Postsurgical pain syndromes: Chronic pain after hysterectomy and cesarean section

Chronic pain syndromes are an important medical problem generated by various molecular, genetic, and pathophysiologic mechanisms. Back pain, neuropathic pain, and posttraumatic pain are the most important pathological processes associated with chronic pain in adults. Standard approaches to the treatment of them do not solve the problem of pain chronicity. This is the reason for the search for new personalized strategies for the prevention and treatment of chronic pain. The nitric oxide (NO) system can play one of the key roles in the development of peripheral pain and its chronicity. The purpose of the study is to review publications devoted to changes in the NO system in patients with peripheral chronical pain syndromes. We have carried out a search for the articles published in e-Library, PubMed, Oxford Press, Clinical Case, Springer, Elsevier, and Google Scholar databases. The search was carried out using keywords and their combinations. The role of NO and NO synthases (NOS) isoforms in peripheral pain development and chronicity was demonstrated primarily from animal models to humans. The most studied is the neuronal NOS (nNOS). The role of inducible NOS (iNOS) and endothelial NOS (eNOS) is still under investigation. Associative genetic studies have shown that single nucleotide variants (SNVs) of NOS1, NOS2, and NOS3 genes encoding nNOS, iNOS, and eNOS may be associated with acute and chronic peripheral pain. Prospects for the use of NOS inhibitors to modulate the effect of drugs used to treat peripheral pain syndrome are discussed. Associative genetic studies of SNVs NOS1, NOS2, and NOS3 genes are important for understanding genetic predictors of peripheral pain chronicity and development of new personalized pharmacotherapy strategies.

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Radiotherapy-Specific Chronic Pain Syndromes in the Cancer Population: An Evidence-Based Narrative Review

Advances in Therapy ◽

10.1007/s12325-021-01640-x ◽

2021 ◽

Author(s):

Jay Karri ◽

Laura Lachman ◽

Alex Hanania ◽

Anuj Marathe ◽

Mani Singh ◽

...

Keyword(s):

Chronic Pain ◽

Narrative Review ◽

Evidence Based ◽

Pain Syndromes ◽

Chronic Pain Syndromes

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Article Commentary: Pain after Mastectomy and Breast Reconstruction

The American Surgeon ◽

10.1177/000313480807400402 ◽

2008 ◽

Vol 74 (4) ◽

pp. 285-296 ◽

Cited By ~ 35

Author(s):

Nalini Vadivelu ◽

Maggie Schreck ◽

Javier Lopez ◽

Gopal Kodumudi ◽

Deepak Narayan

Keyword(s):

Breast Cancer ◽

Chronic Pain ◽

Minimally Invasive ◽

Breast Reconstruction ◽

Sentinel Node ◽

Breast Cancer Surgery ◽

Phantom Pain ◽

Preventative Measures ◽

Pain Syndromes ◽

Post Operative Pain

Breast cancer is a potentially deadly disease affecting one in eight women. With the trend toward minimally invasive therapies for breast cancer, such as breast conserving therapies, sentinel node biopsies, and early treatments of radiation and chemotherapy, life expectancy after breast cancer has increased. However, pain after breast cancer surgery is a major problem and women undergoing mastectomy and breast reconstruction experience postoperative pain syndromes in approximately one-half of all cases. Patients post mastectomy and breast reconstruction can suffer from acute nociceptive pain and chronic neuropathic pain syndromes. Several preventative measures to control acute post operative pain and chronic pain states such as post mastectomy pain and phantom pain have been tried. This review focuses on the recent research done to control acute and chronic pain in patients receiving minimally invasive therapies for breast cancer, such as breast conserving therapies of mastectomies and breast reconstruction, sentinel node biopsies, and early treatments of radiation and chemotherapy.

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P124 Are chronic pain syndromes associated with a unique cytokine profile? A systematic review and meta-analysis

Rheumatology ◽

10.1093/rheumatology/keab247.119 ◽

2021 ◽

Vol 60 (Supplement_1) ◽

Author(s):

Luke Furtado O'Mahony ◽

Arnav Srivastava ◽

Puja Mehta ◽

Coziana Ciurtin

Keyword(s):

Systematic Review ◽

Chronic Pain ◽

Meta Analysis ◽

Pooled Analysis ◽

Cross Sectional ◽

Pain Syndromes ◽

Newcastle Ottawa Scale ◽

Cytokine Milieu ◽

Analysis Models ◽

Chronic Pain Syndromes

Abstract Background/Aims The aetiology of primary chronic pain syndromes (CPS) is highly disputed. One theory suggests that pain is due to a pro-inflammatory cytokine milieu leading to nociceptive activation. We performed a systematic review and meta-analysis aiming to assess differences in cytokines levels in CPS patients versus healthy controls (HC). Methods Human studies published in English from PubMed, MEDLINE/Scopus and Cochrane databases were searched from inception up to January 2020. We included full text cross-sectional or longitudinal studies with cytokine measurements in CPS patients and HC. We excluded studies with underlying organic pathology. Quality assessment was completed using a modified version of the Newcastle-Ottawa Scale. Random-effects meta-analysis models were used to report pooled effects and 95% CIs. Study registered with PROSPERO (CRD42020193774). Results Initial search yielded 324 papers, 36 studies (3229 participants) eligible for systematic review and 26 studies (2048 participants) suitable for metaanalysis. There were reproducible findings supporting trends of cytokine levels comparing CPS patients with HC. Eotaxin (chemokine) however was consistently raised in CPS. Meta-analysis showed significantly increased tumour necrosis factor (TNF) (SMD=0.39, p = 0.0009, %95I=0.16-0.63, p < 0.001; I2=70%, Q2 p < 0.001), interleukin (IL)-6 (SMD=0.15, 8 (SMD=0.26, p = 0.01, 95%CI =0.05-0.47; I2=61%, Q2 p = 0.005) and IL-10 (SMD=0.61; %95 = 0.34-0.89, p < 0.001; I2 = 10%, Q2 p = 0.34) in CPS compared to HC. Conclusion We found significant differences in peripheral blood cytokine profiles of CPS patients compared to HC. However, the distinctive profile associated with CPS includes both pro-inflammatory (TNF-α, IL-6, IL-8), and anti-inflammatory cytokines (IL-10) in pooled analysis, as well as chemokine (eotaxin) signatures. Disclosure L. Furtado O'Mahony: None. A. Srivastava: None. P. Mehta: None. C. Ciurtin: None.

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Sickle cell pain: a critical reappraisal

Blood ◽

10.1182/blood-2012-04-383430 ◽

2012 ◽

Vol 120 (18) ◽

pp. 3647-3656 ◽

Cited By ~ 221

Author(s):

Samir K. Ballas ◽

Kalpna Gupta ◽

Patricia Adams-Graves

Keyword(s):

Chronic Pain ◽

Neuropathic Pain ◽

Sickle Cell ◽

Multiorgan Failure ◽

Organ Damage ◽

Acute Chest Syndrome ◽

Prodromal Phase ◽

Pain Syndromes ◽

Painful Episode ◽

Chronic Pain Syndromes

AbstractSickle cell pain includes 3 types: acute recurrent painful crises, chronic pain syndromes, and neuropathic pain. The acute painful crisis is the hallmark of the disease and the most common cause of hospitalization and treatment in the emergency department. It evolves through 4 phases: prodromal, initial, established, and resolving. Each acute painful episode is associated with inflammation that worsens with recurrent episodes, often culminating in serious complications and organ damage, such as acute chest syndrome, multiorgan failure, and sudden death. Three pathophysiologic events operate in unison during the prodromal phase of the crisis: vaso-occlusion, inflammation, and nociception. Aborting the acute painful episode at the prodromal phase could potentially prevent or minimize tissue damage. Our hypothesis is that managing these events with hydration, anti-inflammatory drugs, aggressive analgesia, and possibly vasodilators could abort the crisis and prevent or minimize further damage. Chronic pain syndromes are associated with or accompany avascular necrosis and leg ulcers. Neuropathic pain is not well studied in patients with sickle cell disease but has been modeled in the transgenic sickle mouse. Management of sickle cell pain should be based on its own pathophysiologic mechanisms rather than borrowing guidelines from other nonsickle pain syndromes.

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HCN2 ion channels: basic science opens up possibilities for therapeutic intervention in neuropathic pain

Biochemical Journal ◽

10.1042/bcj20160287 ◽

2016 ◽

Vol 473 (18) ◽

pp. 2717-2736 ◽

Cited By ~ 23

Author(s):

Christoforos Tsantoulas ◽

Elizabeth R. Mooney ◽

Peter A. McNaughton

Keyword(s):

Chronic Pain ◽

Neuropathic Pain ◽

Ion Channels ◽

Warning Signal ◽

Sensory Nerves ◽

Nociceptive Neurons ◽

Pain Syndromes ◽

Medical Need ◽

Pathological Pain ◽

Genetic Deletion

Nociception — the ability to detect painful stimuli — is an invaluable sense that warns against present or imminent damage. In patients with chronic pain, however, this warning signal persists in the absence of any genuine threat and affects all aspects of everyday life. Neuropathic pain, a form of chronic pain caused by damage to sensory nerves themselves, is dishearteningly refractory to drugs that may work in other types of pain and is a major unmet medical need begging for novel analgesics. Hyperpolarisation-activated cyclic nucleotide (HCN)-modulated ion channels are best known for their fundamental pacemaker role in the heart; here, we review data demonstrating that the HCN2 isoform acts in an analogous way as a ‘pacemaker for pain’, in that its activity in nociceptive neurons is critical for the maintenance of electrical activity and for the sensation of chronic pain in pathological pain states. Pharmacological block or genetic deletion of HCN2 in sensory neurons provides robust pain relief in a variety of animal models of inflammatory and neuropathic pain, without any effect on normal sensation of acute pain. We discuss the implications of these findings for our understanding of neuropathic pain pathogenesis, and we outline possible future opportunities for the development of efficacious and safe pharmacotherapies in a range of chronic pain syndromes.

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