The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial
Repetitive Transcranial Magnetic Stimulation for phantom limb pain in landmine victims: A double-blinded, randomized, sham-controlled trial.
We evaluated the effects of repetitive transcranial magnetic stimulation (rTMS) in the treatment of phantom limb pain (PLP) in land mine victims. Fifty-four patients with PLP were enrolled in a randomized, double-blinded, placebo-controlled, parallel group single-center trial. The intervention consisted of real or sham rTMS of M1 contralateral to the amputated leg. rTMS was given in series of 20 trains of 6-second duration (54-second intertrain, intensity 90% of motor threshold) at a stimulation rate of 10 Hz (1,200 pulses), 20 minutes per day, during 10 days. For the control group, a sham coil was used. The administration of active rTMS induced a significantly greater reduction in pain intensity (visual analogue scale scores) 15 days after treatment compared with sham stimulation (-53.38 ± 53.12% vs -22.93 ± 57.16%; mean between-group difference = 30.44%, 95% confidence interval, .30-60.58; P = .03). This effect was not significant 30 days after treatment. In addition, 19 subjects (70.3%) attained a clinically significant pain reduction (>30%) in the active group compared with 11 in the sham group (40.7%) 15 days after treatment (P = .03). The administration of 10 Hz rTMS on the contralateral primary motor cortex for 2 weeks in traumatic amputees with PLP induced significant clinical improvement in pain. ⋯ High-frequency rTMS on the contralateral primary motor cortex of traumatic amputees induced a clinically significant pain reduction up to 15 days after treatment without any major secondary effect. These results indicate that rTMS is a safe and effective therapy in patients with PLP caused by land mine explosions.
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Review
Systematic review of childhood and adolescent risk and prognostic factors for recurrent headaches.
Little is known about childhood and adolescent risk and prognostic factors for recurrent headaches. This systematic review 1) examined longitudinal evidence about factors associated with onset and course of recurrent headaches in childhood or adolescence, using meta-analysis where possible, and 2) evaluated the quality of this evidence using a modified Grading of Recommendations Assessment, Development and Evaluation framework. Through searching electronic databases, reference lists of included studies, and an electronic mail list we identified and included 23 articles reporting 19 cohorts. From the included studies we explored 27 risk factors for recurrent headaches, 27 prognostic factors for persistence of recurrent headaches, and 6 prognostic factors for presence of headache-related disability. The quality of evidence for most associations is low or very low. There is moderate-quality evidence that women are at risk of developing recurrent headaches and of headaches persisting. There is high-quality evidence suggesting that children with negative emotional states manifested through anxiety, depression, or mental distress are not at risk of developing headache, but moderate-quality evidence suggests that the presence of comorbid negative emotional states in children with headaches is associated with increased risk of headache persistence. Because of the small number of studies, further investigation is needed to increase confidence in existing evidence and to explore new risk and prognostic factors. ⋯ This is a review of the evidence about childhood and adolescent risk and prognostic factors for the onset of recurrent headaches and their course. Understanding these factors can help identify childrens' risk and may suggest ways to reduce this risk.
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Many derivatives of bisphosphonates, which are inhibitors of bone resorption, have been developed as promising agents for painful pathologies in patients with bone resorption-related diseases. The mechanism for pain relief by bisphosphonates remains uncertain. Studies have reported that bisphosphonates could reduce central neurochemical changes involved in the generation and maintenance of bone cancer pain. In this study, we hypothesized that bisphosphonates would inhibit spinal microglial activation and prevent the development of hyperalgesia caused by peripheral tissue injury. We investigated the effects of alendronate (a nitrogen-containing bisphosphonate) on the development of neuropathic pain and its role in modulating microglial activation in vivo and in vitro. Intrathecal and intraperitoneal administration of alendronate relieved neuropathic pain behaviors induced by chronic constriction sciatic nerve injury. Alendronate also significantly attenuated spinal microglial activation and p38 mitogen-activated protein kinase (MAPK) phosphorylation without affecting astrocytes. In vitro, alendronate downregulated phosphorylated p38 and phosphorylated extracellular signal regulated kinase expression in lipopolysaccharide-stimulated primary microglia within 1 hour, and pretreatment with alendronate for 12 and 24 hours decreased the expression of inflammatory cytokines (tumor necrosis factor α, and interleukins 1β and 6). These findings indicate that alendronate could effectively relieve chronic constriction sciatic nerve injury-induced neuropathic pain by at least partially inhibiting the activation of spinal microglia and the p38 MAPK signaling pathway. ⋯ Alendronate could relieve neuropathic pain behaviors in animals by inhibiting the activation of spinal cord microglia and the p38 MAPK cell signaling pathway. Therapeutic applications of alendronate may be extended beyond bone metabolism-related disease.
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The fear-avoidance model postulates that in an initial acute phase chronic low back pain (CLBP) patients acquire a fear of movement that results in avoidance of physical activity and contributes to the pain becoming chronic. The current functional magnetic resonance imaging study investigated the neural correlates of imagining back-straining and neutral movements in CLBP patients with high (HFA) and low fear avoidance (LFA) and healthy pain-free participants. Ninety-three persons (62 CLBP patients, 31 healthy controls; age 49.7 ± 9.2 years) participated. The CLBP patients were divided into an HFA and an LFA group using the Tampa Scale of Kinesiophobia. The participants viewed pictures of back-straining and neutral movements and were instructed to imagine that they themselves were executing the activity shown. When imagining back-straining movements, HFA patients as well as healthy controls showed stronger anterior hippocampus activity than LFA patients. The neural activations of HFA patients did not differ from those of healthy controls. This may indicate that imagining back-straining movements triggered pain-related evaluations in healthy controls and HFA participants, but not in LFA participants. Although heightened pain expectancy in HFA compared with LFA patients fits well with the fear-avoidance model, the difference between healthy controls and LFA patients was unexpected and contrary to the fear-avoidance model. Possibly, negative evaluations of the back-straining movements are common but the LFA patients use some kind of strategy enabling them to react differently to the back-straining events. ⋯ It appears that low fear-avoidant back pain patients use some kind of strategy or underlying mechanism that enables them to react with less fear in the face of potentially painful movements. This warrants further investigation because countering fear and avoidance provide an important advantage with respect to disability.