Articles: neuralgia.
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J. Neurol. Neurosurg. Psychiatr. · Feb 2017
Chronic neuropathic pain severity is determined by lesion level in aquaporin 4-antibody-positive myelitis.
Chronic, intractable neuropathic pain is a common and debilitating consequence of neuromyelitis optica spectrum disorder (NMOSD) myelitis, with no satisfactory treatment; few studies have yet to explore its aetiology. ⋯ Persistent, caudally located (ie, thoracic) cord lesions in AQP4-Ab-positive patients associate with high postmyelitis chronic pain scores, irrespective of number of myelitis relapses, lesion length and lesion burden. Although disability correlated with pain in isolation, it became an insignificant predictor of pain when analysed alongside craniocaudal location of lesions.
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Experimental neurology · Feb 2017
Lentiviral vector-driven inhibition of 5-HT synthesis in B3 bulbo-spinal serotonergic projections - Consequences on nociception, inflammatory and neuropathic pain in rats.
Although it is well established that bulbo-spinal serotonergic projections contribute to pain control mechanisms, whether they exert anti- or pro-nociceptive modulations is still a matter of debate. In order to reappraise the role of 5-HT in descending controls, we used RNA interference to selectively inhibit 5-HT synthesis in B3 neurons and assess resulting changes in nociception. Rats were injected into the bulbar B3 group with a recombinant lentiviral vector, LV-shTPH2, encoding RNA interfering with tryptophan hydroxylase 2 expression. ⋯ Parallel changes in c-Fos immunolabeling within the dorsal horn confirmed that bulbo-spinal serotonergic projections modulate pain signaling under these various conditions. These results suggest that serotonergic neurons of the B3 group are only moderately concerned, if any, by acute nociception but exert modulatory influences under pain sensitizing conditions. The opposite changes in formalin injected- versus sciatic nerve ligated rats might be related to the implication of different receptors in 5-HT-mediated modulation of inflammatory versus neuropathic pain.
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J Oral Facial Pain Headache · Jan 2017
ReviewTopical Review: Potential Use of Botulinum Toxin in the Management of Painful Posttraumatic Trigeminal Neuropathy.
Painful posttraumatic trigeminal neuropathy (PPTTN) is a chronic condition that is difficult to endure and has a poorly understood pathophysiology. Treatment options are limited and often unsatisfactory due to insufficient efficacy and significant adverse effects. Botulinum toxin type A (BTX-A), initially used in the management of pathologically sustained or twisting muscular contractions, has recently been advocated for treatment of neuropathic pain. ⋯ When injected into the painful location, the toxin can be taken up by peripheral terminals of nociceptive afferent nerve fibers, and this action suppresses peripheral and central release of algogenic neurotransmitters such as glutamate or substance P, thus promoting analgesia. Several randomized controlled trials in humans have provided emerging evidence for the therapeutic use of BTX-A in neuropathic pain states, including trigeminal neuralgia. This evidence, in addition to its good safety profile and long-lasting effect, suggests that BTX-A could be a potential novel treatment for PPTTN.
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DNA methylation has been implicated in the pathogenesis of chronic pain. However, the specific genes regulated by DNA methylation under neuropathic pain condition remain largely unknown. Here we investigated how chemokine receptor CXCR3 is regulated by DNA methylation and how it contributes to neuropathic pain induced by spinal nerve ligation (SNL) in mice. ⋯ Superfusing spinal cord slices with CXCL10 enhanced spontaneous EPSCs and potentiated NMDA-induced and AMPA-induced currents of lamina II neurons. Finally, intrathecal injection of CXCL10 induced CXCR3-dependent pain hypersensitivity in naive mice. Collectively, our results demonstrated that CXCR3, increased by DNA demethylation and the enhanced interaction with C/EBPα, can be activated by CXCL10 to facilitate excitatory synaptic transmission and contribute to the maintenance of neuropathic pain.
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Chronic pain is broadly classified into somatic, visceral or neuropathic pain depending upon the location and extent of pain perception. Evidences from different animal studies suggest that inflammatory or neuropathic pain is associated with altered acetylation and deacetylation of histone proteins, which result in abnormal transcription of nociceptive processing genes. There have been a number of studies indicating that nerve injury up-regulates histone deacetylase enzymes, which leads to increased histone deacetylation and induce chronic pain. ⋯ On the other hand, a few studies refer to increased expression of histone acetylase enzymes in response to nerve injury that promotes histone acetylation leading to pain induction. Treatment with histone acetyl transferase inhibitors have been reported to relieve chronic pain by blocking the up-regulation of chemokines and cyclooxygenase-2, the critical factors associated with histone acetylation-induced pain. The present review describes the dual role of histone acetylation/deacetylation in development or attenuation of neuropathic pain along with the underlying mechanisms.