Pressure Pain Thresholds in Chronic Whiplash Associated Disorder: Further Evidence of Altered Central Pain Processing

2002 ◽  
Vol 10 (3) ◽  
pp. 69-81 ◽  
Author(s):  
Michele Sterling ◽  
Julia Treleaven ◽  
Sandra Edwards ◽  
Gwendolen Jull
2020 ◽  
pp. 1-6
Author(s):  
Dhinu J. Jayaseelan ◽  
Cesar Fernandez-de-las-Penas ◽  
Taylor Blattenberger ◽  
Dean Bonneau

Clinical Scenario: Plantar heel pain is a common condition frequently associated with persistent symptoms and functional limitations affecting both the athletic and nonathletic populations. Common interventions target impairments at the foot and ankle and local drivers of symptoms. If symptoms are predominantly perpetuated by alterations in central pain processing, addressing peripheral impairments alone may not be sufficient. Clinical Question: Do individuals with chronic plantar heel pain demonstrate signs potentially associated with altered central pain processing? Summary of Key Findings: After searching 6 electronic databases (PubMed, CINAHL, Scopus, SportDiscus, Cochrane, and PEDro) and filtering titles based on predetermined inclusion and exclusion criteria, 4 case-control studies were included. All studies scored highly on the Newcastle-Ottawa Scale for quality assessment. Using pressure pain thresholds, each study found decreased pressure pain hypersensitivity locally and at a remote site compared to control groups, suggesting the presence, to some extent, of altered nociceptive pain processing. Clinical Bottom Line: In the studies reviewed, reported results suggest a possible presence of centrally mediated symptoms in persons with plantar heel pain. However, despite findings from these studies, limitations in appropriate matching based on body mass index and measures used suggest additional investigation is warranted. Strength of Recommendation: According to the Oxford Centre for Evidence-Based Medicine, there is evidence level C to suggest chronic plantar heel pain is associated with alterations in central pain processing.


2017 ◽  
Vol 14 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Dagmar C. van Rijckevorsel ◽  
Oliver B. Boelens ◽  
Rudi M. Roumen ◽  
Oliver H. Wilder-Smith ◽  
Harry van Goor

AbstractBackground10–30% of chronic abdominal pain originates in the abdominal wall. A common cause for chronic abdominal wall pain is the Anterior Cutaneous Nerve Entrapment Syndrome (ACNES), in which an intercostal nerve branch is entrapped in the abdominal rectus sheath. Treatment consists of local anaesthetics and neurectomy, and is ineffective in 25% of cases for yet unknown reasons.In some conditions, chronic pain is the result of altered pain processing. This so-called sensitization can manifest as segmental or even generalized hyperalgesia, and is generally difficult to treat.ObjectiveThe aim of this study was to assess pain processing in ACNES patients responsive and refractory to treatment by using Quantitative Sensory Testing, in order to explore whether signs of altered central pain processing are present in ACNES and are a possible explanation for poor treatment outcomes.Methods50 patients treated for ACNES with locally orientated treatment were included. They were allocated to a responsive or refractory group based on their response to treatment. Patients showing an improvement of the Visual Analogue Scale (VAS) pain score combined with a current absolute VAS of <40 mm were scored as responsive.Sensation and pain thresholds to pressure and electric skin stimulation were determined in the paravertebral bilateral ACNES dermatomes and at four control areas on the non-dominant side of the body, i.e. the musculus trapezius pars medialis, musculus rectus femoris, musculus abductor hallucis and the thenar. The ACNES dermatomes were chosen to signal segmental hyperalgesia and the sum of the control areas together as a reflection of generalized hyperalgesia. Lower thresholds were interpreted as signs of sensitized pain processing. To test for alterations in endogenous pain inhibition, a conditioned pain modulation (CPM) response to a cold pressor task was determined. Also, patients filled in three pain-related questionnaires, to evaluate possible influence of psychological characteristics on the experienced pain.ResultsPatients refractory to treatment showed significantly lower pressure pain thresholds in the ACNES dermatomes and for the sum of as well as in two individual control areas. No differences were found between groups for electric thresholds or CPM response. Duration of complaints before diagnosis and treatment was significantly longer in the refractory compared to the responsive group, and refractory patients scored higher on the pain-related psychological surveys.Conclusion and ImplicationsIn this hypothesis-generating exploratory study, ACNES patients refractory to treatment showed more signs of sensitized segmental and central pain processing. A longer duration of complaints before diagnosis and treatment may be related to these alterations in pain processing, and both findings could be associated with less effective locally orientated treatment. In order to validate these hypotheses further research is needed.Registration numberNCT01920880 (Clinical Trials Register; http://www.clinicaltrials.gov).


2013 ◽  
Vol 4 (2) ◽  
pp. 65-74 ◽  
Author(s):  
F. Petzke ◽  
K.B. Jensen ◽  
E. Kosek ◽  
E. Choy ◽  
S. Carville ◽  
...  

AbstractBackgroundIn recent years, the prescription of serotonin-noradrenalin reuptake inhibitors (SNRIs) for treatment of fibromyalgia (FM) has increased with reports of their efficacy. The SNRI milnacipran is approved by the U.S. Food and Drug Administration (FDA) for treatment of FM, yet, the mechanisms by which milnacipran reduces FM symptoms are unknown. A large number of neuroimaging studies have demonstrated altered brain function in patients with FM but the effect of milnacipran on central pain processing has not been investigated. The primary objective of this study was to assess the effect of milnacipran on sensitivity to pressure-evoked pain in FM. Secondary objectives were to assess the effect of milnacipran on cerebral processing of pressure-evoked pain using fMRI and the tolerability and safety of milnacipran 200 mg/day in FM.Methods92 patients were randomized to either 13-weeks milnacipran treatment (200 mg/day) or placebo in this double-blind, placebo-controlled multicenter clinical trial. Psychophysical measures and functional MRI (fMRI) assessments were performed before and after treatment using a computer-controlled pressure-pain stimulator. Here, we present the results of several a priori defined statistical analyses.ResultsMilnacipran-treated patients displayed a trend toward lower pressure-pain sensitivity after treatment, compared to placebo, and the difference was greater at higher pain intensities. A single group fMRI analysis of milnacipran-treated patients indicated increased pain-evoked brain activity in the caudatus nucleus, anterior insula and amygdala after treatment, compared to before treatment; regions implicated in pain inhibitory processes. A 2 × 2 repeated measures fMRI analysis, comparing milnacipran and placebo, before and after treatment, showed that milnacipran-treated patients had greater pain-evoked activity in the precuneus/posterior cingulate cortex after treatment; a region previously implicated in intrinsic brain function and FM pathology. This finding was only significant when uncorrected for multiple comparisons. The safety analysis revealed that patients from both treatment groups had treatment-emergent adverse events where nausea was the most common complaint, reported by 43.5% of placebo patients and 71.7% of milnacipran-treated patients. Patients on milnacipran were more likely to discontinue treatment because of side effects.ConclusionsOur results provide preliminary indications of increased pain inhibitory responses in milnacipran-treated FM patients, compared to placebo. The psychophysical assessments did not reach statistical significance but reveal a trend toward higher pressure-pain tolerance after treatment with milnacipran, compared to placebo, especially for higher pain intensities. Our fMRI analyses point toward increased activation of the precuneus/posterior cingulum in patients treated with milnacipran, however results were not corrected for multiple comparisons. The precuneus/posterior cingulum is a key region of the default mode network and has previously been associated with abnormal function in FM. Future studies may further explore activity within the default mode network as a potential biomarker for abnormal central pain processing.ImplicationsThe present study provides novel insights for future studies where functional neuroimaging may be used to elucidate the central mechanisms of common pharmacological treatments for chronic pain. Furthermore, our results point toward a potential mechanism for pain normalization in response to milnacipran, involving regions of the default mode network although this finding needs to be replicated in future studies.


2019 ◽  
Vol 20 (1) ◽  
pp. 11-27 ◽  
Author(s):  
Clare Bartholomew ◽  
Simon Lack ◽  
Bradley Neal

AbstractBackground and aimsPrevious systematic reviews have reported manifestations of pain sensitisation as a feature of painful knee disorders, in particular osteoarthritis, with moderate evidence for pain sensitisation in patellofemoral pain (PFP). However, despite past studies recruiting female mostly adolescent PFP patients, it is unclear if sex or age plays a role. Investigation is required to determine if altered pain processing is a key feature of PFP and if a subgroup of patients is at an increased risk to help provide targeted management. The primary aim of this systematic review was to examine evidence investigating pain processing in PFP. Secondary aims were to evaluate the relationship between pain processing and (1) sex, (2) age and (3) symptom duration.MethodsThe protocol was prospectively registered with PROSPERO (CRD42019129851). PubMed, CINAHL, Web of Science and EMBASE were systematically searched from inception to April 2019 for studies investigating pain processing in PFP patients compared to controls using quantitative sensory testing. Each included paper was assessed for methodological quality using a modified version of Downs and Black. Means and standard deviations were extracted to calculate standardised mean differences (SMD) and 95% confidence intervals (95% CI). Where possible meta-analysis and meta-regression were performed using a random effects model.ResultsEleven studies were identified, two medium and nine high quality. Meta-analysis indicates moderate evidence for decreased pressure pain thresholds (SMD −0.68, 95% CI −0.93 to −0.43), increased tactile detection thresholds (SMD 1.35, 95% CI 0.49–2.22) and increased warmth detection thresholds (SMD 0.61, 95% CI 0.30–0.92) in PFP patients compared to controls. Secondary analysis indicates moderate evidence for decreased pressure pain thresholds in female compared to male patients (SMD −0.75, 95% CI −1.34 to −0.16). Meta-regression indicates a moderate correlation between decreasing local and distal pressure pain thresholds and decreasing patient age (local R2 = 0.556, p = 0.0211; distal R2 = 0.491, p = 0.0354) but no correlation with symptom duration (p > 0.05).ConclusionsEvidence from this systematic review with meta-analysis and meta-regression appears to suggest the presence of altered pain processing and sensitisation in patients with PFP with increased sensitivity indicated in female patients and younger patients.ImplicationsWith evidence of altered pain processing and sensitisation in PFP, it may be beneficial for clinicians to consider management approaches that aim specifically at adressing neuropathic pain, for example neuroscience education, to improve patients outcomes. With female patients and younger patients indicated as experiencing greater degree of sensitivity, this may be a good demographic to start screening for sensitisation, in order to better identify and treat those most affected.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
René F. Castien ◽  
Michel W. Coppieters ◽  
Tom S. C. Durge ◽  
Gwendolyne G. M. Scholten-Peeters

Abstract Background Pressure pain thresholds (PPTs) are commonly assessed to quantify mechanical sensitivity in various conditions, including migraine. Digital and analogue algometers are used, but the concurrent validity between these algometers is unknown. Therefore, we assessed the concurrent validity between a digital and analogue algometer to determine PPTs in healthy participants and people with migraine. Methods Twenty-six healthy participants and twenty-nine people with migraine participated in the study. PPTs were measured interictally and bilaterally at the cephalic region (temporal muscle, C1 paraspinal muscles, and trapezius muscle) and extra-cephalic region (extensor carpi radialis muscle and tibialis anterior muscle). PPTs were first determined with a digital algometer, followed by an analogue algometer. Intraclass correlation coefficients (ICC3.1) and limits of agreement were calculated to quantify concurrent validity. Results The concurrent validity between algometers in both groups was moderate to excellent (ICC3.1 ranged from 0.82 to 0.99, with 95%CI: 0.65 to 0.99). Although PPTs measured with the analogue algometer were higher at most locations in both groups (p < 0.05), the mean differences between both devices were less than 18.3 kPa. The variation in methods, such as a hand-held switch (digital algometer) versus verbal commands (analogue algometer) to indicate when the threshold was reached, may explain these differences in scores. The limits of agreement varied per location and between healthy participants and people with migraine. Conclusion The concurrent validity between the digital and analogue algometer is excellent in healthy participants and moderate in people with migraine. Both types of algometer are well-suited for research and clinical practice but are not exchangeable within a study or patient follow-up.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Morten Pallisgaard Støve ◽  
Rogerio Pessoto Hirata ◽  
Thorvaldur Skuli Palsson

Abstract Objectives The effect of stretching on joint range of motion is well documented, and although sensory perception has significance for changes in the tolerance to stretch following stretching the underlining mechanisms responsible for these changes is insufficiently understood. The aim of this study was to examine the influence of endogenous pain inhibitory mechanisms on stretch tolerance and to investigate the relationship between range of motion and changes in pain sensitivity. Methods Nineteen healthy males participated in this randomized, repeated-measures crossover study, conducted on 2 separate days. Knee extension range of motion, passive resistive torque, and pressure pain thresholds were recorded before, after, and 10 min after each of four experimental conditions; (i) Exercise-induced hypoalgesia, (ii) two bouts of static stretching, (iii) resting, and (iv) a remote, painful stimulus induced by the cold pressor test. Results Exercise-induced hypoalgesia and cold pressor test caused an increase in range of motion (p<0.034) and pressure pain thresholds (p<0.027). Moderate correlations in pressure pain thresholds were found between exercise-induced hypoalgesia and static stretch (Rho>0.507, p=0.01) and exercise-induced hypoalgesia and the cold pressor test (Rho=0.562, p=0.01). A weak correlation in pressure pain thresholds and changes in range of motion were found following the cold pressor test (Rho=0.460, p=0.047). However, a potential carryover hypoalgesic effect may have affected the results of the static stretch. Conclusions These results suggest that stretch tolerance may be linked with endogenous modulation of pain. Present results suggest, that stretch tolerance may merely be a marker for pain sensitivity which may have clinical significance given that stretching is often prescribed in the rehabilitation of different musculoskeletal pain conditions where reduced endogenous pain inhibition is frequently seen.


Pain ◽  
2014 ◽  
Vol 155 (10) ◽  
pp. 2134-2143 ◽  
Author(s):  
Gary D. Slade ◽  
Anne E. Sanders ◽  
Richard Ohrbach ◽  
Roger B. Fillingim ◽  
Ron Dubner ◽  
...  

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