TAILIEUCHUNG - Spinal Disorders: Fundamentals of Diagnosis and Treatment Part 17

Spinal Disorders: Fundamentals of Diagnosis and Treatment Part 171. Spinal disorders are among the most common medical conditions with significant impact on health related quality of life, use of health care resources and socio-economic costs. Spinal surgery is still one of the fastest growing areas in clinical medicine. | PathwaysofSpinal Pain Chapter 5 135 locus ceruleus arousal vigilance behavior parts of the periaqueductal gray fight and flight response stress-induced analgesia Projections from the periaqueductal gray play a role in controlling anti-nociceptive and autonomic responses to nociceptive stimuli 81 . Neuroplasticity Persistent pain is not just a simple prolongation of acute nociceptive pain but results from distinct alterations in the pain pathways. Peripheral tissue damage or nerve injury can result in a pathological state in which there is a reduction in pain threshold allodynia an increased response to noxious stimuli hyperalgesia an increase in the duration of response to brief stimulation persistent pain and a spread of pain and hyperalgesia to uninjured tissue referred pain and secondary hyperalgesia 17 . These alterations in the pain pathways are usually referred to as neuroplasticity. Peripheral Sensitization Tissue damage results in the release of inflammatory mediators including ions H K bradykinin histamine 5-hydroxytryptamine 5-HT ATP and nitric oxide NO . The tissue injury activates the arachidonic acid pathway which results in the production of prostanoids and leukotrienes 60 . Inflammatory mediators are also released from attracted cells such as mast cells fibroblasts neutrophils and platelets 55 . Tissue damage and inflammation leads to low pH which enhances painful sensations by sensitizing and activating the vanilloid receptor 1 TRPV1 49 . Inflammatory mediators . prostaglandin E2 brady- Alterations in the pain pathways characterize neuroplasticity Tissue damage results in inflammatory mediator release Figure 6. Neuroplasticity of the nociceptor a Peripheral sensitization NGF nerve growth factor BK bradykinin TRPV1 transient receptor potential vanilloid 1 channel EP prostaglandin E receptor PK protein kinases AA arachidonic acid PGE2 prostaglandin TrkA tyrosine kinase A receptor Cox2 cyclooxygenase 2 . b Transcriptional change in the DRG PKA .

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