The journal of pain : official journal of the American Pain Society
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Chronic pain is a common complication after thoracic surgery. The cause of chronic post-thoracotomy pain is often suggested to be intercostal nerve damage. Thus chronic pain after thoracic surgery should have an important neuropathic component. The present study investigated the prevalence of the neuropathic component in chronic pain after thoracic surgery. Furthermore, we looked for predictive factors for prevalence and intensity of chronic pain. We contacted 243 patients who underwent a video-assisted thoracoscopy (VATS) or thoracotomy in the period between January 2004 and September 2006 by mail. Patients retrospectively received a questionnaire with the Dutch version of the PainDETECT Questionnaire, a validated screening tool for neuropathic pain. Results were analyzed from 204 patients (144 thoracotomies, 60 VATS). The prevalence of chronic pain was 40% after thoracotomy and 47% after VATS. Definite chronic neuropathic pain was present in 23% of the patients with chronic pain, with an additional 30% having probable neuropathic pain. Greater probability of neuropathic pain (ie, a higher total score of the PainDETECT) correlated with more intense chronic pain. Predictive factors for chronic pain were younger age (P = .01), radiotherapy (P = .043), pleurectomy (P = .04) and more extensive surgery (P < .001). ⋯ Up to half the chronic pain after thoracic surgery is not associated with a neuropathic component, which has not been reported to date. More extensive surgery and pleurectomy are predictive factors for chronic pain after thoracic surgery, suggesting a visceral component apart from nerve injury.
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Preoperative identification of patients at risk for high-intensity postoperative pain may be used to predict patients at risk for development of a persistent pain state and allocate patients to more intensive specific pain therapy. Preoperative pain threshold to electrocutaneus stimulation has recently been shown to correlate to acute postoperative pain after cesarean section, but the findings have not been confirmed in larger studies or other procedures. Preoperative electrical pain detection threshold and pain tolerance were assessed in patients undergoing a primary unilateral groin hernia repair. The correlation between the pain data for electrical stimulation was compared with the postoperative pain during the first week in 165 patients, whereof 3 were excluded. Preoperative electrical pain detection threshold and electrical pain tolerance threshold did not correlate to postoperative pain (rho = -0.13, P = .09, and rho = -1.2, P = .4, respectively. ⋯ Although preoperative electrical nociceptive stimulation may predict patients at risk of high-intensity acute pain after other surgical procedures, this was not the case in groin hernia repair patients receiving concomitant treatment with acetaminophen and ibuprofen.
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Although there are several reports on pain behavioral tests in rat models of knee osteoarthritis (OA), most of them focus on the paw. The aim of this study was to investigate pain-related behaviors on the affected knee joint, the primary source of nociception, in animals with mono-iodoacetate-induced OA, using the knee-bend (which provides information on movement pain) and pin-prick tests, and to evaluate nociception elicited by walking using the CatWalk test. The von Frey and Randall-Selitto tests applied to the paw allowed us to compare our study results with previous studies. A further aim was to compare the behavioral nociceptive responses of the most used doses of mono-iodoacetate, 2 and 3 mg. Knee-bend score of OA animals was higher than those of control animals throughout the study (P < .05). At every time point, the ipsilateral hind-paw load of OA rats, as measured by the CatWalk test, was lower than that of control rats (P < .05), and paw withdraw threshold to von Frey filaments was also decreased (P < .01). No changes were observed in pin-prick and Randall-Selitto tests. Results obtained with the 2 doses of mono-iodoacetate were similar. The knee-bend and CatWalk tests are effective for evaluating movement-related nociception, a hallmark of clinical OA, which was present throughout the experimental period. ⋯ Behavioral characterization of models of OA pain is important and useful for use in future studies to test pharmacological treatments. Furthermore, it is important to find methods that correlate better with the human symptoms of OA.
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Clinical Trial
Impact of chronic somatoform and osteoarthritis pain on conscious and preconscious cognitive processing.
The study investigates the impact of chronic pain (CP) on conscious and preconscious cognitive processes and on guessing behavior and examines the mediating effect of a depressive state. Twenty-eight patients with CP due to hip osteoarthritis, 32 patients with a somatoform disorder including pain symptoms, and 31 participants who did not have CP were examined within the framework of a modified process-dissociation-paradigm. Neutral, health-threatening, and general threatening stimuli were presented acoustically in a lexical decision task. Parameters of conscious processing, preconscious processing, and of chance were estimated by a multinomial modeling procedure. CP patients with osteoarthritis showed the lowest level of conscious processing and the highest level of guessing behavior. Patients with somatoform pain tended to react preconsciously to health threatening stimuli but overall showed a profile similar to that of control subjects who did not have CP. The impact of the threatening quality of stimuli on different levels of cognitive processing was weak. Depression did not mediate between the experience of pain and estimates of conscious and preconscious processing. ⋯ The impact of CP on preconscious and conscious cognitive processing depends on types and causes of pain. The experience of CP caused by inflammation or physical damage tends to reduce the probability of conscious processing and to provoke memory biases. CP in the context of a somatoform disorder appears to have less impact on cognitive functions.
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This study examined whether self-efficacy mediated the relationship between pain catastrophizing and pain and disability. Participants were 192 individuals diagnosed with osteoarthritis (OA) of the knees who were overweight or obese. Multiple mediator analyses were conducted to simultaneously test self-efficacy for pain control, physical function, and emotional symptoms as mediators while controlling for demographic and medical status variables. Higher pain catastrophizing was associated with lower self-efficacy in all 3 domains (Ps < .05). Self-efficacy for pain control fully mediated the relationship between pain catastrophizing and pain (beta = .08, Sobel test Z = 1.97, P < .05). The relationship between pain catastrophizing and physical disability was fully mediated by self-efficacy for physical function (beta = .06, Sobel test Z = 1.95, P = .05). Self-efficacy for emotional symptoms partially mediated the relationship between pain catastrophizing and psychological disability (beta = .12, Sobel test Z = 2.92, P < .05). These results indicate that higher pain catastrophizing contributed to greater pain and disability via lower domain-specific self-efficacy. Efforts to reduce pain and improve functioning in OA patients should consider addressing pain catastrophizing and domain specific self-efficacy. Pain catastrophizing may be addressed through cognitive therapy techniques and self-efficacy may be enhanced through practice of relevant skills and personal accomplishments. ⋯ This study found that higher pain catastrophizing contributed to greater pain and disability via domain specific self-efficacy. These results suggest that treatment efforts to reduce pain and improve functioning in OA patients who are overweight or obese should consider addressing both pain catastrophizing and self-efficacy.