Abstract
Chronic back pain is an actual problem of clinical medicine, the pathogenesis of which includes peripheral nociceptive stimulation, peripheral and/or central inflammation, abnormality of the central pain modulation network and mixed onset of various pathological mechanisms. Sources of nociceptive signal generation include the intervertebral disc, muscles, fasciae, facet joints, sacroiliac joints, pubic symphysis, ligaments and joint capsule, and other structures that contain nociceptors. Any event that causes tissue degeneration activates a massive inflammatory response that infiltrates the MPD, joints, muscles, fascia and other tissues, stimulates nociceptive receptors to produce inflammatory substances, which directly damages the nerve root and causes pain. Simultaneously, the damaged MPD and endplate stimulate pathological and invasive growth and proliferation of vessels and nerves in the MPD. Increasing evidence also suggests that systemic inflammation plays a crucial role in the pathogenesis of chronic back pain. The central mechanism of back pain involves altered sensory processing in the brain. Dysfunction of the descending pain modulation system results in amplification of pain information in the brain. Since monotherapy for chronic back pain is not optimal, it is necessary to promote the comprehensive treatment recommended by current international clinical guidelines and it is reasonable to combine several therapies to improve the clinical effect of therapy. The combination of Tizanidine and Mirtazapine is an effective pharmacotherapy for chronic back pain. KEYWORDS: Chronic back pain, pathogenesis of dorsalgia, Tizanidine, Mirtazapine
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
