Articles: neuropathic-pain.
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The objective of this study was to compare the efficacy and safety of pregabalin for painful diabetic peripheral neuropathy (pDPN) in subjects with type 1 (T1DM) or 2 diabetes mellitus (T2DM). ⋯ Pregabalin significantly improved pain and sleep quality, without a clinically meaningful difference between diabetes types. ClinicalTrial.gov registration: NCT00156078, NCT00159679, NCT00143156, NCT00553475.
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Journal of neurotrauma · Nov 2018
The Amelioration of Pain-Related Behavior in Mice with Chronic Spinal Cord Injury Treated with Neural Stem/Progenitor Cell Transplantation Combined with Treadmill Training.
Progress in regenerative medicine is realizing the possibility of neural regeneration and functional recovery in spinal cord injury (SCI). Recently, rehabilitation has attracted much attention with respect to the synergistic promotion of functional recovery in combination with neural stem/progenitor cell (NS/PC) transplantation, even in the chronic refractory phase of SCI. Nevertheless, sensory disturbance is one of the most prominent sequelae, even though the effects of combination or single therapies have been investigated mostly in the context of motor recovery. ⋯ Although no remarkable histological recovery was found within the lesion epicenter, changes indicating amelioration of pain were observed in the lumbar enlargement of the combination therapy group. Our results suggest that amelioration of thermal allodynia and tactile hyperalgesia can be brought about by the additive effect of NS/PC transplantation and TMT. The degree of recovery seems dependent on the distribution of damage.
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It is widely believed that cortical changes are a consequence of longstanding neuropathic pain (NP). In this article, we demonstrate that NP in individuals with subacute spinal cord injury (SCI) has characteristic electroencephalography markers (EEG) that precede the onset of pain. EEG was recorded in a relaxed state and during motor imagination tasks in 10 able-bodied participants and 31 patients with subacute SCI (11 with NP, 10 without NP, and 10 who had pain develop within 6 months of EEG recording). ⋯ Clinical Trial Registration Number: NCT02178917 PERSPECTIVE: We demonstrate that brain activity in patients with subacute SCI reveals both early markers and predictors of NP, which may manifest before sensory discomfort. These markers and predictors may complement known sensory phenotypes of NP. They may exist in other patient groups suffering from NP of central origin.
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MicroRNAs (miRNAs) are recognized as significant regulators of neuropathic pain. Moreover, neuroinflammation can contribute a lot to the progression of neuropathic pain. MiR-28-5p has been reported to be involved in many pathological diseases. ⋯ Theoverexpression of Zeb1 can disturb neuropathic pain development, which was repressed by the increase of miR-28-5p by upregulating Cox-2, IL-6, and IL-1β levels. By taking all of these together, it was indicated in our study that miR-28-5p can reduce neuropathic pain progression by targeting Zeb1 in vivo. Our data implied that miR-28-5p/Zeb1 axis can be a novel therapeutic target for neuropathic pain treatment.
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Here, we review the literature assessing the role of transient receptor potential ankyrin 1 (TRPA1), a calcium-permeable non-selective cation channel, in various types of pain conditions. In the nervous system, TRPA1 is expressed in a subpopulation of nociceptive primary sensory neurons, astroglia, oligodendrocytes and Schwann cells. In peripheral terminals of nociceptive primary sensory neurons, it is involved in the transduction of potentially harmful stimuli and in their central terminals it is involved in amplification of nociceptive transmission. ⋯ In experimental animal studies, pharmacological or genetic blocking of TRPA1 has effectively attenuated mechanical and cold pain hypersensitivity in various experimental models of pathophysiological pain, with only minor side effects, if any. TRPA1 antagonists acting peripherally are likely to be optimal for attenuating primary hyperalgesia (such as inflammation-induced sensitization of peripheral nerve terminals), while centrally acting TRPA1 antagonists are expected to be optimal for attenuating pain conditions in which central amplification of transmission plays a role (such as secondary hyperalgesia and tactile allodynia caused by various types of peripheral injuries). In an experimental model of peripheral diabetic neuropathy, prolonged blocking of TRPA1 has delayed the loss of nociceptive nerve endings and their function, thereby promising to provide a disease-modifying treatment.