chronic pain
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2022 ◽  
Vol 270 ◽  
pp. 286-292
Colleen M. Trevino ◽  
Timothy Geier ◽  
Rachel Morris ◽  
Susan Cronn ◽  
Terri deRoon-Cassini

Conor G. Loftus ◽  
Jon O. Ebbert ◽  
Christopher A. Aakre ◽  
Natalie A. Caine ◽  
Meredith A. DeZutter ◽  

2022 ◽  
Vol 9 ◽  
Samantha P. Bento ◽  
Amy E. Hale ◽  
Rachael Coakley

Chronic pain is pain that lasts for more than 3 months. About one quarter of kids and teens have this type of pain. Chronic pain includes problems like frequent headaches, stomachaches, or ongoing joint or muscle pain and it often interferes with kids’ sleep, school, activities, and friendships. Even though chronic pain can have a big impact on kids’ lives, “chronic” does not mean “permanent.” Most kids recover from chronic pain. However, many kids are surprised to hear that a part of getting better involves learning a group of skills that are based in psychology. These skills include a combination of mind-body relaxation techniques and strategies for breaking the cycles of pain focused thoughts and avoidance behaviors. Learning these skills helps to boost feelings of comfort, lowers pain, and gets kids back to doing the things they love!

2022 ◽  
Vol 12 ◽  
Amélie Démosthènes ◽  
Benoît Sion ◽  
Fabrice Giraudet ◽  
Xavier Moisset ◽  
Laurence Daulhac ◽  

Among the many symptoms (motor, sensory, and cognitive) associated with multiple sclerosis (MS), chronic pain is a common disabling condition. In particular, neuropathic pain symptoms are very prevalent and debilitating, even in early stages of the disease. Unfortunately, chronic pain still lacks efficient therapeutic agents. Progress is needed (i) clinically by better characterizing pain symptoms in MS and understanding the underlying mechanisms, and (ii) preclinically by developing a more closely dedicated model to identify new therapeutic targets and evaluate new drugs. In this setting, new variants of experimental autoimmune encephalomyelitis (EAE) are currently developed in mice to exhibit less severe motor impairments, thereby avoiding confounding factors in assessing pain behaviors over the disease course. Among these, the optimized relapsing-remitting EAE (QuilA-EAE) mouse model, induced using myelin oligodendrocyte glycoprotein peptide fragment (35–55), pertussis toxin, and quillaja bark saponin, seems very promising. Our study sought (i) to better define sensitive dysfunctions and (ii) to extend behavioral characterization to interfering symptoms often associated with pain during MS, such as mood disturbances, fatigue, and cognitive impairment, in this optimized QuilA-EAE model. We made an in-depth characterization of this optimized QuilA-EAE model, describing for the first time somatic thermal hyperalgesia associated with mechanical and cold allodynia. Evaluation of orofacial pain sensitivity showed no mechanical or thermal allodynia. Detailed evaluation of motor behaviors highlighted slight defects in fine motor coordination in the QuilA-EAE mice but without impact on pain evaluation. Finally, no anxiety-related or cognitive impairment was observed during the peak of sensitive symptoms. Pharmacologically, as previously described, we found that pregabalin, a treatment commonly used in neuropathic pain patients, induced an analgesic effect on mechanical allodynia. In addition, we showed an anti-hyperalgesic thermal effect on this model. Our results demonstrate that this QuilA-EAE model is clearly of interest for studying pain symptom development and so could be used to identify and evaluate new therapeutic targets. The presence of interfering symptoms still needs to be further characterized.

2022 ◽  
Vol 23 (2) ◽  
pp. 955
Hana Ujcikova ◽  
Dagoberto Robles ◽  
Xu Yue ◽  
Petr Svoboda ◽  
Yeon Sun Lee ◽  

Chronic pain is associated with time-dependent structural and functional reorganization of the prefrontal cortex that may reflect adaptive pain compensatory and/or maladaptive pain-promoting mechanisms. However, the molecular underpinnings of these changes and whether there are time-dependent relationships to pain progression are not well characterized. In this study, we analyzed protein composition in the medial prefrontal cortex (mPFC) of rats at two timepoints after spinal nerve ligation (SNL) using two-dimensional gel electrophoresis (2D-ELFO) and liquid chromatography with tandem mass spectrometry (LC–MS/MS). SNL, but not sham-operated, rats developed persistent tactile allodynia and thermal hyperalgesia, confirming the presence of experimental neuropathic pain. Two weeks after SNL (early timepoint), we identified 11 proteins involved in signal transduction, protein transport, cell homeostasis, metabolism, and apoptosis, as well as heat-shock proteins and chaperones that were upregulated by more than 1.5-fold compared to the sham-operated rats. Interestingly, there were only four significantly altered proteins identified at 8 weeks after SNL (late timepoint). These findings demonstrate extensive time-dependent modifications of protein expression in the rat mPFC under a chronic neuropathic pain state that might underlie the evolution of chronic pain characterized by early pain-compensatory and later aberrant mechanisms.

Liangyu Pan ◽  
Tiansheng Li ◽  
Rui Wang ◽  
Weiheng Deng ◽  
Huangsheng Pu ◽  

Medicine ◽  
2022 ◽  
Vol 101 (2) ◽  
pp. e28497
Guangxin Guo ◽  
Boyi Wu ◽  
Shengji Xie ◽  
Jianghan Xu ◽  
Xu Zhou ◽  

2022 ◽  
Vol 15 ◽  
Alison Xiaoqiao Xie ◽  
Sarah Taves ◽  
Ken McCarthy

Chronic neuropathic pain leads to long-term changes in the sensitivity of both peripheral and central nociceptive neurons. Glial fibrillary acidic protein (GFAP)-positive glial cells are closely associated with the nociceptive neurons including astrocytes in the central nervous system (CNS), satellite glial cells (SGCs) in the sensory ganglia, and non-myelinating Schwann cells (NMSCs) in the peripheral nerves. Central and peripheral GFAP-positive cells are involved in the maintenance of chronic pain through a host of inflammatory cytokines, many of which are under control of the transcription factor nuclear factor κB (NFκB) and the enzyme cyclooxygenase 2 (COX2). To test the hypothesis that inhibiting GFAP-positive glial signaling alleviates chronic pain, we used (1) a conditional knockout (cKO) mouse expressing Cre recombinase under the hGFAP promoter and a floxed COX2 gene to inactivate the COX2 gene specifically in GFAP-positive cells; and (2) a tet-Off tetracycline transactivator system to suppress NFκB activation in GFAP-positive cells. We found that neuropathic pain behavior following spared nerve injury (SNI) significantly decreased in COX2 cKO mice as well as in mice with decreased glial NFκB signaling. Additionally, experiments were performed to determine whether central or peripheral glial NFκB signaling contributes to the maintenance of chronic pain behavior following nerve injury. Oxytetracycline (Oxy), a blood-brain barrier impermeable analog of doxycycline was employed to restrict transgene expression to CNS glia only, leaving peripheral glial signaling intact. Signaling inactivation in central GFAP-positive glia alone failed to exhibit the same analgesic effects as previously observed in animals with both central and peripheral glial signaling inhibition. These data suggest that the NFκB-COX2 signaling pathway in NMSCs is necessary for the maintenance of neuropathic pain in vivo.

2022 ◽  
Vol Publish Ahead of Print ◽  
Nicholas F. Rockefeller ◽  
Timothy R. Petersen ◽  
Peter C. Jeppson ◽  
Gena Dunivan ◽  
Cara Ninivaggio ◽  

2022 ◽  
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