Altered pro-nociceptive and anti-nociceptive mechanisms are often implicated in painful conditions and have been increasingly studied over the past decade. For some painful conditions alterations are well-established, but in low back pain (LBP) populations there remains considerable debate whether these mechanisms are altered. The present systematic review aimed to address this issue by identifying studies assessing Conditioned Pain Modulation (CPM) and/or Temporal Summation of Pain (TSP) in LBP patients, comparing to either a healthy control group or using a method with reference data available. Qualitative synthesis and quantitative meta-analysis of group differences were performed. For CPM and TSP, 20 and 29 original articles were eligible, with data for metaanalysis obtainable from 18 (1500 patients, 505 controls) and 27 (1507 patients, 1127 controls) studies, respectively. Most studies were of poor-to-fair quality with significant heterogeneity in study size, population, assessment methodology and outcome. Nonetheless, CPM was impaired in LBP patients compared to controls (standardized mean difference =-0.44 [-0.64,-0.23], P<0.001), and the magnitude of this impairment was related to pain chronicity (acute/recurrent versus chronic, P=0.003), duration (R=-0.62, P=0.006) and severity (R=-0.54, P=0.02). TSP was facilitated in LBP patients compared to controls (standardized mean difference = 0.50 [0.29, 0.72], P<0.001), and the magnitude of this facilitation was weakly related to pain severity (R=0.41, P=0.04) and appeared to be influenced by test modality (P<0.001). Impaired CPM and facilitated TSP was present in LBP patients compared to controls, though the magnitude of differences was small which may direct future research on the clinical utility.
Persistent pain conditions, including low back pain (LBP), are often accompanied by alterations in pronociceptive and antinociceptive mechanisms, as quantified by temporal summation of pain (TSP) and conditioned pain modulation (CPM). It remains unclear whether altered pain sensitivity, CPM, and/or TSP are a consequence of pain presence or determine the degree of pain development. Pressure pain sensitivity, TSP, and CPM were assessed across an episode of exercise-induced LBP maintained for several days. Thirty healthy individuals participated in 3 experimental sessions: before (day 0), 2 days after fatiguing back muscle exercise with exercise-induced LBP present (day 2), and after pain resolution (day 7). Both handheld and cuff pressure-pain thresholds, along with TSP (10-cuff pain stimuli at .5 Hz) and CPM (cuff pain detection threshold prior versus during painful pressure conditioning) were assessed, alongside questionnaires pertaining to pain, disability, mood, sleep, menstruation, physical activity, and catastrophizing. The exercise-induced LBP model produced mild pain and disability, and reductions in pressure pain thresholds over both the lumbar and distant testing sites (p < .007). No pain-related changes were observed for TSP (p > .44) or CPM (p > .17). The baseline TSP was associated with the peak pain intensity of the exercise-induced LBP (p < .003). Perspective: Pressure-pain sensitivity was impacted by the presence of exercise-induced LBP, whereas TSP seemed to be more stable and was instead associated with the intensity of pain developed. No significant pain-related changes or associations were observed for CPM, suggesting this measure may have less usefulness in mild musculoskeletal pain conditions.
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, T. (2019). Assessment of conditioned pain modulation in healthy participants and patients with chronic pain: manifestations and implications for pain progression.
Low back pain (LBP) is a common presentation to the ED, and a frequent cause of disability globally. The ED management is often associated with high rates of imaging, misuse and overuse of pharmacology and subsequent financial implications. Given this, improved quality of care for patients with LBP in ED is essential. This rapid review investigated best practice for the assessment and management of LBP in the ED. PubMed, CINAHL, EMBASE, TRIP and the grey literature, including relevant organisational websites, were searched in 2015. Primary studies, systematic reviews and guidelines were considered for inclusion. English-language articles published in the past 10 years that addressed acute LBP assessment, management or prognosis in the ED or acute setting were included. Data extraction of included articles was conducted, followed by quality appraisal to rate the level of evidence where possible. The search revealed 1538 articles, of which 38 were included in the review (n = 8 primary articles, n = 13 systematic reviews and n = 17 guidelines). This rapid review provides clinicians managing LBP in the ED a summary of the best available evidence to risk stratify and enhance the quality of care, optimising patient outcomes. Consistent evidence was found to support the use of 'red flags' to screen for serious pathologies, diagnostic tests being reserved for use only in the presence of red flags, the judicious prescribing of opioids, identification of psychosocial risk factors as predictors of poorer outcome and promotion of early return to work and function.
Musculoskeletal injuries are a common presentation to the ED, with significant costs involved in the management of these injuries, variances in care within the ED and associated morbidity. A series of rapid review papers were completed to guide best practice for the assessment and management of common musculoskeletal injuries presenting to the ED. This paper presents the methodology used across the rapid reviews. PubMed, CINAHL, EMBASE, TRIP and the grey literature, including relevant organisational websites, were searched in 2015. The search was repeated consistently for each topic area (injuries of the foot and ankle, knee, hand and wrist, elbow, shoulder, lumbar spine and cervical spine). English-language primary studies, systematic reviews and guidelines that were published in the last 10 years and addressed acute musculoskeletal injury management were considered for inclusion. Data extraction of each included article was conducted, followed by a quality appraisal. The extracted data from each article was synthesised to group similar evidence together. For each rapid review, the evidence has been organised in a way that a clinician can direct their attention to a specific component of the clinical cycle of care in the ED, such as the assessment, diagnostic tests, management and follow-up considerations from ED. The series of rapid reviews are designed to foster evidence-based practice within the ED, targeting the injuries most commonly presenting. The reviews provide clinicians in EDs with rapid access to the best current evidence, which has been synthesised and organised to assist decision-making.
Although maximal voluntary contraction (MVC) force is reduced during pain, studies using interpolated twitch show no consistent reduction of voluntary muscle drive. The present study aimed to test if the reduction in MVC force during acute experimental pain could be explained by increased activation of antagonist muscles, weak voluntary activation at baseline, or changes in force direction. Twenty-two healthy volunteers performed maximal voluntary isometric knee extensions before, during, and after the effects of hypertonic (pain) and isotonic (control) saline injections into the infrapatellar fat pad. The MVC force, voluntary activation, electromyographic (EMG) activity of agonist, antagonist, and auxiliary (hip) muscles, and pain cognition and anxiety scores were recorded. MVC force was 9.3% lower during pain than baseline (p < 0.001), but there was no systematic change in voluntary activation. Reduced MVC force during pain was variable between participants (SD: 14%), and was correlated with reduced voluntary activation (r = 0.90), baseline voluntary activation (r = − 0.62), and reduced EMG amplitude of agonist and antagonist muscles (all r > 0.52), but not with changes in force direction, pain or anxiety scores. Hence, reduced MVC force during acute pain was mainly explained by deficits in maximal voluntary drive.
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