The journal of pain : official journal of the American Pain Society
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At present it is unclear if disturbed sensory processing plays a role in the development of the commonly observed motor impairments in patients with complex regional pain syndrome (CRPS). This study aims to investigate the relation between sensory and motor functioning in CRPS patients with and without dystonia. Patients with CRPS of the arm and controls underwent comprehensive quantitative sensory testing and kinematic analysis of repetitive finger movements. Both CRPS groups showed thermal hypoesthesia to cold and warm stimuli and hyperalgesia to cold stimuli. A decreased pressure pain threshold reflecting muscle hyperalgesia emerged as the most prominent sensory abnormality in both patient groups and was most pronounced in CRPS patients with dystonia. Moreover, the decreased pressure pain threshold was the only nociceptive parameter that related to measures of motor function in both patients and controls. CRPS patients with dystonia had an increased 2-point discrimination as compared to controls and CRPS patients without dystonia. This finding was also reported in other types of dystonia and has been associated to cortical reorganization in response to impaired motor function. We hypothesize that increased sensitivity of the circuitry mediating muscle nociception may play a crucial role in impaired motor control in CRPS. ⋯ This is the first study linking a sensory dysfunction, ie, muscle hyperalgesia, to motor impairment in CRPS. Circuitries mediating muscle nociception may therefore play an important role in impaired motor control in CRPS.
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The purpose of this study was to identify alterations in the default mode network of failed back surgery syndrome patients as compared to healthy subjects. Resting state functional magnetic resonance imaging was conducted at 3 Tesla and data were analyzed with an independent component analysis. Results indicate an overall reduced functional connectivity of the default mode network and recruitment of additional pain modulation brain regions, including dorsolateral prefrontal cortex, insula, and additional sensory motor integration brain regions, including precentral and postcentral gyri, for failed back surgery syndrome patients. ⋯ This article presents alterations in the default mode network of chronic low back pain patients with failed back surgery syndrome as compared to healthy participants.
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Randomized Controlled Trial
A randomized controlled pilot study of a cognitive-behavioral therapy approach for painful diabetic peripheral neuropathy.
The purpose of the present pilot study was to assess the efficacy of cognitive-behavioral therapy (CBT) for painful diabetic peripheral neuropathy. This was a randomized, treatment as usual (TAU), controlled, nonblinded intervention pilot study with a 4-month follow-up conducted in a VA medical center. It was hypothesized that participants who received CBT, as compared to those who received TAU, would report significant decreases on self-report measures of pain severity, interference, and depressive symptoms from pretreatment to 4-month follow-up. Participants meeting inclusion criteria were randomly assigned to 1 of the study conditions. Of the 20 eligible participants, 12 were randomized to CBT and 8 were randomized to TAU. Participants randomized to CBT showed significant decreases on measures of pain severity (B = -.54) and pain interference (B = -.77) from pretreatment to 4-month follow-up. There were no significant changes in the TAU participants' scores on measures of pain severity (B = .00) or pain interference (B = -.09). Neither CBT nor TAU participants showed significant changes in their levels of depressive symptoms from pretreatment to 4-month follow-up. CBT may be an effective treatment approach for reducing pain severity and interference associated with painful diabetic peripheral neuropathy. ⋯ The results of this study suggest that engaging patients in CBT for painful diabetic peripheral neuropathy may provide them the skills to become more active and experience less pain.
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Contemporary medical education is inadequate to prepare medical students to competently assess and design care plans for patients with acute and chronic pain. The time devoted to pain education in most medical school curricula is brief and not integrated into case-based clinical experiences, and it is frequently nonexistent during clinical clerkships. Medical student pain curricula have been proposed for over 30 years and are commonly agreed upon, though rarely implemented. As a consequence of poor undergraduate pain education, postgraduate trainees and practicing physicians struggle with both competency and practice satisfaction; their patients are similarly dissatisfied. At the University of Washington School of Medicine, a committee of multidisciplinary pain experts has, between 2009 and 2011, successfully introduced a 4-year integrated pain curriculum that increases required pain education teaching time from 6 to 25 hours, and clinical elective pain courses from 177 to 318 hours. It is expected that increased didactic and case-based multidisciplinary clinical training will increase knowledge and competency in biopsychosocial measurement-based pain narrative and risk assessment, improve understanding of persistent pain as a chronic complex condition, and expand the role of patient-centered interprofessional treatment for medical students, residents, and fellows, leading to better prepared practicing physicians. ⋯ Strategies for improving multidisciplinary pain education at the University of Washington School of Medicine are described and the preliminary results demonstrated.
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We recently showed that during acute muscle pain, C-tactile (CT) fibers mediate allodynia in healthy human subjects. In this study, we pursued the following questions: Do CTs contribute to allodynia observed in delayed onset muscle soreness (DOMS)? Is CT-mediated allodynia reproducible in a clinical pain state? In 30 healthy subjects, DOMS was induced in anterior compartment muscles of the leg by repeated eccentric contractions. DOMS was confirmed by mapping the emergence of tender points (decreased pressure pain thresholds). Furthermore, we measured pressure pain thresholds in a clinical subject who presented with activity-triggered heel pain but no resting pain. Cutaneous vibration (sinusoidal; 200 Hz-200 μm)--an otherwise innocuous stimulus--was applied to anterolateral leg before exercise, during DOMS, and following recovery from DOMS. The peripheral origin of allodynia was determined by employing conduction blocks of unmyelinated (intradermal anesthesia) and myelinated (nerve compression) fibers. In DOMS state, there was no resting pain, but vibration reproducibly evoked pain (allodynia). The blockade of cutaneous C fibers abolished this effect, whereas it persisted during blockade of myelinated fibers. In the clinical subject, without exposure to eccentric exercise, vibration (and brushing) produced a cognate expression of CT-mediated allodynia. These observations attest to a broader role of CTs in pain processing. ⋯ This is the first study to demonstrate the contribution of CT fibers to mechanical allodynia in exercise-induced as well as pathological pain states. These findings are of clinical significance, given the crippling effect of sensory impairments on the performance of competing athletes and patients with chronic pain and neurological disorders.