Pain
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Gastric acid challenge of the rat and mouse stomach is signalled to the brainstem as revealed by expression of c-Fos. The molecular sensors relevant to the detection of gastric mucosal acidosis are not known. Since the acid-sensing ion channels ASIC2 and ASIC3 are expressed by primary afferent neurons, we examined whether knockout of the ASIC2 or ASIC3 gene modifies afferent signalling of a gastric acid insult in the normal and inflamed stomach. ⋯ This gastric acid hyperresponsiveness was absent in ASIC3 knockout mice but fully preserved in ASIC2 knockout mice. The current data indicate that ASIC3 plays a major role in the acid hyperresponsiveness associated with experimental gastritis. In contrast, ASIC2 appears to dampen acid-evoked input from the stomach to the NTS.
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Randomized Controlled Trial
Mindfulness meditation for the treatment of chronic low back pain in older adults: a randomized controlled pilot study.
The objectives of this pilot study were to assess the feasibility of recruitment and adherence to an eight-session mindfulness meditation program for community-dwelling older adults with chronic low back pain (CLBP) and to develop initial estimates of treatment effects. It was designed as a randomized, controlled clinical trial. Participants were 37 community-dwelling older adults aged 65 years and older with CLBP of moderate intensity occurring daily or almost every day. ⋯ Compared to the control group, the intervention group displayed significant improvement in the Chronic Pain Acceptance Questionnaire Total Score and Activities Engagement subscale (P=.008, P=.004) and SF-36 Physical Function (P=.03). An 8-week mindfulness-based meditation program is feasible for older adults with CLBP. The program may lead to improvement in pain acceptance and physical function.
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Randomized Controlled Trial
Chronic low back pain: physical training, graded activity with problem solving training, or both? The one-year post-treatment results of a randomized controlled trial.
Several treatment principles for the reduction of chronic low back pain associated disability have been postulated. To examine whether a combination of a physical training and an operant-behavioral graded activity with problem solving training is more effective than either alone in the long-term, a cluster randomized controlled trial was conducted. In total 172 patients, 18-65 years of age, with chronic disabling non-specific low back pain referred for rehabilitation treatment, were randomized in clusters of four consecutive patients to 10 weeks of aerobic training and muscle strengthening of back extensors (active physical treatment; APT), 10 weeks of gradual assumption of patient relevant activities based on operant-behavioral principles and problem solving training (graded activity plus problem solving training; GAP), or APT combined with GAP (combination treatment; CT). ⋯ During the one-year follow-up, there were no significant differences between each single treatment and the combination treatment on the primary outcome, the Roland Disability Questionnaire. Among multiple other comparisons, only one significant difference emerged, with GAP and APT showing higher self-perceived improvement than CT. We conclude that the combination treatment integrating physical, graded activity with problem solving training is not a better treatment option for patients with chronic low back pain.
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The pathogenesis of dystonia in Complex Regional Pain Syndrome type 1 (CRPS-1) is unclear. In primary dystonia, functional magnetic resonance imaging (fMRI) has revealed changes in cerebral networks during execution of movement. The aim of this study was to determine cerebral network function in CRPS-1 patients with dystonic postures. ⋯ Contralaterally, reduced activation was seen in the inferior parietal and adjacent primary sensory cortex. There were no differences between patients and controls when they executed movements, nor when they imagined moving their unaffected hand. The altered cerebral activation pattern in patients with CRPS-1 linked dystonia most likely reflects an interface between pain-associated circuitry and higher order motor control, which points at a specific mechanistic pathophysiology of this type of dystonia.
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Peripheral nerve injury may lead to the formation of a painful neuroma. In patients, palpating the tissue overlying a neuroma evokes paraesthesias/dysaesthesias in the distribution of the injured nerve. Previous animal models of neuropathic pain have focused on the mechanical hyperalgesia and allodynia that develops at a location distant from the site of injury and not on the pain from direct stimulation of the neuroma. ⋯ The neuroma tenderness (but not the hyperalgesia) was reversed by local lidocaine injection and by proximal transection of the tibial nerve. Afferents originating from the neuroma exhibited spontaneous activity and responses to mechanical stimulation of the neuroma. The TNT model provides a useful tool to investigate the differential mechanisms underlying the neuroma tenderness and mechanical hyperalgesia associated with neuropathic pain.