Articles: neuropathic-pain.
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Members of the miR-183 family are unique in that they are highly abundant in sensory organs. In a recent study, significant downregulation was observed for miR-96 and miR-183 in the L5 dorsal root ganglion (DRG) 2 weeks after spinal nerve ligation (SNL). In this study, we focused on miR-183, which is the most regulated member of the miR-183 family, to look at the specific role on neuropathic pain. ⋯ Intrathecal administration of lentivirions expressing miR-183 downregulated SNL-induced increases in the expression of Nav1.3 and brain-derived neurotrophic factor (BDNF), which correlated with the significant attenuation of SNL-induced mechanical allodynia. Our results show that SNL-induced mechanical allodynia is significantly correlated with the decreased expression of miR-183 in DRG cells. Replacement of miR-183 downregulates SNL-induced increases in Nav1.3 and BDNF expression, and attenuates SNL-induced mechanical allodynia.
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Randomized Controlled Trial
Sensory correlates of pain in peripheral neuropathies.
To characterize sensory threshold alterations in peripheral neuropathies and the relationship between these alterations and the presence of pain. ⋯ There is a complex relationship between the loss or functional deficit of large and especially small sensory nerve fibers and the development of pain in peripheral neuropathy.
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Chronic pain associated with traumatic spinal cord injury (SCI) can be quite challenging to the physiatrist. This highly prevalent condition within the SCI population requires an appropriate evaluative approach including a thorough history, a targeted physical examination, and appropriate use of diagnostic testing. ⋯ A multitude of management approaches exist including nonpharmacologic, pharmacologic, and interventional approaches. This article provides an overview of the epidemiology, classification, evaluation, and management of SCI-associated pain.
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Background: Pulsed radiofrequency (PRF) has been widely used to treat chronic pain, but the effectiveness and mechanisms in preventing early neuropathic pain have not been well explored. Even fewer knowledge is available in its impact on glia-mediated nociceptive sensitization. This study aims to elucidate the modulation of PRF on nerve injury-induced pain development and activation of spinal mitogen-activated protein kinases (MAPKs). ⋯ Conclusions: Low-volt PRF significantly ameliorated SNL-induced acute pain. Inferentially, PRF may inhibit spinal sensitization by down-regulating spinal MAPK activations and activation-mediated cytokine release. We demonstrated that early PRF treatment in acute nerve injury helps to ameliorate neuropathic pain development.
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Experimental neurology · May 2014
Coupling of serotonergic input to NMDA receptor-phosphorylation following peripheral nerve injury via rapid, synaptic up-regulation of ND2.
Evidence implicates serotonergic input to spinal dorsal horn neurons in shifting the NMDA receptor (NMDAR) into a high functional output profile after spinal nerve ligation (SNL). We investigated the involvement of adaptor protein NADH dehydrogenase subunit 2 (ND2) in NMDAR-phosphorylation and spinal hyperexcitability secondary to peripheral nerve injury. Immunofluorescence for ND2 was found in dorsal horn neurons immunopositive for NMDAR subunit NR1. ⋯ Rotenone also abolished enhancement of evoked potentials induced by simultaneous stimulation of NMDA and 5-HR2B receptors in uninjured rats. Increased postsynaptic up-regulation of ND2/pNMDAR 60min after SNL was prevented by prior administration of selective 5-HT2B antagonist SB204741. These results support a pivotal role for ND2 in coupling serotonergic input to NMDAR-activation during neuropathic pain.