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      Enhancing Annular Fissures and High-Intensity Zones: Pain, Internal Derangement, and Anesthetic Response at Provocation Lumbar Discography

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          Magnetic resonance classification of lumbar intervertebral disc degeneration.

          A reliability study was conducted. To develop a classification system for lumbar disc degeneration based on routine magnetic resonance imaging, to investigate the applicability of a simple algorithm, and to assess the reliability of this classification system. A standardized nomenclature in the assessment of disc abnormalities is a prerequisite for a comparison of data from different investigations. The reliability of the assessment has a crucial influence on the validity of the data. Grading systems of disc degeneration based on state of the art magnetic resonance imaging and corresponding reproducibility studies currently are sparse. A grading system for lumbar disc degeneration was developed on the basis of the literature. An algorithm to assess the grading was developed and optimized by reviewing lumbar magnetic resonance examinations. The reliability of the algorithm in depicting intervertebral disc alterations was tested on the magnetic resonance images of 300 lumbar intervertebral discs in 60 patients (33 men and 27 women) with a mean age of 40 years (range, 10-83 years). All scans were analyzed independently by three observers. Intra- and interobserver reliabilities were assessed by calculating kappa statistics. There were 14 Grade I, 82 Grade II, 72 Grade III, 68 Grade IV, and 64 Grade V discs. The kappa coefficients for intra- and interobserver agreement were substantial to excellent: intraobserver (kappa range, 0.84-0.90) and interobserver (kappa range, 0.69-0.81). Complete agreement was obtained, on the average, in 83.8% of all the discs. A difference of one grade occurred in 15.9% and a difference of two or more grades in 1.3% of all the cases. Disc degeneration can be graded reliably on routine T2-weighted magnetic resonance images using the grading system and algorithm presented in this investigation.
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            Central sensitization: implications for the diagnosis and treatment of pain.

            Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity. Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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              High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging.

              The prevalence, validity and reliability of high-intensity zones in the annulus fibrosus seen on T2-weighted magnetic resonance images of patients with intractable low-back pain were determined. This sign was readily recognized by two independent observers. It occurred in 28% of 500 patients undergoing magnetic resonance imaging for back pain. The presence of a high-intensity zone correlated significantly with the presence of Grade 4 annular disruption and with reproduction of the patient's pain. Its sensitivity as a sign of either annular disruption or pain was modest but its specificity was high, and its positive predictive value for a severely disrupted, symptomatic disc was 86%. This sign is diagnostic of painful internal disc disruption.
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                Author and article information

                Contributors
                Journal
                American Journal of Neuroradiology
                AJNR Am J Neuroradiol
                American Society of Neuroradiology (ASNR)
                0195-6108
                1936-959X
                January 11 2023
                January 2023
                January 2023
                December 22 2022
                : 44
                : 1
                : 95-104
                Article
                10.3174/ajnr.A7749
                36549846
                0e8eadef-9b96-4b72-8793-deb7d91e9ae2
                © 2022
                History

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