Готові списки джерел за темами / Pain sensitization

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Добірка наукової літератури з теми "Pain sensitization"

Автор: Grafiati

Опубліковано: 25 січня 2025

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Статті в журналах з теми "Pain sensitization"

Song, Soo Youn, Ye Won Jung, WonKyo Shin, Mia Park, Geon Woo Lee, Soohwa Jeong, Sukjeong An, et al. "Endometriosis-Related Chronic Pelvic Pain." Biomedicines 11, no. 10 (October 23, 2023): 2868. http://dx.doi.org/10.3390/biomedicines11102868.

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Endometriosis, which is the presence of endometrial stroma and glands outside the uterus, is one of the most frequently diagnosed gynecologic diseases in reproductive women. Patients with endometriosis suffer from various pain symptoms such as dysmenorrhea, dyspareunia, and chronic pelvic pain. The pathophysiology for chronic pain in patients with endometriosis has not been fully understood. Altered inflammatory responses have been shown to contribute to pain symptoms. Increased secretion of cytokines, angiogenic factors, and nerve growth factors has been suggested to increase pain. Also, altered distribution of nerve fibers may also contribute to chronic pain. Aside from local contributing factors, sensitization of the nervous system is also important in understanding persistent pain in endometriosis. Peripheral sensitization as well as central sensitization have been identified in patients with endometriosis. These sensitizations of the nervous system can also explain increased incidence of comorbidities related to pain such as irritable bowel disease, bladder pain syndrome, and vulvodynia in patients with endometriosis. In conclusion, there are various possible mechanisms behind pain in patients with endometriosis, and understanding these mechanisms can help clinicians understand the nature of the pain symptoms and decide on treatments for endometriosis-related pain symptoms.

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Aguggia, Marco, M. G. Saracco, M. Cavallini, G. Bussone, and P. Cortelli. "Sensitization and pain." Neurological Sciences 34, S1 (May 2013): 37–40. http://dx.doi.org/10.1007/s10072-013-1382-0.

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Ramalingam, Thangamani, Pooja Desai, Dhruvi Ghoghari, Vidhi Jethva, and Rushvi Shah. "Neurophysiology of pain education knowledge, pain disability, patient satisfaction and central sensitization in chronic musculoskeletal pain." IP Journal of Surgery and Allied Sciences 4, no. 4 (January 15, 2023): 137–41. http://dx.doi.org/10.18231/j.jsas.2022.026.

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Chronic musculoskeletal pains are multifaceted, and Central sensitization is a potential pathophysiological mechanism underlying a group of chronic musculoskeletal pain disorders. Neurophysiology of pain education knowledge and patient satisfaction levels of chronic musculoskeletal pain subjects may contribute to central nervous system sensitization. Hence, the aim of the study was to evaluate the impact of neurophysiology of pain education knowledge and patient satisfaction levels on central sensitization in large population of patient with chronic musculoskeletal pain. The study included 200 chronic musculoskeletal pain subjects that persisted more than 3 months with average age of 43.93±13.62. A cross-sectional study used non probability sampling. Neurophysiology of pain Questionnaire (NPQ) to know the conceptualization of pain, mood rating scale(MRS) to measure patient’s mood fluctuation because of pain, pain disability scale (PDS) for evaluating patients ability to perform certain activity, central sensitization inventory(CSI) to measure nervous system sensitization and patients satisfaction scale(PSS) to understand patient’s satisfaction towards the treatment and health care provider were used. Descriptive and correlation analyses were used for analysis. The correlation analyses showed that patient disability scale negatively correlated with mood scale and positively correlated with the age, duration of the condition, impact of pain on ADL and central sensitization. And there was a positive correlation between patient satisfaction and impact of pain on ADL. The age, mood, duration of the condition and pain disability were the factors behind central sensitization in patients with chronic musculoskeletal pain. And the neuro physiology of pain knowledge had impact on pain disability and patient satisfaction.

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Coderre, Terence J., and Joel Katz. "Peripheral and central hyperexcitability: Differential signs and symptoms in persistent pain." Behavioral and Brain Sciences 20, no. 3 (September 1997): 404–19. http://dx.doi.org/10.1017/s0140525x97251484.

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This target article examines the clinical and experimental evidence for a role of peripheral and central hyperexcitability in persistent pain in four key areas: cutaneous hyperalgesia, referred pain, neuropathic pain, and postoperative pain. Each suggests that persistent pain depends not only on central sensitization, but also on inputs from damaged peripheral tissue. It is instructive to think of central sensitization as comprised of both an initial central sensitization and an ongoing central sensitization driven by inputs from peripheral sources. Each of these factors, initial sensitization, ongoing central sensitization, and inputs from peripheral sources, contributes to the net activity in dorsal horn neurons and thus influences the expression of persistent pain or hyperalgesia. Since each factor, peripheral inputs and central sensitization (initial or ongoing), can contribute to both the initiation and maintenance of persistent pain, therapies should target both peripheral and central sources of pathology.

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Lee, Jaesung, Seohyun Chung, Minkyu Hwang, Yeongkag Kwon, Seung Hyun Han, and Sung Joong Lee. "Estrogen Mediates the Sexual Dimorphism of GT1b-Induced Central Pain Sensitization." Cells 12, no. 5 (March 6, 2023): 808. http://dx.doi.org/10.3390/cells12050808.

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We have previously reported that the intrathecal (i.t.) administration of GT1b, a ganglioside, induces spinal cord microglia activation and central pain sensitization as an endogenous agonist of Toll-like receptor 2 on microglia. In this study, we investigated the sexual dimorphism of GT1b-induced central pain sensitization and the underlying mechanisms. GT1b administration induced central pain sensitization only in male but not in female mice. Spinal tissue transcriptomic comparison between male and female mice after GT1b injection suggested the putative involvement of estrogen (E2)-mediated signaling in the sexual dimorphism of GT1b-induced pain sensitization. Upon ovariectomy-reducing systemic E2, female mice became susceptible to GT1b-induced central pain sensitization, which was completely reversed by systemic E2 supplementation. Meanwhile, orchiectomy of male mice did not affect pain sensitization. As an underlying mechanism, we present evidence that E2 inhibits GT1b-induced inflammasome activation and subsequent IL-1β production. Our findings demonstrate that E2 is responsible for sexual dimorphism in GT1b-induced central pain sensitization.

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De Meulemeester, Kayleigh, Mira Meeus, Robby De Pauw, Barbara Cagnie, Hannah Keppler, and Dorine Lenoir. "Suffering from chronic tinnitus, chronic neck pain, or both: Does it impact the presence of signs and symptoms of central sensitization?" PLOS ONE 18, no. 8 (August 24, 2023): e0290116. http://dx.doi.org/10.1371/journal.pone.0290116.

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Chronic subjective tinnitus is a prevalent symptom, which has many similarities with chronic pain. Central sensitization is considered as a possible underlying mechanism of both symptoms. Central sensitization has already been investigated in chronic pain populations but not in patients with chronic subjective tinnitus. Therefore, the main objective of this cross-sectional study was to compare signs and symptoms, indicative for central sensitization, in tinnitus patients with and without chronic idiopathic neck pain, patients with chronic idiopathic neck pain only, and healthy controls. Also, differences in psychological and lifestyle factors, possibly influencing the association between central sensitization and tinnitus, were examined as well as correlations between signs and symptoms of central sensitization, and tinnitus, pain, psychological and lifestyle factors. Differences in signs and symptoms of central sensitization were examined using the self-report Central Sensitization Inventory and QST protocol (local and distant mechanical and heat hyperalgesia, conditioned pain modulation). Tinnitus, pain, psychological and lifestyle factors were evaluated using self-report questionnaires. Symptoms of central sensitization and local mechanical hyperalgesia were significantly more present in both tinnitus groups, compared to healthy controls, but were most extensive in the group with chronic tinnitus+chronic idiopathic neck pain. Distant mechanical hyperalgesia, indicative for central sensitization, was only observed in the group with both chronic tinnitus+chronic idiopathic neck pain. This group also displayed a significantly higher psychological burden and poorer sleep than patients with chronic tinnitus only and healthy controls. Signs and symptoms of central sensitization were also shown to be associated with tinnitus impact, pain-related disability, psychological burden and sleep disturbances. This study shows preliminary evidence for the presence of central sensitization in patients with chronic tinnitus+chronic idiopathic neck pain. This could be explained by the higher perceived tinnitus impact, psychological burden and sleep problems in this group. Trial registration: This study is registered as NCT05186259 (www.clinicaltrials.gov).

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AKULINUSHKINA, EKATERINA Y., SVETLANA P. YAKUPOVA, EDUARD Z. YAKUPOV, LARISA V. IVANOVA, TATYANA A. BRAGINA, and NIKOLAI I. MAKSIMOV. "CENTRAL SENSITIZATION IN PSORIATIC ARTHRITIS." Bulletin of Contemporary Clinical Medicine 16, no. 5 (October 2023): 16–21. http://dx.doi.org/10.20969/vskm.2023.16(5).16-21.

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Introduction. Chronic pain consists of nociceptive, neuropathic and nociplastic components. Nociplastic pain based on central sensitization. Patients with central sensitization may experience severe pain even with no any signs of clinical and laboratory inflammation, and describe it in descriptors of neuropathic pain. The prevalence and influence of central sensitization in clinical and laboratory activity, the development of mood disorders in patients with psoriatic arthritis are not explored well. Aim. To assess the prevalence of central sensitization in patients with psoriatic arthritis, to compare the parameters of patients with and without central sensitization. Materials and methods. We examined 107 patients with psoriatic arthritis: number of tender and swollen joints, severity of pain, patient global assessment, and C-reactive protein were determined. Activity of disease was assessed with Disease activity in psoriatic arthritis, Ankylosing Spondylitis Disease Activity Score. Central sensitization was determined with Central Sensitization Inventory, presence of anxiety and depression - with Hospital Anxiety and Depression Scale. Descriptors of neuropathic pain were determined with Pain Detect Questionnaire. Statistical processing was carried out with Statistics 26.0. Differences were considered significant at p-value < 0.05. Results and discussion. Central sensitization was found in 46 (43%) patients – they had patient global assessment (p=0.004) and severity of pain (p=0.002) in higher values. The C-reactive protein (p=0.423), Disease activity in psoriatic arthritis (p=0.083) did not differ between groups, but the Ankylosing Spondylitis Disease Activity Score (p=0.002) was higher in patients with central sensitization. High prevalence of anxiety (25.2%) and depression (40.2%) was found; more often in patients with central sensitization (p=0.001 and p=0.004). Most of patients described the tactile allodynia, «electric shocks», and burning. Conclusion. Significant contribution of central sensitization to the persistence of pain in patients with psoriatic arthritis was found. The frequency of clinically significant anxiety and depression in patients with psoriatic arthritis was shown, as well as their higher prevalence among patients with central sensitization. Patients with psoriatic arthritis often described pain like neuropathic pain, which can indicate both local damage to the nervous system and the formation of pain sensitization without direct damage to peripheral nerve structures.

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Previtali, Davide, Gianluigi Capone, Paolo Marchettini, Christian Candrian, Stefano Zaffagnini, and Giuseppe Filardo. "High Prevalence of Pain Sensitization in Knee Osteoarthritis: A Meta-Analysis with Meta-Regression." CARTILAGE 13, no. 1 (January 2022): 194760352210876. http://dx.doi.org/10.1177/19476035221087698.

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Objective The aim of this meta-analysis was to study the evidence on pain sensitization in knee osteoarthritis (OA), providing a quantitative synthesis of its prevalence and impact. Factors associated with pain sensitization were also investigated. Methods Meta-analysis; PubMed (MEDLINE), Cochrane Central Register (CENTRAL), and Web of Science were searched on February 2021. Level I to level IV studies evaluating the presence of pain sensitization in patients with symptomatic knee OA, documented through a validated method (questionnaires or quantitative sensory testing), were included. The primary outcome was the prevalence of pain sensitization. Factors influencing the prevalence were also evaluated, as well as differences in terms of pain thresholds between knee OA patients and healthy controls. Results Fifty-three articles including 7,117 patients were included. The meta-analysis of proportion documented a prevalence of pain sensitization of 20% (95% confidence interval [CI] = 16%-26%) with a significant heterogeneity of results ( I2 = 89%, P < 0.001). The diagnostic tool used was the main factor influencing the documented prevalence of pain sensitization ( P = 0.01). Knee OA patients presented higher pain sensitivity compared with healthy controls, both in terms of local pressure pain threshold (standardized mean difference [SMD] = −1.00, 95% CI = −1.67 to −0.32, P = 0.007) and distant pressure pain threshold (SMD = −0.54, 95% CI = −0.76 to −0.31, P < 0.001). Conclusions Knee OA pain presents features that are consistent with a significant degree of pain sensitization. There is a high heterogeneity in the reported results, mainly based on the diagnostic tool used. The identification of the best methods to detect pain sensitization is warranted to correctly evaluate and manage symptoms of patients affected by knee OA. Registration: PROSPERO CRD42019123347.

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Nijs, Jo. "Applying Modern Pain Neuroscience in Clinical Practice: Criteria for the Classification of Central Sensitization Pain." Pain Physician 5;17, no. 5;9 (September 14, 2014): 447–57. http://dx.doi.org/10.36076/ppj.2014/17/447.

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Background: The awareness is growing that central sensitization is of prime importance for the assessment and management of chronic pain, but its classification is challenging clinically since no gold standard method of assessment exists. Objectives: Designing the first set of classification criteria for the classification of central sensitization pain. Methods: A body of evidence from original research papers was used by 18 pain experts from 7 different countries to design the first classification criteria for central sensitization pain. Results: It is proposed that the classification of central sensitization pain entails 2 major steps: the exclusion of neuropathic pain and the differential classification of nociceptive versus central sensitization pain. For the former, the International Association for the Study of Pain diagnostic criteria are available for diagnosing or excluding neuropathic pain. For the latter, clinicians are advised to screen their patients for 3 major classification criteria, and use them to complete the classification algorithm for each individual patient with chronic pain. The first and obligatory criterion entails disproportionate pain, implying that the severity of pain and related reported or perceived disability are disproportionate to the nature and extent of injury or pathology (i.e., tissue damage or structural impairments). The 2 remaining criteria are 1) the presence of diffuse pain distribution, allodynia, and hyperalgesia; and 2) hypersensitivity of senses unrelated to the musculoskeletal system (defined as a score of at least 40 on the Central Sensitization Inventory). Limitations: Although based on direct and indirect research findings, the classification algorithm requires experimental testing in future studies. Conclusion: Clinicians can use the proposed classification algorithm for differentiating neuropathic, nociceptive, and central sensitization pain. Key words: Chronic pain, diagnosis, hypersensitivity, classification, neuropathic pain

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Wakaizumi, Kenta. "Brain imaging study for central sensitization." PAIN RESEARCH 36, no. 3 (September 30, 2021): 180–85. http://dx.doi.org/10.11154/pain.36.180.

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Більше джерел

Дисертації з теми "Pain sensitization"

McCormick, Emma, and Magdalena Sjöwall. "Central sensitization in orofacial pain." Thesis, Malmö högskola, Odontologiska fakulteten (OD), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-19833.

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Syfte. Att retrospektivt undersöka relationen mellan central sensitisering i det orofacialaområdet och refererad smärta, som kliniskt fynd, samt psykosociala faktorer hos patienter medDC/TMD-muskeldiagnosen myofasciell smärta med refererad smärta (MPR). Studien syftadeäven till att undersöka skillnader gällande psykosociala faktorer mellan patienter somdiagnostiserats med DC/TMD muskeldiagnoserna myofasciell smärta med refererad smärta(MPR), lokal myalgi (LM) och patienter med orofacial smärta eller käkdysfunktion men ejkäkmuskeldiagnos (WMD) som kontrollgrupper.Material och metod. Information från 85 patienters DC/TMD-undersökning utförd påOrofaciala smärtenheten vid Malmö högskola mellan september 2012 till årsslutet 2013insamlades retrospektivt. Undersökta variabler inkluderade smärtintensitet, smärt-relateraddysfunktion, psykosociala faktorer (depression, ångest och stress) samt refererad smärta.Patienterna indelades i grupper baserade på muskeldiagnos enligt DC/TMD samt utbredning avsmärta. Non-parametrisk statistik användes och P < 0,05 betraktades som signifikant.Resultat. Patienter med MPR uppvisade en signifikant korrelation mellan totala antaletrefererade smärtlokalisationer och smärt-relaterad dysfunktion (rs = 0,43, n = 49, p = 0,002),depression (rs = 0,32, n = 49, p = 0,023) och stress (rs = 0,39, n = 49, p = 0,006). Patienter meden generell smärtutbredning uppvisade en signifikant högre grad av stress (p = 0,020) samt flerantal refererade smärtlokalisationer (p = 0,019) jämfört med patienter med lokal och/ellerregional orofacial smärta.Konklusion. Studien indikerar att grad av central sensitisering kan bedömas med hjälp avutbredningen av refererad smärta, undersökt enligt DC/TMD, hos patienter med diagnosenmyofasciell smärta med refererad smärta i det orofaciala området. Studien kunde inte påvisaskillnader gällande psykosociala faktorer mellan de undersökta grupperna.
Objective. The aim of this study was to retrospectively investigate the relation between referredpain, as a clinical finding, and psychosocial factors versus central sensitization in patients withmyofascial pain with referral (MPR) as assessed according to DC/TMD. The study also aimedto investigate differences regarding psychosocial factors between patients demonstratingmyofascial pain with referral (MPR) and patients diagnosed with the DC/TMD muscle diagnoselocal myalgia (LM) as well as OFP/TMD patients without masticatory muscular diagnose(WMD) as control patients.Material and methods. Patients’ medical records of 85 patients examined at the Orofacial PainUnit at Malmö University during September 2012 till the end of 2013 were retrospectivelyexamined for DC/TMD data. Examined variables included pain intensity, pain-related disability,psychosocial factors (depression, anxiety and stress) and referred pain. The patients weredivided into groups based on DC/TMD muscle diagnosis as well as extension of pain. Nonparametricstatistics were used and a probability level of P < 0.05 was considered as significant.Results. Patients with MPR demonstrated significant correlations between the total number ofreferred pain sites and disability score (rs = 0.43, n = 49, p = 0.002), depression (rs = 0.32, n =49, p = 0.023) as well as stress (rs = 0.39, n = 49, p = 0.006). Patients with generalized paindistribution demonstrated a significantly higher degree of stress (p = 0.020) as well as highernumber of referred pain sites (p = 0.019) than patients with local and/or regional orofacial pain.Conclusion. This study indicates that the degree of central sensitization can be estimated bythe extent of referred pain, as assessed according to DC/TMD, in patients with myofascial painwith referred pain in the orofacial region. This study could not detect a difference inpsychosocial factors between the three groups, myofascial pain with referral (MPR), localmyalgia (LM) and no masticatory muscle diagnosis (WMD).

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Seitz, Viola [Verfasser]. "Sensitization and inhibition of pain / Viola Seitz." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1209130866/34.

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Schrepf, Andrew David. "Inflammation and central pain sensitization in Interstitial Cystitis/Bladder Pain Syndrome." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1900.

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Central sensitization refers to abnormal pain modulation present which is characterized by non-aversive or mildly aversive stimuli promoting feelings of pain. Many conditions referred to as Functional Somatic Syndromes (FSS)s are characterized by abnormal pain modulation, including pain in areas of the body not thought to be related to the specific FSS with which the patient has been diagnosed. Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is a diagnosis of exclusion characterized by pelvic pain and urologic symptoms that shares many environmental and psychosocial correlates with FSSs. Treatment is generally non-satisfactory for patients despite substantial healthcare expenditures. Preliminary evidence suggests abnormal pain modulation in IC/BPS. Inflammatory dysregulation is an underexplored mechanism in the pain experience in IC/BPS and FSSs. The purpose of the current project is to explore the role of dysregulated inflammatory processes in IC/BPS with an emphasis on painful symptoms in three distinct papers. Paper one examines the role of inflammation in IC/BPS patients with particular emphasis on the association of Toll-Like Receptor (TLR) - 4 mediated inflammation with symptoms of pelvic pain. Paper two expands on the findings of paper one by exploring the association of TLR-4 mediated inflammation with the presence of comorbid FSSs and widespread pain. Paper three evaluates the predictive ability of these previously explored baseline inflammatory measures by testing the association between TLR-2 and 4-mediated inflammation and diurnal cortisol rhythms with symptom trajectories and symptom flares over one year of observation. Finally, the significance of these novel findings is explored.

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Janke, Elizabeth Amy. "Psychosocial Correlates of Sensitization in Chronic Pain: An Exploratory Analysis." Ohio University / OhioLINK, 2004. http://www.ohiolink.edu/etd/view.cgi?ohiou1108061243.

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Asiedu, Marina N. "Spinal Sensitization Mechanisms Promoting Pain: Gabaergic Disinhibition and Pkmζ-Mediated Plasticity". Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/232496.

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As a major public health problem affecting more that 76.5 million Americans, chronic pain is one main reason why people seek medical attention. It is a pathological nervous system disorder that persists for months or years. Sensitization of nociceptive neurons in the dorsal horn of the spinal cord is crucial in the development of allodynia and hyperalgesia. The work presented in this thesis will focus on spinal protein kinase M zeta (PKMζ)-mediated plasticity and GABAergic disinhibition as spinal amplification mechanisms that orchestrate persistent changes in the dorsal horn of the spinal cord. As a result of central sensitization following peripheral nerve injruy, GABAergic disinhibition occurs due to an alteration in Cl- homeostasis via reduced KCC2 expression and function. Intrathecal administration of acetazolamide (ACT), a carbonic anhydrase inhibitor, attenuated neuropathic allodynia and spinal co-adminitation of ACT and midazolam (MZL), an allosteric modulator of the benzodiazepine class of GABAA receptors, synergistically inhibited neuropathic allodynia. Further studies concerning the impact of altered Cl-homeostasis via reduced KCC2-mediated Cl-extrusion capacity on the analgesic efficacy and potency of GABAA receptor agonist and allosteric modulators revealed that there is a differential regulation of the agonists and allosteric modulators at the GABAA receptor complex when Cl-homeostasis is altered. Another spinal amplification mechanism leading to central sensitization is PKMζ-mediated spinal LTP. In model of persistent nociceptive sensitization, allodynia induced by IL-6 injection or plantar incision was abolished by both the inhibition of protein translation machinery and PKMζ inhibitor, ZIP. However, only PKMζ inhibition prevented the enhanced pain hypersensitivity precipitated by a subsequent stimulus after the initial hypersensitivity had resolved, asserting that spinal PKMζ underlies the maintenance mechanisms of persistent nociceptive sensitization. Also, these results confirmed that the initiation mechanisms of persistent sensitization parallel LTP initiation mechanisms and the maintenance mechanisms of persistent sensitization parallel LTP maintenance mechanisms. Taken together, these results indicate that these amplification mechanisms drive a chronic persistent state in these models such that inhibition of these spinal amplication mechanisms will serve as an effective approach in the quenching chronic pain hypersensitivity in chronic pain models.

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Warwick, Charles A. "The role of complement component C5a in nociceptive sensitization." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5676.

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The complement system is a principal component of innate immunity. Recent studies have underscored the importance of C5a and other complement components in inflammatory and neuropathic pain, although the underlying mechanisms are largely unknown. In particular, it is unclear how the complement system communicates with nociceptors and which ion channels and receptors are involved. Here we demonstrate that inflammatory thermal and mechanical hyperalgesia induced by complete Freund’s adjuvant were accompanied by C5a upregulation and were markedly reduced by C5a receptor (C5aR1) knockout (KO) or treatment with the C5aR1 antagonist PMX53. Direct administration of C5a into the mouse hindpaw produced strong thermal and mechanical hyperalgesia, an effect that was absent in TRPV1 KO mice, and was blocked by the TRPV1 antagonist AMG9810. Immunohistochemistry of mouse plantar skin showed prominent expression of C5aR1 in macrophages. Additionally, C5a evoked strong Ca2+ mobilization in macrophages. Macrophage depletion in transgenic macrophage Fas-induced apoptosis (MAFIA) mice abolished C5a-dependent thermal and mechanical hyperalgesia. Examination of inflammatory mediators following C5a injection revealed a rapid upregulation of nerve growth factor (NGF), a mediator known to sensitize TRPV1. Pre-injection of an NGF-neutralizing antibody or Trk inhibitor GNF-5837 prevented C5a-induced thermal hyperalgesia. Notably, NGF-induced thermal hyperalgesia was unaffected by macrophage depletion. Collectively, these results suggest that C5a induces thermal and mechanical hyperalgesia by triggering macrophage-dependent signaling that involves mobilization of NGF and NGF-dependent sensitization of TRPV1. Our findings highlight the importance of macrophage-to-neuron signaling in pain processing and identify C5a, NGF and TRPV1 as key players in this cross-cellular communication.

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Mickle, Aaron David. "Pain sensitization by parathyroid hormone-related peptide via convergent phosphoregulation of TRPV1." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/5970.

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The neurobiological mechanisms underlying chronic pain in bone-metastasized breast and prostate cancer are not well understood although it is hypothesized that factors released in the tumor microenvironment may modulate sensory nociceptive sensory nerve fibers innervating the bone increasing pain sensation. Advanced metastatic breast and prostate cancer cells secrete high levels of parathyroid hormone-related peptide (PTHrP), which plays a critical role in metastasis to bones and subsequent tumor growth. PTHrP can activate parathyroid hormone receptor 1 (PTH1R), which signaling can activate either protein kinase C (PKC) and/or protein kinase A (PKA) depending on the tissue type. Both of these kinases are well known to modulate the nociceptive ion channel transient receptor potential vanilloid member 1 (TRPV1) due to which PTHrP constitutes an intriguing candidate that could modulate nociceptors, for pain sensitization related to cancer. TRPV1 can be activated by temperatures greater than 43°C and moderately acidic pH, less than pH 6. However, PKC and PKA phosphorylation of TRPV1 can potentiation channel activity by reducing the temperature of activation to 37°C and proton activation to pH 6.8 resulting in a channel that is constitutively active at body temperature or in the mildly acidic tumor microenvironment. Additionally, Src kinase, which under certain circumstances can be activated by PKC, can increase trafficking of TRPV1 to the plasma membrane, and enhance TRPV1-mediated signaling. Therefore, I hypothesize that PTHrP can sensitize TRPV1 and lead to an increase in nociceptive signaling. First I show that intraplantar PTHrP injection causes a TRPV1-dependent increase in thermal and mechanical hypersensitivity in mice. PTHrP treatment of cultured mouse dorsal root ganglion (DRG) neurons enhances TRPV1 activation and increases action potential firing, which was dependent on PKC activation. Furthermore, co-injection of PKC inhibitor attenuated PTHrP-induced thermal hypersensitivity. I also observed that PTHrP activated Src which led to an increase in the number of TRPV1-responsive neurons and an increase in TRPV1 protein level in the plasma membrane. While investigating the role of PTHrP-induced Src phosphorylation of TRPV1 I made a startling observation. Inhibition of Src phosphorylation of TRPV1 completely abolished PKC-induced potentiation of TRPV1. I found that Src phosphorylation of TRPV1 regulated PKC-induced potentiation of channel activity elicited by bradykinin, nerve growth factor and PMA. However, it did not regulate PKA induced potentiation of TRPV1 channel activity. In summary, my results suggest that PTHrP in the tumor microenvironment could induce constitutive pathological sensitization of adjacent nociceptive sensory fibers via upregulation of TRPV1 function, trafficking and expression. These actions are dependent on Src and PKC phosphorylation of TRPV1. Additionally, I found that Src regulates PKC-induced phosphorylation of TRPV1 by PTHrP as well as other inflammatory mediators, suggesting a crucial role for Src in PKC-induced sensitization of TRPV1.

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Öjstedt, Erik, and Simon Pankalla. "Clinical Assessment of Disturbed Central Pain Modulation in Orofacial Pain." Thesis, Malmö universitet, Odontologiska fakulteten (OD), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-19798.

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Syfte. Studiens syfte var att retrospektivt undersöka vilka kliniska variabler, bedömda under specialistundersökning av orofacial smärta, som kan förutsäga närvaro av en störd central smärtmodulering (DCPM). Material och metod. DC/TMD-data hämtades ur patientjournaler från 86 patienter som undersökts på Orofaciala smärtenheten på Malmö Universitet under perioden september 2012 till och med december 2013. Undersökta variabler omfattade smärtintensitet, smärtutbredning, smärtrelaterad nedsatthet, psykosociala variabler, refererad smärta samt kliniska fynd under somatosensoriska undersökningar. Baserat på denna data delades patienterna upp i en DCPM-grupp och en grupp utan DCPM. Allodyni, hyperalgesi, dysestesi, wind-up, regional/generell smärtutbredning samt eftersensation ansågs vara markörer för DCPM. Icke-parametriska statistiska analyser användes och en sannolikhetsnivå på P<0,05 ansågs vara signifikant. Resultat. Graden av ospecifika fysiska symptom och antalet refererande smärtor var signifikant högre i DCPM-gruppen. Den multivariata logistiska regressionen visade att ospecifika fysiska symptom, stress, smärtduration, smärtintensitet, smärtrelaterad nedsatthet, antalet refererande smärtpunkter, maximal gapning med och utan smärta, ångest samt antalet smärtinducerande käkrörelser var signifikanta marörer för DCPM (LR Chi2 = 26.89, p = 0.003, Pseudo R2 = 0.29). Slutsats. Denna studie indikerar att stress, ångest, smärtduration, smärtintensitet, smärtrelaterad nedsatthet, antalet refererande smärtpunkter, maximal gapning med och utan smärta samt antalet smärtinducerande käkrörelser är associerat med DCPM hos patienter med orofacial smärta.
Objective. To retrospectively investigate clinical variables that can predict the presence of disturbed central pain modulation (DCPM). Material and methods Medical records of 86 patients examined at the Orofacial Pain Unit at Malmö University from September 2012 to December 2013 were examined regarding pain intensity, pain distribution, pain-related disability, psychosocial variables, referred pain as well as somatosensory changes. Based on these variables, the patients were divided into a disturbed central pain modulation (DCPM) group and a non-DCPM group. Allodynia, hyperalgesia, dysesthesia, increased wind-up, regional/general pain distribution and aftersensation were considered as markers for DCPM. Non-parametric statistics were used and a probability level of P<0.05 was considered as significant. Results. The degree of unspecific physical symptoms and the number of sites eliciting pain referral were significantly higher in the DCPM group. In the multivariate regression model, the independent variables physical symptoms, stress, pain duration, characteristic pain intensity, pain-related disability, number of sites with referred pain, maximum mouth opening with and without pain, anxiety, and number of pain eliciting jaw movements significantly predicted DCPM (LR Chi2 = 26.89, p = 0.003, Pseudo R2 = 0.29). Conclusion. This study indicates that stress, anxiety, orofacial pain and its consequences, unspecific physical symptoms and jaw dysfunction are clinical signs of DCPM in patients with orofacial pain. Also, high number of palpations sites with referred pain over the masseter and temporal muscles and the TMJ indicate presence of DCPM.

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King, Jacqlyn. "Sensorimotor Abnormalities in Chronic Subacromial Pain: The Influence of Sex, Contribution of Pain, and Utility of Using the Contralateral Limb as a Control." Thesis, University of Oregon, 2018. http://hdl.handle.net/1794/23190.

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Patients with subacromial pain syndrome (SPS) display a number of sensorimotor deficits including alterations in pain processing, poor proprioception, and weakness at the symptomatic limb. The primary purpose of this dissertation was to explore whether the aforementioned deficits: (1) can be quantified by using the non-involved limb as a measure of control, (2) are purely localized to the symptomatic limb or represent a more generalized deficit, (3) are influenced by the presence of subacromial pain, and (4) present similarly in male and female patients. Here, we utilized modern clinical techniques in both a patient cohort with SPS and uninjured control cohort to address these aims. The results of this dissertation are applicable towards treatment of SPS as well as scientific understanding of sex on sensorimotor behavior.

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Bettini, Elizabeth, and Elizabeth Bettini. "Central Sensitization and Associated Factors in Adolescents With Joint Hypermobility and Dysautonomia." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/622947.

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Background: Postural Orthostatic Tachycardia Syndrome (POTS) is a disorder of the autonomic nervous system that has high association with chronic pain syndromes such as fibromyalgia, migraine disorders, and chronic abdominal pain in adolescents with the diagnosis. Many of these disorders are characterized as central sensitization disorders, or pathological pain memory mediated by neural plasticity. Ehlers Danlos Syndrome Type 3 (EDS-3), also called joint hypermobility syndrome (JHS) is a genetic disorder of the connective tissue that causes joint laxity and is also highly associated with chronic pain syndromes as well as POTS. Methods: This study proposed to characterize POTS as a disorder of central sensitization. The hypothesis, presented within the proposed theoretical model, demonstrates that JHS leads to chronic pain that results in central sensitization and autonomic nervous system dysfunction (POTS). Other factors that were evaluated were anxiety and function. A sample size of 40 adolescents between the ages of 12 and 19 years were recruited from the cardiology and pain clinics at Children’s National Medical Center. Analysis of data utilizing Wilcoxon, Chi square, Pearson correlation, and logistic regression tests were completed using SAS 9.3. Results: In comparison to those without POTS, there were no significant associations found between having the diagnosis of POTS and any other variable studied in the model. JHS had a stronger correlation with anxiety, central sensitization, both subjectively, and objectively with hyperalgesia on Aδ sensory nerve fiber when compared to those without JHS. Subjective central sensitization was highly correlated with anxiety, function, age, and female gender. Function and central sensitization had a significant association even when removing anxiety as a covariate. Conclusions: These findings suggest that joint hypermobility may be a factor that contributes to the development of central sensitization in individuals with chronic pain. Dysautonomia is likely not a disorder of central sensitization, but rather a variable related to joint hypermobility and chronic pain in ways yet to be discovered. As previously discussed in other literature, anxiety has strong associations with central sensitization and functional disability in chronic pain syndromes, and when treated effectively may increase function in those that suffer with these disorders.

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Книги з теми "Pain sensitization"

Veldhuijzen, Dieuwke S., Henriët van Middendorp, and Andrea W. M. Evers. Stress and Sensitization in Chronic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190627898.003.0005.

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Stress and sensitization are central concepts in chronic pain. Both can be a consequence and a contributor to the pain experience. This chapter describes the psychobiology of stress and sensitization within a multilevel perspective, indicating the impact of various forms of stress and sensitization on multiple psychoneurobiological processes (i.e., autonomic, endocrine, immune, and central processes) related to chronic pain. As a result of disordered stress regulation, sensitization may occur as a mechanism that explains how acute pain problems can become chronic and how acute pain problems can extend or generalize to other body parts or modalities. The evidence for stress and sensitization as consequences of or as contributors to chronic pain is reviewed, and possible underlying mechanisms are discussed. Next, strategies to reduce stress and sensitization and foster desensitization processes are described. The chapter concludes by introducing a motivational account of chronic pain informed by the stress and sensitization literature.

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Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.

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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.

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Sandkühler, Jürgen. Making the link from “central sensitization” to clinical pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0047.

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The landmark paper discussed in this chapter is ‘Central sensitization: Implications for the diagnosis and treatment of pain’, published by C. J. Woolf in 2011. The phrase ‘central sensitization’ is often used as an umbrella term for all kinds of central nervous system (CNS) mechanisms contributing to pain hypersensitivity. The International Association for the Study of Pain (IASP) defines ‘central sensitization’ as the ‘increased responsiveness of nociceptive neurons in the CNS’. In the CNS, highly distinct mechanisms contribute to pain hypersensitivity depending upon pain aetiology and disease stage. These include modification of synaptic strength, inhibitory tone, and membrane excitability and often involve components of neuroinflammation. It is thus recommended to avoid using the phrase ‘central sensitization’ in the scientific literature all together and replace it with unambiguous technical terms such as ‘CNS mechanisms of pain hypersensitivity’ or with the specific mechanism(s) and CNS location(s) in mind.

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Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization. Humana Press, 2013.

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Goudie, A. J., and M. W. Emmett-Oglesby. Psychoactive Drugs: Tolerance and Sensitization. Humana Press, 1989.

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Pak, Daniel J., and Neel Mehta. Pain Anatomy and Physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0001.

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This chapter focuses on pain anatomy and physiology to provide a comprehensive review of the mechanisms of nociception for preparation for the ABA Pain Medicine (PM) Examination. It reviews the anatomy of pain pathways (particularly the spinothalamic sensory tract), and the process of pain conduction from peripheral nociceptors to the cerebral cortex. It also reviews the different mechanisms of sensitization and inhibition at peripheral nociceptors (manifested as primary and secondary hyperalgesia), the spinal cord (wind-up and sensitization of second-order neurons) and supraspinal structures, which all affect the processing of nociceptive signals in the nervous system and ultimately, the perception of pain.

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Welechew, Edward. Treatment of pain in burns patients. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199234721.003.0009.

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Pain from burns has three components: background, breakthrough, and procedural pain. Central sensitization is an important component of the ongoing pain. Early management of pain, prior to the arrival at hospital is essential. Multimodal treatment including opiates will be necessary and psychological support is key. Procedural pain is of high intensity and short duration, and will require a combination of pharmacological and non-pharmacological methods of analgesia. Central sensitization and opiate tolerance are common problems in burns patients.

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Jarrell, John F. History of Gynecological Treatment of Women's Pelvic Pain and the Recent Emergence of Pain Sensitization. Elsevier Science & Technology, 2024.

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Jarrell, John F. History of Gynecological Treatment of Women's Pelvic Pain and the Recent Emergence of Pain Sensitization. Elsevier Science & Technology Books, 2024.

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Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.

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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ‎ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.

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Частини книг з теми "Pain sensitization"

Jenkinson, Robert H. "Central Sensitization." In Pain, 45–48. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99124-5_11.

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Kam, Peter, Ian Power, Michael J. Cousins, and Philip J. Siddal. "Pain Sensitization." In Principles of Physiology for the Anaesthetist, 445–51. Fourth edition. | Boca Raton : CRC Press, Taylor & Francis Group, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429288210-71.

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Vardeh, Daniel, and Julian F. Naranjo. "Peripheral and Central Sensitization." In Pain Medicine, 15–17. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43133-8_4.

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Bennett, David L. H. "NGF, Sensitization of Nociceptors." In Encyclopedia of Pain, 2144–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_2721.

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Gebhart, Gerald F., and Bin Feng. "Sensitization of Visceral Nociceptors." In Encyclopedia of Pain, 3464–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_3937.

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Ray, Albert L. "Neuroplasticity, Sensitization, and Pain." In Treatment of Chronic Pain by Integrative Approaches, 15–24. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1821-8_2.

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Ray, Albert L. "Neuroplasticity, Sensitization, and Pain." In Comprehensive Treatment of Chronic Pain by Medical, Interventional, and Integrative Approaches, 759–68. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1560-2_71.

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Simone, Donald A. "Spinothalamic Tract Neurons, Central Sensitization." In Encyclopedia of Pain, 3644–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_4170.

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Nicholas, Michael K. "Psychology of Pain, Sensitization, Habituation, and Pain." In Encyclopedia of Pain, 3303–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_3641.

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Arendt-Nielsen, Lars. "Central Sensitization in Humans: Assessment and Pharmacology." In Pain Control, 79–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46450-2_5.

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Тези доповідей конференцій з теми "Pain sensitization"

Isci, Hakan, Polat Şendur, Damla Gezegen, Ramazan Ünal, and Nima Heidari. "Customized Pilot Cervical Spine Protection Orthosis Development." In Vertical Flight Society 80th Annual Forum & Technology Display, 1–8. The Vertical Flight Society, 2024. http://dx.doi.org/10.4050/f-0080-2024-1076.

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Pilots and crew of rotary-wing aircraft can be exposed to inertial and task position stressors that generate pain. Repeated painful exposures with or without tissue damage are precursors to pain sensitization and chronic pain. Chronic pain leads to reduced operational readiness and long-term medical treatment. This study investigated protection orthosis for unrecoverable effects on the cervical spine by heavy helmets and accessories. A user-customized product has been developed and customization has been intended to be done with multi-body dynamic modeling and testing. Although there are many biomechanical models of the human cervical spine in the literature, their analysis capabilities to perform modal analysis and frequency response analysis are limited. Especially for Rotary-wing applications, models with such capabilities will play an essential role in diagnosing and rehabilitating musculoskeletal disorders and designing engineering devices to prevent and heal cervical spine injuries. Therefore, a detailed head-cervical spine model is developed in which frequency domain analysis is possible. Alternative design solutions have been investigated to support helmets to decrease the load exerted on the neck periphery. Finally, tests have been performed to correlate analysis with a real helicopter environment. At the end of the study, a customizable neck orthosis has been developed and verified with the tests that it reduces the adverse effects of heavy helmets on the cervical spine periphery.

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Cruz, AR, F. Sales, J. Chaves Carvalho, E. Oliveira, and L. Agualusa. "B395 Pain interventional treatment after episiotomy sensitization." In ESRA Abstracts, 39th Annual ESRA Congress, 22–25 June 2022. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/rapm-2022-esra.471.

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Narcisse, Darryl, Robert Benkowski, Arman Fijany, and Samarendra K. Mohanty. "Pain modulation by multi-characteristic opsin sensitization of inhibitory network of brain." In Optogenetics and Optical Manipulation 2021, edited by Samarendra K. Mohanty, Anna W. Roe, and Shy Shoham. SPIE, 2021. http://dx.doi.org/10.1117/12.2586107.

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Pettersen, Pernille Steen, Tuhina Neogi, Karin Magnusson, Hilde Berner Hammer, Tore K. Kvien, Till Uhlig, and Ida Kristin Haugen. "THU0417 THE SEVERITY OF STRUCTURAL AND INFLAMMATORY FEATURES OF HAND OSTEOARTHRITIS ASSOCIATE WITH PERIPHERAL PAIN SENSITIZATION." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3960.

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Pettersen, Pernille Steen, Tuhina Neogi, Marthe Gløersen, Karin Magnusson, Hilde Berner Hammer, Tore K. Kvien, Till Uhlig, and Ida Kristin Haugen. "THU0418 NEUROPATHIC-LIKE PAIN IN PERSONS WITH HAND OSTEOARTHRITIS AND ASSOCIATIONS WITH PERIPHERAL AND CENTRAL SENSITIZATION." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4060.

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Sena, Débora de Jesus, Maria Nathalia Gabriela Rocha Pontes de Oliveira, Maria Roberta Melo Pereira Soares, Luís Fábio Barbosa Botelho, and ALESSANDRA DE SOUSA BRAZ. "PRESENCE OF NEUROPATHIC PAIN AND/OR CENTRAL SENSITIZATION IN PATIENTS WITH ANKYLOSING SPONDYLITIS FOLLOWED AT A UNIVERSITY HOSPITAL." In XLI Congresso Brasileiro de Reumatologia, 1. Sociedade Brasileira de Reumatologia, 2024. https://doi.org/10.47660/cbr.2024.2144.

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Oliveira, Maria Nathalia Gabriela Rocha Pontes de, Debora de Jesus Sena, Ana Karla Guedes de Melo, Danielle Christinne Soares do Egypto, Luís Fábio Barbosa Botelho, and ALESSANDRA DE SOUSA BRAZ. "PRESENCE OF NEUROPATHIC PAIN AND/OR CENTRAL SENSITIZATION IN PATIENTS WITH ANKYLOSING SPONDYLITIS FOLLOWED AT A UNIVERSITY HOSPITAL." In XLI Congresso Brasileiro de Reumatologia, 1. Sociedade Brasileira de Reumatologia, 2024. https://doi.org/10.47660/cbr.2024.2143.

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Bordvik, D. H., P. Steen Pettersen, I. Kjeken, M. Gløersen, T. Neogi, and I. K. Haugen. "AB0358 SLEEP PROBLEMS ARE ASSOCIATED WITH HIGHER PAIN INTENSITY AND CENTRAL SENSITIZATION IN PEOPLE WITH HAND OSTEOARTHRITIS: DATA FROM THE NOR-HAND LONGITUDINAL STUDY." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.4441.

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Guimarães, Mário Vicente Campos, Josué Andrade Martins, Ana Lívia Piovezan de Oliveira, and Cecília Procópio Cardoso. "Neuropathic pain as consequence of rifle injury: a case report and literature review." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.585.

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Rifle injuries are relatively common in emergency cases. It may result in several acute damages or it could lead to chronic consequences to the patient. This paper reports a case of a rifle injury on the leg that resulted in neuropathic pain and venous insufficiency. To treat this patient, a multidimensional approach was prefered, using comprehensive therapy, drug treatment and neuromodulation. The case reported in this paper was gathered by appreciation of the patient’s records and interviews and was discussed in the light of the most recent literature. Neuropathic pain is caused by lesion or disease of the somatosensory nervous system, according to The International Association for Study of Pain that affects over 7 to 8 percent of general populations and corresponds to 20 to 25 percent of chronic pain, most frequently in women and man older than 50-years, diagnosed exclusively via clinical criteria. It might be classified by the clinical manifestations: spontaneous pain, evoked pain, after sensations, hyperpathia and referred pain. The details of pathophysiology of neuropathic pain are yet to be clarified once most of the data in the matter comes from animal testing and should be interpreted carefully, majorly in the long-term assessments. It is clear, though, that several mechanisms are involved in the pathogenic process, depending on anatomical location and etiology, and that different classifications of neuropathic pain could be clustered to form several subgroups based on the symptoms combination, each reflecting different mechanisms. Understanding these underlying mechanisms is crucial to a proper treatment of the patient. In this paper, we report a patient who suffered from a fire gun injury in the left feet resulting in a neuropathic pain. A 40-year-old male comes to the office referring to allodynia, hyperalgesia, burning pain and paroxysmal pain, characterizing persistent neuropathic pain, intensity 8 in the one-to-ten scale, and edema during the day in the left inferior member. The patient reports being shot, one year and half before, with a 5.56 caliber rifle at the left feet, riching the fifth metatarsal No remarkable finding was present in the medical history prior to the incident. At physical examination, it was perceived that the patient developed venous insufficiency, for which was prescribed a ⅞ compression socks (30- 40 mmhg). The neuropathic pain was firstly treated with pregabalin 50 mg/ day and Duloxetine 30 mg/day, showing relevant response. Then, electroneuromyography revealed intermedial dorsal cutaneous nerve injury, being managed with a local block, prepared with 8 ml of 2% Lidocaine and 2 ml of 4 mg Dexamethasone, and a 30 Hz neuromodulation, terminating the pain. Ballistic knowledge is essential to a proper management of gunshots injury. In this case report, the patient suffered a 5.56 caliber rifle injury, a high-velocity gun, resulting in an intermediate dorsal cutaneous nerve and the fifth metatarsal lesion. In these injuries, the projectile transfers energy to the affected tissue, expanding and crushing it. This brief expansion creates a subatmospheric pressure resulting in bacterial and foreign material suction into the wound. It is worth to note that gunshot-related injuries in the feet, due to scarce soft tissue, numerous bones and articulations, are more propense to vascular and neural lesions. Although pathophysiological mechanisms of neuropathic pain are not fully understood, it is described post-traumatic peripheral ectopic nerve activity and central sensitization that could help to understand the pain origin. Moreover, coexisting psychological and emotional triggers might be associated with neuropathic pain association. As the electroneuromyography shows, the intermediate dorsal cutaneous nerve, the smallest branch of the fibular nerve, was injured at the fifth metatarsal level rising neuropathic pain. In addition, as mentioned above, gunshot injuries might lead to bacterial invasion, triggering the inflammatory response. In this setting, it is important to point out that evidence suggests inflammatory mediators and proinflammatory cytokines as an inductor factor for pain hypersensitivity. Another possible gunshot related etiology that must be considered is lead toxicity in the composition of gun projectiles, which is reportedly associated with neuropathies. For its heterogeneity of etiologies, mechanisms and presentations, it is essential to understand the underlying causes and its consequences to a proper treatment resulting in partial or full pain relief. In this case, the patient was treated with Duloxetine, a serotonin-norepinephrine reuptake inhibitor and first line to treat neuropathic pain, and pregabalin, an anticonvulsant used to inhibit neuronal excitatory transmission. The synergistic action of these drugs is superior compared to monotherapy. Auxiliary, a local block was performed using Lidocaine analgesic, sodium channel blocker, and Dexamethasone, an antiinflammatory corticosteroid, testifying in favor of mechanical and inflammatory pathogenic mechanism originated by the gunshot injury. Finally, it is worth noting that gunshot wounds might give rise to venous insufficiency as a result of vascular injury and must be carefully considered in order to provide the proper treatment, revascularization for exemple. Another possible cause is deep venous thrombosis and leg injury accounts as a risk factor. In this case, it was opted for compression therapy, a conservative treatment, for increased venous return. Concluding that, neuropathic pain is a heterogeneous condition with a limited action mechanism understanding. It is required from the physicians to comprehend the multiple dimensions and main etiology of this disease in order to provide a proper treatment. As gunshots may contribute to the rise of several damage mechanisms, this case report highlights the importance of acknowledging ballistic properties and possibilities wound-related.

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Popoola, Oluseun, Smile Dzisi, Consolata Mutisya, Matrida Makuluni, Dorcas Kheseli, and Fatoou Janneh. "Digital Technologies Solutions: Strategies for Improving Female Students’ Enrolment into STEM Programme in Some TVET Institutions in Africa." In Tenth Pan-Commonwealth Forum on Open Learning. Commonwealth of Learning, 2022. http://dx.doi.org/10.56059/pcf10.9558.

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Poverty amongst women can be reduced significantly as more women embrace the male dominated skilled and high paying Science, Technology, Engineering and Mathematics (STEM) occupations. Only 24% of graduates in engineering, manufacturing and construction were women (OECD, 2018). Bridging the gender gap remains a global challenge to policy makers especially in Africa. The situation is worrisome considering the social implications. Digital technologies have been known to remove the need for face-to-face interactions in learning thus reducing the difficulties women face in male dominated STEM-TVET. The aim of study is to propose novel attracting and retaining strategies using digital technology solutions for increasing female students’ enrolment and performance in STEM programmes in Technical, Vocational Education and Training (TVET) Institutions. Design of this study was descriptive survey and 109 STEM teachers across five TVET institutions in Africa participated in the study. Data was collected using questionnaire. A blend of existing curriculum with digital technology was infused into the sensitization framework. Well designed and specifically targeted policies were proposed together with the digital solutions to yield more robust outcomes. The results revealed that attracting strategies are crucial initiatives needed to increase students’ enrolment in STEM education. The study recommends that governments and institutions should come up with policies which outline strategies to improve enrolment and retain female students undertaking STEM/TVET courses.

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