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      Female Overrepresentation in Low Back-Related Leg Pain: A Retrospective Study of the Autonomic Response to a Minimally Invasive Procedure

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          The newly proposed low back pain treatment requires case classification according to the pain mechanism (nociceptive, neuropathic or nociplastic) to determine the most effective therapeutic approach. However, there is a lack of objective tools for distinguishing these pain mechanisms. The aim of the study was to identify which symptoms, signs, and standard diagnostic parameters would allow predicting the nociplastic pain (NP) subtype among low back leg pain (LBLP) patients.


          A retrospective analysis of an LBLP case–control study database was carried out. The presence of NP was assumed if the patient presented with myofascial pain syndrome (MPS) and developed a short-term intensive vasodilatation reaction in the perceived lower leg pain area after provocation by a minimally invasive procedure. Clinical data and standard LBLP diagnostic parameters were analyzed to classify patients as NP (+) vs NP (-). Next, to predict NP probability, logistic regression analysis and a diagnostic classification tree were constructed.


          NP was confirmed in 43.75% of LBLP patients. Women represented 95.24% of all NP (+) patients. The diagnostic classification tree indicated that NP was highly probable if the LBLP subject was female and the result of a positive straight leg raise (SLR) test was lower than 45 degrees. If the SLR test result was greater than or equal to 45 degrees, a negative result on the Bragard test would have diagnostic value. This classification tree was approved to a certain extent in the logistic regression model (deviance residuals, min: −1.8519; 1Q: −0.5551; median: −0.1907; 3Q: 0.6565 and max: 2.1058) but should be verified in a larger group of subjects.


          Female sex, but not clinical data or standard diagnostic parameters, is indicative of nociplastic pain in LBLP patients. More sophisticated statistical methods, based on directly measurable parameters, should be proposed to distinguish NP involvement in LBLP.

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          Most cited references 29

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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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            Users' guides to the medical literature: XXII: how to use articles about clinical decision rules. Evidence-Based Medicine Working Group.

            Clinical experience provides clinicians with an intuitive sense of which findings on history, physical examination, and investigation are critical in making an accurate diagnosis, or an accurate assessment of a patient's fate. A clinical decision rule (CDR) is a clinical tool that quantifies the individual contributions that various components of the history, physical examination, and basic laboratory results make toward the diagnosis, prognosis, or likely response to treatment in a patient. Clinical decision rules attempt to formally test, simplify, and increase the accuracy of clinicians' diagnostic and prognostic assessments. Existing CDRs guide clinicians, establish pretest probability, provide screening tests for common problems, and estimate risk. Three steps are involved in the development and testing of a CDR: creation of the rule, testing or validating the rule, and assessing the impact of the rule on clinical behavior. Clinicians evaluating CDRs for possible clinical use should assess the following components: the method of derivation; the validation of the CDR to ensure that its repeated use leads to the same results; and its predictive power. We consider CDRs that have been validated in a new clinical setting to be level 1 CDRs and most appropriate for implementation. Level 1 CDRs have the potential to inform clinical judgment, to change clinical behavior, and to reduce unnecessary costs, while maintaining quality of care and patient satisfaction. JAMA. 2000;284:79-84
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              Sex differences in pain: a brief review of clinical and experimental findings.

              Recent years have witnessed substantially increased research regarding sex differences in pain. The expansive body of literature in this area clearly suggests that men and women differ in their responses to pain, with increased pain sensitivity and risk for clinical pain commonly being observed among women. Also, differences in responsivity to pharmacological and non-pharmacological pain interventions have been observed; however, these effects are not always consistent and appear dependent on treatment type and characteristics of both the pain and the provider. Although the specific aetiological basis underlying these sex differences is unknown, it seems inevitable that multiple biological and psychosocial processes are contributing factors. For instance, emerging evidence suggests that genotype and endogenous opioid functioning play a causal role in these disparities, and considerable literature implicates sex hormones as factors influencing pain sensitivity. However, the specific modulatory effect of sex hormones on pain among men and women requires further exploration. Psychosocial processes such as pain coping and early-life exposure to stress may also explain sex differences in pain, in addition to stereotypical gender roles that may contribute to differences in pain expression. Therefore, this review will provide a brief overview of the extant literature examining sex-related differences in clinical and experimental pain, and highlights several biopsychosocial mechanisms implicated in these male-female differences. The future directions of this field of research are discussed with an emphasis aimed towards further elucidation of mechanisms which may inform future efforts to develop sex-specific treatments.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                18 December 2020
                : 13
                : 3427-3435
                [1 ]Department of Physiotherapy, Poznan University of Medical Sciences , Poznan, Poland
                [2 ]Department of Orthopedics, Traumatology and Hand Surgery Poznan University of Medical Sciences , Poznan, Poland
                [3 ]Department of Virtual Engineering, Poznan University of Technology , Poznan, Poland
                [4 ]Department of Mathematics and Mathematical Economics, Warsaw School of Economics , Warsaw, Poland
                [5 ]Department of Cell Biology, Poznan University of Medical Sciences , Poznan, Poland
                Author notes
                Correspondence: Elzbieta Skorupska Department of Physiotherapy, Poznan University of Medical Sciences , Smoluchowskiego 11, Poznan60-179, PolandTel/Fax +48 61 831-02-17 Email skorupska@ump.edu.pl
                © 2020 Skorupska et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 3, Tables: 3, References: 30, Pages: 9
                Original Research


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