scholarly journals Pain in 1,000 Women Treated for Breast Cancer

2013 ◽  
Vol 119 (6) ◽  
pp. 1410-1421 ◽  
Author(s):  
Mari A. Kaunisto ◽  
Ritva Jokela ◽  
Minna Tallgren ◽  
Oleg Kambur ◽  
Emmi Tikkanen ◽  
...  

Abstract Background: This article describes the methods and results of the early part (experimental pain tests and postoperative analgesia) of a study that assesses genetic and other factors related to acute pain and persistent pain after treatment of breast cancer in a prospective cohort of 1,000 women. Methods: One thousand consenting patients were recruited to the study. Before surgery (breast resection or mastectomy with axillary surgery), the patients filled in questionnaires about health, life style, depression (Beck Depression Inventory), and anxiety (State-Trait Anxiety Inventory). They were also exposed to experimental tests measuring heat (43° and 48°C, 5 s) and cold (2-4°C) pain intensity and tolerance. Anesthesia was standardized with propofol and remifentanil, and postoperative analgesia was optimized with i.v. oxycodone. Results: The patients showed significant interindividual variation in heat and cold pain sensitivity and cold pain tolerance. There was a strong correlation between the experimental pain measures across the tests. Presence of chronic pain, the number of previous operations, and particularly state anxiety were related to increased pain sensitivity. Previous smoking correlated with decreased heat pain sensitivity. These factors explained 4–5% of the total variance in pain sensitivity in these tests. Oxycodone consumption during 20 h was significantly higher in patients who had axillary clearance. Oxycodone consumption had only a weak correlation with the experimental pain measures. Conclusions: Contact heat and cold pressure tests identify variability in pain sensitivity which is modified by factors such as anxiety, chronic pain, previous surgery, and smoking. High levels of anxiety are connected to increased pain sensitivity in experimental and acute postoperative pain. In a study of 1,000 women undergoing breast surgery for cancer, a small portion of the variance in preoperative response to noxious heat and cold testing could be explained by anxiety, the presence of chronic pain, and the number of previous operations. There was a weak correlation between response to experimental pain testing and acute postoperative pain, with largely similar predictive factors across both.

2013 ◽  
Vol 119 (6) ◽  
pp. 1422-1433 ◽  
Author(s):  
Oleg Kambur ◽  
Mari A. Kaunisto ◽  
Emmi Tikkanen ◽  
Suzanne M. Leal ◽  
Samuli Ripatti ◽  
...  

Abstract Background: Catechol-O-methyltransferase (COMT) metabolizes catecholamines in different tissues. Polymorphisms in COMT gene can attenuate COMT activity and increase sensitivity to pain. Human studies exploring the effect of COMT polymorphisms on pain sensitivity have mostly included small, heterogeneous samples and have ignored several important single nucleotide polymorphisms (SNPs). This study examines the effect of COMT polymorphisms on experimental and postoperative pain phenotypes in a large ethnically homogeneous female patient cohort. Methods: Intensity of cold (+2-4°C) and heat (+48°C) pain and tolerance to cold pain were assessed in 1,000 patients scheduled for breast cancer surgery. Acute postoperative pain and oxycodone requirements were recorded. Twenty-two COMT SNPs were genotyped and their association with six pain phenotypes analyzed with linear regression. Results: There was no association between any of the tested pain phenotypes and SNP rs4680. The strongest association signals were seen between rs165774 and heat pain intensity as well as rs887200 and cold pain intensity. In both cases, minor allele carriers reported less pain. Neither of these results remained significant after strict multiple testing corrections. When analyzed further, the effect of rs887200 was, however, shown to be significant and consistent throughout the cold pressure test. No evidence of association between the SNPs and postoperative oxycodone consumption was found. Conclusions: SNPs rs887200 and rs165774 located in the untranslated regions of the gene had the strongest effects on pain sensitivity. Their effect on pain is described here for the first time. These results should be confirmed in further studies and the potential functional mechanisms of the variants studied.


2011 ◽  
Vol 26 (S2) ◽  
pp. 2132-2132
Author(s):  
E. Vermetten

Although posttraumatic stress disorder (PTSD) is associated with chronic pain, preliminary evidence suggests reduced experimental pain sensitivity in this disorder. The questions addressed in the present study were whether pain perception would also be reduced in PTSD patients who are not suffering from chronic pain symptoms, and whether a reduction in pain sensitivity would also be present in combat veterans who did not develop PTSD. For this, we determined thermal detection and pain thresholds in 10 male combat-related PTSD patients, 10 combat control subjects (no PTSD) and 10 healthy controls without combat experience. All subjects were pain free. First, we measured thermal sensory thresholds with ramped heat and cold stimuli using the method of limits. Ramped thermal sensory stimulation revealed no deficits for the detection of (non-noxious) f2.1thermal stimuli between groups. In contrast, heat and cold pain thresholds in both combat groups (PTSD and combat controls) were significantly increased compared to healthy controls. However, these stimuli could not distinguish between the two groups due to ceiling effects. When using longer-lasting heat stimulation at different temperatures (30 s duration; method of fixed stimuli), we found significantly lower frequency of pain reports in PTSD patients compared with both combat and healthy controls, as well as significantly lower pain ratings. Our results suggest an association of PTSD with reduced pain sensitivity, which could be related to PTSD-related (neuro-)psychological alterations or to a pre-existing risk factor for the disorder.


2017 ◽  
Vol 33 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Benno Rehberg ◽  
Stanislas Mathivon ◽  
Christophe Combescure ◽  
Yannick Mercier ◽  
Georges L. Savoldelli

2020 ◽  
Vol 20 (3) ◽  
pp. 545-553
Author(s):  
Sanna Liesto ◽  
Reetta Sipilä ◽  
Tommi Aho ◽  
Hanna Harno ◽  
Marja Hietanen ◽  
...  

AbstractBackground and aimsPsychological resilience refers to successful adaptation or a positive outcome in the context of significant life adversity, such as chronic pain. On the other hand, anxiety closely associates with pain. The aim of this study was to explore how anxiety and psychological resilience together associate with persistent and experimental pain.MethodsIn a cross-sectional design, we studied 160 patients who had previously been treated for breast cancer and who now reported at least moderate pain (NRS ≥ 4) in any area of the body. Psychological resilience was measured on the Resilience Scale-14, anxiety on the Hospital Anxiety and Depression Scale, and intensity and interference of persistent pain by means of the Brief Pain Inventory. The cold pressor test was conducted to assess sensitivity to experimental cold pain.ResultsThe results showed that resilience associated with pain interference in persistent pain, and that anxiety moderated this effect. Higher psychological resilience was associated with lower pain interference and this association was stronger in patients with low anxiety than among patients with high anxiety. These effects were visible with regard to persistent pain but not in experimental cold pain.ConclusionsThese results indicate that chronic pain and experimental pain as well as pain severity and pain interference are psychologically different phenomena. Psychological resilience protects against pain interference but effectively only in patients with low anxiety. It is necessary also to consider protective factors in addition to vulnerability factors in cases of persistent pain.ImplicationsResilience has been considered a potential target for intervention in chronic pain. However, high levels of anxiety might diminish the protective effect of psychological resilience in clinical settings. Therefore, it is important to treat anxiety in addition to resilience enhancing interventions. Patients with low psychological distress might be more suitable for resilience enhancing interventions than patients with high anxiety.


2021 ◽  
Vol 10 (9) ◽  
pp. 1887
Author(s):  
Marium M. Raza ◽  
Ruth Zaslansky ◽  
Debra B. Gordon ◽  
Jeanne M. Wildisen ◽  
Marcus Komann ◽  
...  

Acute postoperative pain is associated with adverse short and long-term outcomes among women undergoing surgery for breast cancer. Previous studies identified preexisting pain as a predictor of postoperative pain, but rarely accounted for pain location or chronicity. This study leveraged a multinational pain registry, PAIN OUT, to: (1) characterize patient subgroups based on preexisting chronic breast pain status and (2) determine the association of preexisting chronic pain with acute postoperative pain-related patient-reported outcomes and opioid consumption following breast cancer surgery. The primary outcome was a composite score comprising the mean of pain intensity and pain interference items from the International Pain Outcomes Questionnaire. The secondary outcome was opioid consumption in the recovery room and ward. Among 1889 patients, we characterized three subgroups: no preexisting chronic pain (n = 1600); chronic preexisting pain elsewhere (n = 128) and; chronic preexisting pain in the breast with/without pain elsewhere (n = 161). Controlling for covariates, women with preexisting chronic breast pain experienced more severe acute postoperative pain and pain interference (β = 1.0, 95% CI = 0.7-1.3, p < 0.001), and required higher doses of opioids postoperatively (β = 2.7, 95% CI = 0.6–4.8, p = 0.013). Preexisting chronic breast pain may be an important risk factor for poor pain-related postoperative outcomes. Targeted intervention of this subgroup may improve recovery.


2014 ◽  
Vol 19 (1) ◽  
pp. e13-e18 ◽  
Author(s):  
Jacob M Vigil ◽  
Lauren N Rowell ◽  
Joe Alcock ◽  
Randy Maestes

BACKGROUND: There is no standardized method for cold pressor pain tasks across experiments. Temperature, apparatus and aspects of experimenters vary widely among studies. It is well known that experimental pain tolerance is influenced by setting as well as the sex of the experimenter. It is not known whether other contextual factors influence experimental pain reporting.OBJECTIVES: The present two-part experiment examines whether minimizing and standardizing interactions with laboratory personnel (eg, limiting interaction with participants to consenting and questions and not during the actual pain task) eliminates the influence of examiner characteristics on subjective pain reports and whether using different cold pain apparatus (cooler versus machine) influences reports.METHODS:The present experiment manipulated the gender of the experimenter (male, female and transgender) and the type of cold pressor task (CPT) apparatus (ice cooler versus refrigerated bath circulator). Participants conducted the CPT at one of two pain levels (5°C or 16°C) without an experimenter present.RESULTS:Men and women showed lower pain sensitivity when they were processed by biological male personnel than by biological female personnel before the CPT. Women who interacted with a transgendered researcher likewise reported higher pain sensitivity than women processed by biological male or female researchers. The type of CPT apparatus, despite operating at equivalent temperatures, also influenced subjective pain reports.DISCUSSION: The findings show that even minimal interactions with laboratory personnel who differ in gender, and differences in laboratory materials impact the reliable measurement of pain.CONCLUSION: More standardized protocols for measuring pain across varying research and clinical settings should be developed.


2018 ◽  
Vol 18 (3) ◽  
pp. 479-489 ◽  
Author(s):  
Kristian Kjær Petersen ◽  
Hjalte Holm Andersen ◽  
Masato Tsukamoto ◽  
Lincoln Tracy ◽  
Julian Koenig ◽  
...  

AbstractBackground and aimsThe autonomic nervous system (ANS) is capable of modulating pain. Aberrations in heart rate variability (HRV), reflective of ANS activity, are associated with experimental pain sensitivity, chronic pain, and more recently, pain modulatory mechanisms but the underlying mechanisms are still unclear. HRV is lowered during experimental pain as well as in chronic pain conditions and HRV can be increased by propranolol, which is a non-selective β-blocker. Sensitization of central pain pathways have been observed in several chronic pain conditions and human mechanistic pain biomarkers for these central pain pathways include temporal summation of pain (TSP) and conditioned pain modulation (CPM). The current study aimed to investigate the effect of the β-blocker propranolol, and subsequently assessing the response to standardized, quantitative, mechanistic pain biomarkers.MethodsIn this placebo-controlled, double-blinded, randomized crossover study, 25 healthy male volunteers (mean age 25.6 years) were randomized to receive 40 mg propranolol and 40 mg placebo. Heart rate, blood pressure, and HRV were assessed before and during experimental pain tests. Cuff pressure pain stimulation was used for assessment of pain detection (cPDTs) and pain tolerance (cPTTs) thresholds, TSP, and CPM. Offset analgesia (OA) was assessed using heat stimulation.ResultsPropranolol significantly reduced heart rate (p<0.001), blood pressure (p<0.02) and increased HRV (p<0.01) compared with placebo. No significant differences were found comparing cPDT (p>0.70), cPTT (p>0.93), TSP (p>0.70), OA-effect (p>0.87) or CPM (p>0.65) between propranolol and placebo.ConclusionsThe current study demonstrated that propranolol increased HRV, but did not affect pressure pain sensitivity or any pain facilitatory or modulatory outcomes.ImplicationsAnalgesic effects of propranolol have been reported in clinical pain populations and the results from the current study could indicate that increased HRV from propranolol is not associated with peripheral and central pain pathways in healthy male subjects.


2016 ◽  
Vol 134 (4) ◽  
pp. 285-291 ◽  
Author(s):  
Eduardo Jun Sadatsune ◽  
Plínio da Cunha Leal ◽  
Rachel Jorge Dino Cossetti ◽  
Rioko Kimiko Sakata

ABSTRACT CONTEXT AND OBJECTIVES: Effective postoperative analgesia is important for reducing the incidence of chronic pain. This study evaluated the effect of preoperative gabapentin on postoperative analgesia and the incidence of chronic pain among patients undergoing carpal tunnel syndrome surgical treatment. DESIGN AND SETTINGS: Randomized, double-blind controlled trial, Federal University of São Paulo Pain Clinic. METHODS: Forty patients aged 18 years or over were randomized into two groups: Gabapentin Group received 600 mg of gabapentin preoperatively, one hour prior to surgery, and Control Group received placebo. All the patients received intravenous regional anesthesia comprising 1% lidocaine. Midazolam was used for sedation if needed. Paracetamol was administered for postoperative analgesia as needed. Codeine was used additionally if the paracetamol was insufficient. The following were evaluated: postoperative pain intensity (over a six-month period), incidence of postoperative neuropathic pain (over a six-month period), need for intraoperative sedation, and use of postoperative paracetamol and codeine. The presence of neuropathic pain was established using the DN4 (Douleur Neuropathique 4) questionnaire. Complex regional pain syndrome was diagnosed using the Budapest questionnaire. RESULTS: No differences in the need for sedation, control over postoperative pain or incidence of chronic pain syndromes (neuropathic or complex regional pain syndrome) were observed. No differences in postoperative paracetamol and codeine consumption were observed. CONCLUSIONS: Preoperative gabapentin (600 mg) did not improve postoperative pain control, and did not reduce the incidence of chronic pain among patients undergoing carpal tunnel syndrome surgery.


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