurement instruments pertaining to 1 particular activity pattern were aggregated, and submitted to factor analysis. Results from 3 separate factor analyses revealed 6 distinct activity patterns: pain avoidance, activity avoidance, task-contingent persistence, excessive persistence, pain-contingent persistence, and pacing. In line with our hypotheses, pain and activity avoidance, and excessive persistence, were related to higher levels of disability and depressive symptomatology. In contrast to hypotheses, pacing was associated with worse outcomes as well. Interestingly, task-contingent persistence was related to lower levels of disability and depressive symptomatology. When controlling for pain and the other activity patterns, excessive persistence and activity avoidance were the most detrimental in terms of relations with depressed mood or disability. Task-contingent persistence appeared to be the least detrimental. ⋯ Our findings suggest the existence of several activity patterns, which are differentially related to disability and depressive symptomatology, in participants with chronic pain. The present results are discussed in the light of previous findings, and may provide a new impetus for future studies on activity patterns in chronic pain research.
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A triad of clinical symptoms, ie, autonomic, motor and sensory dysfunctions, characterizes complex regional pain syndromes (CRPS). Sensory dysfunction comprises sensory loss or spontaneous and stimulus-evoked pain. Furthermore, a disturbance in the body schema may occur. In the present study, patients with CRPS of the upper extremity and healthy controls estimated their hand sizes on the basis of expanded or compressed schematic drawings of hands. In patients with CRPS we found an impairment in accurate hand size estimation; patients estimated their own CRPS-affected hand to be larger than it actually was when measured objectively. Moreover, overestimation correlated significantly with disease duration, neglect score, and increase of two-point-discrimination-thresholds (TPDT) compared to the unaffected hand and to control subjects' estimations. In line with previous functional imaging studies in CRPS patients demonstrating changes in central somatotopic maps, we suggest an involvement of the central nervous system in this disruption of the body schema. Potential cortical areas may be the primary somatosensory and posterior parietal cortices, which have been proposed to play a critical role in integrating visuospatial information. ⋯ CRPS patients perceive their affected hand to be bigger than it is. The magnitude of this overestimation correlates with disease duration, decreased tactile thresholds, and neglect-score. Suggesting a disrupted body schema as the source of this impairment, our findings corroborate the current assumption of a CNS involvement in CRPS.
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Clinical Trial
Predictive value of rTMS in the identification of responders to epidural motor cortex stimulation therapy for pain.
This study was designed to assess the value of repetitive transcranial magnetic stimulation (rTMS) to predict the efficacy of epidural motor cortex stimulation (EMCS) to treat neuropathic pain. We have included 59 patients treated by EMCS for more than 1 year and in whom active and sham 10Hz-rTMS sessions were performed as preoperative tests, targeted over the cortical representation of the painful area. Analgesic effects were rated on a visual analogue scale. The real rTMS efficacy was determined by subtracting the effect of the sham stimulation on pain scores from that of the active stimulation (active-sham calculation). Pain scores were significantly reduced by active rTMS and EMCS, but not by sham rTMS. Twenty-six of the 33 patients (79%) who responded to active rTMS and all the 21 patients (100%) who responded for active-sham calculation also responded to EMCS. The response observed in active-sham calculation had a positive predictive value of 1.0, but a negative predictive value of .6 regarding EMCS outcome. The analgesic effect of rTMS or EMCS was not influenced by the side, origin, or duration of pain or by the presence of motor or sensory deficit in the painful area. Poorer results were observed in case of lower limb pain for rTMS and in older patients for EMCS. This study confirms that neuropathic pain can be significantly relieved by motor cortex rTMS or EMCS. A positive outcome of EMCS can be predicted by a real response to rTMS, but not on clinical grounds. ⋯ Single sessions of sham-controlled preoperative rTMS tests can be used to confirm the indication of EMCS therapy but have no value to exclude patients from this therapy. New rTMS protocols remain to be assessed to improve the usefulness of preoperative rTMS in EMCS practice.
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Myofascial pain syndrome (MPS) is an important clinical condition characterized by chronic muscle pain and a myofascial trigger point (MTrP) located in a taut band (TB). However, its pathogenic mechanism is still unclear. We developed an animal model relevant to conditions of MPS, and analyzed the mechanism of the muscle pain in this model. We applied eccentric contraction (EC) to a rat's gastrocnemius muscle (GM) for 2 weeks, and examined the mechanical withdrawal thresholds, histological changes, and expressions and contents of nerve growth factor (NGF). The mechanical withdrawal threshold decreased significantly at the next day of first EC and continued up to 9 days after EC. TBs were palpable at 3 to 8 days after initiation of EC. In EC animals, necrotic and regenerating muscle cells were found significantly more than in control animals. In EC animals, NGF expressions in regenerating muscle cells and NGF contents of GM were significantly higher than control animals. Administration of NGF receptor (TrkA) inhibitor K252a showed significant suppression of mechanical hyperalgesia in EC animals. Repeated EC induced persistent mechanical muscle hyperalgesia associated with TB. NGF expressed in regenerating muscle cells may have an important role in persistent mechanical muscle hyperalgesia which might be relevant to pathogenesis of MPS. ⋯ The present study shows that NGF expressed in regenerating muscle cells is involved in persistent muscular mechanical hyperalgesia. NGF-TrkA signaling in primary muscle afferent neurons may be one of the most important and promising targets for MPS.
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Although stress induces analgesia, there is evidence that stressful events may exacerbate pain syndromes. Here, we studied the effects of 1 to 3 prestressful events (days 0, 2, and 7), such as non-nociceptive environmental stress, on inflammatory hyperalgesia induced by a carrageenan injection (day 14) in 1 rat hind paw. Changes in nociceptive threshold were evaluated by the paw pressure vocalization test. The higher the number of stress sessions presented to the rats, the greater was the inflammatory hyperalgesia. Blockade of opioid receptors by naltrexone before each stress inhibited stress-induced analgesia and suppressed the exaggerated inflammatory hyperalgesia. Stressed versus nonstressed animals could be discriminated by their response to a fentanyl ultra-low dose (fULD), that produced hyperalgesia or analgesia, respectively. This pharmacological test permitted the prediction of the pain vulnerability level of prestressed rats because fULD analgesic or hyperalgesic indices were positively correlated with inflammatory hyperalgesic indices (r(2) = .84). In prestressed rats, fULD-induced hyperalgesia and the exaggerated inflammatory hyperalgesia were prevented NMDA receptor antagonists. This study provides some preclinical evidence that pain intensity is not only the result of nociceptive input level but is also dependent on the individual history, especially prior life stress events associated with endogenous opioid release. ⋯ Based on these preclinical data, it would be of clinical interest to evaluate whether prior stressful events may also affect further pain sensation in humans. Moreover, this preclinical model could be a good tool for evaluating new therapeutic strategies for relieving pain hypersensitivity.