Articles: neuropathic-pain.
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Journal of pain research · Jan 2018
OnabotulinumtoxinA injections for atypical odontalgia: an open-label study on nine patients.
Atypical odontalgia (AO) manifests as continuous pain in the region of one or several teeth, in the absence of signs of dental pathology. Currently, there is insufficient evidence to establish treatment guidelines for AO. The aim of this study was to describe the effectiveness and safety of treatment with OnabotulinumtoxinA (OnabotA) on a series of patients with AO. ⋯ OnabotA may be a safe and effective option for the treatment of AO.
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Journal of pain research · Jan 2018
Botulinum toxin-A for the treatment of neuralgia: a systematic review and meta-analysis.
This meta-analysis was performed to evaluate the efficacy and safety of botulinum toxin-A (BTX-A) for the treatment of neuralgia. ⋯ Based on the current evidence, BTX-A may be an effective and safe option for the treatment of neuralgia. Due to the limited number of patients included in this meta-analysis, more trials are still needed to confirm these results.
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Introduction Neuropathic pain is a debilitating condition. The importance of neuroimmune interactions in neuropathic pain has been evidenced by the involvement of different immune cells in peripheral and central sensitization of pathological pain. Macrophages and microglia are the most abundant immune cells activated in injured nerves and spinal cord, respectively. ⋯ Microglia activation in dorsal horn of lumbar spinal cord following partial sciatic nerve ligation was significantly inhibited with PLX5622 treatment in both preventive and reversal paradigms. Conclusion Macrophages in peripheral nerve and microglia in the spinal cord are required in the generation and maintenance of injury-associated neuropathic pain. Blocking macrophage-colony stimulating factor/colony stimulating factor 1 receptor signaling on these myeloid cells along the pain transmission pathway is an effective strategy to alleviate neuropathic pain.
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Neuropathic pain is caused by peripheral nerve injury (PNI). One hallmark symptom is allodynia (pain caused by normally innocuous stimuli), but its mechanistic underpinning remains elusive. Notably, whether selective stimulation of non-nociceptive primary afferent Aβ fibers indeed evokes neuropathic pain-like sensory and emotional behaviors after PNI is unknown, because of the lack of tools to manipulate Aβ fiber function in awake, freely moving animals. ⋯ Moreover, illuminating the hindpaw of PNI rats resulted in activation of central amygdaloid neurons and produced an aversion to illumination. Thus, these findings provide the first evidence that optogenetic activation of primary afferent Aβ fibers in PNI rats produces excitation of Lamina I neurons and neuropathic pain-like behaviors that were resistant to morphine treatment. This approach may provide a new path for investigating circuits and behaviors of Aβ fiber-mediated neuropathic allodynia with sensory and emotional aspects after PNI and for discovering novel drugs to treat neuropathic pain.
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Patients with chronic pain often have symptoms similar to neuropathic pain (NeP). Such symptoms are also frequently observed in people with knee osteoarthritis (OA). However, pain quality may be related to psychological problems such as high pain catastrophizing and/or low self-efficacy. The objective of the current study was to investigate whether pain quality is associated with pain catastrophizing and self-efficacy in individuals with symptomatic knee OA. ⋯ High pain catastrophizing and low self-efficacy for pain control are significantly associated with the existence of an NeP component on PDQ in people with symptomatic knee OA.