Self-reported Neuropathic Pain Research Articles

Prevalence and patterns of neuropathic pain in people with chronic post-surgical pain after total knee arthroplasty.

The aim of this study was to describe the prevalence and patterns of neuropathic pain over one year in a cohort of patients with chronic post-surgical pain at three months following total knee arthroplasty (TKA). Between 2016 and 2019, 363 patients with troublesome pain, defined as a score of ≤ 14 on the Oxford Knee Score pain subscale, three months after TKA from eight UK NHS hospitals, were recruited into the Support and Treatment After Replacement (STAR) clinical trial. Self-reported neuropathic pain and postoperative pain was assessed at three, nine, and 15 months after surgery using the painDETECT and Douleur Neuropathique 4 (DN4) questionnaires collected by postal survey. Symptoms of neuropathic pain were common among patients reporting chronic pain at three months post-TKA, with half reporting neuropathic pain on painDETECT (191/363; 53%) and 74% (267/359) on DN4. Of those with neuropathic pain at three months, half continued to have symptoms over the next 12 months (148/262; 56%), one-quarter had improved (67/262; 26%), and for one-tenth their neuropathic symptoms fluctuated over time (24/262; 9%). However, a subgroup of participants reported new, late onset neuropathic symptoms (23/262; 9%). Prevalence of neuropathic symptoms was similar between the screening tools when the lower cut-off painDETECT score (≥ 13) was applied. Overall, mean neuropathic pain scores improved between three and 15 months after TKA. Neuropathic pain is common in patients with chronic pain at three months after TKA. Although neuropathic symptoms improved over time, up to half continued to report painful neuropathic symptoms at 15 months after TKA. Postoperative care should include screening, assessment, and treatment of neuropathic pain in patients with early chronic postoperative pain after TKA.

Neuropathic Pain After Burn Injury: A Severe and Common Problem in Recovery.

The aim of this study was to address the limited understanding of neuropathic pain (NP) among burn survivors by comprehensively examining its prevalence and related factors on a national scale using the Burn Model System (BMS) National Database. NP is a common but underexplored complaint among burn survivors, greatly affecting their quality of life and functionality well beyond the initial injury. Existing data on NP and its consequences in burn survivors are limited to select single-institution studies, lacking a comprehensive national perspective. The BMS National Database was queried to identify burn patients responding to NP-related questions at enrollment, 6 months, 12 months, 2 years, and 5 years postinjury. Descriptive statistics and regression analyses were used to explore associations between demographic/clinical characteristics and self-reported NP at different time points. There were 915 patients included for analysis. At discharge, 66.5% of patients experienced NP in their burn scars. Those with NP had significantly higher Patient-Reported Outcomes Measurement Information System 29 (PROMIS-29) pain inference, itch, anxiety, depression, and sleep disturbance scores and were less able to partake in social roles. Multiple logistic regression revealed male sex, % total body surface area, and moderate-to-severe pain as predictors of NP at 6 months. At 12 months, % total body surface area and moderate-to-severe pain remained significant predictors, while ethnicity and employment status emerged as significant predictors at 24 months. This study highlights the significant prevalence of NP in burn patients and its adverse impacts on their physical, psychological, and social well-being. The findings underscore the necessity of a comprehensive approach to NP treatment, addressing both physical symptoms and psychosocial factors.

PREVALENCE AND PATTERNS OF NEUROPATHIC PAIN IN A COHORT OF PATIENTS WITH CHRONIC POST-SURGICAL PAIN AFTER TOTAL KNEE ARTHROPLASTY

AbstractIntroductionTotal knee replacement (TKR) is a successful operation for many patients, however 15–20% of patients experience chronic post-surgical pain (CPSP). Many will experience neuropathic characteristics.We describe the prevalence and patterns of neuropathic pain in a cohort of patients with CPSP three months after TKR.MethodologyBetween 2016–2019, 363 patients with troublesome pain, ≤14 on Oxford Knee score pain subscale, at three months after TKR from eight NHS hospitals were recruited into the Support and Treatment After Replacement (STAR) trial. Self-reported neuropathic pain was assessed at three, nine and fifteen months after surgery using painDETECT and Douleur Neuropathique 4 (DN4).ResultsAt three months post-operative, 53% reported neuropathic pain on painDETECT and 74% on DN4. Half (56%) remained in neuropathic pain over the twelve-month follow-up period, 26% reported improvement, and 9% reported new neuropathic symtpoms or fluctuated in and out of neuropathic pain (9%). Overall mean neuropathic pain scores improved between three and 15 months after TKR. When the painDETECT cut-off score of ≥13(ambiguous/possible) was used, DN4 and painDETECT measures showed similar prevalence rates at each timepoint.ConclusionNeuropathic pain is common among patients with CPSP at three months after TKR. Although symptoms improved over time, one quarter to one half of our cohort continued to report symptoms at fifteen months. We propose a painDETECT cutoff score of ≥13 be used to identify neuropathic features in the TKR population. Postoperative care should include identification, assessment, and treatment of neuropathic pain in patients with CPSP after TKR.

Somatosensory network functional connectivity differentiates clinical pain phenotypes in diabetic neuropathy

Aims/hypothesisThe aim of this work was to investigate whether different clinical pain phenotypes of diabetic polyneuropathy (DPN) are distinguished by functional connectivity at rest.MethodsThis was an observational, cohort study of 43 individuals with painful DPN, divided into irritable (IR, n = 10) and non-irritable (NIR, n = 33) nociceptor phenotypes using the German Research Network of Neuropathic Pain quantitative sensory testing protocol. In-situ brain MRI included 3D T1-weighted anatomical and 6 min resting-state functional MRI scans. Subgroup differences in resting-state functional connectivity in brain regions involved with somatic (thalamus, primary somatosensory cortex, motor cortex) and non-somatic (insular and anterior cingulate cortices) pain processing were examined. Multidimensional reduction of MRI datasets was performed using a machine-learning approach to classify individuals into each clinical pain phenotype.ResultsIndividuals with the IR nociceptor phenotype had significantly greater thalamic–insular cortex (p false discovery rate [FDR] = 0.03) and reduced thalamus–somatosensory cortex functional connectivity (p-FDR = 0.03). We observed a double dissociation such that self-reported neuropathic pain score was more associated with greater thalamus–insular cortex functional connectivity (r = 0.41; p = 0.01) whereas more severe nerve function deficits were more related to lower thalamus–somatosensory cortex functional connectivity (r = −0.35; p = 0.03). Machine-learning group classification performance to identify individuals with the NIR nociceptor phenotype achieved an accuracy of 0.92 (95% CI 0.08) and sensitivity of 90%.Conclusions/interpretationThis study demonstrates differences in functional connectivity in nociceptive processing brain regions between IR and NIR phenotypes in painful DPN. We also establish proof of concept for the utility of multimodal MRI as a biomarker for painful DPN by using a machine-learning approach to classify individuals into sensory phenotypes.Graphical abstract

Neuropathic pain and symptoms of potential small-fiber neuropathy in fibromyalgic patients: A national on-line survey.

Recent studies have highlighted that about 50% of fibromyalgic patients has a neuropathy of small- and/or large-fibers which could partially explain the puzzling symptoms of fibromyalgia (FM). Our aim was to investigate the estimated prevalence of self-reported neuropathic pain and small-fiber neuropathic symptoms (SFNS) indicative for the presence of small-fiber pathology in FM patients. A nationwide sample of patients was recruited to participate in an on-line survey. Two groups of patients were considered in post-hoc analysis: those positive (FM+) to the Fibromyalgia Research Criteria (FRC) and those complaining typical symptoms of fibromyalgia without fulfilling the FRC (FM-). We collected data from 854 patients (749 FM+ and 105 FM-). Patients that scored=50/100 at the Neuropathic Pain Symptoms Inventory (NPSI), indicating severe neuropathic pain, were 57.3% (62.4% in FM+ and 21.0% in FM-). Around 46% of patients presented three or more SFNS that could be suggestive of small fiber pathology, the most frequent being dry eyes/mouth, allodynia, and dyshidrosis. The NPSI score showed significant moderate/strong associations with disability (Spearman's rho=0.61), pain (rho=0.66), stiffness level (rho=0.46), number of painful sites (rho=0.40), and SFNS (rho=0.44). Despite the high prevalence of neuropathic pain and other symptoms attributable to potential small and/or large fibers pathology, neurophysiologic investigations were performed in 43.6% of cases and skin punch biopsy only in 1.9% of patients enrolled, as well as the assumption of anti-neuropathic pain drugs (13.2%). Our findings underscore the high estimated prevalence of neuropathic pain and SFNS in FM patients.

Interventions for treating neuropathic pain in people with sickle cell disease.

Pain is the hallmark of sickle cell disease (SCD) and it can be severe, frequent and unpredictable. Although nociceptive pain is more common, at times, people with SCD may have neuropathic pain. The latter can occur due to peripheral or central nerve injury. This review is focused on identifying treatment of only painful sensory neuropathy in people with SCD. To determine the effectiveness and safety of any pharmacological or non-pharmacological therapies for treating neuropathic pain in people with SCD. We searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Haemoglobinopathies Trials Register, compiled from electronic database searches and handsearching of journals and conference abstract books. We also searched trial registries, the reference lists of relevant articles and reviews and contacted experts in the field.Date of last search: 31 January 2019. Randomised controlled trials (RCTs) (parallel or cross-over in design), quasi-RCTs of pharmacological or non-pharmacological therapies for treating neuropathic pain in people with SCD compared to placebo or another intervention in any category (i.e. pharmacological or non-pharmacological). Two review authors independently assessed all trials identified by the searches and extracted relevant data. Two authors independently assessed the risk of bias in the selected trials using the Cochrane risk of bias tool. Two review authors independently rated the quality of the evidence for each outcome using the GRADE guidelines. One RCT of 22 participants with SCD, conducted in the USA was included in this review. Participants were randomly assigned to either pregabalin (n = 11) or placebo (n = 11). Oral pregabalin was administered at an initial dose of 75 mg twice daily. The drug was titrated at increments of 75 mg to a maximum of 600 mg daily or decreased by 75 mg per day if necessary, based on clinical presentation and pain level. Neuropathic pain was assessed using self-reports on the Leeds Assessment of Neuropathic Symptoms and Signs (S-LANNS) scale and the Neuropathic Pain Symptom Inventory (NPSI), where higher scores were indicative of more pain. Outcomes included self-reported pain, quality of life and withdrawal due to adverse effects measured at baseline and monthly for three months post-intervention. The overall risk of bias was low with a high risk of bias due to attrition.In relation to this reviews primary outcomes, for self-reported neuropathic pain relief, given the paucity of data, we are very uncertain whether there is a difference between the pregabalin and placebo groups at the end of three months as measured by the S-LANSS scale, mean difference (MD) -2.00 (95% confidence interval (CI) -9.18 to 5.18), or the NPSI scale, MD -11.10 (95% CI -33.97 to 11.77) (very low-quality evidence). There was no report of 'Patient Global Impression of Change' in the included trial.Although the mean quality of life scores (Short Form-36) at three months showed small increases in seven of the eight domains post-intervention in the pregabalin group as compared to the placebo group, this was very low-quality evidence and we are very uncertain whether pregabalin increases quality of life. Neither of our pre-defined outcomes of 'time to improvement of symptoms' or 'changes in sleep quality', were measured in the included trial.While treatment-related adverse effects appeared higher in pregabalin group than the placebo group at three months, this was very low-quality evidence and we are very uncertain whether there is a difference, RR 1.33 (95% CI 0.39 to 4.62) (very low-quality evidence). There was one withdrawal for adverse effects in the pregabalin group while three people withdrew or dropped out from the placebo group due to adverse effects and complications and hospitalisation related to SCD. The included trial provided very low-quality evidence. Self-reported pain relief was greater in the pregabalin group compared to the placebo control group but only using the S-LANSS scale and we are very unsure whether there is a difference. While the pregabalin group tended to have improved quality of life over the duration of the trial, this was very low-quality evidence and we are uncertain whether there is a difference. Adverse effects and withdrawals were similar across the treatment and placebo control group in trial. There are both insufficient trials addressing this review question and insufficient outcomes addressed in the single included RCT. Therefore, there is still a significant gap in evidence on interventions for neuropathic pain in people with SCD.

Effects of omega-3 polyunsaturated fatty-acid supplementation on neuropathic pain symptoms and sphingosine levels in Mexican-Americans with type 2 diabetes.

PurposeTo determine whether dietary supplementation with omega-3 polyunsaturated fatty acids (PUFAs) reduces neuropathic pain symptoms in Mexican-Americans with type 2 diabetes.MethodsForty volunteers with type 2 diabetes enrolled in the “En Balance-PLUS” program, which provided weekly nutrition–diabetes education and daily supplementation with 1,000 mg docosahexaenoic acid (DHA)–200 mg eicosapentaenoic acid over 3 months. The study assessed self-reported neuropathic pain symptoms pre/postintervention using the short-form McGill Pain Questionnaire (SF-MPQ), monitored clinical laboratory values at baseline and 3 months, and performed baseline and 3-month metabolomic analysis of plasma samples.ResultsA total of 26 participants self-reported neuropathic pain symptoms at baseline. After 3 months of omega-3 PUFA supplementation, participants reported significant improvement in SF-MPQ scores (sensory, affective, and visual analogue scale; P<0.001, P=0.012, and P<0.001, respectively). Untargeted metabolomic analysis revealed that participants in the moderate–high SF-MPQ group had the highest relative plasma sphingosine levels at baseline compared to the low SF-MPQ group (P=0.0127) and the nonpain group (P=0.0444). Omega-3 PUFA supplementation increased plasma DHA and reduced plasma sphingosine levels in participants reporting neuropathic pain symptoms (P<0.001 and P<0.001, respectively). Increased plasma DHA levels significantly correlated with improved SF-MPQ sensory scores (r=0.425, P=0.030). Improved SF-MPQ scores, however, did not correlate with clinical/laboratory parameters.ConclusionThe data suggest that omega-3 PUFAs dietary supplementation may reduce neuropathic pain symptoms in individuals with type 2 diabetes and correlates with sphingosine levels in the plasma.

Abstract Animations for the Communication and Assessment of Pain in Adults: Cross-Sectional Feasibility Study.

BackgroundPain is the most common physical symptom requiring medical care, yet the current methods for assessing pain are sorely inadequate. Pain assessment tools can be either too simplistic or take too long to complete to be useful for point-of-care diagnosis and treatment.ObjectiveThe aim was to develop and test Painimation, a novel tool that uses graphic visualizations and animations instead of words or numeric scales to assess pain quality, intensity, and course. This study examines the utility of abstract animations as a measure of pain.MethodsPainimation was evaluated in a chronic pain medicine clinic. Eligible patients were receiving treatment for pain and reported pain more days than not for at least 3 months. Using a tablet computer, participating patients completed the Painimation instrument, the McGill Pain Questionnaire (MPQ), and the PainDETECT questionnaire for neuropathic symptoms.ResultsParticipants (N=170) completed Painimation and indicated it was useful for describing their pain (mean 4.1, SE 0.1 out of 5 on a usefulness scale), and 130 of 162 participants (80.2%) agreed or strongly agreed that they would use Painimation to communicate with their providers. Animations selected corresponded with pain adjectives endorsed on the MPQ. Further, selection of the electrifying animation was associated with self-reported neuropathic pain (r=.16, P=.03), similar to the association between neuropathic pain and PainDETECT (r=.17, P=.03). Painimation was associated with PainDETECT (r=.35, P<.001).ConclusionsUsing animations may be a faster and more patient-centered method for assessing pain and is not limited by age, literacy level, or language; however, more data are needed to assess the validity of this approach. To establish the validity of using abstract animations (“painimations”) for communicating and assessing pain, apps and other digital tools using painimations will need to be tested longitudinally across a larger pain population and also within specific, more homogenous pain conditions.

Sensory profiles are comparable in patients with distal and proximal entrapment neuropathies, while the pain experience differs

Objective: Distal and proximal entrapment neuropathies such as carpal tunnel syndrome (CTS) and cervical radiculopathy (CR) share similar etiologies. Experimental models suggest that, despite comparable etiology, pathomechanisms associated with injuries of the peripheral and central axon branches are distinct. This study therefore compared self-reported and elicited sensory profiles in patients with distal and proximal entrapment neuropathies.Methods: Patients with electrodiagnostically confirmed CTS (n = 103) and patients with CR (n = 23) were included in this study. A group of healthy participants served as controls (n = 39). Symptoms and sensory profiles were evaluated using quantitative sensory testing (QST) and a self-reported neuropathic pain questionnaire (painDETECT).Results: Both patient groups were characterized by a loss of function in thermal and mechanical detection in the main pain area and dermatome compared to healthy reference data (p < .001). There was no significant difference between patients with CTS and CR in pain and detection thresholds except for reduced vibration sense in the main pain area (p < .001) and reduced pressure pain sensitivity in the dermatome in patients with CR (p < .001). However, patients with CR reported higher pain intensities (p = .008), more severe pain attacks (p = .009) and evoked pain by light pressure (p = .002) compared to patients with CTS.Conclusion: While QST profiles were similar between patients with CTS and CR, self-reported pain profiles differed and may suggest distinct underlying mechanisms in these patient cohorts.

Epidural Spinal Cord Stimulation Acutely Reduces Efferent Postganglionic Sympathetic Nerve Activity in Humans

Evidence in clinical and animal studies demonstrates that epidural spinal cord stimulation (SCS) mimics the effects of sympathetic block or sympathectomy and increases peripheral blood flow. However, the extent to which SCS lowers sympathetic nerve activity in humans remains unclear because no studies have directly assessed muscle sympathetic nerve activity (MSNA) responses to SCS. We tested the hypothesis that acute SCS (60 min) at the lower thoracic spine would 1) lead to reduced MSNA in the peroneal nerve, and 2) increase blood flow in the legs, but not the arms. Twelve patients (54 ± 3 yrs, 5 men/7 women) that previously underwent surgical implantation of a SCS device for management of neuropathic pain were studied. Following 48 hours of no SCS, femoral and brachial artery blood flow was assessed using Doppler ultrasound at baseline and at 15, 30, 45, 60 min of SCS, and 15 min post SCS. MSNA was assessed using microneurography under the same conditions during a second visit (n=5). Femoral artery blood flow was significantly increased throughout SCS and 15 min post SCS (15 min: 26 ± 1%, 30 min: 32 ± 14%, 45 min: 30 ± 13%, 60 min: 26 ± 13%, 15 min post SCS: 40 ± 14% ml/min, P=0.02), but no change in brachial artery blood flow was observed (15 min: 4 ± 6%, 30 min: 5 ± 8%, 45 min: 5 ± 7%, 60 min: 7 ± 7% ml/min, 15 min post SCS: 6 ± 11% ml/min, P=0.86). MSNA was progressively reduced during SCS, reaching significance at 45 and 60 min, and returned toward baseline following SCS (15 min: −1 ± 6%, 30 min: −13 ± 4%, 45 min: −17 ± 6%, 60 min: −21 ± 7%, 15 min post SCS: −4 ± 5% bursts/100heartbeats, P=0.01). Similar results were observed for MSNA total activity (AU/min) (P&lt;0.042). During measures of MSNA, self‐reported neuropathic pain was low at baseline and not significantly changed by SCS (scale 0–10; BL: 2.8 ± 0.8, 15 min: 1.7 ± 0.9, 30 min: 1.5 ± 1, 45 min: 1.7 ± 1, 60 min: 1.5 ± 1, P=0.07), suggesting that reductions in MSNA were SCS‐mediated and not primarily a result of pain relief. These preliminary results demonstrate proof of principle that acute lower thoracic SCS significantly reduces peroneal MSNA in humans.Support or Funding InformationAHA 17POST33440101, T32 HL07121, NHLBI (P01HL014388), U54 TR001356 and AHA (13DG143400012)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Interventions for treating neuropathic pain in people with sickle cell disease

BACKGROUND Pain is the hallmark of sickle cell disease (SCD) and it can be severe, frequent and unpredictable. Although nociceptive pain is more common, at times, people with SCD may have neuropathic pain. The latter can occur due to peripheral or central nerve injury. This review is focused on identifying treatment of only painful sensory neuropathy in people with SCD. OBJECTIVES To determine the effectiveness and safety of any pharmacological or non-pharmacological therapies for treating neuropathic pain in people with SCD. SEARCH METHODS We searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Haemoglobinopathies Trials Register, compiled from electronic database searches and handsearching of journals and conference abstract books. We also searched trial registries, the reference lists of relevant articles and reviews and contacted experts in the field.Date of last search: 31 January 2019. SELECTION CRITERIA Randomised controlled trials (RCTs) (parallel or cross-over in design), quasi-RCTs of pharmacological or non-pharmacological therapies for treating neuropathic pain in people with SCD compared to placebo or another intervention in any category (i.e. pharmacological or non-pharmacological). DATA COLLECTION AND ANALYSIS Two review authors independently assessed all trials identified by the searches and extracted relevant data. Two authors independently assessed the risk of bias in the selected trials using the Cochrane risk of bias tool. Two review authors independently rated the quality of the evidence for each outcome using the GRADE guidelines. MAIN RESULTS One RCT of 22 participants with SCD, conducted in the USA was included in this review. Participants were randomly assigned to either pregabalin (n = 11) or placebo (n = 11). Oral pregabalin was administered at an initial dose of 75 mg twice daily. The drug was titrated at increments of 75 mg to a maximum of 600 mg daily or decreased by 75 mg per day if necessary, based on clinical presentation and pain level. Neuropathic pain was assessed using self-reports on the Leeds Assessment of Neuropathic Symptoms and Signs (S-LANNS) scale and the Neuropathic Pain Symptom Inventory (NPSI), where higher scores were indicative of more pain. Outcomes included self-reported pain, quality of life and withdrawal due to adverse effects measured at baseline and monthly for three months post-intervention. The overall risk of bias was low with a high risk of bias due to attrition.In relation to this reviews primary outcomes, for self-reported neuropathic pain relief, given the paucity of data, we are very uncertain whether there is a difference between the pregabalin and placebo groups at the end of three months as measured by the S-LANSS scale, mean difference (MD) -2.00 (95% confidence interval (CI) -9.18 to 5.18), or the NPSI scale, MD -11.10 (95% CI -33.97 to 11.77) (very low-quality evidence). There was no report of 'Patient Global Impression of Change' in the included trial.Although the mean quality of life scores (Short Form-36) at three months showed small increases in seven of the eight domains post-intervention in the pregabalin group as compared to the placebo group, this was very low-quality evidence and we are very uncertain whether pregabalin increases quality of life. Neither of our pre-defined outcomes of 'time to improvement of symptoms' or 'changes in sleep quality', were measured in the included trial.While treatment-related adverse effects appeared higher in pregabalin group than the placebo group at three months, this was very low-quality evidence and we are very uncertain whether there is a difference, RR 1.33 (95% CI 0.39 to 4.62) (very low-quality evidence). There was one withdrawal for adverse effects in the pregabalin group while three people withdrew or dropped out from the placebo group due to adverse effects and complications and hospitalisation related to SCD. AUTHORS' CONCLUSIONS The included trial provided very low-quality evidence. Self-reported pain relief was greater in the pregabalin group compared to the placebo control group but only using the S-LANSS scale and we are very unsure whether there is a difference. While the pregabalin group tended to have improved quality of life over the duration of the trial, this was very low-quality evidence and we are uncertain whether there is a difference. Adverse effects and withdrawals were similar across the treatment and placebo control group in trial. There are both insufficient trials addressing this review question and insufficient outcomes addressed in the single included RCT. Therefore, there is still a significant gap in evidence on interventions for neuropathic pain in people with SCD.

Self-Reported Neuropathic Pain Characteristics of Women With Provoked Vulvar Pain: A Preliminary Investigation

BackgroundProvoked vestibulodynia (PVD) is a common chronic genital pain condition affecting approximately 12% of premenopausal women. Although parallels have been drawn between PVD and neuropathic pain (NP), no studies have examined self-reported NP characteristics in PVD. AimTo explore pain symptoms that resemble NP reported by those with PVD and compare responses with those with an established NP condition. MethodsWomen with provoked vulvar pain (PVP; n = 65) completed online questionnaires designed to assess characteristics of NP. Responses were compared with those of women with postherpetic neuralgia (PHN; n = 30). OutcomesIn addition to a range of descriptive questions, participants completed the McGill Pain Questionnaire, the Self-Complete Leeds Assessment of Neuropathic Signs and Symptoms (S-LANSS), the Neuropathic Pain Symptom Inventory (NPSI), and the Pain Quality Assessment Scale (PQAS). ResultsPVP exhibits some neuropathic characteristics, typically evoked pain (as opposed to the more constant pain of PHN) indicative of allodynia and hyperalgesia. Specifically, women with PVP scored, on average, higher than the NP cutoff on the S-LANSS, and there were no significant differences between women with PVP and those with PHN on some NPSI subscales. However, women with PHN reported more NP symptoms on the PQAS, S-LANSS, and other NPSI subscales. Clinical ImplicationsValidated NP questionnaires could be of particular use for health care professionals who need a more efficient way to assess symptoms of patients with PVP and should be included in future studies investigating the mechanisms and treatment of this pain. Strengths and LimitationsThis study takes a unique approach to the examination of PVP by using multiple validated NP measures to compare pain characteristics with those of a group of participants with PHN, an established NP condition. However, it is limited by self-reported data not confirmed with clinical examination, small size of the PHN group, and the severity of the pain experienced in the PVP group. ConclusionWomen with PVP report some symptoms suggestive of NP characteristics, and future research should use NP measures in addition to physical examinations to further investigate the mechanisms that maintain this pain condition.Dargie E, Gilron I, Pukall CF. Self-Reported Neuropathic Pain Characteristics of Women With Provoked Vulvar Pain: A Preliminary Investigation. J Sex Med 2017;14:577–591.

The effect of monitoring 'processing style' on post-surgical neuropathic pain in women with breast cancer.

Pain is a commonly reported symptom following surgery that is more likely to occur in individuals psychologically distressed prior to surgery. Monitoring processing style, a cognitive tendency to focus on health-related threats, has been associated with increased reporting of somatic symptoms, but no studies have specifically addressed the link between this cognitive style and pain. This prospective clinical study aimed to investigate whether monitoring processing style predicted post-surgical pain in women undergoing breast surgery, controlling for pre-surgical psychological distress. Women scheduled to undergo breast cancer surgery (N = 106) completed pre-surgical assessments of monitoring processing style (Miller Behavioral Style Scale) and psychological distress (Depression Anxiety Stress Scales-21). Demographic and medical characteristics were documented. Self-reported neuropathic pain (Neuropathic Pain Scale) was assessed at 3 months post surgery. Post-surgical neuropathic pain levels were low to moderate (M = 19.3, SD = 21.1). Higher pre-surgical monitoring processing style scores significantly predicted higher post-surgical neuropathic pain (β = 0.23, p = 0.023), over and above psychological stress (β = 0.22, p = 0.020) and age (β = -0.25, p = 0.011). Pre-surgical monitoring processing style was an independent predictor of post-surgical neuropathic pain, even when accounting for pre-surgical psychological distress. Since the reduction of post-surgical pain is a key goal of healthcare, efforts should be made prior to breast cancer surgery to counsel and support individuals with high monitoring processing styles irrespective of their level of distress.

Predictors of severe pain in a cohort of 5271 individuals with self-reported neuropathic pain

The influence of pain descriptors and mechanical hypersensitivity on pain severity in neuropathic pain has not been well researched and is poorly understood. The aim of this study was to determine the relationship between pain severity and other factors describing chronic neuropathic pain in a large cohort of patients with self-reported neuropathic pain potentially recruited as subjects for a Phase IIa study. A questionnaire specific to the study parameters covering demographics and pain characteristics was sent to potential participants. Overall, 9185 questionnaires were returned from potential subjects who self-reported neuropathic pain. Adjusted odds ratios with 95% confidence intervals were used as a measure of association. These were estimated by unconditional logistic regression. Pain descriptors in the questionnaire were: burning, shooting, shocking, and aching. The presence of self-reported allodynia and hyperalgesia was strongly indicative of both moderate and severe pain, with a significant interaction of both factors in moderate and severe pain. Having 3 or 4 pain descriptors was also strongly indicative of both moderate and severe pain. Female gender, age, and history of serious mental disorders were found to be weaker indicators of both moderate and severe pain. Given the large and varied population with many neuropathic pain diagnoses in the study, the findings are not likely to be merely chance, but are likely to reflect important relationships between pain severity and other factors in those who suffer from chronic neuropathic pain.

Quantitative Sensory Testing in Measurement of Neuropathic Pain Phenomena and Other Sensory Abnormalities

Neuropathic pain disorders are usually characterized by spontaneous ongoing or intermittent symptoms, stimulus-evoked positive sensory phenomena, and negative sensory phenomena. Spontaneous individual subject specific phenomena are identified in the neurologic history and are quantifiable by means of self-reported neuropathic pain symptoms tools such as scales, inventories, and questionnaires. Negative and positive sensory phenomena are assessed by the neurologic bedside examination and quantitative sensory testing (QST), which refers to psychophysical tests of sensory perception during the administration of stimuli with predetermined physical properties and following specific protocols. QST is able to capture and quantify stimulus-evoked negative and positive sensory phenomena, and as such should become standard if not a critical tool in neuropathic pain research and practice. Although the advent of anatomic and functional imaging modalities is revolutionizing our understanding of the mechanisms of neuropathic pain, only by anchoring such test results to individual subjects' own perceptions via QST can they provide meaningful information about neuropathic pain, which is based on perceptual experience. To yield useful results, QST requires a cooperative subject and carefully standardized methods, including standardization of the stimulus parameters as well as the testing environment, instructions, and evaluation methods. This manuscript provides a concise review of fundamental concepts necessary for understanding the role of QST in the process of eliciting information about sensory abnormalities associated with neuropathic pain and the place of that information in analysis of pain mechanisms. Together with the companion manuscript, this review provides definitions that should help further the use of QST as a diagnostic tool as well.