Articles: neuropathic-pain.
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It is clear that implicit motor imagery (IMI) is impaired by chronic pain in peripheral regions (hand, feet), but unclear in axial regions (neck, shoulder, back). Previous IMI tasks displayed small-amplitude movements of axial regions, which limits person-centered IMI processes mobilization. This study aimed to assess the impact of chronic low back pain (CLBP) on IMI processes with a new task displaying large-amplitude whole-body movements mobilizing the lumbar spine. ⋯ The laterality judgment task proposed here confirmed that CLBP impacts IMI processes, and that the nature of pain (neuropathic or mechanical) needs to be considered because it seems to modulate IMI processes. PERSPECTIVE: A laterality judgment task with large-amplitude lumbar movements is key to show that CLBP alters processing speed of sensorimotor information originating from the painful region. This task could become an objective tool, transferable in clinical settings, for assessing the impact and the progression of CLBP on motor control processes.
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Pain management in patients with complete spinal cord injury is complex. ⋯ The effectiveness of this approach may be attributed to its ability to modulate supraspinal pain processing, allowing for targeted relief of various pain mechanisms below the level of injury.
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Neuropathic pain occurs for various reasons involving adenosine receptors. One of several drugs used to control neuropathic pain is amitriptyline, a tricyclic antidepressant. Amitriptyline has an antinociceptive effect on the A3 adenosine receptor (A3AR). However, the exact mechanisms underlying A3AR activation remain unclear. ⋯ The release of proinflammatory cytokines via NF-kB expression and subsequent inflammatory responses is significantly associated with the development of neuropathic pain. Our study reveals that AMI effectively suppresses NF-kB-related proinflammatory cytokines, offering a promising avenue for treating pain related to peripheral nerve injuries. These findings provide valuable insights into neuropathic pain management.
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Neuropathic pain is one of the most challenging types of pain to diagnose and treat, a problem exacerbated by the lack of a quantitative biomarker. Recently, several clinical and preclinical studies have shown that neuropathic pain induces cerebral hemodynamic changes as a result of neuroplasticity in the brain. Our hypothesis in this study is that neuropathic pain leads to cerebral hemodynamic changes over postoperative time in a spinal nerve ligation (SNL) rat model, which has not been longitudinally explored previously. ⋯ We investigate cerebral hemodynamic changes using dynamic susceptibility contrast magnetic resonance imaging in a rat model up to 28 days after ligating L5/L6 spinal nerves. We trained a linear support vector machine with relative cerebral blood volume data from different brain regions and found that the prediction model trained on the nucleus accumbens, motor cortex, pretectal area, and thalamus classified the SNL group and sham group at a 79.27% balanced accuracy, regardless of when the onset of pain occurred (SNL/sham: 60/45 data points). From the use of the SNL model without prior knowledge of the onset time of pain, the current findings highlight the potential of relative cerebral blood volume in the 4 highlighted brain regions as a biomarker for neuropathic pain.
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Pharmacological ablation of rostral ventromedial medulla (RVM) mu opioid receptor-expressing cells before peripheral nerve injury prevents the development of neuropathic pain. However, whether these neurons are required for the expression of established neuropathic pain is not known. Male Oprm1Cre heterozygous (MOR Cre ) or wild-type (MOR WT ) mice received AAV8-hSyn-DIO-hM4D(Gi)-mCherry in the RVM. ⋯ Sustained CNO in drinking water before PSNL prevented expression of chronic pain without affecting acute surgical pain; however, relief of chronic pain required sustained CNO treatment. Thus, in male mice, activity of spinally projecting RVM-MOR cells is required (1) for expression and manifestation of both sensory and affective dimensions of established neuropathic pain and (2) to promote descending facilitation that overcomes apparently intact descending inhibition to maintain chronic pain. Enhanced descending facilitation likely regulates the output signal from the spinal cord to the brain to shape the pain experience and may provide a mechanism for nonopioid management of pain.