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Narrative Review of Pathophysiology and Endoscopic Management of Basivertebral and Sinuvertebral Neuropathy for Chronic Back Pain.

Chronic lower back pain is a leading cause of disability in musculoskeletal system. Degenerative disc disease is one of the main contributing factor of chronic back pain in the aging population in the world. It is postulated that sinuvertebral nerve and basivertebral nerve main mediator of the nociceptive response in degenerative disc disease as a result of neurotization of sinuvertebral and basivertebral nerve. A review in literature is done on the pathoanatomy, pathophysiology and pain generation pathway in degenerative disc disease and chronic back pain and management strategy is discussed in this review to aid understanding of sinuvertebral and basivertebral neuropathy treatment strategies.

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Characterization of health concerns in people with neurofibromatosis type 1.

Neurofibromatosis 1 (NF1) is a common cancer predisposition syndrome. Affected individuals require lifelong surveillance and often suffer progressive disfigurement due to cutaneous neurofibromas. The aim of this research was to characterize health concerns and quality of life (QOL) in a population cohort.

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Structural and functional properties of spinal dorsal horn neurons after peripheral nerve injury change overtime via astrocyte activation.

Chronic pain remains challenging to treat, despite numerous reports of its pathogenesis, including neuronal plasticity in the spinal dorsal horn (SDH). We hypothesized that understanding plasticity only at a specific time point after peripheral nerve injury (PNI) is insufficient to solve chronic pain. Here, we analyzed the temporal changes in synaptic transmission and astrocyte-neuron interactions in SDH after PNI. We found that synaptic transmission in the SDH after PNI changed in a time-dependent manner, which was accompanied by astrocyte proliferation and loss of inhibitory and excitatory neurons. Furthermore, neuronal loss was accompanied by necroptosis. Short-term inhibition of astrocytes after PNI suppressed these physiological and morphological changes and long-term pain-related behaviors. These results are the first to demonstrate that the inhibition of astrocyte proliferation after PNI contributes to the long-term regulation of plasticity and of necroptosis development in the SDH.

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Rheumatoid arthritis and the risk of preterm birth.

During pregnancy, many diseases are correlated with different adverse outcomes. In turn, pregnancy affects the body, leading to increased disease susceptibility. This interplay between diseased states and pregnancy outcomes is illustrated in the effect of the chronic autoimmune disorder, rheumatoid arthritis (RA), and the adverse outcome, preterm birth (PTB). RA is a systemic disorder characterized by inflammation of the joints and other body organs. Joint pain and swelling are the most prominent manifestations of RA during pregnancy. However, the exact role of RA on PTB among pregnant women has yet to be established. This review highlighted the immunologic mechanisms involved in PTB in pregnant patients with RA. The immune cell population in pregnant women with RA exhibits higher activity of macrophages, dendritic cells, neutrophils, helper T (Th) 1 cells, and Vδ1 cells, but lower activity of CD4 + CD25 T regulatory (CD24 + CD25 T ), Th2, and Vδ2 cells. Increased pro-inflammatory cytokines IL-6, TNF-α, and IFN-γ and decreased anti-inflammatory cytokines IL-12 and IL-10 are also exhibited by pregnant patients with RA. This review also discussed factors that may predict the risk of PTB in RA. These include disease activity and severity of RA, laboratory parameters (cytokines and immune cell population), and sociodemographic factors such as ethnicity, smoking, alcohol intake, and the level of education. Current findings on the underlying immunological mechanisms of RA can help identify possible strategies to prevent PTB. This article is protected by copyright. All rights reserved.

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Nation-wide decrease in the prevalence of pediatric chronic pain during the COVID-19 pandemic.

The COVID-19 pandemic was expected to increase prevalence and severity of chronic pain. We compared pandemic-era and pre-pandemic prevalence of chronic pain among children in the US.

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Tapentadol and the opioid epidemic: a simple solution or short-lived sensation?

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Micromagnetic Stimulation (μMS) Dose-Response of the Rat Sciatic Nerve.

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Monoaminergic mediation of hyperalgesic and analgesic descending control of nociception in mice.

Descending control of nociception (DCN; also known as conditioned pain modulation [CPM], the behavioral correlate of diffuse noxious inhibitory controls) is the phenomenon whereby pain inhibits pain in another part of the body and is the subject of increasing study because it may represent a biomarker of chronic pain. We recently discovered that pain modulation on the application of a DCN paradigm involving low-intensity test stimuli occurs in the direction of hyperalgesia in healthy mice and rats, whereas the use of high-intensity stimuli produces analgesia. To elucidate the physiological mechanisms underlying hyperalgesic DCN, we administered agonists and antagonists of norepinephrine (NE) and serotonin (5-HT) receptors, key neurochemical players in the production of analgesic DCN. We find that 3 different monoamine reuptake inhibitors-the NE-selective reboxetine, the 5-HT-selective fluoxetine, and the dual NE/5-HT agonist duloxetine-all abolish hyperalgesic DCN when administered into the spinal cord (but not systemically), with no effect on heat or mechanical pain sensitivity. The reversal by reboxetine of hyperalgesic DCN is mediated by α2-adrenergic receptors (ie, blocked by atipamezole), and the fluoxetine reversal is mediated by 5-HT7 receptors (ie, blocked by SB269970). By contrast, analgesic DCN was found to be reversed by atipamezole and SB269970 themselves, with no effect of reboxetine or fluoxetine. Thus, hyperalgesic DCN seems to be the neurochemical opposite to analgesic DCN. These data further validate and help elucidate a preclinical paradigm that mimics dysfunctional CPM and thus may form the basis of translational experiments that aim to reveal preventative pharmacological strategies for individuals predisposed to persistent pain.

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Macrophage and neutrophil heterogeneity at single-cell spatial resolution in inflammatory bowel disease.

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Clinical hypnosis for Procedural Pain and Distress in Children: A Scoping Review.

Pain and distress are common in children undergoing medical procedures, exposing them to acute and chronic biopsychosocial impairments if inadequately treated. Clinical hypnosis has emerged as a potentially beneficial treatment for children's procedural pain and distress due to evidence of effectiveness and potential superiority to other psychological interventions. However, systematic reviews of clinical hypnosis for children's procedural pain and distress have been predominantly conducted in children undergoing oncology and needle procedures and are lacking in broader paediatric contexts. This scoping review maps the evidence of clinical hypnosis for children's procedural pain and distress across broad paediatric contexts while highlighting knowledge gaps and areas requiring further investigation.

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